TripSit Wiki - User contributions [en]

Drug combinations

2015-12-03T16:19:28Z

Roi:

'''WARNING! For educational purposes: We do not endorse any of these combinations. This page will always be 'work in progress'. It is extremely important to be safe at all times! '''

[[File:Combo_2.png|1000px|center]]

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If you want to give us some feedback/recommendation/comment on the chart, you can contact us:

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'''[http://wiki.tripsit.me/images/d/d4/TripSitDrugComboChart-German.png German]'''

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== Specific Combinations ==

=== Amphetamine & Mescaline ===

The focus and anxiety caused by stimulants is magnified by psychedelics and results in an increased risk of thought loops.

=== Cocaine & Mescaline ===

The focus and anxiety caused by stimulants is magnified by psychedelics and results in an increased risk of thought loops.

=== Caffeine & Mescaline ===

High doses of caffeine are uncomfortable and this will be magnified by psychedelics.

=== 5-MeO-xxT & Mescaline ===

The 5-MeO class of tryptamines can be unpredictable in their interactions.

=== Tramadol & Mescaline ===

This combination can cause seizures due to the lowering of the threshold by tramadol and the potential of mescaline to cause seziures.

=== 5-MeO-xxT & DOx ===

The 5-MeO class of tryptamines can be unpredictable in their interactions, particularly increasing the risk of unpleasant physical side effects.

=== Ketamine & DOx ===

Ketamine and psychedelics tend to potentiate each other - go slowly.

=== MXE & DOx ===

As an NMDA antagonist MXE potentiates DOx which can be unpleasantly intense.

=== DXM & DOx ===

The DOx class as psychedelic stimulants have the potential to mask the effects of DXM and could lead to redosing to an unsafe level. DXM can also potentiate DOx resulting in an unpleasantly intense experience.

=== PCP & DOx ===

Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.

=== Amphetamine & DOx ===

The combined stimulating effects of the two can lead to an uncomfortable body-load, while the focusing effects of amphetamine can easily lead to thought loops. Coming down from amphetamines while the DOx is still active can be quite anxiogenic.

=== MDMA & DOx ===

The combined stimulating effects of the two can be uncomfortable. Coming down on the MDMA while the DOx is still active can be quite anxiogenic.

=== Cocaine & DOx ===
The combined stimulating effects of the two can lead to an uncomfortable body-load, while the focusing effects of cocaine can easily lead to thought loops. Coming down from cocaine while the DOx is still active can be quite anxiogenic.

=== Caffeine & DOx ===

High doses of caffeine may cause anxiety which is less manageable when tripping, and since both are stimulating it may cause some physical discomfort.

=== Alcohol & DOx ===

Drinking on stimulants is risky because the sedative effects of the alcohol are reduced, and these are what the body uses to gauge drunkenness. This typically leads to excessive drinking with greatly reduced inhibitions, high risk of liver damage and increased dehydration. They will also allow you to drink past a point where you might normally pass out, increasing the risk.

=== Opioids & DOx ===

No unexpected interactions.

=== Tramadol & DOx ===

Tramadol is well known to lower seizure threshold and psychedelics also cause occasional seizures.

=== 5-MeO-xxT & NBOMes ===

The 5-MeO class of tryptamines can be unpredictable in their interactions and the NBOMes are known to be unpredictable even alone. This combination is best avoided.

=== Amphetamine & NBOMes ===

Amphetamines and NBOMes both provide considerable stimulation. When combined they can result in tachycardia, hypertension, vasoconstriction and in extreme cases heart failure. The anxiogenic and focusing effects of stimulants are also not good in combination with psychedelics as they can lead to unpleasant thought loops. NBOMes are known to cause seizures and stimulants can increase this risk.

=== Cocaine & NBOMes ===

Cocaine and NBOMes both provide considerable stimulation. When combined they can result in severe vasoconstriction, tachycardia, hypertension, and in extreme cases heart failure.

=== Caffeine & NBOMes ===

Caffiene can bring out the natural stimulation from psychedelic drugs to make it uncomfortable. High doses can cause anxiety which is hard to handle while tripping.

=== Tramadol & NBOMes ===

Tramadol is well known to lower seizure threshold and NBOMes have also shown a tendency to cause severe seizures.

=== 5-MeO-xxT & 2c-x ===

The 5-MeO psychedelics can interact unpredictably to potentiate other psychedelics.

=== Amphetamine & 2c-x ===

The anxiogenic and focusing effects of stimulants increase the chance of unpleasant thought loops. The combination is generally uneccessary because of the stimulating effects of psychedelics. Combination of the stimulating effects may be uncomfortable.

=== Cocaine & 2c-x ===

The anxiogenic and focusing effects of stimulants increase the chance of unpleasant thought loops. The combination is generally unnecessary because of the stimulating effects of psychedelics. Combination of the stimulating effects may be uncomfortable.

=== Caffeine & 2c-x ===

High doses of caffeine may cause anxiety which is less manageable when tripping, and since both are stimulating the combination may cause some physical discomfort.

=== Tramadol & 2c-x ===

Tramadol is well known to lower seizure threshold and psychedelics raise the risk of seizures.

=== Caffeine & 2C-T-x ===

High doses of caffeine may cause anxiety which is less manageable when tripping, and since both are stimulating the combination may cause some physical discomfort.

=== Alcohol & 2C-T-x ===

Both these classes of compound can interact unpredictably. Caution should be exercised.

=== Opioids & 2C-T-x ===

No expected interactions, some Opioids have Serotonin action, and could lead to Serotonin Syndrome or a seizure. These are pretty much only to Pentazocine, Methadone, Tramadol, Tapenatdol.

=== Caffeine & αMT ===

High doses of caffeine may cause anxiety which is less manageable when tripping, and since both are stimulating the combination may cause some physical discomfort.

=== Alcohol & αMT ===

αMT has a broad mechanism of action in the brain and so does alcohol so the combination can be unpredictable.

=== Opioids & αMT ===

No unexpected interactions

=== Amphetamine & 5-MeO-xxT ===

The anxiogenic and focusing effects of stimulants increase the chance of unpleasant thought loops. The combination is generally unnecessary because of the stimulating effects of psychedelics.

=== MDMA & 5-MeO-xxT ===

Some of the 5-MeO tryptamines are a bit unpredictable and should be mixed with MDMA with care.

=== Cocaine & 5-MeO-xxT ===

The anxiogenic and focusing effects of stimulants increase the chance of unpleasant thought loops. The combination is generally unnecessary because of the stimulating effects of psychedelics.

=== Amphetamine & Ketamine ===

Amphetamine worsens Ketamines ataxia.

=== Caffeine & Ketamine ===

No unexpected interactions.

=== Alcohol & Ketamine ===

Both substances cause ataxia and bring a very high risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position.

=== GHB/GBL & Ketamine ===

Both substances cause ataxia and bring a risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position.

=== Opioids & Ketamine ===

Both substances bring a risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position.

=== Tramadol & Ketamine ===

No unexpected interactions.

=== Benzodiazepines & Ketamine ===

Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position.

=== Amphetamine & MXE ===

Risk of tachycardia, hypertension, and manic states.

=== MDMA & MXE ===

There have been reports of risky serotonergic interactions when the two are taken at the same time, but MXE taken to the end of an MDMA experience does not appear to cause the same issues.

=== Cocaine & MXE ===

Stimulants taken with MXE can lead to hypermanic states much more easily, especially if sleep is avoided.

=== Caffeine & MXE ===

No likely interactions.

=== Alcohol & MXE ===

There is a high risk of memory loss, vomiting and severe ataxia from this combination.

=== GHB/GBL & MXE ===

Both substances cause ataxia and bring a risk of vomiting and unconsciousness. If the patient falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position.

=== Opioids & MXE ===

This combination can potentiate the effects of the opioid.

=== Benzodiazepines & MXE ===

Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess.

=== SSRIs & MXE ===

Depending on the SSRI this combination can be unpredictable.

=== Amphetamine & DXM ===

Both substances raise heart rate, in extreme cases, panic attacks caused by these drugs have led to more serious heart issues.

=== MAOIs & DXM ===

High risk of serotonin syndrome.

=== Cocaine & DXM ===

Both substances raise heart rate, in extreme cases, panic attacks caused by these drugs have led to more serious heart issues.

=== SSRIs & DXM ===

High risk of serotonin syndrome.

=== Caffeine & DXM ===

High doses of caffeine may cause anxiety which is less manageable when tripping, and since both are stimulating the combination may cause some physical discomfort.

=== Alcohol & DXM ===

Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess. Additionally CNS depression can lead to difficulty breathing. Avoid on anything higher than 1st plateau.

=== GHB/GBL & DXM ===

Both substances cause ataxia and bring a risk of vomiting and unconsciousness. If the patient falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position. This combination is hard to predict.

=== Opioids & DXM ===
CNS depression, difficult breathing, heart issues, hepatoxic, just very unsafe combination all around. Additionally, there is a reverse cross tolerance between opiates/dxm. I.E. if one takes dxm, their tolerance of opiates goes down slightly, thus causing additional synergistic effects.

=== Benzodiazepines & DXM ===

Small doses of benzos can end a bad trip, but both substances potentiate the ataxia and sedation caused by the other and this can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position.

=== Amphetamine & PCP ===

This combination can easily lead to hypermanic states.

=== MDMA & PCP ===

This combination can easily lead to hypermanic states.

=== Cocaine & PCP ===

This combination can easily lead to hypermanic states.

=== Caffeine & PCP ===

Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.

=== Alcohol & PCP ===

Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.

=== GHB/GBL & PCP ===

Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.

=== Opioids & PCP ===

PCP can reduce opioid tolerance, increasing the risk of overdose.

=== Benzodiazepines & PCP ===

Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position. Memory blackouts are likely.

=== SSRIs & PCP ===

Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.

=== Alcohol & N2O ===

This combination can lead to vomiting.

=== MDMA & Amphetamine ===

Amphetamines increase the neurotoxic effects of MDMA.

=== Cocaine & Amphetamine ===

This combination of stimulants will increase strain on the heart. It is not generally worth it as cocaine has a mild blocking effect on dopamine releasers like amphetamine.

=== Caffeine & Amphetamine ===

This combination of stimulants is not generally necessary and may increase strain on the heart, as well as potentially causing anxiety and greater physical discomfort.

=== Alcohol & Amphetamine ===

Drinking on stimulants is risky because the sedative effects of the alcohol are reduced, and these are what the body uses to gauge drunkenness. This typically leads to excessive drinking with greatly reduced inhibitions, high risk of liver damage and increased dehydration. They will also allow you to drink past a point where you might normally pass out, increasing the risk. If you do decide to do this then you should set a limit of how much you will drink each hour and stick to it, bearing in mind that you will feel the alcohol and the stimulant less. Extended release formulations may severely impede sleep, further worsening the hangover.

=== GHB/GBL & Amphetamine ===

Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.

=== Opioids & Amphetamine ===

Stimulants increase respiration rate allowing a higher dose of opiates. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.

=== Tramadol & Amphetamine ===

Tramadol and stimulants both increase the risk of seizures.

=== Cocaine & MDMA ===

Cocaine blocks some of the desirable effects of MDMA while increasing the risk of heart attack.

=== Caffeine & MDMA ===

Caffiene is not really necessary with MDMA and increases any neurotoxic effects from MDMA.

=== Alcohol & MDMA ===

Both MDMA and alcohol cause severe dehydration. Approach this combination with caution, moderation and sufficient hydration.

=== Tramadol & MDMA ===

Tramadol and stimulants both increase the risk of seizures.

=== Caffeine & Cocaine ===

Both stimulants, risk of tachycardia, hypertension, and in extreme cases heart failure.

=== Alcohol & Cocaine ===

Drinking on stimulants is risky because the sedative effects of the alcohol are reduced, and these are what the body uses to gauge drunkenness. This typically leads to excessive drinking with greatly reduced inhibitions, high risk of liver damage and increased dehydration. They will also allow you to drink past a point where you might normally pass out, increasing the risk. If you do decide to do this then you should set a limit of how much you will drink each hour and stick to it, bearing in mind that you will feel he alcohol less. Cocaine is potentiated somewhat by alcohol because of the formation of cocaethylene.

=== GHB/GBL & Cocaine ===

Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest. Likewise the G can wear off and leave a dangerous concentration of cocaine behind.

=== Opioids & Cocaine ===

Stimulants increase respiration rate allowing a higher dose of opiates. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.

=== Tramadol & Cocaine ===

Tramadol and stimulants both increase the risk of seizures.

=== SSRIs & Cocaine ===

Risk of serotonin syndrome, Likely to make the SSRI's innefective with regular cocaine use. The SSRIs may also make the cocaine less effective. Mental stability and cocaine don't go together.

=== GHB/GBL & Alcohol ===

Even in very low doses this combination rapidly leads to memory loss, severe ataxia and unconsciousness. There is a high risk of vomit aspiration while unconscious.

=== Opioids & Alcohol ===

Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess. Memory blackouts are likely.

=== Tramadol & Alcohol ===

Heavy CNS depressants, risk of seizures. Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess. Memory blackouts are likely.

=== Benzodiazepines & Alcohol ===

Ethanol ingestion may potentiate the CNS effects of many benzodiazepines. The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position. Blacking out and memory loss is almost certain.

=== MAOIs & Alcohol ===

The chemical tyramine in alcoholic beverages can have dangerous reactions with MAOIs, causing an increase in blood pressure.

=== SSRIs & Alcohol ===

Alcohol may potentiate some of the pharmacologic effects of CNS-active agents. Use in combination may result in additive central nervous system depression and/or impairment of judgment, thinking, and psychomotor skills.

=== Opioids & GHB/GBL ===

The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position.

=== Tramadol & GHB/GBL ===

The sedative effects of this combination can lead to dangerous respiratory depression.

=== Benzodiazepines & GHB/GBL ===

The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position.

=== Tramadol & Opioids ===

Concomitant use of tramadol increases the seizure risk in patients taking other opioids. These agents are often individually epileptogenic and may have additive effects on seizure threshold during coadministration. Central nervous system- and/or respiratory-depressant effects may be additively or synergistically present.

=== Benzodiazepines & Opioids ===

Central nervous system and/or respiratory-depressant effects may be additively or synergistically present. The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position Blackouts/memory loss likely.

=== MAOIs & Opioids ===

Coadministration of monoamine oxidase inhibitors (MAOIs) with certain opioids has been associated with rare reports of severe and fatal adverse reactions. There appear to be two types of interaction, an excitatory and a depressive one. Symptoms of the excitatory reaction may include agitation, headache, diaphoresis, hyperpyrexia, flushing, shivering, myoclonus, rigidity, tremor, diarrhea, hypertension, tachycardia, seizures, and coma. Death has occurred in some cases.

=== Benzodiazepines & Tramadol ===

Central nervous system- and/or respiratory-depressant effects may be additively or synergistically present. Vomit aspiration a risk when passed out, lay down in recovery position if ingested.

== References ==

=== LSD & DMT ===

http://www.ncbi.nlm.nih.gov/pubmed/3006089
http://deepblue.lib.umich.edu/bitstream/handle/2027.42/26285/0000370.pdf

===LSD & GHB/GBL===

http://www.ncbi.nlm.nih.gov/pubmed/16483730

===LSD & Opioids===

http://www.ncbi.nlm.nih.gov/pubmed/547279

http://www.ncbi.nlm.nih.gov/pubmed/3006089

"Low doses antagonized the effects of both hallucinogens, whereas larger doses enhanced their effects."

http://www.ncbi.nlm.nih.gov/pubmed/3006089

http://deepblue.lib.umich.edu/bitstream/handle/2027.42/26285/0000370.pdf

===LSD & Tramadol===

http://www.ncbi.nlm.nih.gov/pubmed/3006089

===LSD & MAOIs===

http://www.ncbi.nlm.nih.gov/pubmed/8788508

http://www.ncbi.nlm.nih.gov/pubmed/108709

https://www.erowid.org/references/refs_view.php?A=ShowDocPartFrame&ID=2439&DocPartID=2199

===LSD & SSRIs===

http://www.nature.com/npp/journal/v14/n6/full/1380431a.html

http://www.ncbi.nlm.nih.gov/pubmed/8726753

===DMT & Opioids===

http://www.ncbi.nlm.nih.gov/pubmed/3006089

===DMT & Tramadol===

http://www.ncbi.nlm.nih.gov/pubmed/3006089

===MDMA & GHB/GBL===

http://www.ncbi.nlm.nih.gov/pubmed/16234132

http://www.ncbi.nlm.nih.gov/pubmed/22554869

http://www.ncbi.nlm.nih.gov/pubmed/20730418

http://www.ncbi.nlm.nih.gov/pubmed/16483730

===DOx & Amphetamines===

http://www.ncbi.nlm.nih.gov/pubmed/1208759

===Ketamine & Caffeine===

http://onlinelibrary.wiley.com/doi/10.1111/j.1742-7843.2009.00382.x/full

===Ketamine & Amphetamine===

http://www.ncbi.nlm.nih.gov/pubmed/23660488

===Ketamine & Alcohol===

http://onlinelibrary.wiley.com/doi/10.1002/jemt.22045/abstract

===Ketamine & GHB/GBL===

http://www.ncbi.nlm.nih.gov/pubmed/16483730

===Ketamine & Opioids===

http://www.ncbi.nlm.nih.gov/pubmed/21224020

===Tramadol & SSRIs===

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2714818/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750095/

===MXE & DXM===

http://i.imgur.com/zmqaw.jpg

http://www.sciencedirect.com/science/article/pii/S0014488607002543

===MXE & Amphetamines===

http://www.ncbi.nlm.nih.gov/pubmed/25060403

===DXM & PCP===

http://i.imgur.com/zmqaw.jpg

http://www.sciencedirect.com/science/article/pii/S0014488607002543

===PCP & SSRIs===

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1224745/

===Amphetamines & Benzodiazepines===

http://www.ncbi.nlm.nih.gov/pubmed/17320309

===MDMA & Caffeine===

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492978/

http://link.springer.com/article/10.1007/s00213-010-1864-1

http://www.sciencedirect.com/science/article/pii/S0028390805003114

http://www.ncbi.nlm.nih.gov/pubmed/24211539

===MDMA & Alcohol===

http://www.ncbi.nlm.nih.gov/pubmed/21040238

http://www.ncbi.nlm.nih.gov/pubmed/21756931

===Cocaine & SSRIs===

http://www.ncbi.nlm.nih.gov/pubmed/23761390

http://www.ncbi.nlm.nih.gov/pubmed/20195220

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3377381

===Caffeine & Alcohol===

http://www.ncbi.nlm.nih.gov/pubmed/20001110

===Caffeine & Tramadol===

http://www.ncbi.nlm.nih.gov/pubmed/20837047

===Caffeine & SSRIs===

http://journals.lww.com/jpharmacogenetics/abstract/1996/06000/a_fluvoxamine_caffeine_interaction_study.3.aspx

===Alcohol & GHB/GBL===

http://www.ncbi.nlm.nih.gov/pubmed/15274975

===Alcohol & SSRIs===

http://www.ncbi.nlm.nih.gov/pubmed/15739105

===GHB/GBL & Opioids===

http://www.ncbi.nlm.nih.gov/pubmed/7782758

===GHB/GBL & Tramadol===

http://www.ncbi.nlm.nih.gov/pubmed/7782758

===GHB/GBL & Benzodiazepines===

http://www.ncbi.nlm.nih.gov/pubmed/16483730

===GHB/GBL & MAOIs===

No study, but MAO B inhibitors should enhance the effects, no interaction with MAO A.

===Opioids & Benzodiazepines===

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3454351/

===Opioids & MAOIs===

http://www.ncbi.nlm.nih.gov/pubmed/17157368 (?)

http://www.ncbi.nlm.nih.gov/pubmed/2891392

http://www.if-pan.krakow.pl/pjp/pdf/2013/3_593.pdf

===Opioids & SSRIs===

http://www.ncbi.nlm.nih.gov/pubmed/23391344

http://www.ncbi.nlm.nih.gov/pubmed/20513454

http://www.ncbi.nlm.nih.gov/pubmed/16005413

http://www.ncbi.nlm.nih.gov/pubmed/18676387

http://www.ncbi.nlm.nih.gov/pubmed/17381671

===Tramadol & Benzodiazepines===

http://www.ncbi.nlm.nih.gov/pubmed/12842359

===Tramadol & MAOIs===

http://www.ncbi.nlm.nih.gov/pubmed/16051647

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750095/

===Benzodiazepines & SSRIs===

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2446479/

http://www.ncbi.nlm.nih.gov/pubmed/9435993

===MAOIs & SSRIs===

http://www.ncbi.nlm.nih.gov/pubmed/24577320

[[Category:Guides]]

Drug combinations

2015-10-28T17:04:02Z

Roi: spelling

'''WARNING! For educational purposes: We do not endorse any of these combinations. This page will always be 'work in progress'. It is extremely important to be safe at all times! '''

[[File:Combo_2.png|1000px|center]]

== Overview ==
If you want to give us some feedback/recommendation/comment on the chart, you can contact us:

[http://chat.tripsit.me/?nick=AskContent?#content Join #content channel on IRC]

Email: '''content@tripsit.me''', or email GrimReaper directly at '''grimreaper@tripsit.me'''

== Chart versions ==

'''[http://wiki.tripsit.me/images/d/d6/TripSitDrugComboChart.gif English]'''

'''[http://wiki.tripsit.me/images/5/5b/TripSitDrugComboChart-Portuguese.png Portuguese]'''

'''[http://wiki.tripsit.me/images/d/d4/TripSitDrugComboChart-German.png German]'''

'''[http://wiki.tripsit.me/wiki/File:TripSitDrugComboChart-Polish.gif Polish]'''

== Specific Combinations ==

=== Amphetamine & Mescaline ===

The focus and anxiety caused by stimulants is magnified by psychedelics and results in an increased risk of thought loops.

=== Cocaine & Mescaline ===

The focus and anxiety caused by stimulants is magnified by psychedelics and results in an increased risk of thought loops.

=== Caffeine & Mescaline ===

High doses of caffeine are uncomfortable and this will be magnified by psychedelics.

=== 5-MeO-xxT & Mescaline ===

The 5-MeO class of tryptamines can be unpredictable in their interactions.

=== Tramadol & Mescaline ===

This combination can cause seizures due to the lowering of the threshold by tramadol and the potential of mescaline to cause seziures.

=== 5-MeO-xxT & DOx ===

The 5-MeO class of tryptamines can be unpredictable in their interactions, particularly increasing the risk of unpleasant physical side effects.

=== Ketamine & DOx ===

Ketamine and psychedelics tend to potentiate each other - go slowly.

=== MXE & DOx ===

As an NMDA antagonist MXE potentiates DOx which can be unpleasantly intense.

=== DXM & DOx ===

The DOx class as psychedelic stimulants have the potential to mask the effects of DXM and could lead to redosing to an unsafe level. DXM can also potentiate DOx resulting in an unpleasantly intense experience.

=== PCP & DOx ===

Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.

=== Amphetamine & DOx ===

The combined stimulating effects of the two can lead to an uncomfortable body-load, while the focusing effects of amphetamine can easily lead to thought loops. Coming down from amphetamines while the DOx is still active can be quite anxiogenic.

=== MDMA & DOx ===

The combined stimulating effects of the two can be uncomfortable. Coming down on the MDMA while the DOx is still active can be quite anxiogenic.

=== Cocaine & DOx ===
The combined stimulating effects of the two can lead to an uncomfortable body-load, while the focusing effects of cocaine can easily lead to thought loops. Coming down from cocaine while the DOx is still active can be quite anxiogenic.

=== Caffeine & DOx ===

High doses of caffeine may cause anxiety which is less manageable when tripping, and since both are stimulating it may cause some physical discomfort.

=== Alcohol & DOx ===

Drinking on stimulants is risky because the sedative effects of the alcohol are reduced, and these are what the body uses to gauge drunkenness. This typically leads to excessive drinking with greatly reduced inhibitions, high risk of liver damage and increased dehydration. They will also allow you to drink past a point where you might normally pass out, increasing the risk.

=== Opioids & DOx ===

No unexpected interactions.

=== Tramadol & DOx ===

Tramadol is well known to lower seizure threshold and psychedelics also cause occasional seizures.

=== 5-MeO-xxT & NBOMes ===

The 5-MeO class of tryptamines can be unpredictable in their interactions and the NBOMes are known to be unpredictable even alone. This combination is best avoided.

=== Amphetamine & NBOMes ===

Amphetamines and NBOMes both provide considerable stimulation. When combined they can result in tachycardia, hypertension, vasoconstriction and in extreme cases heart failure. The anxiogenic and focusing effects of stimulants are also not good in combination with psychedelics as they can lead to unpleasant thought loops. NBOMes are known to cause seizures and stimulants can increase this risk.

=== Cocaine & NBOMes ===

Cocaine and NBOMes both provide considerable stimulation. When combined they can result in severe vasoconstriction, tachycardia, hypertension, and in extreme cases heart failure.

=== Caffeine & NBOMes ===

Caffiene can bring out the natural stimulation from psychedelic drugs to make it uncomfortable. High doses can cause anxiety which is hard to handle while tripping.

=== Tramadol & NBOMes ===

Tramadol is well known to lower seizure threshold and NBOMes have also shown a tendency to cause severe seizures.

=== 5-MeO-xxT & 2c-x ===

The 5-MeO psychedelics can interact unpredictably to potentiate other psychedelics.

=== Amphetamine & 2c-x ===

The anxiogenic and focusing effects of stimulants increase the chance of unpleasant thought loops. The combination is generally uneccessary because of the stimulating effects of psychedelics. Combination of the stimulating effects may be uncomfortable.

=== Cocaine & 2c-x ===

The anxiogenic and focusing effects of stimulants increase the chance of unpleasant thought loops. The combination is generally unnecessary because of the stimulating effects of psychedelics. Combination of the stimulating effects may be uncomfortable.

=== Caffeine & 2c-x ===

High doses of caffeine may cause anxiety which is less manageable when tripping, and since both are stimulating the combination may cause some physical discomfort.

=== Tramadol & 2c-x ===

Tramadol is well known to lower seizure threshold and psychedelics raise the risk of seizures.

=== Caffeine & 2C-T-x ===

High doses of caffeine may cause anxiety which is less manageable when tripping, and since both are stimulating the combination may cause some physical discomfort.

=== Alcohol & 2C-T-x ===

Both these classes of compound can interact unpredictably. Caution should be exercised.

=== Opioids & 2C-T-x ===

No expected interactions, some Opioids have Serotonin action, and could lead to Serotonin Syndrome or a seizure. These are pretty much only to Pentazocine, Methadone, Tramadol, Tapenatdol.

=== Caffeine & αMT ===

High doses of caffeine may cause anxiety which is less manageable when tripping, and since both are stimulating the combination may cause some physical discomfort.

=== Alcohol & αMT ===

αMT has a broad mechanism of action in the brain and so does alcohol so the combination can be unpredictable.

=== Opioids & αMT ===

No unexpected interactions

=== Amphetamine & 5-MeO-xxT ===

The anxiogenic and focusing effects of stimulants increase the chance of unpleasant thought loops. The combination is generally unnecessary because of the stimulating effects of psychedelics.

=== MDMA & 5-MeO-xxT ===

Some of the 5-MeO tryptamines are a bit unpredictable and should be mixed with MDMA with care.

=== Cocaine & 5-MeO-xxT ===

The anxiogenic and focusing effects of stimulants increase the chance of unpleasant thought loops. The combination is generally unnecessary because of the stimulating effects of psychedelics.

=== Amphetamine & Ketamine ===

Amphetamine worsens Ketamines ataxia.

=== Caffeine & Ketamine ===

No unexpected interactions.

=== Alcohol & Ketamine ===

Both substances cause ataxia and bring a very high risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position.

=== GHB/GBL & Ketamine ===

Both substances cause ataxia and bring a risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position.

=== Opioids & Ketamine ===

Both substances bring a risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position.

=== Tramadol & Ketamine ===

No unexpected interactions.

=== Benzodiazepines & Ketamine ===

Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position.

=== Amphetamine & MXE ===

Risk of tachycardia, hypertension, and manic states.

=== MDMA & MXE ===

There have been reports of risky serotonergic interactions when the two are taken at the same time, but MXE taken to the end of an MDMA experience does not appear to cause the same issues.

=== Cocaine & MXE ===

Stimulants taken with MXE can lead to hypermanic states much more easily, especially if sleep is avoided.

=== Caffeine & MXE ===

No likely interactions.

=== Alcohol & MXE ===

There is a high risk of memory loss, vomiting and severe ataxia from this combination.

=== GHB/GBL & MXE ===

Both substances cause ataxia and bring a risk of vomiting and unconsciousness. If the patient falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position.

=== Opioids & MXE ===

This combination can potentiate the effects of the opioid.

=== Benzodiazepines & MXE ===

Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess.

=== SSRIs & MXE ===

Depending on the SSRI this combination can be unpredictable.

=== Amphetamine & DXM ===

Both substances raise heart rate, in extreme cases, panic attacks caused by these drugs have led to more serious heart issues.

=== MAOIs & DXM ===

High risk of serotonin syndrome.

=== Cocaine & DXM ===

Both substances raise heart rate, in extreme cases, panic attacks caused by these drugs have led to more serious heart issues.

=== SSRIs & DXM ===

High risk of serotonin syndrome.

=== Caffeine & DXM ===

High doses of caffeine may cause anxiety which is less manageable when tripping, and since both are stimulating the combination may cause some physical discomfort.

=== Alcohol & DXM ===

Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess. Additionally CNS depression can lead to difficulty breathing. Avoid on anything higher than 1st plateau.

=== GHB/GBL & DXM ===

Both substances cause ataxia and bring a risk of vomiting and unconsciousness. If the patient falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position. This combination is hard to predict.

=== Opioids & DXM ===
CNS depression, difficult breathing, heart issues, hepatoxic, just very unsafe combination all around. Additionally, there is a reverse cross tolerance between opiates/dxm. I.E. if one takes dxm, their tolerance of opiates goes down slightly, thus causing additional synergistic effects.

=== Benzodiazepines & DXM ===

Small doses of benzos can end a bad trip, but both substances potentiate the ataxia and sedation caused by the other and this can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position.

=== Amphetamine & PCP ===

This combination can easily lead to hypermanic states.

=== MDMA & PCP ===

This combination can easily lead to hypermanic states.

=== Cocaine & PCP ===

This combination can easily lead to hypermanic states.

=== Caffeine & PCP ===

Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.

=== Alcohol & PCP ===

Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.

=== GHB/GBL & PCP ===

Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.

=== Opioids & PCP ===

PCP can reduce opioid tolerance, increasing the risk of overdose.

=== Benzodiazepines & PCP ===

Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position. Memory blackouts are likely.

=== SSRIs & PCP ===

Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.

=== Alcohol & N2O ===

This combination can lead to vomiting.

=== MDMA & Amphetamine ===

Amphetamines increase the neurotoxic effects of MDMA.

=== Cocaine & Amphetamine ===

This combination of stimulants will increase strain on the heart. It is not generally worth it as cocaine has a mild blocking effect on dopamine releasers like amphetamine.

=== Caffeine & Amphetamine ===

This combination of stimulants is not generally necessary and may increase strain on the heart, as well as potentially causing anxiety and greater physical discomfort.

=== Alcohol & Amphetamine ===

Drinking on stimulants is risky because the sedative effects of the alcohol are reduced, and these are what the body uses to gauge drunkenness. This typically leads to excessive drinking with greatly reduced inhibitions, high risk of liver damage and increased dehydration. They will also allow you to drink past a point where you might normally pass out, increasing the risk. If you do decide to do this then you should set a limit of how much you will drink each hour and stick to it, bearing in mind that you will feel the alcohol and the stimulant less. Extended release formulations may severely impede sleep, further worsening the hangover.

=== GHB/GBL & Amphetamine ===

Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.

=== Opioids & Amphetamine ===

Stimulants increase respiration rate allowing a higher dose of opiates. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.

=== Tramadol & Amphetamine ===

Tramadol and stimulants both increase the risk of seizures.

=== Cocaine & MDMA ===

Cocaine blocks some of the desirable effects of MDMA while increasing the risk of heart attack.

=== Caffeine & MDMA ===

Caffiene is not really necessary with MDMA and increases any neurotoxic effects from MDMA.

=== Alcohol & MDMA ===

Both MDMA and alcohol cause severe dehydration. Approach this combination with caution, moderation and sufficient hydration.

=== Tramadol & MDMA ===

Tramadol and stimulants both increase the risk of seizures.

=== Caffeine & Cocaine ===

Both stimulants, risk of tachycardia, hypertension, and in extreme cases heart failure.

=== Alcohol & Cocaine ===

Drinking on stimulants is risky because the sedative effects of the alcohol are reduced, and these are what the body uses to gauge drunkenness. This typically leads to excessive drinking with greatly reduced inhibitions, high risk of liver damage and increased dehydration. They will also allow you to drink past a point where you might normally pass out, increasing the risk. If you do decide to do this then you should set a limit of how much you will drink each hour and stick to it, bearing in mind that you will feel he alcohol less. Cocaine is potentiated somewhat by alcohol because of the formation of cocaethylene.

=== GHB/GBL & Cocaine ===

Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest. Likewise the G can wear off and leave a dangerous concentration of cocaine behind.

=== Opioids & Cocaine ===

Stimulants increase respiration rate allowing a higher dose of opiates. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.

=== Tramadol & Cocaine ===

Tramadol and stimulants both increase the risk of seizures.

=== SSRIs & Cocaine ===

Risk of serotonin syndrome, Likely to make the SSRI's innefective with regular cocaine use. The SSRIs may also make the cocaine less effective. Mental stability and cocaine don't go together.

=== GHB/GBL & Alcohol ===

Even in very low doses this combination rapidly leads to memory loss, severe ataxia and unconsciousness. There is a high risk of vomit aspiration while unconscious.

=== Opioids & Alcohol ===

Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess. Memory blackouts are likely.

=== Tramadol & Alcohol ===

Heavy CNS depressants, risk of seizures. Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess. Memory blackouts are likely.

=== Benzodiazepines & Alcohol ===

Ethanol ingestion may potentiate the CNS effects of many benzodiazepines. The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position. Blacking out and memory loss is almost certain.

=== MAOIs & Alcohol ===

The chemical tyramine in alcoholic beverages can have dangerous reactions with MAOIs, causing an increase in blood pressure.

=== SSRIs & Alcohol ===

Alcohol may potentiate some of the pharmacologic effects of CNS-active agents. Use in combination may result in additive central nervous system depression and/or impairment of judgment, thinking, and psychomotor skills.

=== Opioids & GHB/GBL ===

The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position.

=== Tramadol & GHB/GBL ===

The sedative effects of this combination can lead to dangerous respiratory depression.

=== Benzodiazepines & GHB/GBL ===

The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position.

=== Tramadol & Opioids ===

Concomitant use of tramadol increases the seizure risk in patients taking other opioids. These agents are often individually epileptogenic and may have additive effects on seizure threshold during coadministration. Central nervous system- and/or respiratory-depressant effects may be additively or synergistically present.

=== Benzodiazepines & Opioids ===

Central nervous system and/or respiratory-depressant effects may be additively or synergistically present. The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position Blackouts/memory loss likely.

=== MAOIs & Opioids ===

Coadministration of monoamine oxidase inhibitors (MAOIs) with certain opioids has been associated with rare reports of severe and fatal adverse reactions. There appear to be two types of interaction, an excitatory and a depressive one. Symptoms of the excitatory reaction may include agitation, headache, diaphoresis, hyperpyrexia, flushing, shivering, myoclonus, rigidity, tremor, diarrhea, hypertension, tachycardia, seizures, and coma. Death has occurred in some cases.

=== Benzodiazepines & Tramadol ===

Central nervous system- and/or respiratory-depressant effects may be additively or synergistically present. Vomit aspiration a risk when passed out, lay down in recovery position if ingested.

== References ==

=== LSD & DMT ===

http://www.ncbi.nlm.nih.gov/pubmed/3006089
http://deepblue.lib.umich.edu/bitstream/handle/2027.42/26285/0000370.pdf

===LSD & GHB/GBL===

http://www.ncbi.nlm.nih.gov/pubmed/16483730

===LSD & Opioids===

http://www.ncbi.nlm.nih.gov/pubmed/547279

http://www.ncbi.nlm.nih.gov/pubmed/3006089

"Low doses antagonized the effects of both hallucinogens, whereas larger doses enhanced their effects."

http://www.ncbi.nlm.nih.gov/pubmed/3006089

http://deepblue.lib.umich.edu/bitstream/handle/2027.42/26285/0000370.pdf

===LSD & Tramadol===

http://www.ncbi.nlm.nih.gov/pubmed/3006089

===LSD & MAOIs===

http://www.ncbi.nlm.nih.gov/pubmed/8788508

http://www.ncbi.nlm.nih.gov/pubmed/108709

https://www.erowid.org/references/refs_view.php?A=ShowDocPartFrame&ID=2439&DocPartID=2199

===LSD & SSRIs===

http://www.nature.com/npp/journal/v14/n6/full/1380431a.html

http://www.ncbi.nlm.nih.gov/pubmed/8726753

===DMT & Opioids===

http://www.ncbi.nlm.nih.gov/pubmed/3006089

===DMT & Tramadol===

http://www.ncbi.nlm.nih.gov/pubmed/3006089

===MDMA & GHB/GBL===

http://www.ncbi.nlm.nih.gov/pubmed/16234132

http://www.ncbi.nlm.nih.gov/pubmed/22554869

http://www.ncbi.nlm.nih.gov/pubmed/20730418

http://www.ncbi.nlm.nih.gov/pubmed/16483730

===DOx & Amphetamines===

http://www.ncbi.nlm.nih.gov/pubmed/1208759

===Ketamine & Caffeine===

http://onlinelibrary.wiley.com/doi/10.1111/j.1742-7843.2009.00382.x/full

===Ketamine & Amphetamine===

http://www.ncbi.nlm.nih.gov/pubmed/23660488

===Ketamine & Alcohol===

http://onlinelibrary.wiley.com/doi/10.1002/jemt.22045/abstract

===Ketamine & GHB/GBL===

http://www.ncbi.nlm.nih.gov/pubmed/16483730

===Ketamine & Opioids===

http://www.ncbi.nlm.nih.gov/pubmed/21224020

===Tramadol & SSRIs===

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2714818/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750095/

===MXE & DXM===

http://i.imgur.com/zmqaw.jpg

http://www.sciencedirect.com/science/article/pii/S0014488607002543

===MXE & Amphetamines===

http://www.ncbi.nlm.nih.gov/pubmed/25060403

===DXM & PCP===

http://i.imgur.com/zmqaw.jpg

http://www.sciencedirect.com/science/article/pii/S0014488607002543

===PCP & SSRIs===

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1224745/

===Amphetamines & Benzodiazepines===

http://www.ncbi.nlm.nih.gov/pubmed/17320309

===MDMA & Caffeine===

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492978/

http://link.springer.com/article/10.1007/s00213-010-1864-1

http://www.sciencedirect.com/science/article/pii/S0028390805003114

http://www.ncbi.nlm.nih.gov/pubmed/24211539

===MDMA & Alcohol===

http://www.ncbi.nlm.nih.gov/pubmed/21040238

http://www.ncbi.nlm.nih.gov/pubmed/21756931

===Cocaine & SSRIs===

http://www.ncbi.nlm.nih.gov/pubmed/23761390

http://www.ncbi.nlm.nih.gov/pubmed/20195220

===Caffeine & Alcohol===

http://www.ncbi.nlm.nih.gov/pubmed/20001110

===Caffeine & Tramadol===

http://www.ncbi.nlm.nih.gov/pubmed/20837047

===Caffeine & SSRIs===

http://journals.lww.com/jpharmacogenetics/abstract/1996/06000/a_fluvoxamine_caffeine_interaction_study.3.aspx

===Alcohol & GHB/GBL===

http://www.ncbi.nlm.nih.gov/pubmed/15274975

===Alcohol & SSRIs===

http://www.ncbi.nlm.nih.gov/pubmed/15739105

===GHB/GBL & Opioids===

http://www.ncbi.nlm.nih.gov/pubmed/7782758

===GHB/GBL & Tramadol===

http://www.ncbi.nlm.nih.gov/pubmed/7782758

===GHB/GBL & Benzodiazepines===

http://www.ncbi.nlm.nih.gov/pubmed/16483730

===GHB/GBL & MAOIs===

No study, but MAO B inhibitors should enhance the effects, no interaction with MAO A.

===Opioids & Benzodiazepines===

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3454351/

===Opioids & MAOIs===

http://www.ncbi.nlm.nih.gov/pubmed/17157368 (?)

http://www.ncbi.nlm.nih.gov/pubmed/2891392

http://www.if-pan.krakow.pl/pjp/pdf/2013/3_593.pdf

===Opioids & SSRIs===

http://www.ncbi.nlm.nih.gov/pubmed/23391344

http://www.ncbi.nlm.nih.gov/pubmed/20513454

http://www.ncbi.nlm.nih.gov/pubmed/16005413

http://www.ncbi.nlm.nih.gov/pubmed/18676387

http://www.ncbi.nlm.nih.gov/pubmed/17381671

===Tramadol & Benzodiazepines===

http://www.ncbi.nlm.nih.gov/pubmed/12842359

===Tramadol & MAOIs===

http://www.ncbi.nlm.nih.gov/pubmed/16051647

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750095/

===Benzodiazepines & SSRIs===

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2446479/

http://www.ncbi.nlm.nih.gov/pubmed/9435993

===MAOIs & SSRIs===

http://www.ncbi.nlm.nih.gov/pubmed/24577320

[[Category:Guides]]

Editing Factsheets

2015-10-17T21:28:40Z

Roi:

This document describes how staff members can edit our [[Factsheets]], which provides a database of concise drug information - upon which our IRC-based ~drug information is built, along with our web-based [http://drugs.tripsit.me/ factsheets] and its associated API.

=Web Editing=

Factsheet information can be edited live on the tripbot web interface on the specific factsheet pages after logging in - simply click 'edit.' Currently this does not support modifying aliases, adding properties or creating new drugs. These features are soon to come.

=Commands=

Factsheets can also be edited through IRC.

==~setdrug==

Set a property of a drug.

Syntax: '''~setdrug [drugname] [fieldname] [Content here]'''

Standard fields are generally: onset, duration, after-effects, effects, wiki, summary, categories and avoid. However, for certain drugs custom fields may be added. Wiki is a link to our own TripSit Wiki page on the subject.

===Dose===

The dosage field currently requires a bit of a strict syntax. Information for different ROAs e.g. 2-FA is done like so:

'''~setdrug 2-FA dose Oral Light: 5-15mg Common: 15-30mg Strong: 30-50mg Heavy: 50+mg. | Insufflated Light: 10-30mg Common: 30-60mg Strong: 60-120mg Heavy: 120mg+ | NOTE: Insufflating does not appear to provide better bioavailability than oral ingestion, and will cause damage to nasal cavity.'''

ROAs are separated with the pipe symbol, starting each with the ROA name and then each level followed by a colon e.g. Light: is important. You can check that the data has been picked up correctly by testing if the 'formatted_dose' property exists under e.g. http://tripbot.tripsit.me/api/tripsit/getDrug?name=2-FA

The values which should be used for doses are (in ascending order):
* Threshold
* Light
* Common
* Strong
* Heavy
* Dangerous

Any notes should be added under a separate piped section titled 'NOTE', as if it were a separate ROA.

===Onset, Duration and After-effects===

All three duration properties work in a similar way to above. They can either have one duration for all ROAs, like so:

'''3-5 hours'''

or one for each, seperated by a pipe:

'''Oral: 3-5 hours | Insufflated: 3-7 hours'''

In terms of unit, either hours or minutes is fine. Ensure that the ROA names are the same in each field - for example, don't use Plugged and Insufflated and Oral in one property, but then use Plugged/Insufflated and Oral in another.

==~rmdrug==

Remove a drug or a property of a drug.

Syntax: '''~rmdrug [drugname] ([fieldname])'''

Field name is optional, and if called without one the entire entry for the drug will be removed.

==~setdrugcategory==

This gives a drug a category.

Syntax: '''~setdrugcategory [drugname] [category]'''

Currently accepted categories are: psychedelic, benzodiazepine, dissociative, opioid, depressant, stimulant, habit-forming, research-chemical, empathogen, deliriant, nootropic, tentative, inactive.

==~rmdrugcategory==

Remove drug category.

Syntax: '''~rmdrugcategory [drugname] [category]'''

==~setdrugalias==

This sets an alias of a drug.

Syntax: '''~setdrugalias [drugname] [altname]'''

==~rmdrugalias==

Removes an alias of a drug.

Syntax: '''~rmdrugalias [drugname] [altname]'''

==~setdrugprettyname==

Changes display name.

Syntax: '''~setdrugprettyname [drugname] [prettyname]'''

[[Category:IRC]]
[[Category:TripSit]]

Main Page

2015-10-17T21:26:06Z

Roi:

{{DISPLAYTITLE:Welcome to TripSit Wiki!<span style="display: none"></span>}}
<table style="display:block;" cellpadding=0>
<tr>
<td valign=top width=30% bgcolor=#f1f1f1>
== Drug Knowledge ==
*'''List of [[:Category:Drugs|Psychoactive Substances]]'''
*Main pages for drug classes:
**[[Hallucinogens]]
***[[Psychedelics]]
***[[Dissociatives]]
**[[Stimulants]]
**[[Depressants]]
***[[Opioids]]
***[[Benzodiazepines]]
**[[Antidepressants]]
**[[Deliriants]]
**[[:Category:Ethnobotanical|Ethnobotanicals]]
**[[Research Chemicals]]

* [[Drug combinations]]
* [http://drugs.tripsit.me/ Factsheets]
* [[Glossary]]

== [[Guides]] ==

* [[Addiction]]
* [[Overdose]]
* [[Panic Attacks]]
* [[How To Deal With A Bad Trip]]
* [[Common Misconceptions About Psychedelics]]
* [[Quick Guide to Plugging]]
* [[Quick Guide to Stimulant Comedowns]]
* [[Quick Guide to Volumetric Dosing]]
* [[Cold Water Extraction]]

== Tripsitting ==
* [[How_To_Tripsit_Online|How to Tripsit online]]
* [[How_To_Tripsit_In_Real_Life|How to Tripsit in real life]]

== Harm Reduction Supplies & Testing ==
* [[Scales]]
* [[Test Kits]]
* [[Sources for Laboratory Analysis]]

</td>
<td valign=top width=30% bgcolor=#f1f1f1>
== [[:Category:Common Drugs|Common Drugs]] ==

* '''[[:Category:Psychedelic|Psychedelics]]'''
** [[Mushrooms]]
** [[DMT]]
** [[LSD]]
** [[LSA]]
** [[Mescaline]]
** [[2C-X|2C-X series]]
** [[NBOMes|NBOMe series]]
** [[DOx|DOx series]]
** [[AMT|αMT]]
** [[Cannabis]]

* '''[[:Category:Dissociative|Dissociatives]]'''
** [[PCP]]
** [[3-MeO-PCP]]
** [[Ketamine]]
** [[MXE]]
** [[DXM]]
** [[Diphenidine]]
** [[Salvia]]
** [[Nitrous Oxide]]

* '''[[:Category:Stimulant|Stimulants]]'''
** [[Adderall]]
** [[Amphetamine]]
** [[Methamphetamine]]
** [[MDMA]]
** [[MDA]]
** [[Mephedrone]]
** [[Cocaine]]
** [[Methylphenidate]]

* '''[[:Category:Depressant|Depressants]]'''
** [[Alcohol]]
** [[Etizolam]]
** [[GHB]]
** [[Kava]]
** [[Zolpidem]]

* '''[[:Category:Opioid|Opioids]]'''
** [[Kratom]]
** [[Morphine]]
** [[Heroin]]
** [[Codeine]]
** [[Tramadol]]
** [[Hydrocodone]]
** [[Oxycodone]]
** [[Buprenorphine]]
</td>

<td valign=top width=20%>
== Community ==
=== Important Pages ===
* [[TripSit Rules]]
* [[Network Terms of Service]]
* [[List of staff and their roles]]
* [[TripSit's Plans]]
* [[How to help TripSit]]

=== IRC ===
* [[IRC_User_Guide|'''New user guide''']]
* [http://tripsit.me/tripsitapp/ Tripsit's portable IRC distribution]
* [[Channels]]
** [http://chat.tripsit.me/?nick=Social?#tripsit #tripsit]
** [http://chat.tripsit.me/?nick=Social?#home #home]
** [http://chat.tripsit.me/?nick=Social?#drugs #drugs]
* [[How_to_connect_through_Tor|How to Connect through Tor]]
* [[List of IRC bot commands]]
* Moderation [[Commands reference]]

=== TripRadio ===
* [http://radio.tripsit.me Listen Now]

* [[Radio|General info]]
* [[DJ Application|We need DJs!]]
* [[How to DJ|How to setup DJ software]]
</td>

</tr>
</table>

[[About|About Tripsit wiki]]

TripSit wiki currently has [[Special:Statistics|{{NUMBEROFPAGES}} pages]].

View a [[Special:AllPages|list of all pages]].

Research Chemicals

2015-10-17T21:19:06Z

Roi: /* Research */

'Research Chemical' is a term used to refer to any chemical that has not been well researched, and does not have an established long-term safety-profile.

==Definition==

'Research chemical' is simply a term used to indicate that a chemical has not had a history of research or use and therefore is at the research stage of it's development. There is no official body which determines a research chemical, or when a research chemical has accrued enough history of use to cease its classification as one. Some have suggested that these chemicals should be called "unresearched chemicals" or another term "Experimental chemicals". Some are new, while others have been around for years; and little is known about most of them besides first hand accounts of use. There are research chemicals of many different types of drugs: while many drugs are qualified as research chemicals, the term itself is more of a flag than a category.

The expression can be considered somewhat of a misnomer, as drugs in this category have often not actually been researched, or at least have almost no history of human use. Many research chemicals in use today were originally discovered and published by Alexander Shulgin in PiHKAL and TiHKAL, and many more have been found based on these works. The term partially came from the fact that substances in the recreational markets were drugs that had been discovered in labs and only examined in-vitro or low-level animal studies. However, the 'research' more readily applies to the fact that these drugs were usually found through a process of research - such as through exploring analogues of existing psychoactive substances. Very little to no research has been used to establish the toxicology or human pharmacology of these drugs.

'Legal highs' commonly sold on grey-area market are usually one or more research chemicals made to mimic the effects of other illicit drugs. There is currently a very large market for the production, sale and use of research chemicals, driven by their implicit legality; vendors and users alike pursue research chemicals to avoid legal troubles encountered from being involved with the more traditional chemicals. Governments tend to ban research chemicals a short while after they become popular, and this in turn leads to more being discovered and sold. Some legal systems, such as that of the USA, have moved against research chemicals with acts of law implicitly banning analogues of drugs which are already banned.

==Risks==

As many of these drugs are very new and may not have a well-established safety profile, there are a variety of stronger risk-factors in using them. It is likely that many research chemicals have undocumented side-effects, interactions or contraindications.

===Misrepresentation===

One major risk associated with research chemicals is that they are often misrepresented; it is relatively common for a purportedly new chemical to actually consist of a blend of other research chemicals or banned chemicals.

When seeking to acquire research chemicals it is strongly advised to avoid 'blends', or branded products for which the active ingredients are often unknown or unlisted.

Not only does buying research chemicals in this manner keep you from being able to use any of what little research there may be on the active ingredient(s), but there have been published analysis results indicating that there is a very real risk of chemical synergy.

Consider the case of URB-754, wherein a blend marketed as a cannabinoid product was sold with some of the active ingredients listed. Upon analysis researchers learned that it contained not only unlisted cannabinoids but was also found to contain a previously unreported cathinone. While misrepresentation in the RC market is not uncommon, in this case closer inspection revealed an unexpected chemical reaction upon combustion, where some of the cannabinoids actually formed an entirely new previously unknown class of chemical when they reacted with the unlisted cathinone!

To put it simply, often the vendors themselves don't even really know what their product contains or the potential outcome of mixing chemicals.

===Analogue Misconception===

Remember, just because it is an analogue of something, does not mean it will behave the same way.

An example of this can be seen in the following comparison of two structurally related chemicals [[MDAI]] and [[MDMA]]. MDMA has been documented since the late 60's. MDAI is an analogue of MDMA, and while it produces some similar effects to MDMA it differs in that it's non-nuerotoxic.

Or we can take [[2C-B]] and its analogues such as [[BK-2C-B]], 25B-NBXXX, TCB-2, DOB, Bromo-Dragon-Fly, 2C-B-FLY. The parent drug in this example is much safer than the rest. There is no record of a death from 2C-B alone, with 25B-NBOMe there have been reports of multiple deaths during its short history of release.

==Harm Reduction Precautions==

While there is a certain element of risk involved in all experimentation / use of research chemicals. There are some basic precautions one can take in an effort to make an inherently risky behavior less dangerous than otherwise.

===Research===

While most readily available anecdotal information on research chemicals cannot be entirely trusted (due to the nature of research chemicals most data available on RC's is just that, a series of anecdotes), even for very new drugs there is usually a fair amount of information available which can give a good idea about what to expect. It is important that you do your own research and make your own informed decisions; don't take people's word for what a drug can/will do to/for you at face value as the same drug can effect people differently.

* The TripSit [http://drugs.tripsit.me/ factsheets] often have data on new drugs, and our Wiki includes harm reduction information for research chemicals in each drug class on their respective pages.

* While Erowid is usually slow to publish full vaults on research chemicals, there are usually a number of experience reports published for even very new drugs. These can give a good idea about what can be expected from the experience itself, as well as more anecdotal information about dosages and the like.

* Forums such as Bluelight.org and drugs-forum.com often have the first discussions and experience reports for very new chemicals, however reports can be somewhat dubious as in many cases very new drugs are often falsely sold, so the reports actually pertain to another chemical.

===Preparation===

When experimenting with any new drug a little forethought can go a long way, especially when it comes to drugs about which very little is actually known.

Usually if you're experimenting with a new drug (or even just a drug that is new to you) it's best practice to have a sober sitter with you, just in case something goes wrong. Some types of drugs produce effects that are more risky to go into alone than others but if you're using something new and you are unaware of how it will effect you, it's never a bad idea to be accompanied by a trustworthy person, such as a close friend to help guide you through a difficult experience or just someone to keep an eye on how your body reacts to something.

===Dosing===

As these chemicals are generally very new, and little information exists as to their effect on humans, there is also a lack of information about recommended doses. Often, speculative doses can be found on the Internet. When a new research chemical is released, the first results can often be found on forums such as Bluelight or drugs-forum. These consist of anecdotal trip reports, and cannot be trusted very much since in the early days of a drug's release, vendors will often sell other drugs under the newer name. After a time, and once some verifiable reports about the drug have been collected, tiered summaries are compiled by resources such as [http://factsheet.tripsit.me/factsheet/ TripSit Factsheets] and [https://www.erowid.org Erowid], which can provide more conclusive dosage guidelines. However, even when speculative doses are published, they should not be fully trusted due to the lack of long-term testing a drug has received at this point. Drugs which do not have much reliable information pertaining to their dose will generally be tagged.

With a chemical that has never been tested in vivo (animal subjects) for most substances you would want to start around 25ug's and titrate your dosage up to 50ug's in increments of 25ug's Leaving a week minimum between the 25ug test and 50ug, and work your way up. But this isn't needed for every chemical, such as BK-2C-I. You can use BK-2C-B as a "reference" of sorts, of it being 10x weaker than the parent compound(BK-2C-B). It is much safer to start at a lower dose than what would be an active dose to see if your body can handle the drug.Some might say that you can gauge an activity with just SAR's (Structure-Activity relationship) which in the most part true, yet in cases such as Lophophine and IRIS, there is a very good reason why it should be active, yet it isn't. That can also go in the other way, as IRIS is one of the "Ten Classic Ladies" or the ten possible homologues of DOM. While DOM is active around 3mg's, yet IRIS is inactive.

Therefor, because of the importance of using sub-threshold tester-doses, and since many of these new chemicals are highly potent anyways it is imperative that one has a reliable way to accurately measure chemicals in low doses.

It is not safe to assume any consumer-grade scale will be reliably accurate <50mg, however there is a way to measure accurately low doses of chemicals using a method known as 'volumetric dosing', [[Quick guide to volumetric dosing]]. While this technique is not particularly difficult it does require some planning and precision.

If you intend to employ volumetric measuring techniques, or when working with new chemicals (or any chemicals for that matter) it is important to be sure to use the most accurate scale available on a consumer level. Unfortunately, there are no scales that are reliably accurate for weights under approximately 25 mg that are readily available to the average consumer. That being said, there are some scales for sale for under $100, which if used correctly, can be safely used to prepare a solution for volumetric dosing of a substance. For more information on how to correctly use a scale, and sources for reasonably reliable scales to buy, check [[Scales]].

==Links==

* [https://erowid.org/psychoactives/research_chems/research_chems.shtml Erowid Research Chemicals Vault]

==References==

(1) * [http://www.fsijournal.org/article/S0379-0738(12)00434-3/abstract URB-754: A new class of designer drug and 12 synthetic cannabinoids detected in illegal products]

[[Category:Drug class]]

Editing Factsheets

2015-05-16T09:01:05Z

Roi: /* ~setdrugcategory */

This document describes how staff members can edit our [[Factsheets]], which provides a database of concise drug information - upon which our IRC-based ~drug information is built, along with our web-based [http://factsheet.tripsit.me/factsheet/ factsheets] and its associated API.

=Web Editing=

Factsheet information can be edited live on the tripbot web interface on the specific factsheet pages after logging in - simply click 'edit.' Currently this does not support modifying aliases, adding properties or creating new drugs. These features are soon to come.

=Commands=

Factsheets can also be edited through IRC.

==~setdrug==

Set a property of a drug.

Syntax: '''~setdrug [drugname] [fieldname] [Content here]'''

Standard fields are generally: onset, duration, after-effects, effects, wiki, summary, categories and avoid. However, for certain drugs custom fields may be added. Wiki is a link to our own TripSit Wiki page on the subject.

===Dose===

The dosage field currently requires a bit of a strict syntax. Information for different ROAs e.g. 2-FA is done like so:

'''~setdrug 2-FA dose Oral Light: 5-15mg Common: 15-30mg Strong: 30-50mg Heavy: 50+mg. | Insufflated Light: 10-30mg Common: 30-60mg Strong: 60-120mg Heavy: 120mg+ | NOTE: Insufflating does not appear to provide better bioavailability than oral ingestion, and will cause damage to nasal cavity.'''

ROAs are separated with the pipe symbol, starting each with the ROA name and then each level followed by a colon e.g. Light: is important. You can check that the data has been picked up correctly by testing if the 'formatted_dose' property exists under e.g. http://tripbot.tripsit.me/api/tripsit/getDrug?name=2-FA

The values which should be used for doses are (in ascending order):
* Threshold
* Light
* Common
* Strong
* Heavy
* Dangerous

Any notes should be added under a separate piped section titled 'NOTE', as if it were a separate ROA.

===Onset, Duration and After-effects===

All three duration properties work in a similar way to above. They can either have one duration for all ROAs, like so:

'''3-5 hours'''

or one for each, seperated by a pipe:

'''Oral: 3-5 hours | Insufflated: 3-7 hours'''

In terms of unit, either hours or minutes is fine. Ensure that the ROA names are the same in each field - for example, don't use Plugged and Insufflated and Oral in one property, but then use Plugged/Insufflated and Oral in another.

==~rmdrug==

Remove a drug or a property of a drug.

Syntax: '''~rmdrug [drugname] ([fieldname])'''

Field name is optional, and if called without one the entire entry for the drug will be removed.

==~setdrugcategory==

This gives a drug a category.

Syntax: '''~setdrugcategory [drugname] [category]'''

Currently accepted categories are: psychedelic, benzodiazepine, dissociative, opioid, depressant, stimulant, habit-forming, research-chemical, empathogen, deliriant, nootropic, tentative, inactive.

==~rmdrugcategory==

Remove drug category.

Syntax: '''~rmdrugcategory [drugname] [category]'''

==~setdrugalias==

This sets an alias of a drug.

Syntax: '''~setdrugalias [drugname] [altname]'''

==~rmdrugalias==

Removes an alias of a drug.

Syntax: '''~rmdrugalias [drugname] [altname]'''

==~setdrugprettyname==

Changes display name.

Syntax: '''~setdrugprettyname [drugname] [prettyname]'''

[[Category:IRC]]
[[Category:TripSit]]

Editing Factsheets

2015-05-16T00:56:08Z

Roi: /* ~setprettyname */

This document describes how staff members can edit our [[Factsheets]], which provides a database of concise drug information - upon which our IRC-based ~drug information is built, along with our web-based [http://factsheet.tripsit.me/factsheet/ factsheets] and its associated API.

=Web Editing=

Factsheet information can be edited live on the tripbot web interface on the specific factsheet pages after logging in - simply click 'edit.' Currently this does not support modifying aliases, adding properties or creating new drugs. These features are soon to come.

=Commands=

Factsheets can also be edited through IRC.

==~setdrug==

Set a property of a drug.

Syntax: '''~setdrug [drugname] [fieldname] [Content here]'''

Standard fields are generally: onset, duration, after-effects, effects, wiki, summary, categories and avoid. However, for certain drugs custom fields may be added. Wiki is a link to our own TripSit Wiki page on the subject.

===Dose===

The dosage field currently requires a bit of a strict syntax. Information for different ROAs e.g. 2-FA is done like so:

'''~setdrug 2-FA dose Oral Light: 5-15mg Common: 15-30mg Strong: 30-50mg Heavy: 50+mg. | Insufflated Light: 10-30mg Common: 30-60mg Strong: 60-120mg Heavy: 120mg+ | NOTE: Insufflating does not appear to provide better bioavailability than oral ingestion, and will cause damage to nasal cavity.'''

ROAs are separated with the pipe symbol, starting each with the ROA name and then each level followed by a colon e.g. Light: is important. You can check that the data has been picked up correctly by testing if the 'formatted_dose' property exists under e.g. http://tripbot.tripsit.me/api/tripsit/getDrug?name=2-FA

The values which should be used for doses are (in ascending order):
* Threshold
* Light
* Common
* Strong
* Heavy
* Dangerous

Any notes should be added under a separate piped section titled 'NOTE', as if it were a separate ROA.

===Onset, Duration and After-effects===

All three duration properties work in a similar way to above. They can either have one duration for all ROAs, like so:

'''3-5 hours'''

or one for each, seperated by a pipe:

'''Oral: 3-5 hours | Insufflated: 3-7 hours'''

In terms of unit, either hours or minutes is fine. Ensure that the ROA names are the same in each field - for example, don't use Plugged and Insufflated and Oral in one property, but then use Plugged/Insufflated and Oral in another.

==~rmdrug==

Remove a drug or a property of a drug.

Syntax: '''~rmdrug [drugname] ([fieldname])'''

Field name is optional, and if called without one the entire entry for the drug will be removed.

==~setdrugcategory==

This gives a drug a category.

Syntax: '''~setdrugcategory [drugname] [category]'''

Currently accepted categories are: psychedelic, dissociative, stimulant, depressant, opioid, benzodiazepine, other.

==~rmdrugcategory==

Remove drug category.

Syntax: '''~rmdrugcategory [drugname] [category]'''

==~setdrugalias==

This sets an alias of a drug.

Syntax: '''~setdrugalias [drugname] [altname]'''

==~rmdrugalias==

Removes an alias of a drug.

Syntax: '''~rmdrugalias [drugname] [altname]'''

==~setdrugprettyname==

Changes display name.

Syntax: '''~setdrugprettyname [drugname] [prettyname]'''

[[Category:IRC]]
[[Category:TripSit]]

Editing Factsheets

2015-05-16T00:54:29Z

Roi:

This document describes how staff members can edit our [[Factsheets]], which provides a database of concise drug information - upon which our IRC-based ~drug information is built, along with our web-based [http://factsheet.tripsit.me/factsheet/ factsheets] and its associated API.

=Web Editing=

Factsheet information can be edited live on the tripbot web interface on the specific factsheet pages after logging in - simply click 'edit.' Currently this does not support modifying aliases, adding properties or creating new drugs. These features are soon to come.

=Commands=

Factsheets can also be edited through IRC.

==~setdrug==

Set a property of a drug.

Syntax: '''~setdrug [drugname] [fieldname] [Content here]'''

Standard fields are generally: onset, duration, after-effects, effects, wiki, summary, categories and avoid. However, for certain drugs custom fields may be added. Wiki is a link to our own TripSit Wiki page on the subject.

===Dose===

The dosage field currently requires a bit of a strict syntax. Information for different ROAs e.g. 2-FA is done like so:

'''~setdrug 2-FA dose Oral Light: 5-15mg Common: 15-30mg Strong: 30-50mg Heavy: 50+mg. | Insufflated Light: 10-30mg Common: 30-60mg Strong: 60-120mg Heavy: 120mg+ | NOTE: Insufflating does not appear to provide better bioavailability than oral ingestion, and will cause damage to nasal cavity.'''

ROAs are separated with the pipe symbol, starting each with the ROA name and then each level followed by a colon e.g. Light: is important. You can check that the data has been picked up correctly by testing if the 'formatted_dose' property exists under e.g. http://tripbot.tripsit.me/api/tripsit/getDrug?name=2-FA

The values which should be used for doses are (in ascending order):
* Threshold
* Light
* Common
* Strong
* Heavy
* Dangerous

Any notes should be added under a separate piped section titled 'NOTE', as if it were a separate ROA.

===Onset, Duration and After-effects===

All three duration properties work in a similar way to above. They can either have one duration for all ROAs, like so:

'''3-5 hours'''

or one for each, seperated by a pipe:

'''Oral: 3-5 hours | Insufflated: 3-7 hours'''

In terms of unit, either hours or minutes is fine. Ensure that the ROA names are the same in each field - for example, don't use Plugged and Insufflated and Oral in one property, but then use Plugged/Insufflated and Oral in another.

==~rmdrug==

Remove a drug or a property of a drug.

Syntax: '''~rmdrug [drugname] ([fieldname])'''

Field name is optional, and if called without one the entire entry for the drug will be removed.

==~setdrugcategory==

This gives a drug a category.

Syntax: '''~setdrugcategory [drugname] [category]'''

Currently accepted categories are: psychedelic, dissociative, stimulant, depressant, opioid, benzodiazepine, other.

==~rmdrugcategory==

Remove drug category.

Syntax: '''~rmdrugcategory [drugname] [category]'''

==~setdrugalias==

This sets an alias of a drug.

Syntax: '''~setdrugalias [drugname] [altname]'''

==~rmdrugalias==

Removes an alias of a drug.

Syntax: '''~rmdrugalias [drugname] [altname]'''

==~setprettyname==

Changes display name.

Syntax: '''~setprettyname[drugname] [prettyname]'''

[[Category:IRC]]
[[Category:TripSit]]

Factsheets

2015-05-15T21:43:58Z

Roi:

The TripSit team has collected information about a number of drugs, which is being updated and revised continually as more information becomes available. You can access this repository [http://drugs.tripsit.me/ online] or through our [http://tripsit.me/chat/chat-overview/ IRC network] using the ~drug command.

==API==

The factsheet system also has an open JSON API, which you can use to integrate the drug data into your own applications or use for your own purposes.

===Usage===

The API is a simple rest-based JSON API, which can be accessed by sending a GET request to the following path:

http://tripbot.tripsit.me/api/tripsit/getDrug?name=lsd

Substituting the name parameter for the drug of your choice.

===Attribution===
Use of this API is free-of-charge for non-commercial purposes, we only require that your application links back to either this page or [http://drugs.tripsit.me/ Factsheets], citing TripSit as the source for the information.

tripbot is based on the open-source [https://github.com/reality/dbot dbot] software.

==Disclaimer and Updates==

This information has been researched to the best ability by the TripSit team, and the greatest effort has been made not to include incorrect or misleading information - though some information may not be 100% accurate. These factsheets are designed as a quick reference, not a definitive source on drug information. Use at your own risk, and please try to be safe.

In the case that there is any ambiguity in terms of dosing guidelines, we have tended towards the lower dosage range.

If you spot any incorrect information on the factsheets or have any feature requests, then please get in contact with us by sending an email to '''reality @ tripsit.me'''.

==Donations==

The development of this software and the cultivation of the data in it takes a lot of work from the TripSit team, so if you wish to support the TripSit project then please check out our [http://tripsit.me/donate/ donations] page.

[[Category:TripSit]]

Editing Factsheets

2015-05-15T21:36:44Z

Roi:

This document describes how staff members can edit our [[Factsheets]], which provides a database of concise drug information - upon which our IRC-based ~drug information is built, along with our web-based [http://factsheet.tripsit.me/factsheet/ factsheets] and its associated API.

=Web Editing=

Factsheet information can be edited live on the tripbot web interface on the specific factsheet pages after logging in - simply click 'edit.' Currently this does not support modifying aliases, adding properties or creating new drugs. These features are soon to come.

=Commands=

Factsheets can also be edited through IRC.

==~setdrug==

Set a property of a drug.

Syntax: '''~setdrug [drugname] [fieldname] [Content here]'''

Standard fields are generally: onset, duration, after-effects, effects, wiki, summary, categories and avoid. However, for certain drugs custom fields may be added. Wiki is a link to our own TripSit Wiki page on the subject.

===Dose===

The dosage field currently requires a bit of a strict syntax. Information for different ROAs e.g. 2-FA is done like so:

'''~setdrug 2-FA dose Oral Light: 5-15mg Common: 15-30mg Strong: 30-50mg Heavy: 50+mg. | Insufflated Light: 10-30mg Common: 30-60mg Strong: 60-120mg Heavy: 120mg+ | NOTE: Insufflating does not appear to provide better bioavailability than oral ingestion, and will cause damage to nasal cavity.'''

ROAs are separated with the pipe symbol, starting each with the ROA name and then each level followed by a colon e.g. Light: is important. You can check that the data has been picked up correctly by testing if the 'formatted_dose' property exists under e.g. http://tripbot.tripsit.me/api/tripsit/getDrug?name=2-FA

The values which should be used for doses are (in ascending order):
* Threshold
* Light
* Common
* Strong
* Heavy
* Dangerous

Any notes should be added under a separate piped section titled 'NOTE', as if it were a separate ROA.

===Onset, Duration and After-effects===

All three duration properties work in a similar way to above. They can either have one duration for all ROAs, like so:

'''3-5 hours'''

or one for each, seperated by a pipe:

'''Oral: 3-5 hours | Insufflated: 3-7 hours'''

In terms of unit, either hours or minutes is fine. Ensure that the ROA names are the same in each field - for example, don't use Plugged and Insufflated and Oral in one property, but then use Plugged/Insufflated and Oral in another.

==~rmdrug==

Remove a drug or a property of a drug.

Syntax: '''~rmdrug [drugname] ([fieldname])'''

Field name is optional, and if called without one the entire entry for the drug will be removed.

==~setdrugcategory==

This gives a drug a category.

Syntax: '''~setdrugcategory [drugname] [category]'''

Currently accepted categories are: psychedelic, dissociative, stimulant, depressant, opioid, benzodiazepine, other.

==~rmdrugcategory==

Remove drug category.

Syntax: '''~rmdrugcategory [drugname] [category]'''

==~setdrugalias==

This sets an alias of a drug.

Syntax: '''~setdrugalias [drugname] [altname]'''

==~rmdrugalias==

Removes an alias of a drug.

Syntax: '''~rmdrugalias [drugname] [altname]'''

[[Category:IRC]]
[[Category:TripSit]]

Rules

2015-02-25T17:14:10Z

Roi: /add TC password rule

= Contact Us =
== Technical problems with can be brought up in #help.==

{| class="mw-collapsible mw-collapsed wikitable"
! The '''#help''' room has staff there to address anything related to technical problems with the IRC network, subreddit, or website.
|-
| If you need help connecting via our TOR client, this is the channel to get assistance.
|-
| This is not a room to get help with drug information, and you will be kindly redirected to #tripsit or #drugs for that.
|}

==You may talk to the TripSit Managers to ask questions or give feedback via IRC in the #tripsit.me channel.==

{| class="mw-collapsible mw-collapsed wikitable"

! You can access this room on IRC by saying '''/join #tripsit.me'' or using [http://chat.tripsit.me/?nick=Problem?#tripsit.me this link].
|-

| Please join this room if you are unclear or need further explanation about any IRC rules.
|-

| We ask that non-staff do not idle in this room, so when you are finished, please leave the channel using the /part #channel command.
|}

==If rules are broken, use the ~report command to notify staff.==
{| class="mw-collapsible mw-collapsed wikitable"
! Syntax is: '''~report <#channel> <user> <reason>'''
|-
| Rules are enforced by the TripSit staff; as much as we try, we cannot monitor every aspect of our network all the time.
|-
| We encourage users to use reports to get attention to a situation quickly.
|-
| Should you witness a user breaking one of the following rules, use the ‘~report’ command to notify the TripSit [http://wiki.tripsit.me/wiki/List_of_staff_and_their_roles staff].
|-
| Try to be as clear and detailed as possible when explaining the nature of the event.
|}

== To appeal a ban, /join the #tripsit.me channel.==

{| class="mw-collapsible mw-collapsed wikitable"
! Do not evade a ban issued to you, this will result in a removal from the server (k-line).
|-
| Ban-evasion is when you enter a TripSit room while still under the effect of a ban.
|-
| While banned, you can still enter non-TripSit rooms and #tripsit.me
| -
|If you wish to discuss a ban, please PM a TripSit [http://wiki.tripsit.me/wiki/List_of_staff_and_their_roles staff member] or join '''#tripsit.me'''.
|}

== To appeal a k-line, email the admins. ==
{| class="mw-collapsible mw-collapsed wikitable"
! If you have been removed from the network with a k-line, you can send an email to admin (at) tripsit (dot) me.
|-
| We will investigate and get back to you as soon as we can.
|-
| You can also send a modmail to /r/tripsit, but please, do not make a post on /r/tripsit.
|}

= Acceptance of terms =

== Using our network is an acceptance of the rules and terms of service. ==

'''By using and remaining connected to this site and any other site owned and operated by TripSit (TripSit.me), you signify your agreement to the terms, conditions and notices of this policy.'''

'''By continuing to enter and browse TripSit and its systems, you are implying that you have read, understand and are in agreement with all of the terms stated in this document.'''

= Network-Wide Prohibited Use =

== Rules have been established to protect TripSit and its members against abuse. ==
== Do not use our network for illegal activity. ==

{| class="mw-collapsible mw-collapsed wikitable"
! TripSit is an informational and community resource, which does not advocate breaking any laws.
|-
| Do not use TripSit for unlawful purposes, including, without limitation:
|-
| Posting or exchanging any information on ongoing or future criminal activity, any information that can be construed as discussing such activity or actively encouraging others to engage in criminal activities.
|}

== Do not post torrents or other pirating sites. ==

{| class="mw-collapsible mw-collapsed wikitable"
! Do not post any content that is copyrighted by another, or invasive of another's privacy.
|-
| This includes linking to any peer-to-peer sites, such as torrent search engines that allow access to copyrighted material.
|}

== Do not harass people. ==
{| class="mw-collapsible mw-collapsed wikitable"
! TripSit is a positive place and is not the community for harassment or other negative behavior.
|-
| Do not post any content that victimizes, harasses, degrades, or intimidates an individual or group of individuals based on race, ethnicity, religion, sexual orientation or any other reason.
|-
| Depending on the severity, you may either be quieted, banned or removed entirely.
|}

== Do not impersonate staff. ==
{| class="mw-collapsible mw-collapsed wikitable"
! Do not act as an official representative of TripSit.
|-
| Do not use other Internet sites to promote libelous or slanderous messages about TripSit or incite abuse against TripSit.
|-
| Do not associate a third-party website with TripSit without authorization.
|}

== Do not take down TripBot or any of our systems. ==
{| class="mw-collapsible mw-collapsed wikitable"
! Do not intentionally overload any of our systems.
|-
| Do not interfere with service to any user or host including, without limitation, mail bombing, flooding, and attempting to deliberately overload the system.
|-
| This includes any of our web services such as the IRC network and TripBot.
|}

== Do not hack us or otherwise take unauthorized control of our systems. ==
{| class="mw-collapsible mw-collapsed wikitable"
! Do not attempt to gain unauthorized access to data, accounts or systems of this service.
|-
| This includes probing, scaning or testing the vulnerability of a system of this service; disseminate in any way, content originally posted in any staff-only area of this service.
|}

== Do not collect or post personal information on people. ==
{| class="mw-collapsible mw-collapsed wikitable"
! Posting personal information about channel members, or doxing, is grounds for a permanent network ban.

|-
| Trying to collect personal info of users is dealt with in the same manner.
|}

== Do not ruin the TripSit community for others. ==

{| class="mw-collapsible mw-collapsed wikitable"
! Do not use TripSit for any purpose which could impair any other party's use or enjoyment of this site.
|-
| We are a community, and everyone on the internet deserves to enjoy being here.
|-
| Actions that make this community anything less than a pleasant place to be will be deal with appropriately.
|}

=== No information is better than wrong information. ===
{| class="mw-collapsible mw-collapsed wikitable"
! If you are not 100% positive about the advice you are thinking about giving, do not say it.
|-
| It is still better to inform the person there may be no current information rather than staying silent and having them wonder if anyone noticed it.
|-
| In most instances, people on the internet are not qualified to provide medical advice.
|-
| Members of the TripSit community are extremely knowledgeable, wise, and often have ample life experience in a range of situations pertaining to drug use; however, they are no substitute for a personal doctor.
|-
| If you do not have sources to validate your advice, do not say anything related to medical advice.
|}

==Do not suggest harmful actions to others.==

{| class="mw-collapsible mw-collapsed wikitable"
! It is against the rules to endorse or encourage dangerous behavior regarding drug consumption.
|-
| The TripSit community is devoted to [http://wiki.tripsit.me/wiki/Harm_Reduction_Supplies harm reduction], support, and positvitiy, and we will never recommend or tolerate dangerous or reckless drug use.
|-
| Users identified as continually engaging in reckless drug-use behavior are seen as a bad influence on the community as a whole, actively working against our [http://tripsit.me/about-tripsit/about-tripsit/ mission] to be a a harm-reduction community devoted to positive support.
|-
| All users are expected to discourage drug dosages, [http://wiki.tripsit.me/wiki/Drug_combinations drug combinations], or any drug experimentation which could be reliably considered unsafe.
|}

== Do not try to buy or sell substances, currencies or services. ==

'''<font color="#888888">A</font>ttempting to solicit or obtain currencies/bitcoins, contraband substances or substances of a quasi-legal status or information on how to do so is not allowed.'''

===Sourcing is defined as:===

Discussion, requesting or posting the personally identifying information of websites, online vendors (this includes websites such as Amazon) and real-life people who sell or coordinate the purchase, distribution, or production of: Chemicals (legal, grey-area, or illegal), paraphernalia, services and currencies (bitcoin).

Keep in mind sarcasm is hard to tell on the internet, it's better to err on the side of caution when considering to jokingly ask for sources.

{| class="mw-collapsible mw-collapsed wikitable"
! Definitions
|-
| Vendor || A person or group selling or distributing specific goods.
|-
| Marketplace || A trade hub on which Vendors’ trade goods.
|-
| Linking || Posting a URL hyperlink into a channel.
|}

=== We do not allow ===
==== Linking to chemical or currency vendors. Legal, clearnet, or otherwise (Also known as 'sourcing'). ====
{| class="mw-collapsible mw-collapsed wikitable"
! This includes, but is not limited to:
|-
| Legal psychoactives, such as caffeine, nootropics, or tobacco
|-
| Darknet marketplaces
|-
| Research Chemicals
|-
| "Legal Highs"
|-
| Herbal supplements or blends
|-
| Bitcoins
|}

==== Linking to E-juice or other nicotine vendors. ====
{| class="mw-collapsible mw-collapsed wikitable"
! Nicotine is a mild psychoactive and potentially deadly.
|-
| Flavored glycerin with nicotine, otherwise known as E-juice, contains nicotine, a mild psychoactive and potentially deadly substance.
|-
| Since we cannot establish the quality of the product, for the safety of our members, we do not allow the linking to E-juice vendors.
|}

==== Soliciting currencies (bitcoin) and/or substances, and services of a quasi-legal or illegal nature. ====
{| class="mw-collapsible mw-collapsed wikitable"
! This includes, but is not limited to:
|-
| Asking for currencies in a public channel.
|-
| Asking for drugs in a public channel (Remember, sarcasm is hard to tell on the internet).
|-
| Asking for a vendors or dealers name '''(This includes doctors)''', URL, PGP key or any other contact information.
|-
| Selling currencies or drugs in a public channel.
|-
| Services of a quasi-legal or illegal nature, including prostitutes, sex workers, or hitmen.
|}

==== Discussion of vendors.====
{| class="mw-collapsible mw-collapsed wikitable"
! The following are unacceptable questions:
|-
| "How is reliable is [vendor]?"
|-
| "Hey how much does Vendor's weed sell for?"
|-
| "How much does [Chemical] cost on Chemicals.com?"
|-
| "Does [Vendor] on [Marketplace] have good [Drug]"
|-
| Discussing the specifics or otherwise going in depth to the mechanics of online vending.
|}

===We Allow===
==== Discussion of brand name products. ====
==== Linking to a [http://wiki.tripsit.me/wiki/Clearnet_Vendor_Discussion discussion page for clearnet vendors], not the vendor itself. ====

==== Linking to harm reduction equipment is allowed (Such as scales or test kits) but please check that the source doesn't contain any chemicals. ====

==== Linking to paraphernalia and [http://wiki.tripsit.me/wiki/Harm_Reduction_Supplies harm reduction equipment] ====
{| class="mw-collapsible mw-collapsed wikitable"
! Harm reduction equipment includes:
|-
| Scales
|-
| Test Kits
|-
| Sterile needles
|-
| Sterile water
|-
| Nitrous dispensers
|-
| Water Pipes
|-
| Vaporizers
|}

==== Talking about marketplaces or prices in a GENERAL sense.====
{| class="mw-collapsible mw-collapsed wikitable"
! For example, the following are acceptable questions:
|-
| "Can SR 2.0 be trusted?"
|-
| "Is it safe to trade on Agora?"
|-
| Asking the price of a drug in a general sense.
|-
| "How much does weed cost in [given area]?"
|-
| "How much does [substance] usually cost?"
|}

= TripSit Channel Policies =

== Use common sense and do not do questionable things. ==
{| class="mw-collapsible mw-collapsed wikitable"
! If you have any doubt over whether your topic, question, advice, or comment is acceptable, feel free to join '''#tripsit.me'''.
|-
| We are happy to give you a solid judgement on whether your topic is acceptable in private without judgement or consequence.
|-
| We like to deal with other behaviors in a softer manner, by guiding the user and explaining to them what is and isn't allowed.
|-
| In the case of repeated offences or a bad attitude, we reserve the right to forego these protocols in favor of the community.
|-
| Every case is unique and will be dealt with to the best of the ability of the [http://wiki.tripsit.me/wiki/List_of_staff_and_their_roles staff] on duty at the time.
|}

== Keep It Positive Please. ==
{| class="mw-collapsible mw-collapsed wikitable"
! This basically means no rude, mean, or judgmental discussion.
|-
| We are a network devoted to harm reduction and positivity.
|-
| One of our policies is to try and Keep It Positive (KIP).
|-
| Please refrain from racial slurs, homophobia, and all other prejudice against any person or group of people.
|-
| Do not insult other users; take intense arguments to private chat.
|}

== Keep the #tripsit channel awesome. ==
{| class="mw-collapsible mw-collapsed wikitable"
! This channel should always be ready to help fellow members.
|-
| The #tripsit channel is for people currently under the influence of drugs and those there to sit them.
|-
| Please take any drug discussion, arguments or otherwise distracting chatter to #drugs instead.
|-
| Only light-hearted and positive conversation here: We all know how easily a trip can turn bad just by a simple thought.
|-
| Anyone caught being facetious will be warned and then banned if need be.
|-
| Rules are '''STRICTLY''' enforced in this channel.
|}

== Do not post the TripSit Tinychat password in public channels. ==
{| class="mw-collapsible mw-collapsed wikitable"
! Just don't!
|}

== Do not post gore, mark NSFW links as such. ==
{| class="mw-collapsible mw-collapsed wikitable"
! Do not post any gore. Please mark any content 18+ with a NSFW label.
|-
| The general subject of our network is not work appropriate, but there is a difference between text and pictures that are not safe for work.
|-
| Please be courteous to those with the luxury of being on the network while at work.
|}

== Do not argue rules in public channels, take it to #tripsit.me. ==

{| class="mw-collapsible mw-collapsed wikitable"
! Arguing a ban, quiet, or general rule is not allowed in public channels, but is encouraged in #tripsit.me
|-
| Arguing against established practices in large channels is rarely productive.
|-
| However, the TripSit team wants to hear your opinion, and welcomes rule discussion in #tripsit.me
|-
| We are happy to discuss any ambiguity in our rules that is not covered on this page.
|}

== Do not use poor language. ==
{| class="mw-collapsible mw-collapsed wikitable"
! To ensure maintaining a comfortable atmosphere, certain words trigger a auto-kick.
|-
| We believe in free speech, but certain words have proven to only lead to a degradation in community discussion. They are:
|-
| Jenkem
|-
| Yolo
|-
| Nigger
|-
| Swag
|}

== Do not impersonate law enforcement. ==

{| class="mw-collapsible mw-collapsed wikitable"
! For the sake of everyone's peace of mind, impersonating law enforcement is against our rules.
|-
| Impersonating an officer of the law will first result in a warning.
|-
| If the user does not comply, the user will be kicked.
|-
| Repeated attempts to impersonate law enforcement will result in a temporary or permanent ban.
|}

== Do not perform risky actions when using our TinyChat room.==
{| class="mw-collapsible mw-collapsed wikitable"
! Please refrain from IV activities while on camera.
|-
| We are sensitive to our former addicts and appreciate you keeping the room a nice place to be.
|}

==Do not give wrong or misleading medical advice to others.==
{| class="mw-collapsible mw-collapsed wikitable"
! Please avoid spreading misinformation about drug use.
|-
| Do not post any content that is libelous, deceptive, fraudulent, tortuous or inaccurate.
|-
| Misinformation is harmful to our community.
|}
== You may be removed if you continue to chat after receiving advice to seek medical attention ==

{| class="mw-collapsible mw-collapsed wikitable"
! If a user has taken a dangerous drug dose or combination they cannot continue to chat, they should get help.
|-
| Note that if a situation is identified as life threatening, or one in which the community's users believe immediate medical attention is required, we will always attempt to contact local medical personnel to help you.
|-
| As such, these behaviors are considered against the rules and violators may be subjected to temporary or permanent bans (situation depending).
|}

== Do not threaten suicide. ==
{| class="mw-collapsible mw-collapsed wikitable"
! While TripSitters will try their best to help member cope with down feelings of depression or worse, we cannot tolerate threats of suicide.
|-
| Suicide, depression and mental illness are not the focus of our network and our staff is not adequately trained to deal with suicidal situations, nor is it fair to our network's members to have the onus of guilt placed upon them for potential outcomes of such situations.
|-
| If a member is experiencing suicidal thoughts or tendencies, we kindly ask them to consider professional therapeutic assistance.
|-
| In a situation in which we fear for a user’s life, we will remind them of the guidelines stated above and do everything in our power to assist the member find qualified help.
|-
| In a dangerous overdose situation in which we believe immediate medical attention is required, we will always attempt to contact local medical personnel.
|-
| These behaviors disrupt the primary objectives of our community.
|-
| Therefore, suicide threats and attempts are considered against the rules, and while we will try our best to help in the immediate timescale, such threats and attempts may result in either a temporary or permanent ban from the community (under discretion from the administrators).
|-
| We endorse Reddit's [http://reddit.com/r/suicidewatch SuicideWatch] community.
|-
| '''Suicide prevention hotlines'''
|-
| *USA, National Suicide Prevention Lifeline: 1-800-273-8255
|-
| *[https://en.wikipedia.org/wiki/List_of_suicide_crisis_lines List of international suicide crisis hotlines]
|-
| '''Poison control hotlines'''
|-
| USA: 888 888 8822
|-
| UK: 111
|}

== Do not use mix drugs and mental illness. ==
{| class="mw-collapsible mw-collapsed wikitable"
! The TripSit community will not serve as enabler for the destruction of mental or physical health.
|-
| While we are very accepting of members who may have mental illnesses and/or disorders, we do not condone or encourage the use or abuse of drugs that could interact, worsen, or otherwise negatively affect your health.
|-
| Please seek medical assistance if you have a question regarding mental illnesses or disorders and their interactions with drugs.
|-
| We are not qualified to provide professional medical advice on drug interactions with mental illnesses.
|-
| If you want to discuss the topic, feel free to bring it up in our IRC channels or message the TripSit team.
|-
| We are happy to discuss any topic at length with you, warn you of any potential drug interactions as well as give you advice, love, respect and positive energy to the best of our ability.
|-
| The TripSit community is always here to help and support you, no matter what. We love you and want to keep you with us!
|}

= Disclaimer of Liability =

== We assume no liability for actions as a result of using our service. ==
{| class="mw-collapsible mw-collapsed wikitable"
! You indemnify TripSit, it's managers, and it's users.
|-
| TripSit's managers (any owner, operator, or associate of this website, including but not limited to the administrators, moderators, webmaster, technical contacts, and officers; henceforth to be referred to simply as 'managers') take no responsibility or liability for anything that happens as a result of you reading or posting any information at TripSit.
|}

== You are responsible for your own actions. ==
{| class="mw-collapsible mw-collapsed wikitable"
! You agree to hold responsible yourself, and no other, for the consequences of your actions while here.
|-
| We want to provide you with the best network ever, but it is ultimately your responsibility what you post in chat.
|-
| Be aware that legislation differs depending on location and do not suggest illegal acts.
|}

== We are not responsible for what other users tell you. ==

{| class="mw-collapsible mw-collapsed wikitable"
! You acknowledge that all data submitted to this website expresses the views and opinions of the author and not necessarily of TripSit or its managers.
|-
| You acknowledge IRC is a free, real-time, un-moderated media, and as such, TripSit Managers have little-to-no control over what users say in a chat room and cannot delete comments once users say them.
|-
| Neither TripSit nor its managers assume any legal liability or responsibility for the accuracy, completeness, or usefulness of any information, document, link, product, or post disclosed within this website.
|-
| Reference herein to any specific post, process, service or product offered by a member of this forum, or otherwise, does not necessarily constitute or imply its endorsement, recommendation, or favoring by TripSit or its managers.
|-
| Nothing on the board is to be taken as real and these may be games or fantasies people are expressing, therefore: Research on your own before taking someone's advice or following their example.
|}

= Privacy =

== Everything on the internet is public. ==

{| class="mw-collapsible mw-collapsed wikitable"
! Everything you post on the internet can be recorded in some way and can/will make its way back to you.
|-
| It is for your own safety and the safety of the network that these rules are in place.
|-
| TripSit does not keep data logs of our users, but our public channels are open to anyone who wants to gather logs. We simply cannot stop this in a public channel.
|-
| Any communication that you transmit to TripSit should be considered non-confidential, and you agree that TripSit will not be liable or responsible if information that belongs to you is intercepted or used by an unintended recipient.
|-
| As an internet user, you agree to any information you have entered on the internet being stored in a database somewhere else on the internet.
|}

== TripSit itself does not collect any personal information. ==
{| class="mw-collapsible mw-collapsed wikitable"
! This website uses cookies to store information on your local computer.
|-
| These cookies do not contain any of the registration information you have entered; they serve only to improve your viewing experience.
|}

== We do not share what personal information we have. ==
{| class="mw-collapsible mw-collapsed wikitable"
! We will never share what little information we have with anyone, unless Terms of Service are broken.
|-
| TripSit will not share member information with any party, unless the member has violated the TripSit User Agreement, in which case TripSit may take all necessary measures to ensure its security, including publishing the information or sharing it with private investigators.
|-
| Please note: This has never happened.
|}

== We do not watch private messages. ==
{| class="mw-collapsible mw-collapsed wikitable"
! TripSit does not have the capacity to store or read private messages.
|-
| TripSit does not monitor private communications; however, it should be assumed that any other party is logging what they see in public chat or a private message.
|-
| For additional privacy: TripSit provides a Tor hidden service to protect the identity of users, and you are welcome to use this hidden service at your own discretion.
|}

== We are not responsible if the security of our systems is compromised. ==
{| class="mw-collapsible mw-collapsed wikitable"
! The managers cannot be held responsible for any hacking attempt that may lead to the data being compromised.
|-
| To prevent unauthorized access, maintain data accuracy, and ensure the appropriate use of information, TripSit has put in place physical, electronic, and managerial procedures to safeguard and secure the information it collects online
|-
| Any unauthorized access to this system is prohibited and is subject to criminal and civil penalties under Federal Laws including but not limited to Public Laws 83-703 and 99-47
|-
| IP addresses may be recorded to aid in enforcing these conditions.
|}

= Measures =

== We can and will remove users and accounts if we feel it is necessary. ==

{| class="mw-collapsible mw-collapsed wikitable"
! TripSit reserves the right to take action to restrict or terminate your access to TripSit at any time for any reason.
|-
| In the case of repeated offences or a bad attitude, we reserve the right to forgo established protocols in favor of the community.
|-
| TripSit and its managers have the right to remove, edit, move or close any submitted data at any time should they choose to.
|}

== We do not work with law enforcement. ==

== If we are required by law to do give information, then we will need to comply. ==
{| class="mw-collapsible mw-collapsed wikitable"
! In case TripSit receives a court order with a properly authorized request, any stored information may be provided to law enforcement officials.
|-
| We will need to comply with the appliciable laws when necessary.
|-
| A lawyer will be contacted in this event, as well as yourself.

|}
=== Please note this has never happened. ===

= Non-TripSit rooms =

== We do not watch every channel created, but if we hear a report, we will take action. ==
{| class="mw-collapsible mw-collapsed wikitable"
! We reserve the right to take action in non-TripSit rooms if the Terms of Service have been broken.
|-
| The TripSit Team will not police rooms created by users, however, if there are reports of activity going against our rules we reserve the right to intervene, including the permanent takeover or shutdown of a channel.
|-
| Channels that are created on our network, official or otherwise, still adhere to our terms of service.
|-
| If a channel is in violation of the terms of service, the Tripsit administrative team reserves the right to permanently close or delete a channel, and ban the users in violation of the terms of service.
|}

= Underage users =
== We do not allow anyone under the age of 13 to be on the network. ==
{| class="mw-collapsible mw-collapsed wikitable"
! '''This is in accordance with the Child Online Protection Act, and is required by law.'''
|-
| While TripSit welcomes users and communities from all ends of the spectrum, our network is not designed for nor aimed at children.
|-
| In accordance with the United States government and the Children's Online Privacy Protection Act of 1998, individuals under the age of 13 are not permitted to browse TripSit nor create user accounts.
|-
| We require (in accordance with the Children's Online Privacy Act of 1998) that minors 13 years of age or older ask their parents for permission before logging on, and to refrain from posting any information about themselves, personal or otherwise, on the network.
|-
| If you have collected information from or about a child under the age of 13, both parties will face a network ban.
|}
== Minors (Users under the age of 18) are not allowed in the #opiates channel. ==
While TripSit tries to welcome everyone to our network, and will answer questions to anyone in our #tripsit room, we do not agree with letting minors getting involved with the more serious communities, and thus do not allow anyone under the age of 18 to enter the #opiates room.

= Accounts =

== Nicknames or channels cannot be offensive. ==
{| class="mw-collapsible mw-collapsed wikitable"
! [http://wiki.tripsit.me/wiki/Nicknames Nicknames] and channels may not contain any racial slurs or bigotry.
|-
| In this case the user will be forced to choose another name, multiple offenses may result in bans.
|-

{| class="mw-collapsible mw-collapsed wikitable"
! Nickname suffixes cannot be disruptive to the community.

|-
| It's customary for users to post-pend their nickname with their current substance, to help others let them know that they're not sober.
|-
| For example, User1 may change his nick to User1|THC to show that they have ingested marijuana.
|-
| Users who choose to postpend disruptive words/phrases at the end of their nick will be asked to change it.
|-
| Examples of disruptive phrases are: Jenkem and krokodil.
|-
| Users who refuse to change their nick may have their nickname changed for them.
|-

{| class="mw-collapsible mw-collapsed wikitable"
! Abandoned accounts will be removed after a period of inactivity.
|-
| The administrators of TripSit reserve the right to delete any and all data associated with abandoned accounts including, but not limited to: Profile information entered by the user, channels owned by the user or blog posts made by the user.
|-
| Further, TripSit reserves the right to reissue the username & any channels associated with an abandoned account.
|-
| An account is deemed to be abandoned if the account has no activity in the last six months.
|-
| A channel is deemed to be abandoned if the channel has no operator activity in the last six months.
|}

= Third party sites =

== This is a list of our online presence. ==
{| class="mw-collapsible mw-collapsed wikitable"
! The TripSit staff maintains an offsite presence (to some extent) on the following sites:
|-
| Facebook: https://www.facebook.com/tripsitme
|-
| Reddit: http://reddit.com/r/tripsit
|-
| GoFundMe: http://www.gofundme.com/tripsit

|-
| TinyChat: http://tinychat.com/coconutkingdom

|-
| Mumble: coconut.tripsit.me

|-
| Bitcoin: 1EDqf32gw73tc1WtgdT2FymfmDN4RyC9RN

|-
| Any links to Facebook groups, chat rooms, or other online communities other than those listed here are not affiliated with TripSit in any way.
|-
| The administration of TripSit cannot enforce our policies off site.
|}

= Thanks for reading! =

Alprazolam

2015-01-13T23:26:54Z

Roi: fix link

[[File:Xanax.jpg|250px|right]]
Alprazolam is a short acting anxiolytic of the benzodiazepine class of drugs. It is commonly used and FDA approved for the treatment of panic disorders and anxiety disorders, such as GAD/SAD. It is available in both instant and time released version.

= History =

Alprazolam was first released by Upjohn, under the brand name Xanax. The patent was filed in October 1969, granted in October of 1976, and expired in September of 1993. It was first released in 1981, for the treatment of panic disorders.

= Formulations =

Instant release tablets are available in 0.25mg, 0.5mg, 1mg, and 2mg.

Extended Release tablets are available in 0.5mg, 1mg, 2mg, and 3mg.

Oral solutions are available in 0.5mg/5mL and as 1mg/1mL solutions.

= Dosage =

Note: Higher doses have an increased risk of blacking out.

{| class="wikitable"
|+ Oral
| Light ||.25-.5mg

|-

| Common ||0.5-1.5mg

|-

| Strong ||1.5-2mg

|-

|Heavy ||2-3mg

|}

= Duration =

Note: Duration can be significantly longer with higher doses.

{| class="wikitable"
|+ Oral

| Onset || 20-40 minutes

|-

| Duration || 5-8 hours

|}

= Effects =

== Positive ==

*Euphoria

*Relaxation

*Anti-Anxiety effects
== Neutral ==

*Drowsiness

*Appetite fluctuation
== Negative ==

*Memory loss

*Blackout potential

*Motor skill impairment

*Dizziness

*Depression

*Irritability, aggression, rage

*Personality changes

*Emotional and social dissociation or de-realization (long term use)

= Harm Reduction =

When on high doses of benzodiazepines, users are likely to black out and potentially hurt themselves through a variety of adventures. If you are using it as a sleep aid, it's reccomended to continue doing what you're doing until you begin to feel drowsy, then go to bed.

Some users report Alprazolam (and benzodiazepines in general) to lead to compulsive redosing, trying to find a “high” which is where a fair amount of the point above comes from. To avoid this keep doses low and be wary of reduced inhibitions while under the influence of Alprazolam.

== Interactions ==

As with other depressants, Alprazolam should not be combined with any other CNS depressants (such as [[Alcohol]]), at the risk of respiratory depression, which can lead to death.
See the [[Drug combinations]] chart for more information.

= Chemistry and Pharmacology =

Alprazolam is absorbed fairly rapidly, with peak plasma levels achieved around the one-two hour mark.

It is primarily metabilised via CYP3A4. Alprazolam is a chemical analogue of triazolam. It is a triazolobenzodiazepine. It binds to the GABA(a) receptor and modulates the function of the GABA receptor. You can learn more about the GABA(a) receptor [[GABA Receptors and Subunits Info|here]].

The LD50 of Alprazolam in rats is 331-2171mg/kg.

= Legal Status =
==USA==
Alprazolam is a schedule IV substance.
==UK==
Under the UK drug misuse classification system benzodiazepines are class C drugs (Schedule 4).
==Ireland==
Alprazolam is a schedule 4 medicine.
==Sweden==
Alprazolam is a prescription drug in List IV under the Narcotic Drugs Act (1968).
==Netherlands==
Alprazolam is a List 2 substance of the Opium Law and is available for prescription.
==Australia==
Alprazolam was orginally a Schedule 4 (prescription only) medication; yet as of February 2014 it has become a Schedule 8 medication.

[[Category:Drugs]]

[[Category:Benzodiazepine]]

[[Category:Depressant]]

Alprazolam

2015-01-13T23:25:18Z

Roi:

[[File:Xanax.jpg|250px|right]]
Alprazolam is a short acting anxiolytic of the benzodiazepine class of drugs. It is commonly used and FDA approved for the treatment of panic disorders and anxiety disorders, such as GAD/SAD. It is available in both instant and time released version.

= History =

Alprazolam was first released by Upjohn, under the brand name Xanax. The patent was filed in October 1969, granted in October of 1976, and expired in September of 1993. It was first released in 1981, for the treatment of panic disorders.

= Formulations =

Instant release tablets are available in 0.25mg, 0.5mg, 1mg, and 2mg.

Extended Release tablets are available in 0.5mg, 1mg, 2mg, and 3mg.

Oral solutions are available in 0.5mg/5mL and as 1mg/1mL solutions.

= Dosage =

Note: Higher doses have an increased risk of blacking out.

{| class="wikitable"
|+ Oral
| Light ||.25-.5mg

|-

| Common ||0.5-1.5mg

|-

| Strong ||1.5-2mg

|-

|Heavy ||2-3mg

|}

= Duration =

Note: Duration can be significantly longer with higher doses.

{| class="wikitable"
|+ Oral

| Onset || 20-40 minutes

|-

| Duration || 5-8 hours

|}

= Effects =

== Positive ==

*Euphoria

*Relaxation

*Anti-Anxiety effects
== Neutral ==

*Drowsiness

*Appetite fluctuation
== Negative ==

*Memory loss

*Blackout potential

*Motor skill impairment

*Dizziness

*Depression

*Irritability, aggression, rage

*Personality changes

*Emotional and social dissociation or de-realization (long term use)

= Harm Reduction =

When on high doses of benzodiazepines, users are likely to black out and potentially hurt themselves through a variety of adventures. If you are using it as a sleep aid, it's reccomended to continue doing what you're doing until you begin to feel drowsy, then go to bed.

Some users report Alprazolam (and benzodiazepines in general) to lead to compulsive redosing, trying to find a “high” which is where a fair amount of the point above comes from. To avoid this keep doses low and be wary of reduced inhibitions while under the influence of Alprazolam.

== Interactions ==

As with other depressants, Alprazolam should not be combined with any other CNS depressants (such as [[Alcohol]]), at the risk of respiratory depression, which can lead to death.
See the [[Drug combinations]] chart for more information.

= Chemistry and Pharmacology =

Alprazolam is absorbed fairly rapidly, with peak plasma levels achieved around the one-two hour mark.

It is primarily metabilised via CYP3A4. Alprazolam is a chemical analogue of triazolam. It is a triazolobenzodiazepine. It binds to the GABA(a) receptor and modulates the function of the GABA receptor. You can learn more about the GABA(a) receptor here. [url][[http://wiki.tripsit.me/wiki/GABA_Receptors_and_Subunits_Info]][/url]

The LD50 of Alprazolam in rats is 331-2171mg/kg.

= Legal Status =
==USA==
Alprazolam is a schedule IV substance.
==UK==
Under the UK drug misuse classification system benzodiazepines are class C drugs (Schedule 4).
==Ireland==
Alprazolam is a schedule 4 medicine.
==Sweden==
Alprazolam is a prescription drug in List IV under the Narcotic Drugs Act (1968).
==Netherlands==
Alprazolam is a List 2 substance of the Opium Law and is available for prescription.
==Australia==
Alprazolam was orginally a Schedule 4 (prescription only) medication; yet as of February 2014 it has become a Schedule 8 medication.

[[Category:Drugs]]

[[Category:Benzodiazepine]]

[[Category:Depressant]]

Opioid Notes

2014-11-04T17:21:46Z

Roi: /* Morphinones and Morphols */

=== Opium Derivatives ===

== Opium Alkaloids ==
:Thebaine - 6,14 Dimethoxy version of Oxymorphone. Stimulant rather than an analgesic.
:Narceine - Bitter, Crystalline, formerly used as a substitute for Morphine.
:Noscapine - Acts on the Sigma receptor. Non painkilling. Used commonly in Antitussives. Blocks Bradykinine B-2 receptors in Stroke patients.

== Alkaloid Salt Mixtures ==
:Pantopon - Preparation of all alkaloids present in opium without plant matter. Injectable and slightly less potent than Morphine.

== Morphine Family ==
:6-MDDM - 80x Morphine, has a faster onset and less body load then the prior.
:Azidomorphine - 40x Morphine, has a high affinity for μ.
:Hydromorphinol - Derivative of Morphine, yet more potent, with a steeper-dose-response curve and a longer half life. Scripted in Sweden.
:Methyldesorphin - 15x Morphine. Is found in some mixtures of Krokodil.
:MR-2096 - Oxymorphone analogue that is roughly the same potency.
:N-Phenethylnormorphine - 8-14x Morphine.
:RAM-378 - N-Phenethyl analogue of Hydromorphinol. It is probably more potent as a result.

== 3,6 Morphine Diesters ==
:Diacetyldihydromorphine - Occasionally used as an alternative to diamorphine, of which it is faster acting, longer lasting and has less side effects such as euphoria and addiction. However it is equipotent with Morphine.
:Dipropanoylmorphine - Ester of Morphine used to treat severe pain. Rarely used but considered to be safer and less addictive than Morphine. As such carries less side effects, such as euphoria. Slower acting, longer lasting and slightly more potent than Morphine.
:Nicomorphone - 2-3x Morphine and commonly prescribed in German speaking countries.

== Codeine-Dionine Family ==
:Heterocodeine - Reverse isomer of codeine. 6x Morphine, while Codeine is a prodrug, Heterocodeine is a direct agonist.
:Myrophine - Acts as a prodrug to Morphine. Has a slow onset and longer duration, but reduced potency. Does NOT produce addiction or dependence regardless of dose.
:Acetyldihydrocodeine - Used in Germany. Close relative of Thebacon, where only the 6-7 bond is unsaturated. 6-Acetyl derivative of Dihydrocodeine. Metabolizes into Dihydromorphine. Higher lipophilicity than codeine. Would probably be more potent and longer lasting as a result. Higher oral BA than Codeine.

== Morphinones and Morphols ==
:14-Cinnamoyloxycodeinone - 100x Morphine.
:14-Methoxymetopon - 500x Morphine. Can be up to one million times Morphine if injected into the spine.
:14-Phenylpropoxymetopon - 2000x potency of Morphine. When injected into the spine up to one million times Morphine. 14-Methoxymetopon has a ceiling effect on respiratory depression, but the above has been left untested.
:3-Acetyloxymorphone - Acetylated analogue of Oxymorphone.
:7-Spiroindanyloxymorphone - Odd Oxymorphone analogue that is selective at dopamine.
:Acetylmorphone - Acetoxy version of Hydromorphone, has a higher bioavailability as a result.
:Chloroxymorphamine - Derivative of Oxymorphone and irreversible full agonist.
:Methyldihydromorphone - Related to Heterocodieine not Dihydrocodeine. Is 6-9x Morphine.
:Metopon - Methylated Hydromorphone, less potent. More than likely would have more euphoria as a result.
:N-Phenethyl - 14-Ethoxymetopon - 60x Morphine, but produces less constipation. d & u agonist.
:Oxymorphol - 6-Hydrogenated Oxymorphone.
:Pentamorphone - Few times more potent than Fentanyl. Short duration, yet low respiratory depression.
:Semorphone - 2x Morphine. Partial u agonist and has a ceiling effect on both analgesia and respiratory depression.
:Thebacon - Thebaine analogue, that is fairly uninteresting. 6-8x Codeine.

== Hydrazones ==
:Oxymorphazone - Half Oxymorphone, yet higher doses last up to 48 hours.

== Morphians ==
:Butorphanol - Partial agonist-antagonist at μ opioid and competitive antagonist/partial agonist at κ opioid. dysphoria is common at normal dose.
:Drotebanol - Morphinan derivative synthesised from Thebaine with analgesic effects several times more potent than codeine but weaker than morphine. Moderately addictive but limited physical dependance. Under Metabanyl when available as a script.
:Dextromethorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, (very weak) μ, δ & κ opioid agonist, SERT & NET inhibitor, NADPH Oxidase inhibitor. (Race)Methorphan = racemic
:Dextrorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, L-Type voltage-gated calcium channel (LVGCC) blocker, SRI.
:Cyclorphan - Mixed antagonist-agonist with affinity for κ.
:Levophenacylmorphan - 10x potency of Morphine.
:Levofurethylnormorphanol (Ro4-1539) - potent μ opioid agonist 30-60x potency of Levorphanol.
:Levomethorphan (+) - NDMA antagonist, σ1 & σ2 sigma agonist, μ, δ & κ opioid agonist.
:Levorphanol (+) - μ, κ & δ agonist, 4-8x potency of M, long duration, no cross tolerance with morphine.
:Norlevorphanol - Opioid analgesic, uninteresting.
:Phenomorphan - 10x potency of Levorphanol. :└--> N-(2-(2-furyl)ethyl) analogue - 60x Levorphanol :└--> N-(2-(2-thienyl)ethyl) analogue - 45x Levorphanol.
:Proxorphan - Partial κ agonist, lesser partial μ agonist.
:Ro4-1539 (Furethylnorlevorphanol) - 30-60x Morphine. One of the more potent u agonists from the Morphans.

:(Race)Methorphan: L(eft) (+) Levomethorphan >< Dextromethorphan (-) D(exter) :--> l = Opioid >< d = Hallucinogenic opioid.
:└--> Racemic mix of both isomers, embodying their properties.

:Morphinan (Racemorphan): l (+) Levorphanol >< Dextrorphan (-) d --> l = Opioid >< :d = Hallucinogenic opioid.
:└--> Racemic mix of both isomers, embodying their properties.

:(Race)Allorphan: l (+) Levallorphan >< Dextrallorphan (-) d --> l = Opioid antagonist >< d = NMDA antagonist.
:└--> Racemic mix of both isomers, embodying their properties.

:3-Hydroxymorphinan: l (+) Norlevorphanol >< Nordextrorphan (-) d --> l = :Opioid >< d = Nootropic.
└--> Racemic mix of both isomers, embodying their properties.

:Oxilorphan: μ antagonist & weak partial κ agonist.
:Dimemorfan - Sigmaergic drug.
:Xorphanol - Mixed agonist-antagonist produces convulsions at highest dose tested.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors.
:Samidorphan - selective μ antagonist. potential for addiction treatment.

== Benzomorphans ==

:Butinazocine - Benzomorphan opioid that was never marketed.
:Carbazocine - Benzomorphan opioid that was never marketed.
:Etazocine - Partial opioid agonist with mixed agonist-antagonist effects. Low potency.
:Ethylketocyclozocine - Partial opioid agonist with mixed agonist-antagonist effects.
:Ibazocine - Benzomorphan opioid that was never marketed.
:Moxazocine - 10x potency of Morphine, partial/mixed agonist-antagonist.
:Tonazocine - Partial agonist at μ & δ, no adverse effects on breathing.
:Volazocine - Benzomorphan opioid that was never marketed.
:Fluorophen - Radioligand, full μ agonist (6x Morphine) & lower affinity for δ.
:Zenazocine - Partial agonist at μ & δ.
:Eptazocine - Japanese κ agonist & μ antagonist.
:Pentazocine - Mixed agonist-antagonist (-) is the κ agonist side, the (+) displays 10x the affinity for sigma receptors. NO μ agonism.
:Phenazocine - Related to ^ but stronger analgesic, 4x potency of Morphine.
:Cyclazocine - Mixed agonist-antagonist.
:Dezocine - Mixed agonist-antagonist with high κ antagonism. Low dose=euphoria (μ), high dose=dysphoria (κ). Weird structure.
:8-Carboxamidocyclazocine (8-CAC) - κ & μ agonist, long duration.
:Bremazocine - κ agonist related to Pentazocine.
:Metazocine - Analgesic; mixed agonist-antagonist at μ, activity also at κ and sigma.
:Alazocine - σ1 agonist, κ opioid agonist & slight NMDA antagonist.

== 4-Phenylpiperidines ==
:4-Fluoropethidine - In comparison to Pethidine, it is 50% less potent as an analgesic but 50% more potent as a DRI. (4-iodo & 3, 4-dichloro only increase these differences)
:Anileridine - Another banned Pethidine analogue, probably abused. Higher analgesia than Meperidine due to n-aminophenyl group and acts withing 15 mins orally, lasting 2-3 hours.
:Benzethidine - 4-Phenylpiperidine analogue of Pethidine. Probably somewhat more potent and euphoric. Never scripted.
:Carperidine - Fairly normal opioid but unused in medicine.
:Furethidine - 4-Phenylpiperidine analogue of Pethidine. Probably a lot more potent and abuse prone. Never prescribed.
:Morpheridine - Related to Meperidine but 4x the potency and does not cause convulsions.
:Phenoperidine - 20-200x Pethidine. Less hypnotic and than morphine but more emetic (nausea). This can be cured by Haloperidol.
:Piminodine - Similar dose to Morphine, used in 60's and 70's but was banned. It was probably abused widely.

== Prodines ==
:Alphaprodine - 1.5x Morphine.
:Allylprodine - Prodine analogue 23x potency of Morphine.
:Betaprodine - 7.5x Morphine.
:Prosidol - Russian Prodine analogue.

== Ketobemidones ==
:Acetoxyketobemidone - Unschedualed analogue of Ketobemidone.
:Bemidone - Analogue of Pethidine but significantly less potent, however it has NMDA antagonism like Ketobemidone.
:Ketobemidone - μ opioid antagonist & NMDA antagonist. More addictive than Morphine.

== Others ==
:Loperamide - Peripheral opioid so it cannot cross BBB. useful anti-Diarrhoea med. When used in conjuction with Quinine or Omerprazole can cross BBB and opioid effects are seen.
:Picenadol - R isomer (or Levopicenadol) is pure μ agonist while S is antagonist. Racemic is mixed that casues low abuse potential but has low κ activity.

== Amidones ==
:Dipipadone - Lost Ark of the Covenant.
:Phenadoxone - Methadone analogue, similar dose to M, lasts 1-4 hours.
:Levacetylmethadol - Methadone analogue with u agonism and noncompetitive a3b4 NACh antagonisMorphine. Brand name Orlaam, prescribed to those unresponsive to methadone or subutex. Long half life (3 days) and heavier affect.
:Norpipanone - Was not under international control until case reports of addiction arose.
:Isomethadone - Previously used in medicine. μ- δ- agonisMorphine. S-isomer more potent.

==Methadols ==
:Dimepheptanol - Related to Methadone, has two isomers which also have two isomers so 6 possible isomers including racemic.

== Moramides ==
:Palfium (Dextomoramide) - 3x potency of M but shorter acting. High BA & fast acting, oral feels like shooting. Low LD50 & inconsistent potency (one day you may need 5mg, next day 3mg)

== Thiambutens ==
:Thiambutenes - Dimethyl-TAB, Diethyl-TAB, Ethylmethyl-TAB. Used in vetinary medicine in Japan. Banned in virtually all countried due to high abuse potential. Anticholinergic and antihistamine properties!

== Phenalkoxams ==
:Dextropropoxyphene - Low potency opioid not absorbed by CYP2D6. Also is a potent, noncompetitive α3β4 NACh antagonist and a weak SRI.
:Dimenoxadol - Benzillic Acid derivative related to methadone. Banned due to high abuse potential it seems.
:Dioxaphetyl butyrate - Banned opioid similar to methadone. Possibly in use or previously in use as a med under the names Amidalgon & Spasmoxal.

== Ampromides ==
:Diampromide - Banned Analgesic related to PropiraMorphine. Similar potency to Morphine.
:Propiram - Slightly more potent than codeine, 3-6hr duration. mixed μ agonist-antagonist favouring agonisMorphine. affinity for κ & δ, sigma and NMDA. 97% oral BA!

== Others ==
:IC-26 Methadone analogue with similar potency, but unscheduled.
:Lefetamine - Weak opioid on the same scale as codeine but has DRI properties.
:R-4066 - Methadone analogue with 212x the potency, but a much shorter duration. (3 hours)

== Amilidopiperidines ==

:3-Methylfentanyl - 400-6000x potency of Morphine depending on isomer (cis-iso more potent).
:4-Fluorobutyrfentanyl - Short duration.
:Acetylfentanyl - 80x Morphine.
:Alfentanil - 1/4 the potency and 1/3 the duration of fent but 4x quicker onset. The businessman's lunch of opioids.
:Betahydroxythiofentanyl - One of the more favoured fentanyl analogues by addicts, implying euphoria.
:Butyrfentanyl - 20-25x Morphine.
:Carfentanil - 100x potency of fent., 10000x Morphine. Used in spetznaz hostage crisis. 10,000x potency of Morphine. Activity in humans starts at 1μg.
:Lofentanil - More potent and with a longer duration than carfentanil.
:Mirfentanil - Fentanyl analogue with strong selevtivity over μ. Lower doses it antagonises effects caused by lesser opioids but at higher doses is resistant to antagonists, suggesting it has non-opioid mechanisms.
:Ohmefentanyl - 6300x morphine at it's most active isomer. Analogues of this are even stronger with one possessing 30,000x Morphine.
:Parofluorofentanyl - 150-200x morphine. Sold breifly in 1980.
:R-30490 - Analogue of carfentanil. Most selective μ agonist of all fentanyl analogues.
:Remifentanil - Potent ultra short acting fent. analogue. Potency from between 20 and 100ug. Used in medicine as an anaesthetic under Ultiva.
:Sufentanil - 5-10x potency of fentanyl.

== Opipavine Derivatives ==
:7-PET - 300x potency of M, 3-OH derivative is 2200x potency of Morphine. Unscheduled.
:Acetorphine - 8700x potency of Morphine.
:BU-48 - Etorphine derivative. Selective δ agonist and produces only convulsions with slight antidepression.
:Buprenorphin - Subutex.
:Cyprenorphine - Buprenorphine analogue, agonist-antagonist effects but with higher affinity towards κ.
:Dihydroetorphine -1000-12000x potency of M depending on RoA. Less addictive than other opioids and is used in a similar fashion to Subutex in China.
:Etorphine - 1000-3000x potency of Morphine. μ, κ & δ opioid agonist. weak affinity for ORL1 nociceptin/orphanin FQ receptor.

== Indoles ==
:18-Methoxycoronaridine - Ibogaine derivative, selective α3β4 nicotinic antagonist, however no affinity for α4β2, NMDA or seretonin. Retains modest affinity at μ & κ opioid.
:7-Hydroxymitragynine - Alkaloid in KratoMorphine. Some 17x potency of Morphine. 30x potency of Mitragynine.
:Eseroline - Metabolite of the ACh inhibitor physostigmine but potent μ agonist.
:Hodgkinsine - Alkaloid found in Psychotria colorata plants. Has antiviral, antibacterial and antifungal properties. Also μ opioid agonist & NMDA antagonist.
:Ibogaine - Addiction CURE. HT2a agonist, κ opioid agonist, NMDA antagonist.
:Mitragynine - Alkaloid in KratoMorphine. Fairly selective μ agonist but little affinity for δ & κ.
:Noribogaine - Metabolite of Ibogaine. Potent SRI, κ antagonist, weak μ full agonist.
:Voacangine - Precursor to Ibogine used by iboga plant. Displays similar effects towards addiction as Ibogaine.

== Pyrroles ==
:Viminol - Mixed agonist-antagonist, 5.5x Morphine.
:Pyrollidone-Viminol - 318x Morphine.

== Diphenylmethylpiperazines ==
:BW373U86 - Selective δ agonist at 15x stronger affinity. Analgesic and anti-depressant properties along with BDNF release. Produces convulsions at high doses and reverses respiratory depression produced by μ agonisMorphine. Also protects heart muscle cells from death during oxygen deprivation, a result of heart attacks.
:DPI-227 - Highly selective δ agonist with antidepressant effects but produces fewer convulsions than most other dugs in it's family.
:DPI-3290 - Potent δ & μ agonist but produces little respiratory depression.

== Opioid Peptides ==

:Biphalin - Endogenous eptide with high affinity for δ & μ receptors. Potency almost 7x greater than Etorphine and 7000x Morphine. Low side effects; no dependancy caused.
:Casomorphins - Opioids found in Cow's milk.
:DAMGO - Synthetic opioid peptide with high μ selectivity. When administered alongside M for 7 days, M had the same effect at the same dose as the first day. I.e. removes tolerance.
:Deltorphin - High affinity and selectivity, naturally occuring δ opioid agonist.
:Dermorphin - South American Tree frog skin. Natural opioid peptide. High potency (30-40x M) and selectivity to μ but may be less likely to cause tolerance and addiction.
:Dynorphins - Endogenous opioid peptides, primarily k agonists. Useful in the analysis of addiction.
:Leu-enkephalin - Endogeneous opioid petide that acts as a δ & μ agonist with strong selectivity for δ.
:Met-enkephalin - Opioid Growth Factor (OGF), Endogenous opioid peptide. Primary ligand of the δ receptor along with Leu-enkephalin (high potency and selectivity at δ). Low BA & is metabolised rapidly.
:Opiorphin - Endogenous opioid isolated from human saliva.

== Others ==

:3-HO-TCP - PCP analogue. More glutamergic than the PCP analogue.
:3-HO-BCP - Substitutes for both cocaine and morphine at ~5mg (made-up).
:AD-1211 - Structure looks unrelated to /most/ other opioid drugs. Mixed Agonist-antagonist at opioid recepts similar to pentazocine. Little to no developement of tolerance/dependence in animal studies.
:AH-7921 - Selective μ agonist, with 80% potency of Morphine. Distributed as an RC, TRs show that it has very little euphoria, indicating euphoria comes from somewhere else. Perhaps sigma? Other opioids are heavily potentiated by it. Perhaps μ agonism is purely analgesic and high comes from a combination of μ & δ with each multiplying the affect of the other. This indicates ultimate opioid high would be moderately selective δ agonist.
:Azaprocin - Azaprocin - ~10x potency of Morphine. Faster onset and short duration of actin. Discoved in 1963, never been marketed. The derivative subbed on the phenyl ring with a p-nitro group would be more potent by roughly 2.5. (So 25x potency of M) The open ringed 2,6-dimethylpiperazine analouges would also be active.
:BRL-52537 - Highly potent and selective κ agonist. Neuroprotective.
:Bromadol (BDPC) - 500-10,000x potency of Morphine. Similar to PCP analogues & -HO bonds within them.
:C-8813 (Thiobromadol) - 591x potency of Morphine. μ agonist & δ antagonist to reduce repiratory depression. Making the drug safer.
:Ciramadol - Opioid related to PCP, Tramadol & Tapentadol. mixed agonist-antagonist for μ, low abuse potential and ceiling on respiratory depression.
:Enadoline - Highly selective κ agonist. Produces visual distortions, dissociation and of course dysphoria similar to Salvia.
:Herkinorin - Analogue of Salvinorin A but the complete opposite. 100x higher μ affinity and 50x lower κ affinity. Also; "does not promote the recruitment of β-arrestin-2 to the intracellular domain of the μ-opioid receptor, or induce receptor internalization". This means Herkinorin may not produce tolerance or dependance.
:HZ-2 - κ-opioid agonist, same potency as morphine, long duration, high oral BA.
:ICI-199,441 - High potency, highly selective κ agonist with analgesic effects.
:Methopholine - Isoquinilone derivative with same efficacy as Codeine. Could produces corneal opacity. Analogues are more potent with 4'-Nitromethopholine at 20x Codeine.
:MT-45 - 80% of Morphine. mixed agonist-antagonist and mild NMDA antagonist.
:Nortilidine - Equipotency of Morphine. Opioid activity is in (1S,2R) iso, NMDA antagonism is in (1R,2S) iso. Also acts as a DRI.
:O-Desmethyltramadol - Metabolite of Tramadol. Considerably more potent than Tramadol. Both (+) & (-) isomers lose SRI function but (-) retains NRI functionality. RC.
:Salvinorin A - Highly potent κ agonist and even more potent D2 partial agonist. Used in therapy for addiction.
:Salvinorin B ethoxymethyl ether - Semi-synthetic analogue of Salvinorin A. Longer duration @ ~3hrs, active at 50ug & 3000x (!) selectivity over μ & δ.
:Salvinorin B methoxymethyl ether - Similar to ^^ but less selective. 5x potency as Salvinorin A. Deacetylised from Salvinorin A.
:SC-17599 - Selective μ agonist with little or no affinity for δ & κ. Potency in between Pethidine & Morphine.
:RWJ-394674 - Potent and selective δ agonist, however once inside body it is dealkylated to its monodesethyl metabolite RWJ-413216 which is a potent μ agonist with less affinity for δ. δ activity counteracts the respiratory depression the μ causes. Only prominent side effect is sedation (and euphoria!).
:TAN-67 - Potent and selective δ1 agonist. Has analgesic properties & releases dopamine in the brain. Neuro & cardiac protective properties.
:Tapentadol - μ & σ agonist & SNRI. Potency in between Morphine & Tramadol.
:Tifluadom - Benzo derivative but without GABAa agonism. Instead selective κ agonism.
:U-47700 - Overlays betaprodine, 7.5x morphine.
:U-50488 - Highly selective κ agonist with analgesic effects.
:U-69,593 - Potent and selective κ1 agonist. Produces: Antinociception, anti-inflammation, anxiolysis (low doses), respiratory depression & diuresis. Also inhibits periphery oxytocin secretion. Not sure if hallucinogenic.
:W-15 - 5.4x Morphine. RC.
:W-18 - 10,000x potency of M, structure abstract from any other drug. These super potent opioids are used in vetenarian practice for tranquilising elephants.

== Opioid Antagonists and Inverse Agonists ==
(selective δ antagonists may reduce physical addiction without causing w/d if attatched to an opioid).
:Chlornaltrexamine - Irreversible mixed agonist-antagonist at μ opioid. 22x more potent than Morphine.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors.
:Diprenorphine - Strongest opioid antagonist available. 100x potency of Nalorphine. Used to reverse effects of super-potent opioids.
:Levallorphan - μ opioid antagonist, when used with opioids, it potentiates it and removes addiction potential or induces withdrawal in addicts.
:Nalbuphine - Mixed agonist-antagonist as is common with this class, there occurs analgesia with no addictive properties.
:Naloxazone - Irreversible μ opioid receptor antagonist.
:Naloxonazine - Very Potent Irreversible μ opioid antagonist. Dimerizes from Naloxazone under acidic conditions.
:Naltrexone - Competitive antagonist at μ & κ receptors, and to a lesser extent, δ. Modulation of the dopaminergic mesolimbic pathway makes it good for countering alcohol dependance as well as opioid addiction. Blocks the euphoric effects of opioids and is used in rapid detoxification and attenuation of withdrawal. If opioids are used simultaneously, oD may occur.
:Samidorphan - Selective μ antagonist. potential for addiction treatment.

== Uncategorised Opioids ==

:FE 200665 - Is an all D-Amino acid peptide that acts as a restucted K-opioid receptor agnoist. Was dosed at 0.36mg/kg IV. Was compared to 15mg oxycodone. Slightly less than hydrocodone. Caused Hyperalgesic response in a skin pinch test. Also known as CR665.
:SoRI-9409 - Mixed μ agonist & δ antagonist. moderate analgesia without development of tolerance. Anti-addictive effects for all dopaminergic drugs.
:Synthetic Conotoxin - Snail toxin derived painkiller 1000x potency of morphine. Non-addictive.

==RELATED COMPOUNDS==
:Amiphenazole - Treatment for OD. counteracts respiratory depression. If Morphine-N-oxide is taken on this, M's potency will increase.
:Chitosan - Linear polysaccharide that can give Morphine up to 60% BA intranasally. Powdered & the ratio is 1.3g : 6.7g (morphine : chitosan).
:BIMU-8 - Nootropic.

:NMDA antagonists - Inhibit development of tolerance to morphine.
:Tezampanel - Anxiolytic.
:Ibudilast - Nootropic.
:Nuciferine
:Tetrahydropalmatine - Anxiolytic.
:Lofexidine - Anxiolytic.
:d & l Phenylalanine (DLPA) - Increases dopamine and endorphin levels, reducing opioid tolerance and even providing an analgesic effect of it's own.

== CCK Antagonists ==

:Proglumide - Acts as a δ-opioid agonist and non selective CCK antagonist. Enhances analgesia produced by opioids and can prevent or even reverse the development of tolerance.
:Devazepide - No affinity for GABAa, selective CCKa antagonist.
:Lorglumide - Selective CCKa antagonist for treatment of gastrointestinal problems and some forms of cancer as well as opioid interacting properties.

== Nocieceptinergic drugs ==
(ORL-1 ant. & ag.'s)
:J-113,397 - Highly selective ORL-1 antagonist. Prevents development of opioid tolerance, stimulates dopamine release, cognitive enhancer
:SB-612,111 - Selective ORL-1 antagonist but several times ^^
:MCOPPB - Potent, selective ORL-1 agonist with only moderate affinity for μ, even less for δ & κ. Anxiolytic with no inhibition of memory, motor function or sedation.
:NNC 63-0532 - Potent, selective ORL-1 agonist.
:Ro64-6198 - Potent, selective ORL-1 agonist with 100x selectivity over others. In rats produced anxiolytic but no anticonvulsant effects. Impairs short term memory & increases appetite. Reduces analgesic effects of Morphine but does not prevent tolerance. In primates it showed analgesic behaviour without respiratory depression.
:Menabitan - Potent cannabinoid receptor agonist with anti-nociceptive effects.

== Enkephalin Potease Inhibitors ==

:RB-101*** - Inhibits enzymes responsible for breaking down enkephalin (regulates nociceptin). Weak μ & δ affinity and slight σ1. Potentiates opioids, stops withdrawal symptoms, no addiction potential, produces no respiratory depression. Also exerts very potent antidepressant and anxiolytic effects. Not orally active so analogues vv were developed.
:RB-120 - Orally active version of the above.
:RB-3007 - Another Enkeph. PI & Nociceptin antagonist.

Opioid Notes

2014-11-04T17:20:30Z

Roi: /* Benzomorphans */

=== Opium Derivatives ===

== Opium Alkaloids ==
:Thebaine - 6,14 Dimethoxy version of Oxymorphone. Stimulant rather than an analgesic.
:Narceine - Bitter, Crystalline, formerly used as a substitute for Morphine.
:Noscapine - Acts on the Sigma receptor. Non painkilling. Used commonly in Antitussives. Blocks Bradykinine B-2 receptors in Stroke patients.

== Alkaloid Salt Mixtures ==
:Pantopon - Preparation of all alkaloids present in opium without plant matter. Injectable and slightly less potent than Morphine.

== Morphine Family ==
:6-MDDM - 80x Morphine, has a faster onset and less body load then the prior.
:Azidomorphine - 40x Morphine, has a high affinity for μ.
:Hydromorphinol - Derivative of Morphine, yet more potent, with a steeper-dose-response curve and a longer half life. Scripted in Sweden.
:Methyldesorphin - 15x Morphine. Is found in some mixtures of Krokodil.
:MR-2096 - Oxymorphone analogue that is roughly the same potency.
:N-Phenethylnormorphine - 8-14x Morphine.
:RAM-378 - N-Phenethyl analogue of Hydromorphinol. It is probably more potent as a result.

== 3,6 Morphine Diesters ==
:Diacetyldihydromorphine - Occasionally used as an alternative to diamorphine, of which it is faster acting, longer lasting and has less side effects such as euphoria and addiction. However it is equipotent with Morphine.
:Dipropanoylmorphine - Ester of Morphine used to treat severe pain. Rarely used but considered to be safer and less addictive than Morphine. As such carries less side effects, such as euphoria. Slower acting, longer lasting and slightly more potent than Morphine.
:Nicomorphone - 2-3x Morphine and commonly prescribed in German speaking countries.

== Codeine-Dionine Family ==
:Heterocodeine - Reverse isomer of codeine. 6x Morphine, while Codeine is a prodrug, Heterocodeine is a direct agonist.
:Myrophine - Acts as a prodrug to Morphine. Has a slow onset and longer duration, but reduced potency. Does NOT produce addiction or dependence regardless of dose.
:Acetyldihydrocodeine - Used in Germany. Close relative of Thebacon, where only the 6-7 bond is unsaturated. 6-Acetyl derivative of Dihydrocodeine. Metabolizes into Dihydromorphine. Higher lipophilicity than codeine. Would probably be more potent and longer lasting as a result. Higher oral BA than Codeine.

== Morphinones and Morphols ==
:14-Cinnamoyloxycodeinone - 100x Morphine.
:14-Methoxymetopon - 500x Morphine. Can be up to one million times Morphine if injected into the spine.
:14-Phenylpropoxymetopon - 2000x potency of Morphine. When injected into the spine up to one million times Morphine. 14-Methoxymetopon has a ceiling effect on respiratory depression, but the above has been left untested.
:3-Acetyloxymorphone - Acetylated analogue of Oxymorphone.
:7-Spiroindanyloxymorphone - Odd Oxymorphone analogue that is selective at dopamine.
:Acetylmorphone - Acetoxy version of Hydromorphone, has a higher bioavailability as a result.
:Chloroxymorphamine - Derivative of Oxymorphone and irreversible full agonist.
:Methyldihydromorphone - Related to Heterocodieine not dihydrocodeine. Is 6-9x Morphine.
:Metopon - Methylated Hydromorphone, less potent. More than likely would have more euphoria as a result.
:N-Phenethyl - 14-Ethoxymetopon - 60x Morphine, but produces less constipation. d & u agonist.
:Oxymorphol - 6-Hydrogenated Oxymorphone.
:Pentamorphone - Few times more potent than Fentanyl. Short duration, yet low respiratory depression.
:Semorphone - 2x Morphine. Partial u agonist and has a ceiling effect on both analgesia and respiratory depression.
:Thebacon - Thebaine analogue, that is fairly uninteresting. 6-8x Codeine.

== Hydrazones ==
:Oxymorphazone - Half Oxymorphone, yet higher doses last up to 48 hours.

== Morphians ==
:Butorphanol - Partial agonist-antagonist at μ opioid and competitive antagonist/partial agonist at κ opioid. dysphoria is common at normal dose.
:Drotebanol - Morphinan derivative synthesised from Thebaine with analgesic effects several times more potent than codeine but weaker than morphine. Moderately addictive but limited physical dependance. Under Metabanyl when available as a script.
:Dextromethorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, (very weak) μ, δ & κ opioid agonist, SERT & NET inhibitor, NADPH Oxidase inhibitor. (Race)Methorphan = racemic
:Dextrorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, L-Type voltage-gated calcium channel (LVGCC) blocker, SRI.
:Cyclorphan - Mixed antagonist-agonist with affinity for κ.
:Levophenacylmorphan - 10x potency of Morphine.
:Levofurethylnormorphanol (Ro4-1539) - potent μ opioid agonist 30-60x potency of Levorphanol.
:Levomethorphan (+) - NDMA antagonist, σ1 & σ2 sigma agonist, μ, δ & κ opioid agonist.
:Levorphanol (+) - μ, κ & δ agonist, 4-8x potency of M, long duration, no cross tolerance with morphine.
:Norlevorphanol - Opioid analgesic, uninteresting.
:Phenomorphan - 10x potency of Levorphanol. :└--> N-(2-(2-furyl)ethyl) analogue - 60x Levorphanol :└--> N-(2-(2-thienyl)ethyl) analogue - 45x Levorphanol.
:Proxorphan - Partial κ agonist, lesser partial μ agonist.
:Ro4-1539 (Furethylnorlevorphanol) - 30-60x Morphine. One of the more potent u agonists from the Morphans.

:(Race)Methorphan: L(eft) (+) Levomethorphan >< Dextromethorphan (-) D(exter) :--> l = Opioid >< d = Hallucinogenic opioid.
:└--> Racemic mix of both isomers, embodying their properties.

:Morphinan (Racemorphan): l (+) Levorphanol >< Dextrorphan (-) d --> l = Opioid >< :d = Hallucinogenic opioid.
:└--> Racemic mix of both isomers, embodying their properties.

:(Race)Allorphan: l (+) Levallorphan >< Dextrallorphan (-) d --> l = Opioid antagonist >< d = NMDA antagonist.
:└--> Racemic mix of both isomers, embodying their properties.

:3-Hydroxymorphinan: l (+) Norlevorphanol >< Nordextrorphan (-) d --> l = :Opioid >< d = Nootropic.
└--> Racemic mix of both isomers, embodying their properties.

:Oxilorphan: μ antagonist & weak partial κ agonist.
:Dimemorfan - Sigmaergic drug.
:Xorphanol - Mixed agonist-antagonist produces convulsions at highest dose tested.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors.
:Samidorphan - selective μ antagonist. potential for addiction treatment.

== Benzomorphans ==

:Butinazocine - Benzomorphan opioid that was never marketed.
:Carbazocine - Benzomorphan opioid that was never marketed.
:Etazocine - Partial opioid agonist with mixed agonist-antagonist effects. Low potency.
:Ethylketocyclozocine - Partial opioid agonist with mixed agonist-antagonist effects.
:Ibazocine - Benzomorphan opioid that was never marketed.
:Moxazocine - 10x potency of Morphine, partial/mixed agonist-antagonist.
:Tonazocine - Partial agonist at μ & δ, no adverse effects on breathing.
:Volazocine - Benzomorphan opioid that was never marketed.
:Fluorophen - Radioligand, full μ agonist (6x Morphine) & lower affinity for δ.
:Zenazocine - Partial agonist at μ & δ.
:Eptazocine - Japanese κ agonist & μ antagonist.
:Pentazocine - Mixed agonist-antagonist (-) is the κ agonist side, the (+) displays 10x the affinity for sigma receptors. NO μ agonism.
:Phenazocine - Related to ^ but stronger analgesic, 4x potency of Morphine.
:Cyclazocine - Mixed agonist-antagonist.
:Dezocine - Mixed agonist-antagonist with high κ antagonism. Low dose=euphoria (μ), high dose=dysphoria (κ). Weird structure.
:8-Carboxamidocyclazocine (8-CAC) - κ & μ agonist, long duration.
:Bremazocine - κ agonist related to Pentazocine.
:Metazocine - Analgesic; mixed agonist-antagonist at μ, activity also at κ and sigma.
:Alazocine - σ1 agonist, κ opioid agonist & slight NMDA antagonist.

== 4-Phenylpiperidines ==
:4-Fluoropethidine - In comparison to Pethidine, it is 50% less potent as an analgesic but 50% more potent as a DRI. (4-iodo & 3, 4-dichloro only increase these differences)
:Anileridine - Another banned Pethidine analogue, probably abused. Higher analgesia than Meperidine due to n-aminophenyl group and acts withing 15 mins orally, lasting 2-3 hours.
:Benzethidine - 4-Phenylpiperidine analogue of Pethidine. Probably somewhat more potent and euphoric. Never scripted.
:Carperidine - Fairly normal opioid but unused in medicine.
:Furethidine - 4-Phenylpiperidine analogue of Pethidine. Probably a lot more potent and abuse prone. Never prescribed.
:Morpheridine - Related to Meperidine but 4x the potency and does not cause convulsions.
:Phenoperidine - 20-200x Pethidine. Less hypnotic and than morphine but more emetic (nausea). This can be cured by Haloperidol.
:Piminodine - Similar dose to Morphine, used in 60's and 70's but was banned. It was probably abused widely.

== Prodines ==
:Alphaprodine - 1.5x Morphine.
:Allylprodine - Prodine analogue 23x potency of Morphine.
:Betaprodine - 7.5x Morphine.
:Prosidol - Russian Prodine analogue.

== Ketobemidones ==
:Acetoxyketobemidone - Unschedualed analogue of Ketobemidone.
:Bemidone - Analogue of Pethidine but significantly less potent, however it has NMDA antagonism like Ketobemidone.
:Ketobemidone - μ opioid antagonist & NMDA antagonist. More addictive than Morphine.

== Others ==
:Loperamide - Peripheral opioid so it cannot cross BBB. useful anti-Diarrhoea med. When used in conjuction with Quinine or Omerprazole can cross BBB and opioid effects are seen.
:Picenadol - R isomer (or Levopicenadol) is pure μ agonist while S is antagonist. Racemic is mixed that casues low abuse potential but has low κ activity.

== Amidones ==
:Dipipadone - Lost Ark of the Covenant.
:Phenadoxone - Methadone analogue, similar dose to M, lasts 1-4 hours.
:Levacetylmethadol - Methadone analogue with u agonism and noncompetitive a3b4 NACh antagonisMorphine. Brand name Orlaam, prescribed to those unresponsive to methadone or subutex. Long half life (3 days) and heavier affect.
:Norpipanone - Was not under international control until case reports of addiction arose.
:Isomethadone - Previously used in medicine. μ- δ- agonisMorphine. S-isomer more potent.

==Methadols ==
:Dimepheptanol - Related to Methadone, has two isomers which also have two isomers so 6 possible isomers including racemic.

== Moramides ==
:Palfium (Dextomoramide) - 3x potency of M but shorter acting. High BA & fast acting, oral feels like shooting. Low LD50 & inconsistent potency (one day you may need 5mg, next day 3mg)

== Thiambutens ==
:Thiambutenes - Dimethyl-TAB, Diethyl-TAB, Ethylmethyl-TAB. Used in vetinary medicine in Japan. Banned in virtually all countried due to high abuse potential. Anticholinergic and antihistamine properties!

== Phenalkoxams ==
:Dextropropoxyphene - Low potency opioid not absorbed by CYP2D6. Also is a potent, noncompetitive α3β4 NACh antagonist and a weak SRI.
:Dimenoxadol - Benzillic Acid derivative related to methadone. Banned due to high abuse potential it seems.
:Dioxaphetyl butyrate - Banned opioid similar to methadone. Possibly in use or previously in use as a med under the names Amidalgon & Spasmoxal.

== Ampromides ==
:Diampromide - Banned Analgesic related to PropiraMorphine. Similar potency to Morphine.
:Propiram - Slightly more potent than codeine, 3-6hr duration. mixed μ agonist-antagonist favouring agonisMorphine. affinity for κ & δ, sigma and NMDA. 97% oral BA!

== Others ==
:IC-26 Methadone analogue with similar potency, but unscheduled.
:Lefetamine - Weak opioid on the same scale as codeine but has DRI properties.
:R-4066 - Methadone analogue with 212x the potency, but a much shorter duration. (3 hours)

== Amilidopiperidines ==

:3-Methylfentanyl - 400-6000x potency of Morphine depending on isomer (cis-iso more potent).
:4-Fluorobutyrfentanyl - Short duration.
:Acetylfentanyl - 80x Morphine.
:Alfentanil - 1/4 the potency and 1/3 the duration of fent but 4x quicker onset. The businessman's lunch of opioids.
:Betahydroxythiofentanyl - One of the more favoured fentanyl analogues by addicts, implying euphoria.
:Butyrfentanyl - 20-25x Morphine.
:Carfentanil - 100x potency of fent., 10000x Morphine. Used in spetznaz hostage crisis. 10,000x potency of Morphine. Activity in humans starts at 1μg.
:Lofentanil - More potent and with a longer duration than carfentanil.
:Mirfentanil - Fentanyl analogue with strong selevtivity over μ. Lower doses it antagonises effects caused by lesser opioids but at higher doses is resistant to antagonists, suggesting it has non-opioid mechanisms.
:Ohmefentanyl - 6300x morphine at it's most active isomer. Analogues of this are even stronger with one possessing 30,000x Morphine.
:Parofluorofentanyl - 150-200x morphine. Sold breifly in 1980.
:R-30490 - Analogue of carfentanil. Most selective μ agonist of all fentanyl analogues.
:Remifentanil - Potent ultra short acting fent. analogue. Potency from between 20 and 100ug. Used in medicine as an anaesthetic under Ultiva.
:Sufentanil - 5-10x potency of fentanyl.

== Opipavine Derivatives ==
:7-PET - 300x potency of M, 3-OH derivative is 2200x potency of Morphine. Unscheduled.
:Acetorphine - 8700x potency of Morphine.
:BU-48 - Etorphine derivative. Selective δ agonist and produces only convulsions with slight antidepression.
:Buprenorphin - Subutex.
:Cyprenorphine - Buprenorphine analogue, agonist-antagonist effects but with higher affinity towards κ.
:Dihydroetorphine -1000-12000x potency of M depending on RoA. Less addictive than other opioids and is used in a similar fashion to Subutex in China.
:Etorphine - 1000-3000x potency of Morphine. μ, κ & δ opioid agonist. weak affinity for ORL1 nociceptin/orphanin FQ receptor.

== Indoles ==
:18-Methoxycoronaridine - Ibogaine derivative, selective α3β4 nicotinic antagonist, however no affinity for α4β2, NMDA or seretonin. Retains modest affinity at μ & κ opioid.
:7-Hydroxymitragynine - Alkaloid in KratoMorphine. Some 17x potency of Morphine. 30x potency of Mitragynine.
:Eseroline - Metabolite of the ACh inhibitor physostigmine but potent μ agonist.
:Hodgkinsine - Alkaloid found in Psychotria colorata plants. Has antiviral, antibacterial and antifungal properties. Also μ opioid agonist & NMDA antagonist.
:Ibogaine - Addiction CURE. HT2a agonist, κ opioid agonist, NMDA antagonist.
:Mitragynine - Alkaloid in KratoMorphine. Fairly selective μ agonist but little affinity for δ & κ.
:Noribogaine - Metabolite of Ibogaine. Potent SRI, κ antagonist, weak μ full agonist.
:Voacangine - Precursor to Ibogine used by iboga plant. Displays similar effects towards addiction as Ibogaine.

== Pyrroles ==
:Viminol - Mixed agonist-antagonist, 5.5x Morphine.
:Pyrollidone-Viminol - 318x Morphine.

== Diphenylmethylpiperazines ==
:BW373U86 - Selective δ agonist at 15x stronger affinity. Analgesic and anti-depressant properties along with BDNF release. Produces convulsions at high doses and reverses respiratory depression produced by μ agonisMorphine. Also protects heart muscle cells from death during oxygen deprivation, a result of heart attacks.
:DPI-227 - Highly selective δ agonist with antidepressant effects but produces fewer convulsions than most other dugs in it's family.
:DPI-3290 - Potent δ & μ agonist but produces little respiratory depression.

== Opioid Peptides ==

:Biphalin - Endogenous eptide with high affinity for δ & μ receptors. Potency almost 7x greater than Etorphine and 7000x Morphine. Low side effects; no dependancy caused.
:Casomorphins - Opioids found in Cow's milk.
:DAMGO - Synthetic opioid peptide with high μ selectivity. When administered alongside M for 7 days, M had the same effect at the same dose as the first day. I.e. removes tolerance.
:Deltorphin - High affinity and selectivity, naturally occuring δ opioid agonist.
:Dermorphin - South American Tree frog skin. Natural opioid peptide. High potency (30-40x M) and selectivity to μ but may be less likely to cause tolerance and addiction.
:Dynorphins - Endogenous opioid peptides, primarily k agonists. Useful in the analysis of addiction.
:Leu-enkephalin - Endogeneous opioid petide that acts as a δ & μ agonist with strong selectivity for δ.
:Met-enkephalin - Opioid Growth Factor (OGF), Endogenous opioid peptide. Primary ligand of the δ receptor along with Leu-enkephalin (high potency and selectivity at δ). Low BA & is metabolised rapidly.
:Opiorphin - Endogenous opioid isolated from human saliva.

== Others ==

:3-HO-TCP - PCP analogue. More glutamergic than the PCP analogue.
:3-HO-BCP - Substitutes for both cocaine and morphine at ~5mg (made-up).
:AD-1211 - Structure looks unrelated to /most/ other opioid drugs. Mixed Agonist-antagonist at opioid recepts similar to pentazocine. Little to no developement of tolerance/dependence in animal studies.
:AH-7921 - Selective μ agonist, with 80% potency of Morphine. Distributed as an RC, TRs show that it has very little euphoria, indicating euphoria comes from somewhere else. Perhaps sigma? Other opioids are heavily potentiated by it. Perhaps μ agonism is purely analgesic and high comes from a combination of μ & δ with each multiplying the affect of the other. This indicates ultimate opioid high would be moderately selective δ agonist.
:Azaprocin - Azaprocin - ~10x potency of Morphine. Faster onset and short duration of actin. Discoved in 1963, never been marketed. The derivative subbed on the phenyl ring with a p-nitro group would be more potent by roughly 2.5. (So 25x potency of M) The open ringed 2,6-dimethylpiperazine analouges would also be active.
:BRL-52537 - Highly potent and selective κ agonist. Neuroprotective.
:Bromadol (BDPC) - 500-10,000x potency of Morphine. Similar to PCP analogues & -HO bonds within them.
:C-8813 (Thiobromadol) - 591x potency of Morphine. μ agonist & δ antagonist to reduce repiratory depression. Making the drug safer.
:Ciramadol - Opioid related to PCP, Tramadol & Tapentadol. mixed agonist-antagonist for μ, low abuse potential and ceiling on respiratory depression.
:Enadoline - Highly selective κ agonist. Produces visual distortions, dissociation and of course dysphoria similar to Salvia.
:Herkinorin - Analogue of Salvinorin A but the complete opposite. 100x higher μ affinity and 50x lower κ affinity. Also; "does not promote the recruitment of β-arrestin-2 to the intracellular domain of the μ-opioid receptor, or induce receptor internalization". This means Herkinorin may not produce tolerance or dependance.
:HZ-2 - κ-opioid agonist, same potency as morphine, long duration, high oral BA.
:ICI-199,441 - High potency, highly selective κ agonist with analgesic effects.
:Methopholine - Isoquinilone derivative with same efficacy as Codeine. Could produces corneal opacity. Analogues are more potent with 4'-Nitromethopholine at 20x Codeine.
:MT-45 - 80% of Morphine. mixed agonist-antagonist and mild NMDA antagonist.
:Nortilidine - Equipotency of Morphine. Opioid activity is in (1S,2R) iso, NMDA antagonism is in (1R,2S) iso. Also acts as a DRI.
:O-Desmethyltramadol - Metabolite of Tramadol. Considerably more potent than Tramadol. Both (+) & (-) isomers lose SRI function but (-) retains NRI functionality. RC.
:Salvinorin A - Highly potent κ agonist and even more potent D2 partial agonist. Used in therapy for addiction.
:Salvinorin B ethoxymethyl ether - Semi-synthetic analogue of Salvinorin A. Longer duration @ ~3hrs, active at 50ug & 3000x (!) selectivity over μ & δ.
:Salvinorin B methoxymethyl ether - Similar to ^^ but less selective. 5x potency as Salvinorin A. Deacetylised from Salvinorin A.
:SC-17599 - Selective μ agonist with little or no affinity for δ & κ. Potency in between Pethidine & Morphine.
:RWJ-394674 - Potent and selective δ agonist, however once inside body it is dealkylated to its monodesethyl metabolite RWJ-413216 which is a potent μ agonist with less affinity for δ. δ activity counteracts the respiratory depression the μ causes. Only prominent side effect is sedation (and euphoria!).
:TAN-67 - Potent and selective δ1 agonist. Has analgesic properties & releases dopamine in the brain. Neuro & cardiac protective properties.
:Tapentadol - μ & σ agonist & SNRI. Potency in between Morphine & Tramadol.
:Tifluadom - Benzo derivative but without GABAa agonism. Instead selective κ agonism.
:U-47700 - Overlays betaprodine, 7.5x morphine.
:U-50488 - Highly selective κ agonist with analgesic effects.
:U-69,593 - Potent and selective κ1 agonist. Produces: Antinociception, anti-inflammation, anxiolysis (low doses), respiratory depression & diuresis. Also inhibits periphery oxytocin secretion. Not sure if hallucinogenic.
:W-15 - 5.4x Morphine. RC.
:W-18 - 10,000x potency of M, structure abstract from any other drug. These super potent opioids are used in vetenarian practice for tranquilising elephants.

== Opioid Antagonists and Inverse Agonists ==
(selective δ antagonists may reduce physical addiction without causing w/d if attatched to an opioid).
:Chlornaltrexamine - Irreversible mixed agonist-antagonist at μ opioid. 22x more potent than Morphine.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors.
:Diprenorphine - Strongest opioid antagonist available. 100x potency of Nalorphine. Used to reverse effects of super-potent opioids.
:Levallorphan - μ opioid antagonist, when used with opioids, it potentiates it and removes addiction potential or induces withdrawal in addicts.
:Nalbuphine - Mixed agonist-antagonist as is common with this class, there occurs analgesia with no addictive properties.
:Naloxazone - Irreversible μ opioid receptor antagonist.
:Naloxonazine - Very Potent Irreversible μ opioid antagonist. Dimerizes from Naloxazone under acidic conditions.
:Naltrexone - Competitive antagonist at μ & κ receptors, and to a lesser extent, δ. Modulation of the dopaminergic mesolimbic pathway makes it good for countering alcohol dependance as well as opioid addiction. Blocks the euphoric effects of opioids and is used in rapid detoxification and attenuation of withdrawal. If opioids are used simultaneously, oD may occur.
:Samidorphan - Selective μ antagonist. potential for addiction treatment.

== Uncategorised Opioids ==

:FE 200665 - Is an all D-Amino acid peptide that acts as a restucted K-opioid receptor agnoist. Was dosed at 0.36mg/kg IV. Was compared to 15mg oxycodone. Slightly less than hydrocodone. Caused Hyperalgesic response in a skin pinch test. Also known as CR665.
:SoRI-9409 - Mixed μ agonist & δ antagonist. moderate analgesia without development of tolerance. Anti-addictive effects for all dopaminergic drugs.
:Synthetic Conotoxin - Snail toxin derived painkiller 1000x potency of morphine. Non-addictive.

==RELATED COMPOUNDS==
:Amiphenazole - Treatment for OD. counteracts respiratory depression. If Morphine-N-oxide is taken on this, M's potency will increase.
:Chitosan - Linear polysaccharide that can give Morphine up to 60% BA intranasally. Powdered & the ratio is 1.3g : 6.7g (morphine : chitosan).
:BIMU-8 - Nootropic.

:NMDA antagonists - Inhibit development of tolerance to morphine.
:Tezampanel - Anxiolytic.
:Ibudilast - Nootropic.
:Nuciferine
:Tetrahydropalmatine - Anxiolytic.
:Lofexidine - Anxiolytic.
:d & l Phenylalanine (DLPA) - Increases dopamine and endorphin levels, reducing opioid tolerance and even providing an analgesic effect of it's own.

== CCK Antagonists ==

:Proglumide - Acts as a δ-opioid agonist and non selective CCK antagonist. Enhances analgesia produced by opioids and can prevent or even reverse the development of tolerance.
:Devazepide - No affinity for GABAa, selective CCKa antagonist.
:Lorglumide - Selective CCKa antagonist for treatment of gastrointestinal problems and some forms of cancer as well as opioid interacting properties.

== Nocieceptinergic drugs ==
(ORL-1 ant. & ag.'s)
:J-113,397 - Highly selective ORL-1 antagonist. Prevents development of opioid tolerance, stimulates dopamine release, cognitive enhancer
:SB-612,111 - Selective ORL-1 antagonist but several times ^^
:MCOPPB - Potent, selective ORL-1 agonist with only moderate affinity for μ, even less for δ & κ. Anxiolytic with no inhibition of memory, motor function or sedation.
:NNC 63-0532 - Potent, selective ORL-1 agonist.
:Ro64-6198 - Potent, selective ORL-1 agonist with 100x selectivity over others. In rats produced anxiolytic but no anticonvulsant effects. Impairs short term memory & increases appetite. Reduces analgesic effects of Morphine but does not prevent tolerance. In primates it showed analgesic behaviour without respiratory depression.
:Menabitan - Potent cannabinoid receptor agonist with anti-nociceptive effects.

== Enkephalin Potease Inhibitors ==

:RB-101*** - Inhibits enzymes responsible for breaking down enkephalin (regulates nociceptin). Weak μ & δ affinity and slight σ1. Potentiates opioids, stops withdrawal symptoms, no addiction potential, produces no respiratory depression. Also exerts very potent antidepressant and anxiolytic effects. Not orally active so analogues vv were developed.
:RB-120 - Orally active version of the above.
:RB-3007 - Another Enkeph. PI & Nociceptin antagonist.

Opioid Notes

2014-11-04T17:19:16Z

Roi: /* Others */

=== Opium Derivatives ===

== Opium Alkaloids ==
:Thebaine - 6,14 Dimethoxy version of Oxymorphone. Stimulant rather than an analgesic.
:Narceine - Bitter, Crystalline, formerly used as a substitute for Morphine.
:Noscapine - Acts on the Sigma receptor. Non painkilling. Used commonly in Antitussives. Blocks Bradykinine B-2 receptors in Stroke patients.

== Alkaloid Salt Mixtures ==
:Pantopon - Preparation of all alkaloids present in opium without plant matter. Injectable and slightly less potent than Morphine.

== Morphine Family ==
:6-MDDM - 80x Morphine, has a faster onset and less body load then the prior.
:Azidomorphine - 40x Morphine, has a high affinity for μ.
:Hydromorphinol - Derivative of Morphine, yet more potent, with a steeper-dose-response curve and a longer half life. Scripted in Sweden.
:Methyldesorphin - 15x Morphine. Is found in some mixtures of Krokodil.
:MR-2096 - Oxymorphone analogue that is roughly the same potency.
:N-Phenethylnormorphine - 8-14x Morphine.
:RAM-378 - N-Phenethyl analogue of Hydromorphinol. It is probably more potent as a result.

== 3,6 Morphine Diesters ==
:Diacetyldihydromorphine - Occasionally used as an alternative to diamorphine, of which it is faster acting, longer lasting and has less side effects such as euphoria and addiction. However it is equipotent with Morphine.
:Dipropanoylmorphine - Ester of Morphine used to treat severe pain. Rarely used but considered to be safer and less addictive than Morphine. As such carries less side effects, such as euphoria. Slower acting, longer lasting and slightly more potent than Morphine.
:Nicomorphone - 2-3x Morphine and commonly prescribed in German speaking countries.

== Codeine-Dionine Family ==
:Heterocodeine - Reverse isomer of codeine. 6x Morphine, while Codeine is a prodrug, Heterocodeine is a direct agonist.
:Myrophine - Acts as a prodrug to Morphine. Has a slow onset and longer duration, but reduced potency. Does NOT produce addiction or dependence regardless of dose.
:Acetyldihydrocodeine - Used in Germany. Close relative of Thebacon, where only the 6-7 bond is unsaturated. 6-Acetyl derivative of Dihydrocodeine. Metabolizes into Dihydromorphine. Higher lipophilicity than codeine. Would probably be more potent and longer lasting as a result. Higher oral BA than Codeine.

== Morphinones and Morphols ==
:14-Cinnamoyloxycodeinone - 100x Morphine.
:14-Methoxymetopon - 500x Morphine. Can be up to one million times Morphine if injected into the spine.
:14-Phenylpropoxymetopon - 2000x potency of Morphine. When injected into the spine up to one million times Morphine. 14-Methoxymetopon has a ceiling effect on respiratory depression, but the above has been left untested.
:3-Acetyloxymorphone - Acetylated analogue of Oxymorphone.
:7-Spiroindanyloxymorphone - Odd Oxymorphone analogue that is selective at dopamine.
:Acetylmorphone - Acetoxy version of Hydromorphone, has a higher bioavailability as a result.
:Chloroxymorphamine - Derivative of Oxymorphone and irreversible full agonist.
:Methyldihydromorphone - Related to Heterocodieine not dihydrocodeine. Is 6-9x Morphine.
:Metopon - Methylated Hydromorphone, less potent. More than likely would have more euphoria as a result.
:N-Phenethyl - 14-Ethoxymetopon - 60x Morphine, but produces less constipation. d & u agonist.
:Oxymorphol - 6-Hydrogenated Oxymorphone.
:Pentamorphone - Few times more potent than Fentanyl. Short duration, yet low respiratory depression.
:Semorphone - 2x Morphine. Partial u agonist and has a ceiling effect on both analgesia and respiratory depression.
:Thebacon - Thebaine analogue, that is fairly uninteresting. 6-8x Codeine.

== Hydrazones ==
:Oxymorphazone - Half Oxymorphone, yet higher doses last up to 48 hours.

== Morphians ==
:Butorphanol - Partial agonist-antagonist at μ opioid and competitive antagonist/partial agonist at κ opioid. dysphoria is common at normal dose.
:Drotebanol - Morphinan derivative synthesised from Thebaine with analgesic effects several times more potent than codeine but weaker than morphine. Moderately addictive but limited physical dependance. Under Metabanyl when available as a script.
:Dextromethorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, (very weak) μ, δ & κ opioid agonist, SERT & NET inhibitor, NADPH Oxidase inhibitor. (Race)Methorphan = racemic
:Dextrorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, L-Type voltage-gated calcium channel (LVGCC) blocker, SRI.
:Cyclorphan - Mixed antagonist-agonist with affinity for κ.
:Levophenacylmorphan - 10x potency of Morphine.
:Levofurethylnormorphanol (Ro4-1539) - potent μ opioid agonist 30-60x potency of Levorphanol.
:Levomethorphan (+) - NDMA antagonist, σ1 & σ2 sigma agonist, μ, δ & κ opioid agonist.
:Levorphanol (+) - μ, κ & δ agonist, 4-8x potency of M, long duration, no cross tolerance with morphine.
:Norlevorphanol - Opioid analgesic, uninteresting.
:Phenomorphan - 10x potency of Levorphanol. :└--> N-(2-(2-furyl)ethyl) analogue - 60x Levorphanol :└--> N-(2-(2-thienyl)ethyl) analogue - 45x Levorphanol.
:Proxorphan - Partial κ agonist, lesser partial μ agonist.
:Ro4-1539 (Furethylnorlevorphanol) - 30-60x Morphine. One of the more potent u agonists from the Morphans.

:(Race)Methorphan: L(eft) (+) Levomethorphan >< Dextromethorphan (-) D(exter) :--> l = Opioid >< d = Hallucinogenic opioid.
:└--> Racemic mix of both isomers, embodying their properties.

:Morphinan (Racemorphan): l (+) Levorphanol >< Dextrorphan (-) d --> l = Opioid >< :d = Hallucinogenic opioid.
:└--> Racemic mix of both isomers, embodying their properties.

:(Race)Allorphan: l (+) Levallorphan >< Dextrallorphan (-) d --> l = Opioid antagonist >< d = NMDA antagonist.
:└--> Racemic mix of both isomers, embodying their properties.

:3-Hydroxymorphinan: l (+) Norlevorphanol >< Nordextrorphan (-) d --> l = :Opioid >< d = Nootropic.
└--> Racemic mix of both isomers, embodying their properties.

:Oxilorphan: μ antagonist & weak partial κ agonist.
:Dimemorfan - Sigmaergic drug.
:Xorphanol - Mixed agonist-antagonist produces convulsions at highest dose tested.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors.
:Samidorphan - selective μ antagonist. potential for addiction treatment.

== Benzomorphans ==

:Butinazocine - Benzomorphan opioid that was never marketed.
:Carbazocine - Benzomorphan opioid that was never marketed.
:Etazocine - Partial opioid agonist with mixed agonist-antagonist effects. low potency.
:Ethylketocyclozocine - Partial opioid agonist with mixed agonist-antagonist effects.
:Ibazocine - Benzomorphan opioid that was never marketed.
:Moxazocine - 10x potency of Morphine, partial/mixed agonist-antagonist.
:Tonazocine - Partial agonist at μ & δ, no adverse effects on breathing.
:Volazocine - Benzomorphan opioid that was never marketed.
:Fluorophen - Radioligand, full μ agonist (6x M) & lower affinity for δ.
:Zenazocine - Partial agonist at μ & δ.
:Eptazocine - Japanese κ agonist & μ antagonist.
:Pentazocine - Mixed agonist-antagonist (-) is the κ agonist side, the (+) displays 10x the affinity for sigma receptors. NO μ agonism.
:Phenazocine - Related to ^ but stronger analgesic, 4x potency of Morphine.
:Cyclazocine - Mixed agonist-antagonist.
:Dezocine - Mixed agonist-antagonist with high κ antagonisMorphine. Low dose=euphoria (μ) High dose=dysphoria (κ). Weird structure.
:8-Carboxamidocyclazocine (8-CAC) - κ & μ agonist, long duration.
:Bremazocine - κ agonist related to Pentazocine.
:Metazocine - Analgesic; mixed agonist-antagonist at μ, activity also at κ and sigma.
:Alazocine - σ1 agonist, κ opioid agonist & slight NMDA antagonist.

== 4-Phenylpiperidines ==
:4-Fluoropethidine - In comparison to Pethidine, it is 50% less potent as an analgesic but 50% more potent as a DRI. (4-iodo & 3, 4-dichloro only increase these differences)
:Anileridine - Another banned Pethidine analogue, probably abused. Higher analgesia than Meperidine due to n-aminophenyl group and acts withing 15 mins orally, lasting 2-3 hours.
:Benzethidine - 4-Phenylpiperidine analogue of Pethidine. Probably somewhat more potent and euphoric. Never scripted.
:Carperidine - Fairly normal opioid but unused in medicine.
:Furethidine - 4-Phenylpiperidine analogue of Pethidine. Probably a lot more potent and abuse prone. Never prescribed.
:Morpheridine - Related to Meperidine but 4x the potency and does not cause convulsions.
:Phenoperidine - 20-200x Pethidine. Less hypnotic and than morphine but more emetic (nausea). This can be cured by Haloperidol.
:Piminodine - Similar dose to Morphine, used in 60's and 70's but was banned. It was probably abused widely.

== Prodines ==
:Alphaprodine - 1.5x Morphine.
:Allylprodine - Prodine analogue 23x potency of Morphine.
:Betaprodine - 7.5x Morphine.
:Prosidol - Russian Prodine analogue.

== Ketobemidones ==
:Acetoxyketobemidone - Unschedualed analogue of Ketobemidone.
:Bemidone - Analogue of Pethidine but significantly less potent, however it has NMDA antagonism like Ketobemidone.
:Ketobemidone - μ opioid antagonist & NMDA antagonist. More addictive than Morphine.

== Others ==
:Loperamide - Peripheral opioid so it cannot cross BBB. useful anti-Diarrhoea med. When used in conjuction with Quinine or Omerprazole can cross BBB and opioid effects are seen.
:Picenadol - R isomer (or Levopicenadol) is pure μ agonist while S is antagonist. Racemic is mixed that casues low abuse potential but has low κ activity.

== Amidones ==
:Dipipadone - Lost Ark of the Covenant.
:Phenadoxone - Methadone analogue, similar dose to M, lasts 1-4 hours.
:Levacetylmethadol - Methadone analogue with u agonism and noncompetitive a3b4 NACh antagonisMorphine. Brand name Orlaam, prescribed to those unresponsive to methadone or subutex. Long half life (3 days) and heavier affect.
:Norpipanone - Was not under international control until case reports of addiction arose.
:Isomethadone - Previously used in medicine. μ- δ- agonisMorphine. S-isomer more potent.

==Methadols ==
:Dimepheptanol - Related to Methadone, has two isomers which also have two isomers so 6 possible isomers including racemic.

== Moramides ==
:Palfium (Dextomoramide) - 3x potency of M but shorter acting. High BA & fast acting, oral feels like shooting. Low LD50 & inconsistent potency (one day you may need 5mg, next day 3mg)

== Thiambutens ==
:Thiambutenes - Dimethyl-TAB, Diethyl-TAB, Ethylmethyl-TAB. Used in vetinary medicine in Japan. Banned in virtually all countried due to high abuse potential. Anticholinergic and antihistamine properties!

== Phenalkoxams ==
:Dextropropoxyphene - Low potency opioid not absorbed by CYP2D6. Also is a potent, noncompetitive α3β4 NACh antagonist and a weak SRI.
:Dimenoxadol - Benzillic Acid derivative related to methadone. Banned due to high abuse potential it seems.
:Dioxaphetyl butyrate - Banned opioid similar to methadone. Possibly in use or previously in use as a med under the names Amidalgon & Spasmoxal.

== Ampromides ==
:Diampromide - Banned Analgesic related to PropiraMorphine. Similar potency to Morphine.
:Propiram - Slightly more potent than codeine, 3-6hr duration. mixed μ agonist-antagonist favouring agonisMorphine. affinity for κ & δ, sigma and NMDA. 97% oral BA!

== Others ==
:IC-26 Methadone analogue with similar potency, but unscheduled.
:Lefetamine - Weak opioid on the same scale as codeine but has DRI properties.
:R-4066 - Methadone analogue with 212x the potency, but a much shorter duration. (3 hours)

== Amilidopiperidines ==

:3-Methylfentanyl - 400-6000x potency of Morphine depending on isomer (cis-iso more potent).
:4-Fluorobutyrfentanyl - Short duration.
:Acetylfentanyl - 80x Morphine.
:Alfentanil - 1/4 the potency and 1/3 the duration of fent but 4x quicker onset. The businessman's lunch of opioids.
:Betahydroxythiofentanyl - One of the more favoured fentanyl analogues by addicts, implying euphoria.
:Butyrfentanyl - 20-25x Morphine.
:Carfentanil - 100x potency of fent., 10000x Morphine. Used in spetznaz hostage crisis. 10,000x potency of Morphine. Activity in humans starts at 1μg.
:Lofentanil - More potent and with a longer duration than carfentanil.
:Mirfentanil - Fentanyl analogue with strong selevtivity over μ. Lower doses it antagonises effects caused by lesser opioids but at higher doses is resistant to antagonists, suggesting it has non-opioid mechanisms.
:Ohmefentanyl - 6300x morphine at it's most active isomer. Analogues of this are even stronger with one possessing 30,000x Morphine.
:Parofluorofentanyl - 150-200x morphine. Sold breifly in 1980.
:R-30490 - Analogue of carfentanil. Most selective μ agonist of all fentanyl analogues.
:Remifentanil - Potent ultra short acting fent. analogue. Potency from between 20 and 100ug. Used in medicine as an anaesthetic under Ultiva.
:Sufentanil - 5-10x potency of fentanyl.

== Opipavine Derivatives ==
:7-PET - 300x potency of M, 3-OH derivative is 2200x potency of Morphine. Unscheduled.
:Acetorphine - 8700x potency of Morphine.
:BU-48 - Etorphine derivative. Selective δ agonist and produces only convulsions with slight antidepression.
:Buprenorphin - Subutex.
:Cyprenorphine - Buprenorphine analogue, agonist-antagonist effects but with higher affinity towards κ.
:Dihydroetorphine -1000-12000x potency of M depending on RoA. Less addictive than other opioids and is used in a similar fashion to Subutex in China.
:Etorphine - 1000-3000x potency of Morphine. μ, κ & δ opioid agonist. weak affinity for ORL1 nociceptin/orphanin FQ receptor.

== Indoles ==
:18-Methoxycoronaridine - Ibogaine derivative, selective α3β4 nicotinic antagonist, however no affinity for α4β2, NMDA or seretonin. Retains modest affinity at μ & κ opioid.
:7-Hydroxymitragynine - Alkaloid in KratoMorphine. Some 17x potency of Morphine. 30x potency of Mitragynine.
:Eseroline - Metabolite of the ACh inhibitor physostigmine but potent μ agonist.
:Hodgkinsine - Alkaloid found in Psychotria colorata plants. Has antiviral, antibacterial and antifungal properties. Also μ opioid agonist & NMDA antagonist.
:Ibogaine - Addiction CURE. HT2a agonist, κ opioid agonist, NMDA antagonist.
:Mitragynine - Alkaloid in KratoMorphine. Fairly selective μ agonist but little affinity for δ & κ.
:Noribogaine - Metabolite of Ibogaine. Potent SRI, κ antagonist, weak μ full agonist.
:Voacangine - Precursor to Ibogine used by iboga plant. Displays similar effects towards addiction as Ibogaine.

== Pyrroles ==
:Viminol - Mixed agonist-antagonist, 5.5x Morphine.
:Pyrollidone-Viminol - 318x Morphine.

== Diphenylmethylpiperazines ==
:BW373U86 - Selective δ agonist at 15x stronger affinity. Analgesic and anti-depressant properties along with BDNF release. Produces convulsions at high doses and reverses respiratory depression produced by μ agonisMorphine. Also protects heart muscle cells from death during oxygen deprivation, a result of heart attacks.
:DPI-227 - Highly selective δ agonist with antidepressant effects but produces fewer convulsions than most other dugs in it's family.
:DPI-3290 - Potent δ & μ agonist but produces little respiratory depression.

== Opioid Peptides ==

:Biphalin - Endogenous eptide with high affinity for δ & μ receptors. Potency almost 7x greater than Etorphine and 7000x Morphine. Low side effects; no dependancy caused.
:Casomorphins - Opioids found in Cow's milk.
:DAMGO - Synthetic opioid peptide with high μ selectivity. When administered alongside M for 7 days, M had the same effect at the same dose as the first day. I.e. removes tolerance.
:Deltorphin - High affinity and selectivity, naturally occuring δ opioid agonist.
:Dermorphin - South American Tree frog skin. Natural opioid peptide. High potency (30-40x M) and selectivity to μ but may be less likely to cause tolerance and addiction.
:Dynorphins - Endogenous opioid peptides, primarily k agonists. Useful in the analysis of addiction.
:Leu-enkephalin - Endogeneous opioid petide that acts as a δ & μ agonist with strong selectivity for δ.
:Met-enkephalin - Opioid Growth Factor (OGF), Endogenous opioid peptide. Primary ligand of the δ receptor along with Leu-enkephalin (high potency and selectivity at δ). Low BA & is metabolised rapidly.
:Opiorphin - Endogenous opioid isolated from human saliva.

== Others ==

:3-HO-TCP - PCP analogue. More glutamergic than the PCP analogue.
:3-HO-BCP - Substitutes for both cocaine and morphine at ~5mg (made-up).
:AD-1211 - Structure looks unrelated to /most/ other opioid drugs. Mixed Agonist-antagonist at opioid recepts similar to pentazocine. Little to no developement of tolerance/dependence in animal studies.
:AH-7921 - Selective μ agonist, with 80% potency of Morphine. Distributed as an RC, TRs show that it has very little euphoria, indicating euphoria comes from somewhere else. Perhaps sigma? Other opioids are heavily potentiated by it. Perhaps μ agonism is purely analgesic and high comes from a combination of μ & δ with each multiplying the affect of the other. This indicates ultimate opioid high would be moderately selective δ agonist.
:Azaprocin - Azaprocin - ~10x potency of Morphine. Faster onset and short duration of actin. Discoved in 1963, never been marketed. The derivative subbed on the phenyl ring with a p-nitro group would be more potent by roughly 2.5. (So 25x potency of M) The open ringed 2,6-dimethylpiperazine analouges would also be active.
:BRL-52537 - Highly potent and selective κ agonist. Neuroprotective.
:Bromadol (BDPC) - 500-10,000x potency of Morphine. Similar to PCP analogues & -HO bonds within them.
:C-8813 (Thiobromadol) - 591x potency of Morphine. μ agonist & δ antagonist to reduce repiratory depression. Making the drug safer.
:Ciramadol - Opioid related to PCP, Tramadol & Tapentadol. mixed agonist-antagonist for μ, low abuse potential and ceiling on respiratory depression.
:Enadoline - Highly selective κ agonist. Produces visual distortions, dissociation and of course dysphoria similar to Salvia.
:Herkinorin - Analogue of Salvinorin A but the complete opposite. 100x higher μ affinity and 50x lower κ affinity. Also; "does not promote the recruitment of β-arrestin-2 to the intracellular domain of the μ-opioid receptor, or induce receptor internalization". This means Herkinorin may not produce tolerance or dependance.
:HZ-2 - κ-opioid agonist, same potency as morphine, long duration, high oral BA.
:ICI-199,441 - High potency, highly selective κ agonist with analgesic effects.
:Methopholine - Isoquinilone derivative with same efficacy as Codeine. Could produces corneal opacity. Analogues are more potent with 4'-Nitromethopholine at 20x Codeine.
:MT-45 - 80% of Morphine. mixed agonist-antagonist and mild NMDA antagonist.
:Nortilidine - Equipotency of Morphine. Opioid activity is in (1S,2R) iso, NMDA antagonism is in (1R,2S) iso. Also acts as a DRI.
:O-Desmethyltramadol - Metabolite of Tramadol. Considerably more potent than Tramadol. Both (+) & (-) isomers lose SRI function but (-) retains NRI functionality. RC.
:Salvinorin A - Highly potent κ agonist and even more potent D2 partial agonist. Used in therapy for addiction.
:Salvinorin B ethoxymethyl ether - Semi-synthetic analogue of Salvinorin A. Longer duration @ ~3hrs, active at 50ug & 3000x (!) selectivity over μ & δ.
:Salvinorin B methoxymethyl ether - Similar to ^^ but less selective. 5x potency as Salvinorin A. Deacetylised from Salvinorin A.
:SC-17599 - Selective μ agonist with little or no affinity for δ & κ. Potency in between Pethidine & Morphine.
:RWJ-394674 - Potent and selective δ agonist, however once inside body it is dealkylated to its monodesethyl metabolite RWJ-413216 which is a potent μ agonist with less affinity for δ. δ activity counteracts the respiratory depression the μ causes. Only prominent side effect is sedation (and euphoria!).
:TAN-67 - Potent and selective δ1 agonist. Has analgesic properties & releases dopamine in the brain. Neuro & cardiac protective properties.
:Tapentadol - μ & σ agonist & SNRI. Potency in between Morphine & Tramadol.
:Tifluadom - Benzo derivative but without GABAa agonism. Instead selective κ agonism.
:U-47700 - Overlays betaprodine, 7.5x morphine.
:U-50488 - Highly selective κ agonist with analgesic effects.
:U-69,593 - Potent and selective κ1 agonist. Produces: Antinociception, anti-inflammation, anxiolysis (low doses), respiratory depression & diuresis. Also inhibits periphery oxytocin secretion. Not sure if hallucinogenic.
:W-15 - 5.4x Morphine. RC.
:W-18 - 10,000x potency of M, structure abstract from any other drug. These super potent opioids are used in vetenarian practice for tranquilising elephants.

== Opioid Antagonists and Inverse Agonists ==
(selective δ antagonists may reduce physical addiction without causing w/d if attatched to an opioid).
:Chlornaltrexamine - Irreversible mixed agonist-antagonist at μ opioid. 22x more potent than Morphine.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors.
:Diprenorphine - Strongest opioid antagonist available. 100x potency of Nalorphine. Used to reverse effects of super-potent opioids.
:Levallorphan - μ opioid antagonist, when used with opioids, it potentiates it and removes addiction potential or induces withdrawal in addicts.
:Nalbuphine - Mixed agonist-antagonist as is common with this class, there occurs analgesia with no addictive properties.
:Naloxazone - Irreversible μ opioid receptor antagonist.
:Naloxonazine - Very Potent Irreversible μ opioid antagonist. Dimerizes from Naloxazone under acidic conditions.
:Naltrexone - Competitive antagonist at μ & κ receptors, and to a lesser extent, δ. Modulation of the dopaminergic mesolimbic pathway makes it good for countering alcohol dependance as well as opioid addiction. Blocks the euphoric effects of opioids and is used in rapid detoxification and attenuation of withdrawal. If opioids are used simultaneously, oD may occur.
:Samidorphan - Selective μ antagonist. potential for addiction treatment.

== Uncategorised Opioids ==

:FE 200665 - Is an all D-Amino acid peptide that acts as a restucted K-opioid receptor agnoist. Was dosed at 0.36mg/kg IV. Was compared to 15mg oxycodone. Slightly less than hydrocodone. Caused Hyperalgesic response in a skin pinch test. Also known as CR665.
:SoRI-9409 - Mixed μ agonist & δ antagonist. moderate analgesia without development of tolerance. Anti-addictive effects for all dopaminergic drugs.
:Synthetic Conotoxin - Snail toxin derived painkiller 1000x potency of morphine. Non-addictive.

==RELATED COMPOUNDS==
:Amiphenazole - Treatment for OD. counteracts respiratory depression. If Morphine-N-oxide is taken on this, M's potency will increase.
:Chitosan - Linear polysaccharide that can give Morphine up to 60% BA intranasally. Powdered & the ratio is 1.3g : 6.7g (morphine : chitosan).
:BIMU-8 - Nootropic.

:NMDA antagonists - Inhibit development of tolerance to morphine.
:Tezampanel - Anxiolytic.
:Ibudilast - Nootropic.
:Nuciferine
:Tetrahydropalmatine - Anxiolytic.
:Lofexidine - Anxiolytic.
:d & l Phenylalanine (DLPA) - Increases dopamine and endorphin levels, reducing opioid tolerance and even providing an analgesic effect of it's own.

== CCK Antagonists ==

:Proglumide - Acts as a δ-opioid agonist and non selective CCK antagonist. Enhances analgesia produced by opioids and can prevent or even reverse the development of tolerance.
:Devazepide - No affinity for GABAa, selective CCKa antagonist.
:Lorglumide - Selective CCKa antagonist for treatment of gastrointestinal problems and some forms of cancer as well as opioid interacting properties.

== Nocieceptinergic drugs ==
(ORL-1 ant. & ag.'s)
:J-113,397 - Highly selective ORL-1 antagonist. Prevents development of opioid tolerance, stimulates dopamine release, cognitive enhancer
:SB-612,111 - Selective ORL-1 antagonist but several times ^^
:MCOPPB - Potent, selective ORL-1 agonist with only moderate affinity for μ, even less for δ & κ. Anxiolytic with no inhibition of memory, motor function or sedation.
:NNC 63-0532 - Potent, selective ORL-1 agonist.
:Ro64-6198 - Potent, selective ORL-1 agonist with 100x selectivity over others. In rats produced anxiolytic but no anticonvulsant effects. Impairs short term memory & increases appetite. Reduces analgesic effects of Morphine but does not prevent tolerance. In primates it showed analgesic behaviour without respiratory depression.
:Menabitan - Potent cannabinoid receptor agonist with anti-nociceptive effects.

== Enkephalin Potease Inhibitors ==

:RB-101*** - Inhibits enzymes responsible for breaking down enkephalin (regulates nociceptin). Weak μ & δ affinity and slight σ1. Potentiates opioids, stops withdrawal symptoms, no addiction potential, produces no respiratory depression. Also exerts very potent antidepressant and anxiolytic effects. Not orally active so analogues vv were developed.
:RB-120 - Orally active version of the above.
:RB-3007 - Another Enkeph. PI & Nociceptin antagonist.

Opioid Notes

2014-11-04T17:15:34Z

Roi: /* CCK Antagonists */

=== Opium Derivatives ===

== Opium Alkaloids ==
:Thebaine - 6,14 Dimethoxy version of Oxymorphone. Stimulant rather than an analgesic.
:Narceine - Bitter, Crystalline, formerly used as a substitute for Morphine.
:Noscapine - Acts on the Sigma receptor. Non painkilling. Used commonly in Antitussives. Blocks Bradykinine B-2 receptors in Stroke patients.

== Alkaloid Salt Mixtures ==
:Pantopon - Preparation of all alkaloids present in opium without plant matter. Injectable and slightly less potent than Morphine.

== Morphine Family ==
:6-MDDM - 80x Morphine, has a faster onset and less body load then the prior.
:Azidomorphine - 40x Morphine, has a high affinity for μ.
:Hydromorphinol - Derivative of Morphine, yet more potent, with a steeper-dose-response curve and a longer half life. Scripted in Sweden.
:Methyldesorphin - 15x Morphine. Is found in some mixtures of Krokodil.
:MR-2096 - Oxymorphone analogue that is roughly the same potency.
:N-Phenethylnormorphine - 8-14x Morphine.
:RAM-378 - N-Phenethyl analogue of Hydromorphinol. It is probably more potent as a result.

== 3,6 Morphine Diesters ==
:Diacetyldihydromorphine - Occasionally used as an alternative to diamorphine, of which it is faster acting, longer lasting and has less side effects such as euphoria and addiction. However it is equipotent with Morphine.
:Dipropanoylmorphine - Ester of Morphine used to treat severe pain. Rarely used but considered to be safer and less addictive than Morphine. As such carries less side effects, such as euphoria. Slower acting, longer lasting and slightly more potent than Morphine.
:Nicomorphone - 2-3x Morphine and commonly prescribed in German speaking countries.

== Codeine-Dionine Family ==
:Heterocodeine - Reverse isomer of codeine. 6x Morphine, while Codeine is a prodrug, Heterocodeine is a direct agonist.
:Myrophine - Acts as a prodrug to Morphine. Has a slow onset and longer duration, but reduced potency. Does NOT produce addiction or dependence regardless of dose.
:Acetyldihydrocodeine - Used in Germany. Close relative of Thebacon, where only the 6-7 bond is unsaturated. 6-Acetyl derivative of Dihydrocodeine. Metabolizes into Dihydromorphine. Higher lipophilicity than codeine. Would probably be more potent and longer lasting as a result. Higher oral BA than Codeine.

== Morphinones and Morphols ==
:14-Cinnamoyloxycodeinone - 100x Morphine.
:14-Methoxymetopon - 500x Morphine. Can be up to one million times Morphine if injected into the spine.
:14-Phenylpropoxymetopon - 2000x potency of Morphine. When injected into the spine up to one million times Morphine. 14-Methoxymetopon has a ceiling effect on respiratory depression, but the above has been left untested.
:3-Acetyloxymorphone - Acetylated analogue of Oxymorphone.
:7-Spiroindanyloxymorphone - Odd Oxymorphone analogue that is selective at dopamine.
:Acetylmorphone - Acetoxy version of Hydromorphone, has a higher bioavailability as a result.
:Chloroxymorphamine - Derivative of Oxymorphone and irreversible full agonist.
:Methyldihydromorphone - Related to Heterocodieine not dihydrocodeine. Is 6-9x Morphine.
:Metopon - Methylated Hydromorphone, less potent. More than likely would have more euphoria as a result.
:N-Phenethyl - 14-Ethoxymetopon - 60x Morphine, but produces less constipation. d & u agonist.
:Oxymorphol - 6-Hydrogenated Oxymorphone.
:Pentamorphone - Few times more potent than Fentanyl. Short duration, yet low respiratory depression.
:Semorphone - 2x Morphine. Partial u agonist and has a ceiling effect on both analgesia and respiratory depression.
:Thebacon - Thebaine analogue, that is fairly uninteresting. 6-8x Codeine.

== Hydrazones ==
:Oxymorphazone - Half Oxymorphone, yet higher doses last up to 48 hours.

== Morphians ==
:Butorphanol - Partial agonist-antagonist at μ opioid and competitive antagonist/partial agonist at κ opioid. dysphoria is common at normal dose.
:Drotebanol - Morphinan derivative synthesised from Thebaine with analgesic effects several times more potent than codeine but weaker than morphine. Moderately addictive but limited physical dependance. Under Metabanyl when available as a script.
:Dextromethorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, (very weak) μ, δ & κ opioid agonist, SERT & NET inhibitor, NADPH Oxidase inhibitor. (Race)Methorphan = racemic
:Dextrorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, L-Type voltage-gated calcium channel (LVGCC) blocker, SRI.
:Cyclorphan - Mixed antagonist-agonist with affinity for κ.
:Levophenacylmorphan - 10x potency of Morphine.
:Levofurethylnormorphanol (Ro4-1539) - potent μ opioid agonist 30-60x potency of Levorphanol.
:Levomethorphan (+) - NDMA antagonist, σ1 & σ2 sigma agonist, μ, δ & κ opioid agonist.
:Levorphanol (+) - μ, κ & δ agonist, 4-8x potency of M, long duration, no cross tolerance with morphine.
:Norlevorphanol - Opioid analgesic, uninteresting.
:Phenomorphan - 10x potency of Levorphanol. :└--> N-(2-(2-furyl)ethyl) analogue - 60x Levorphanol :└--> N-(2-(2-thienyl)ethyl) analogue - 45x Levorphanol.
:Proxorphan - Partial κ agonist, lesser partial μ agonist.
:Ro4-1539 (Furethylnorlevorphanol) - 30-60x Morphine. One of the more potent u agonists from the Morphans.

:(Race)Methorphan: L(eft) (+) Levomethorphan >< Dextromethorphan (-) D(exter) :--> l = Opioid >< d = Hallucinogenic opioid.
:└--> Racemic mix of both isomers, embodying their properties.

:Morphinan (Racemorphan): l (+) Levorphanol >< Dextrorphan (-) d --> l = Opioid >< :d = Hallucinogenic opioid.
:└--> Racemic mix of both isomers, embodying their properties.

:(Race)Allorphan: l (+) Levallorphan >< Dextrallorphan (-) d --> l = Opioid antagonist >< d = NMDA antagonist.
:└--> Racemic mix of both isomers, embodying their properties.

:3-Hydroxymorphinan: l (+) Norlevorphanol >< Nordextrorphan (-) d --> l = :Opioid >< d = Nootropic.
└--> Racemic mix of both isomers, embodying their properties.

:Oxilorphan: μ antagonist & weak partial κ agonist.
:Dimemorfan - Sigmaergic drug.
:Xorphanol - Mixed agonist-antagonist produces convulsions at highest dose tested.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors.
:Samidorphan - selective μ antagonist. potential for addiction treatment.

== Benzomorphans ==

:Butinazocine - Benzomorphan opioid that was never marketed.
:Carbazocine - Benzomorphan opioid that was never marketed.
:Etazocine - Partial opioid agonist with mixed agonist-antagonist effects. low potency.
:Ethylketocyclozocine - Partial opioid agonist with mixed agonist-antagonist effects.
:Ibazocine - Benzomorphan opioid that was never marketed.
:Moxazocine - 10x potency of Morphine, partial/mixed agonist-antagonist.
:Tonazocine - Partial agonist at μ & δ, no adverse effects on breathing.
:Volazocine - Benzomorphan opioid that was never marketed.
:Fluorophen - Radioligand, full μ agonist (6x M) & lower affinity for δ.
:Zenazocine - Partial agonist at μ & δ.
:Eptazocine - Japanese κ agonist & μ antagonist.
:Pentazocine - Mixed agonist-antagonist (-) is the κ agonist side, the (+) displays 10x the affinity for sigma receptors. NO μ agonism.
:Phenazocine - Related to ^ but stronger analgesic, 4x potency of Morphine.
:Cyclazocine - Mixed agonist-antagonist.
:Dezocine - Mixed agonist-antagonist with high κ antagonisMorphine. Low dose=euphoria (μ) High dose=dysphoria (κ). Weird structure.
:8-Carboxamidocyclazocine (8-CAC) - κ & μ agonist, long duration.
:Bremazocine - κ agonist related to Pentazocine.
:Metazocine - Analgesic; mixed agonist-antagonist at μ, activity also at κ and sigma.
:Alazocine - σ1 agonist, κ opioid agonist & slight NMDA antagonist.

== 4-Phenylpiperidines ==
:4-Fluoropethidine - In comparison to Pethidine, it is 50% less potent as an analgesic but 50% more potent as a DRI. (4-iodo & 3, 4-dichloro only increase these differences)
:Anileridine - Another banned Pethidine analogue, probably abused. Higher analgesia than Meperidine due to n-aminophenyl group and acts withing 15 mins orally, lasting 2-3 hours.
:Benzethidine - 4-Phenylpiperidine analogue of Pethidine. Probably somewhat more potent and euphoric. Never scripted.
:Carperidine - Fairly normal opioid but unused in medicine.
:Furethidine - 4-Phenylpiperidine analogue of Pethidine. Probably a lot more potent and abuse prone. Never prescribed.
:Morpheridine - Related to Meperidine but 4x the potency and does not cause convulsions.
:Phenoperidine - 20-200x Pethidine. Less hypnotic and than morphine but more emetic (nausea). This can be cured by Haloperidol.
:Piminodine - Similar dose to Morphine, used in 60's and 70's but was banned. It was probably abused widely.

== Prodines ==
:Alphaprodine - 1.5x Morphine.
:Allylprodine - Prodine analogue 23x potency of Morphine.
:Betaprodine - 7.5x Morphine.
:Prosidol - Russian Prodine analogue.

== Ketobemidones ==
:Acetoxyketobemidone - Unschedualed analogue of Ketobemidone.
:Bemidone - Analogue of Pethidine but significantly less potent, however it has NMDA antagonism like Ketobemidone.
:Ketobemidone - μ opioid antagonist & NMDA antagonist. More addictive than Morphine.

== Others ==
:Loperamide - Peripheral opioid so it cannot cross BBB. useful anti-Diarrhoea med. When used in conjuction with Quinine or Omerprazole can cross BBB and opioid effects are seen.
:Picenadol - R isomer (or Levopicenadol) is pure μ agonist while S is antagonist. Racemic is mixed that casues low abuse potential but has low κ activity.

== Amidones ==
:Dipipadone - Lost Ark of the Covenant.
:Phenadoxone - Methadone analogue, similar dose to M, lasts 1-4 hours.
:Levacetylmethadol - Methadone analogue with u agonism and noncompetitive a3b4 NACh antagonisMorphine. Brand name Orlaam, prescribed to those unresponsive to methadone or subutex. Long half life (3 days) and heavier affect.
:Norpipanone - Was not under international control until case reports of addiction arose.
:Isomethadone - Previously used in medicine. μ- δ- agonisMorphine. S-isomer more potent.

==Methadols ==
:Dimepheptanol - Related to Methadone, has two isomers which also have two isomers so 6 possible isomers including racemic.

== Moramides ==
:Palfium (Dextomoramide) - 3x potency of M but shorter acting. High BA & fast acting, oral feels like shooting. Low LD50 & inconsistent potency (one day you may need 5mg, next day 3mg)

== Thiambutens ==
:Thiambutenes - Dimethyl-TAB, Diethyl-TAB, Ethylmethyl-TAB. Used in vetinary medicine in Japan. Banned in virtually all countried due to high abuse potential. Anticholinergic and antihistamine properties!

== Phenalkoxams ==
:Dextropropoxyphene - Low potency opioid not absorbed by CYP2D6. Also is a potent, noncompetitive α3β4 NACh antagonist and a weak SRI.
:Dimenoxadol - Benzillic Acid derivative related to methadone. Banned due to high abuse potential it seems.
:Dioxaphetyl butyrate - Banned opioid similar to methadone. Possibly in use or previously in use as a med under the names Amidalgon & Spasmoxal.

== Ampromides ==
:Diampromide - Banned Analgesic related to PropiraMorphine. Similar potency to Morphine.
:Propiram - Slightly more potent than codeine, 3-6hr duration. mixed μ agonist-antagonist favouring agonisMorphine. affinity for κ & δ, sigma and NMDA. 97% oral BA!

== Others ==
:IC-26 Methadone analogue with similar potency, but unscheduled.
:Lefetamine - Weak opioid on the same scale as codeine but has DRI properties.
:R-4066 - Methadone analogue with 212x the potency, but a much shorter duration. (3 hours)

== Amilidopiperidines ==

:3-Methylfentanyl - 400-6000x potency of Morphine depending on isomer (cis-iso more potent).
:4-Fluorobutyrfentanyl - Short duration.
:Acetylfentanyl - 80x Morphine.
:Alfentanil - 1/4 the potency and 1/3 the duration of fent but 4x quicker onset. The businessman's lunch of opioids.
:Betahydroxythiofentanyl - One of the more favoured fentanyl analogues by addicts, implying euphoria.
:Butyrfentanyl - 20-25x Morphine.
:Carfentanil - 100x potency of fent., 10000x Morphine. Used in spetznaz hostage crisis. 10,000x potency of Morphine. Activity in humans starts at 1μg.
:Lofentanil - More potent and with a longer duration than carfentanil.
:Mirfentanil - Fentanyl analogue with strong selevtivity over μ. Lower doses it antagonises effects caused by lesser opioids but at higher doses is resistant to antagonists, suggesting it has non-opioid mechanisms.
:Ohmefentanyl - 6300x morphine at it's most active isomer. Analogues of this are even stronger with one possessing 30,000x Morphine.
:Parofluorofentanyl - 150-200x morphine. Sold breifly in 1980.
:R-30490 - Analogue of carfentanil. Most selective μ agonist of all fentanyl analogues.
:Remifentanil - Potent ultra short acting fent. analogue. Potency from between 20 and 100ug. Used in medicine as an anaesthetic under Ultiva.
:Sufentanil - 5-10x potency of fentanyl.

== Opipavine Derivatives ==
:7-PET - 300x potency of M, 3-OH derivative is 2200x potency of Morphine. Unscheduled.
:Acetorphine - 8700x potency of Morphine.
:BU-48 - Etorphine derivative. Selective δ agonist and produces only convulsions with slight antidepression.
:Buprenorphin - Subutex.
:Cyprenorphine - Buprenorphine analogue, agonist-antagonist effects but with higher affinity towards κ.
:Dihydroetorphine -1000-12000x potency of M depending on RoA. Less addictive than other opioids and is used in a similar fashion to Subutex in China.
:Etorphine - 1000-3000x potency of Morphine. μ, κ & δ opioid agonist. weak affinity for ORL1 nociceptin/orphanin FQ receptor.

== Indoles ==
:18-Methoxycoronaridine - Ibogaine derivative, selective α3β4 nicotinic antagonist, however no affinity for α4β2, NMDA or seretonin. Retains modest affinity at μ & κ opioid.
:7-Hydroxymitragynine - Alkaloid in KratoMorphine. Some 17x potency of Morphine. 30x potency of Mitragynine.
:Eseroline - Metabolite of the ACh inhibitor physostigmine but potent μ agonist.
:Hodgkinsine - Alkaloid found in Psychotria colorata plants. Has antiviral, antibacterial and antifungal properties. Also μ opioid agonist & NMDA antagonist.
:Ibogaine - Addiction CURE. HT2a agonist, κ opioid agonist, NMDA antagonist.
:Mitragynine - Alkaloid in KratoMorphine. Fairly selective μ agonist but little affinity for δ & κ.
:Noribogaine - Metabolite of Ibogaine. Potent SRI, κ antagonist, weak μ full agonist.
:Voacangine - Precursor to Ibogine used by iboga plant. Displays similar effects towards addiction as Ibogaine.

== Pyrroles ==
:Viminol - Mixed agonist-antagonist, 5.5x Morphine.
:Pyrollidone-Viminol - 318x Morphine.

== Diphenylmethylpiperazines ==
:BW373U86 - Selective δ agonist at 15x stronger affinity. Analgesic and anti-depressant properties along with BDNF release. Produces convulsions at high doses and reverses respiratory depression produced by μ agonisMorphine. Also protects heart muscle cells from death during oxygen deprivation, a result of heart attacks.
:DPI-227 - Highly selective δ agonist with antidepressant effects but produces fewer convulsions than most other dugs in it's family.
:DPI-3290 - Potent δ & μ agonist but produces little respiratory depression.

== Opioid Peptides ==

:Biphalin - Endogenous eptide with high affinity for δ & μ receptors. Potency almost 7x greater than Etorphine and 7000x Morphine. Low side effects; no dependancy caused.
:Casomorphins - Opioids found in Cow's milk.
:DAMGO - Synthetic opioid peptide with high μ selectivity. When administered alongside M for 7 days, M had the same effect at the same dose as the first day. I.e. removes tolerance.
:Deltorphin - High affinity and selectivity, naturally occuring δ opioid agonist.
:Dermorphin - South American Tree frog skin. Natural opioid peptide. High potency (30-40x M) and selectivity to μ but may be less likely to cause tolerance and addiction.
:Dynorphins - Endogenous opioid peptides, primarily k agonists. Useful in the analysis of addiction.
:Leu-enkephalin - Endogeneous opioid petide that acts as a δ & μ agonist with strong selectivity for δ.
:Met-enkephalin - Opioid Growth Factor (OGF), Endogenous opioid peptide. Primary ligand of the δ receptor along with Leu-enkephalin (high potency and selectivity at δ). Low BA & is metabolised rapidly.
:Opiorphin - Endogenous opioid isolated from human saliva.

== Others ==

:3-HO-TCP - PCP analogue. More glutamergic than the PCP analogue.
:3-HO-BCP - Substitutes for both cocaine and morphine at ~5mg (made-up).
:AD-1211 - Structure looks unrelated to /most/ other opioid drugs. Mixed Agonist-antagonist at opioid recepts similar to pentazocine. Little to no developement of tolerance/dependence in animal studies.
:AH-7921 - Selective μ agonist, with 80% potency of Morphine. distributed as an RC, TRs show that it has very little euphoria, indicating euphoria comes from somewhere else. Perhaps sigma? Other opioids are heavily potentiated by it. Perhaps μ agonism is purely analgesic and high comes from a combination of μ & δ with each multiplying the affect of the other. This indicates ultimate opioid high would be moderately selective δ agonist.
:Azaprocin - Azaprocin - ~10x potency of Morphine. Faster onset and short duration of actin. Discoved in 1963, never been marketed. The derivative subbed on the phenyl ring with a p-nitro group would be more potent by roughly 2.5. (So 25x potency of M) The open ringed 2,6-dimethylpiperazine analouges would also be active.
:BRL-52537 - Highly potent and selective κ agonist. Neuroprotective.
:Bromadol (BDPC) - 500-10,000x potency of Morphine. Similar to PCP analogues & -HO bonds within theMorphine.
:C-8813 (Thiobromadol) - 591x potency of Morphine. μ agonist & δ antagonist to reduce repiratory depression. Making the drug safer.
:Ciramadol - Opioid related to PCP, Tramadol & Tapentadol. mixed agonist-antagonist for μ, low abuse potential and ceiling on respiratory depression.
:Enadoline - Highly selective κ agonist. Produces visual distortions, dissociation and of course dysphoria similar to Salvia.
:Herkinorin - Analogue of Salvinorin A but the complete opposite. 100x higher μ affinity and 50x lower κ affinity. Also; "does not promote the recruitment of β-arrestin-2 to the intracellular domain of the μ-opioid receptor, or induce receptor internalization". This means Herkinorin may not produce tolerance or dependance.
:HZ-2 - κ-opioid agonist, same potency as morphine, long duration, high oral BA.
:ICI-199,441 - High potency, highly selective κ agonist with analgesic effects.
:Methopholine - Isoquinilone derivative with same efficacy as codeine. Could produces corneal opacity. Analogues are more potent with 4'-nitromethopholine at 20x codeine.
:MT-45 - 80% of Morphine. mixed agonist-antagonist and mild NMDA antagonist.
:Nortilidine - Equipotency of Morphine. Opioid activity is in (1S,2R) iso, NMDA antagonism is in (1R,2S) iso. Also acts as a DRI.
:O-Desmethyltramadol - Metabolite of Tramadol. Considerably more potent than Tramadol. Both (+) & (-) isomers lose SRI function but (-) retains NRI functionality. RC.
:Salvinorin A - Highly potent κ agonist and even more potent D2 partial agonist. Use in therapy for addiction.
:Salvinorin B ethoxymethyl ether - Semi-synthetic analogue of Salv. A. Longer duration @ ~3hrs, active at 50ug & 3000x (!) selectivity over μ & δ.
:Salvinorin B methoxymethyl ether - Similar to ^^ but less selective. 5x potency as Salvinorin A. Deacetylised from Salvinorin A.
:SC-17599 - Selective μ agonist with little or no affinity for δ & κ. Potency in between pethidine & morphine.
:RWJ-394674 - Potent and selective δ agonist, however once inside body it is dealkylated to its monodesethyl metabolite RWJ-413216 which is a potent μ agonist with less affinity for δ. δ activity counteracts the respiratory depression the μ causes. Only prominent side effect is sedation (and euphoria!).
:TAN-67 - Potent and selective δ1 agonist. Has analgesic properties & releases dopamine in the brain. Neuro & cardiac protective properties.
:Tapentadol - μ & σ agonist & SNRI. Potency in between M & TraMorphine.
:Tifluadom - Benzo derivative but without GABAa agonisMorphine. Instead selective κ agonisMorphine.
:U-47700 - Overlays betaprodine, 7.5x morphine.
:U-50488 - Highly selective κ agonist with analgesic effects.
:U-69,593 - Potent and selective κ1 agonist. Produces; antinociception, anti-inflammation, anxiolysis (low doses), respiratory depression & diuresis. Also inhibits periphery oxytocin secretion. Not sure if Hallucinogenic.
:W-15 - 5.4x Morphine. RC.
:W-18 - 10,000x potency of M, structure abstract from any other drug. These super potent opioids are used in vetenarian practice for tranquilising elephants.

== Opioid Antagonists and Inverse Agonists ==
(selective δ antagonists may reduce physical addiction without causing w/d if attatched to an opioid).
:Chlornaltrexamine - Irreversible mixed agonist-antagonist at μ opioid. 22x more potent than Morphine.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors.
:Diprenorphine - Strongest opioid antagonist available. 100x potency of Nalorphine. Used to reverse effects of super-potent opioids.
:Levallorphan - μ opioid antagonist, when used with opioids, it potentiates it and removes addiction potential or induces withdrawal in addicts.
:Nalbuphine - Mixed agonist-antagonist as is common with this class, there occurs analgesia with no addictive properties.
:Naloxazone - Irreversible μ opioid receptor antagonist.
:Naloxonazine - Very Potent Irreversible μ opioid antagonist. Dimerizes from Naloxazone under acidic conditions.
:Naltrexone - Competitive antagonist at μ & κ receptors, and to a lesser extent, δ. Modulation of the dopaminergic mesolimbic pathway makes it good for countering alcohol dependance as well as opioid addiction. Blocks the euphoric effects of opioids and is used in rapid detoxification and attenuation of withdrawal. If opioids are used simultaneously, oD may occur.
:Samidorphan - Selective μ antagonist. potential for addiction treatment.

== Uncategorised Opioids ==

:FE 200665 - Is an all D-Amino acid peptide that acts as a restucted K-opioid receptor agnoist. Was dosed at 0.36mg/kg IV. Was compared to 15mg oxycodone. Slightly less than hydrocodone. Caused Hyperalgesic response in a skin pinch test. Also known as CR665.
:SoRI-9409 - Mixed μ agonist & δ antagonist. moderate analgesia without development of tolerance. Anti-addictive effects for all dopaminergic drugs.
:Synthetic Conotoxin - Snail toxin derived painkiller 1000x potency of morphine. Non-addictive.

==RELATED COMPOUNDS==
:Amiphenazole - Treatment for OD. counteracts respiratory depression. If Morphine-N-oxide is taken on this, M's potency will increase.
:Chitosan - Linear polysaccharide that can give Morphine up to 60% BA intranasally. Powdered & the ratio is 1.3g : 6.7g (morphine : chitosan).
:BIMU-8 - Nootropic.

:NMDA antagonists - Inhibit development of tolerance to morphine.
:Tezampanel - Anxiolytic.
:Ibudilast - Nootropic.
:Nuciferine
:Tetrahydropalmatine - Anxiolytic.
:Lofexidine - Anxiolytic.
:d & l Phenylalanine (DLPA) - Increases dopamine and endorphin levels, reducing opioid tolerance and even providing an analgesic effect of it's own.

== CCK Antagonists ==

:Proglumide - Acts as a δ-opioid agonist and non selective CCK antagonist. Enhances analgesia produced by opioids and can prevent or even reverse the development of tolerance.
:Devazepide - No affinity for GABAa, selective CCKa antagonist.
:Lorglumide - Selective CCKa antagonist for treatment of gastrointestinal problems and some forms of cancer as well as opioid interacting properties.

== Nocieceptinergic drugs ==
(ORL-1 ant. & ag.'s)
:J-113,397 - Highly selective ORL-1 antagonist. Prevents development of opioid tolerance, stimulates dopamine release, cognitive enhancer
:SB-612,111 - Selective ORL-1 antagonist but several times ^^
:MCOPPB - Potent, selective ORL-1 agonist with only moderate affinity for μ, even less for δ & κ. Anxiolytic with no inhibition of memory, motor function or sedation.
:NNC 63-0532 - Potent, selective ORL-1 agonist.
:Ro64-6198 - Potent, selective ORL-1 agonist with 100x selectivity over others. In rats produced anxiolytic but no anticonvulsant effects. Impairs short term memory & increases appetite. Reduces analgesic effects of Morphine but does not prevent tolerance. In primates it showed analgesic behaviour without respiratory depression.
:Menabitan - Potent cannabinoid receptor agonist with anti-nociceptive effects.

== Enkephalin Potease Inhibitors ==

:RB-101*** - Inhibits enzymes responsible for breaking down enkephalin (regulates nociceptin). Weak μ & δ affinity and slight σ1. Potentiates opioids, stops withdrawal symptoms, no addiction potential, produces no respiratory depression. Also exerts very potent antidepressant and anxiolytic effects. Not orally active so analogues vv were developed.
:RB-120 - Orally active version of the above.
:RB-3007 - Another Enkeph. PI & Nociceptin antagonist.

Main Page

2014-11-03T21:32:24Z

Roi:

{{DISPLAYTITLE:Welcome to TripSit Wiki!<span style="display: none"></span>}}
<table style="max-width: 1000px; display:block;" cellpadding=5><tr><td valign=top width=20%>
== Community ==

=== IRC ===

* [[IRC_User_Guide|New user guide]]
* [http://tripsit.me/chat/tripsitapp/ '''Tripsit's portable IRC distribution''']
* [[Channels]]
** [http://chat.tripsit.me/?nick=Social?#home #home]
** [http://chat.tripsit.me/?nick=Social?#home,#tripsit #tripsit]
** [http://chat.tripsit.me/?nick=Social?#home,#drugs #drugs]
* [[How_to_connect_through_Tor|Connect through Tor]]
* [[List of IRC bot commands]]
* [[Commands reference]]

=== TripRadio ===
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* [[Radio|General info]]
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* [[How to DJ|How to setup DJ software]]

</td>

<td valign=top width=25%>
== Important Pages ==
* [[TripSit Rules]]
* [[Network Terms of Service]]
* [[List of staff and their roles]]
* [[TripSit's Plans]]

<td valign=top width=30% bgcolor=#f1f1f1>
== Drug Knowledge ==
*List of [[:Category:Drugs|Psychoactive Substances]]
*Main pages for drug classes:
**[[Psychedelics]]
**[[Dissociatives]]
**[[Stimulants]]
**[[Depressants]]
***[[Opioids]]
***[[Benzodiazepines]]
**[[Antidepressants]]
**[[Deliriants]]

* [[Drug combinations]]
* [http://factsheet.tripsit.me Factsheets]
* [[Glossary]]

== [[Guides]] ==

* [[Addiction]]
* [[Overdose]]
* [[Panic Attacks]]
* [[How To Deal With A Bad Trip]]
* [[Common Misconceptions About Psychedelics]]
* [[Quick Guide to Stimulant Comedowns]]
* [[Quick Guide to Volumetric Dosing]]
* [[Cold Water Extraction]]

== Tripsitting ==
* [[How_To_Tripsit_Online|How to Tripsit online]]
* [[How_To_Tripsit_In_Real_Life|How to Tripsit in real life]]

== Harm Reduction Supplies & Testing ==
* [[Scales]]
* [[Test Kits]]
* [[Sources for Laboratory Analysis]]

</td>
<td valign=top width=30% bgcolor=#f1f1f1>
== Common Drugs ==

* '''[[:Category:Psychedelic|Psychedelics]]'''
** [[Mushrooms]]
** [[DMT]]
** [[LSD]]
** [[LSA]]
** [[Mescaline]]
** [[2C-X|2C-X series]]
** [[NBOMes|NBOMe series]]
** [[DOx|DOx series]]
** [[AMT|αMT]]
** [[Cannabis]]

* '''[[:Category:Dissociative|Dissociatives]]'''
** [[PCP]]
** [[3-MeO-PCP]]
** [[Ketamine]]
** [[MXE]]
** [[DXM]]
** [[Diphenidine]]
** [[Salvia]]
** [[Nitrous Oxide]]

* '''[[:Category:Stimulant|Stimulants]]'''
** [[Adderall]]
** [[Amphetamine]]
** [[Methamphetamine]]
** [[MDMA]]
** [[MDA]]
** [[Mephedrone]]
** [[Cocaine]]
** [[Methylphenidate]]

* '''[[:Category:Depressant|Depressants]]'''
** [[Alcohol]]
** [[Etizolam]]
** [[GHB]]
** [[Kava]]
** [[Zolpidem]]

* '''[[:Category:Opioid|Opioids]]'''
** [[Kratom]]
** [[Morphine]]
** [[Heroin]]
** [[Codeine]]
** [[Tramadol]]
** [[Hydrocodone]]
** [[Oxycodone]]
** [[Buprenorphine]]
</td>

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[[About|About Tripsit wiki]]

TripSit wiki currently has [[Special:Statistics|{{NUMBEROFPAGES}} pages]].

View a [[Special:AllPages|list of all pages]].

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Main Page

2014-10-23T14:42:42Z

Roi:

{{DISPLAYTITLE:Welcome to TripSit Wiki!<span style="display: none"></span>}}
<table style="max-width: 1000px; display:block;" cellpadding=5><tr><td valign=top width=20%>
== Community ==

=== IRC ===

* [[IRC_User_Guide|New user guide]]
* [http://tripsit.me/chat/tripsitapp/ '''Tripsit's portable IRC distribution''']
* [[Channels]]
** [http://chat.tripsit.me/?nick=Social?#home #home]
** [http://chat.tripsit.me/?nick=Social?#home,#tripsit #tripsit]
** [http://chat.tripsit.me/?nick=Social?#home,#drugs #drugs]
* [[How_to_connect_through_Tor|Connect through Tor]]
* [[List of IRC bot commands]]
* [[Commands reference]]

=== TripRadio ===
* [http://radio.tripsit.me Listen Now]

* [[Radio|General info]]
* [[DJ Application|We need DJs!]]
* [[How to DJ|How to setup DJ software]]

</td>

<td valign=top width=25%>
== Important Pages ==
* [[TripSit Rules]]
* [[Network Terms of Service]]
* [[List of staff and their roles]]
* [[TripSit's Plans]]

<td valign=top width=30% bgcolor=#f1f1f1>
== Drug Knowledge ==
*List of [[:Category:Drugs|Psychoactive Substances]]
*Main pages for drug classes:
**[[Psychedelics]]
**[[Dissociatives]]
**[[Stimulants]]
**[[Depressants]]
***[[Opioids]]
***[[Benzodiazepines]]
**[[Antidepressants]]
**[[Deliriants]]

* [[Drug combinations]]
* [http://factsheet.tripsit.me Factsheets]
* [[Glossary]]

== [[Guides]] ==

* [[Addiction]]
* [[Overdose]]
* [[Panic Attacks]]
* [[How To Deal With A Bad Trip]]
* [[Common Misconceptions About Psychedelics]]
* [[Quick Guide to Stimulant Comedowns]]
* [[Quick Guide to Volumetric Dosing]]
* [[Cold Water Extraction]]

== Tripsitting ==
* [[How_To_Tripsit_Online|How to Tripsit online]]
* [[How_To_Tripsit_In_Real_Life|How to Tripsit in real life]]

== Harm Reduction Supplies & Testing ==
* [[Scales]]
* [[Test Kits]]
* [[Sources for Laboratory Analysis]]

</td>
<td valign=top width=30% bgcolor=#f1f1f1>
== Common Drugs ==

* '''[[:Category:Psychedelic|Psychedelics]]'''
** [[Mushrooms]]
** [[DMT]]
** [[LSD]]
** [[LSA]]
** [[Mescaline]]
** [[2C-X|2C-X series]]
** [[NBOMes|NBOMe series]]
** [[DOx|DOx series]]
** [[AMT|αMT]]
** [[Cannabis]]

* '''[[:Category:Dissociative|Dissociatives]]'''
** [[PCP]]
** [[3-MeO-PCP]]
** [[Ketamine]]
** [[MXE]]
** [[DXM]]
** [[Diphenidine]]
** [[Salvia]]
** [[Nitrous Oxide]]

* '''[[:Category:Stimulant|Stimulants]]'''
** [[Adderall]]
** [[Street amphetamine]]
** [[Methamphetamine]]
** [[MDMA]]
** [[MDA]]
** [[Mephedrone]]
** [[Cocaine]]
** [[Methylphenidate]]

* '''[[:Category:Depressant|Depressants]]'''
** [[Alcohol]]
** [[Etizolam]]
** [[GHB]]
** [[Kava]]
** [[Zolpidem]]

* '''[[:Category:Opioid|Opioids]]'''
** [[Kratom]]
** [[Morphine]]
** [[Heroin]]
** [[Codeine]]
** [[Tramadol]]
** [[Hydrocodone]]
** [[Oxycodone]]
** [[Buprenorphine]]
</td>

</tr>
</table>

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Opioid Notes

2014-10-18T03:24:39Z

Roi:

=== Opium Derivatives ===

== Opium Alkaloids ==
:Thebaine - 6,14 Dimethoxy version of Oxymorphone. Stimulant rather than an analgesic.
:Narceine - Bitter, Crystalline, formerly used as a substitute for Morphine.
:Noscapine - Acts on the Sigma receptor. Non painkilling. Used commonly in Antitussives. Blocks Bradykinine B-2 receptors in Stroke patients.

== Alkaloid Salt Mixtures ==
:Pantopon - Preparation of all alkaloids present in opium without plant matter. Injectable and slightly less potent than Morphine.

== Morphine Family ==
:6-MDDM - 80x Morphine, has a faster onset and less body load then the prior.
:Azidomorphine - 40x Morphine, has a high affinity for μ.
:Hydromorphinol - Derivative of Morphine, yet more potent, with a steeper-dose-response curve and a longer half life. Scripted in Sweden.
:Methyldesorphin - 15x Morphine. Is found in some mixtures of Krokodil.
:MR-2096 - Oxymorphone analogue that is roughly the same potency.
:N-Phenethylnormorphine - 8-14x Morphine.
:RAM-378 - N-Phenethyl analogue of Hydromorphinol. It is probably more potent as a result.

== 3,6 Morphine Diesters ==
:Diacetyldihydromorphine - Occasionally used as an alternative to diamorphine, of which it is faster acting, longer lasting and has less side effects such as euphoria and addiction. However it is equipotent with Morphine.
:Dipropanoylmorphine - Ester of Morphine used to treat severe pain. Rarely used but considered to be safer and less addictive than Morphine. As such carries less side effects, such as euphoria. Slower acting, longer lasting and slightly more potent than Morphine.
:Nicomorphone - 2-3x Morphine and commonly prescribed in German speaking countries.

== Codeine-Dionine Family ==
:Heterocodeine - Reverse isomer of codeine. 6x Morphine, while Codeine is a prodrug, Heterocodeine is a direct agonist.
:Myrophine - Acts as a prodrug to Morphine. Has a slow onset and longer duration, but reduced potency. Does NOT produce addiction or dependence regardless of dose.
:Acetyldihydrocodeine - Used in Germany. Close relative of Thebacon, where only the 6-7 cond is unsaturated. 6-Acetyl derivative of Dihydrocodeine. Metabolizes into Dihydromorphine. Higher lipophilicity than codeine. Would probably be more potent and longer lasting as a result. Higher oral BA than Codeine.

== Morphinones and Morphols ==
:14-Cinnamoyloxycodeinone - 100x Morphine.
:14-Methoxymetopon - 500x Morphine. Can be up to one million times Morphine if injected into the spine.
:14-Phenylpropoxymetopon - 2000x potency of Morphine. When injected into the spine up to one million times Morphine. 14-Methoxymetopon has a ceiling effect on respiratory depression, but the above has been left untested.
:3-Acetyloxymorphone - Acetylated analogue of Oxymorphone.
:7-Spiroindanyloxymorphone - Odd Oxymorphone analogue that is selective at dopamine.
:Acetylmorphone - Acetoxy version of Hydromorphone, has a higher bioavailability as a result.
:Chloroxymorphamine - Derivative of Oxymorphone and irreversible full agonist.
:Methyldihydromorphone - Related to Heterocodieine not dihydrocodeine. Is 6-9x Morphine.
:Metopon - Methylated Hydromorphone, less potent. More than likely would have more euphoria as a result.
:N-Phenethyl - 14-Ethoxymetopon - 60x Morphine, but produces less constipation. d & u agonist.
:Oxymorphol - 6-Hydrogenated Oxymorphone.
:Pentamorphone - Few times more potent than Fentanyl. Short duration, yet low respiratory depression.
:Semorphone - 2x Morphine. Partial u agonist and has a ceiling effect on both analgesia and respiratory depression.
:Thebacon - Thebaine analogue, that is fairly uninteresting. 6-8x Codeine.

== Hydrazones ==
:Oxymorphazone - Half Oxymorphone, yet higher doses last up to 48 hours.

== Morphians ==
:Butorphanol - Partial agonist-antagonist at μ opioid and competitive antagonist/partial agonist at κ opioid. dysphoria is common at normal dose.
:Drotebanol - Morphinan derivative synthesised from Thebaine with analgesic effects several times more potent than codeine but weaker than morphine. Moderately addictive but limited physical dependance. Under Metabanyl when available as a script.
:Dextromethorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, (very weak) μ, δ & κ opioid agonist, SERT & NET inhibitor, NADPH Oxidase inhibitor. (Race)Methorphan = racemic
:Dextrorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, L-Type voltage-gated calcium channel (LVGCC) blocker, SRI.
:Cyclorphan - Mixed antagonist-agonist with affinity for κ.
:Levophenacylmorphan - 10x potency of Morphine.
:Levofurethylnormorphanol (Ro4-1539) - potent μ opioid agonist 30-60x potency of Levorphanol.
:Levomethorphan (+) - NDMA antagonist, σ1 & σ2 sigma agonist, μ, δ & κ opioid agonist.
:Levorphanol (+) - μ, κ & δ agonist, 4-8x potency of M, long duration, no cross tolerance with morphine.
:Norlevorphanol - Opioid analgesic, uninteresting.
:Phenomorphan - 10x potency of Levorphanol. :└--> N-(2-(2-furyl)ethyl) analogue - 60x Levorphanol :└--> N-(2-(2-thienyl)ethyl) analogue - 45x Levorphanol.
:Proxorphan - Partial κ agonist, lesser partial μ agonist.
:Ro4-1539 (Furethylnorlevorphanol) - 30-60x Morphine. One of the more potent u agonists from the Morphans.

:(Race)Methorphan: L(eft) (+) Levomethorphan >< Dextromethorphan (-) D(exter) --> l = Opioid >< d = Hallucinogenic opioid.
└--> Racemic mix of both isomers, embodying their properties.

:Morphinan (Racemorphan): l (+) Levorphanol >< Dextrorphan (-) d --> l = Opioid >< :d = Hallucinogenic opioid.
:└--> Racemic mix of both isomers, embodying their properties.

:(Race)Allorphan: l (+) Levallorphan >< Dextrallorphan (-) d --> l = Opioid antagonist >< d = NMDA antagonist.
: └--> Racemic mix of both isomers, embodying their properties.

:3-Hydroxymorphinan: l (+) Norlevorphanol >< Nordextrorphan (-) d --> l = Opioid >< d = Nootropic.
└--> Racemic mix of both isomers, embodying their properties.

:Oxilorphan: μ antagonist & weak partial κ agonist.
:Dimemorfan - Sigmaergic drug.
:Xorphanol - Mixed agonist-antagonist produces convulsions at highest dose tested.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors.
:Samidorphan - selective μ antagonist. potential for addiction treatment.

== Benzomorphans ==

:Butinazocine - Benzomorphan opioid that was never marketed.
:Carbazocine - Benzomorphan opioid that was never marketed.
:Etazocine - Partial opioid agonist with mixed agonist-antagonist effects. low potency.
:Ethylketocyclozocine - Partial opioid agonist with mixed agonist-antagonist effects.
:Ibazocine - Benzomorphan opioid that was never marketed.
:Moxazocine - 10x potency of Morphine, partial/mixed agonist-antagonist.
:Tonazocine - Partial agonist at μ & δ, no adverse effects on breathing.
:Volazocine - Benzomorphan opioid that was never marketed.
:Fluorophen - Radioligand, full μ agonist (6x M) & lower affinity for δ.
:Zenazocine - Partial agonist at μ & δ.
:Eptazocine - Japanese κ agonist & μ antagonist.
:Pentazocine - Mixed agonist-antagonist (-) is the κ agonist side, the (+) displays 10x the affinity for sigma receptors. NO μ agonism.
:Phenazocine - Related to ^ but stronger analgesic, 4x potency of Morphine.
:Cyclazocine - Mixed agonist-antagonist.
:Dezocine - Mixed agonist-antagonist with high κ antagonisMorphine. Low dose=euphoria (μ) High dose=dysphoria (κ). Weird structure.
:8-Carboxamidocyclazocine (8-CAC) - κ & μ agonist, long duration.
:Bremazocine - κ agonist related to Pentazocine.
:Metazocine - Analgesic; mixed agonist-antagonist at μ, activity also at κ and sigma.
:Alazocine - σ1 agonist, κ opioid agonist & slight NMDA antagonist.

== 4-Phenylpiperidines ==
:4-Fluoropethidine - In comparison to pethidine, it is 50% less potent as an analgesic but 50% more potent as a DRI. (4-iodo & 3, 4-dichloro only increase these differences)
:Anileridine - Another banned pethidine analogue, probably abused. Higher analgesia than Meperidine due to n-aminophenyl group and acts withing 15 mins orally, lasting 2-3 hours.
:Benzethidine - 4-phenylpiperidine analogue of pethidine. Probably somewhat more potent and euphoric. Never scripted.
:Carperidine - Fairly normal opioid but unused in medicine and currently legal (08/06/2013).
:Furethidine - 4-Phenylpiperidine analogue of pethidine. Probably a lot more potent and abuse prone. Never prescribed.
:Morpheridine - Related to meperidine but 4x the potency and does not cause convulsions.
:Phenoperidine - 20-200x Pethidine. Less hypnotic and than morphine but more emetic (nausea). This can be cured by Haloperidol.
:Piminodine - Similar dose to Morphine, used in 60's and 70's but was banned. It was probably abused widely.

== Prodines ==
:Alphaprodine - 1.5x Morphine.
:Allylprodine - Prodine analogue 23x potency of Morphine.
:Betaprodine - 7.5x Morphine.
:Prosidol - Russian Prodine analogue.

== Ketobemidones ==
:Acetoxyketobemidone - Unschedualed analogue of Ketobemidone.
:Bemidone - Analogue of Pethidine but significantly less potent, however it has NMDA antagonism like Ketobemidone.
:Ketobemidone - μ opioid antagonist & NMDA antagonist. More addictive than Morphine.

== Others ==
:Loperamide - Peripheral opioid so it cannot cross BBB. useful anti-Diarrhoea med. When used in conjuction with Quinine or Omerprazole can cross BBB and opioid effects are seen.
:Picenadol - R isomer (or Levopicenadol) is pure μ agonist while S is antagonist. Racemic is mixed that casues low abuse potential but has low κ activity.

=== Open Chain Opioids ===
== Amidones ==
:Dipipadone - Lost Ark of the Covenant.
:Phenadoxone - Methadone analogue, similar dose to M, lasts 1-4 hours.
:Levacetylmethadol - Methadone analogue with u agonism and noncompetitive a3b4 NACh antagonisMorphine. Brand name Orlaam, prescribed to those unresponsive to methadone or subutex. Long half life (3 days) and heavier affect.
:Norpipanone - Was not under international control until case reports of addiction arose.
:Isomethadone - Previously used in medicine. μ- δ- agonisMorphine. S-isomer more potent.

==Methadols ==
:Dimepheptanol - Related to Methadone, has two isomers which also have two isomers so 6 possible isomers including racemic.

== Moramides ==
:Palfium (Dextomoramide) - 3x potency of M but shorter acting. High BA & fast acting, oral feels like shooting. Low LD50 & inconsistent potency (one day you may need 5mg, next day 3mg)

== Thiambutens ==
:Thiambutenes - Dimethyl-TAB, Diethyl-TAB, Ethylmethyl-TAB. Used in vetinary medicine in Japan. Banned in virtually all countried due to high abuse potential. Anticholinergic and antihistamine properties!

== Phenalkoxams ==
:Dextropropoxyphene - Low potency opioid not absorbed by CYP2D6. Also is a potent, noncompetitive α3β4 NACh antagonist and a weak SRI.
:Dimenoxadol - Benzillic Acid derivative related to methadone. Banned due to high abuse potential it seems.
:Dioxaphetyl butyrate - Banned opioid similar to methadone. Possibly in use or previously in use as a med under the names Amidalgon & Spasmoxal.

== Ampromides ==
:Diampromide - Banned Analgesic related to PropiraMorphine. Similar potency to Morphine.
:Propiram - Slightly more potent than codeine, 3-6hr duration. mixed μ agonist-antagonist favouring agonisMorphine. affinity for κ & δ, sigma and NMDA. 97% oral BA!

== Others ==
:IC-26 Methadone analogue with similar potency, but unscheduled.
:Lefetamine - Weak opioid on the same scale as codeine but has DRI properties.
:R-4066 - Methadone analogue with 212x the potency, but a much shorter duration. (3 hours)

== Amilidopiperidines ==

:3-Methylfentanyl - 400-6000x potency of Morphine depending on isomer (cis-iso more potent).
:4-Fluorobutyrfentanyl - Short duration.
:Acetylfentanyl - 80x Morphine.
:Alfentanil - 1/4 the potency and 1/3 the duration of fent but 4x quicker onset. The businessman's lunch of opioids.
:Betahydroxythiofentanyl - One of the more favoured fentanyl analogues by addicts, implying euphoria.
:Butyrfentanyl - 20-25x Morphine.
:Carfentanil - 100x potency of fent., 10000x Morphine. Used in spetznaz hostage crisis. 10,000x potency of Morphine. Activity in humans starts at 1μg.
:Lofentanil - More potent and with a longer duration than carfentanil.
:Mirfentanil - Fentanyl analogue with strong selevtivity over μ. Lower doses it antagonises effects caused by lesser opioids but at higher doses is resistant to antagonists, suggesting it has non-opioid mechanisms.
:Ohmefentanyl - 6300x morphine at it's most active isomer. Analogues of this are even stronger with one possessing 30,000x Morphine.
:Parofluorofentanyl - 150-200x morphine. Sold breifly in 1980.
:R-30490 - Analogue of carfentanil. Most selective μ agonist of all fentanyl analogues.
:Remifentanil - Potent ultra short acting fent. analogue. Potency from between 20 and 100ug. Used in medicine as an anaesthetic under Ultiva.
:Sufentanil - 5-10x potency of fentanyl.

== Opipavine Derivatives ==
:7-PET - 300x potency of M, 3-OH derivative is 2200x potency of Morphine. Unscheduled.
:Acetorphine - 8700x potency of Morphine.
:BU-48 - Etorphine derivative. Selective δ agonist and produces only convulsions with slight antidepression.
:Buprenorphin - Subutex.
:Cyprenorphine - Buprenorphine analogue, agonist-antagonist effects but with higher affinity towards κ.
:Dihydroetorphine -1000-12000x potency of M depending on RoA. Less addictive than other opioids and is used in a similar fashion to Subutex in China.
:Etorphine - 1000-3000x potency of Morphine. μ, κ & δ opioid agonist. weak affinity for ORL1 nociceptin/orphanin FQ receptor.

== Indoles ==
:18-Methoxycoronaridine - Ibogaine derivative, selective α3β4 nicotinic antagonist, however no affinity for α4β2, NMDA or seretonin. Retains modest affinity at μ & κ opioid.
:7-Hydroxymitragynine - Alkaloid in KratoMorphine. Some 17x potency of Morphine. 30x potency of Mitragynine.
:Eseroline - Metabolite of the ACh inhibitor physostigmine but potent μ agonist.
:Hodgkinsine - Alkaloid found in Psychotria colorata plants. Has antiviral, antibacterial and antifungal properties. Also μ opioid agonist & NMDA antagonist.
:Ibogaine - Addiction CURE. HT2a agonist, κ opioid agonist, NMDA antagonist.
:Mitragynine - Alkaloid in KratoMorphine. Fairly selective μ agonist but little affinity for δ & κ.
:Noribogaine - Metabolite of Ibogaine. Potent SRI, κ antagonist, weak μ full agonist.
:Voacangine - Precursor to Ibogine used by iboga plant. Displays similar effects towards addiction as Ibogaine.

== Pyrroles ==
:Viminol - Mixed agonist-antagonist, 5.5x Morphine.
:Pyrollidone-Viminol - 318x Morphine.

== Diphenylmethylpiperazines ==
:BW373U86 - Selective δ agonist at 15x stronger affinity. Analgesic and anti-depressant properties along with BDNF release. Produces convulsions at high doses and reverses respiratory depression produced by μ agonisMorphine. Also protects heart muscle cells from death during oxygen deprivation, a result of heart attacks.
:DPI-227 - Highly selective δ agonist with antidepressant effects but produces fewer convulsions than most other dugs in it's family.
:DPI-3290 - Potent δ & μ agonist but produces little respiratory depression.

== Opioid Peptides ==

:Biphalin - Endogenous eptide with high affinity for δ & μ receptors. Potency almost 7x greater than Etorphine and 7000x Morphine. Low side effects; no dependancy caused.
:Casomorphins - Opioids found in Cow's milk.
:DAMGO - Synthetic opioid peptide with high μ selectivity. When administered alongside M for 7 days, M had the same effect at the same dose as the first day. I.e. removes tolerance.
:Deltorphin - High affinity and selectivity, naturally occuring δ opioid agonist.
:Dermorphin - South American Tree frog skin. Natural opioid peptide. High potency (30-40x M) and selectivity to μ but may be less likely to cause tolerance and addiction.
:Dynorphins - Endogenous opioid peptides, primarily k agonists. Useful in the analysis of addiction.
:Leu-enkephalin - Endogeneous opioid petide that acts as a δ & μ agonist with strong selectivity for δ.
:Met-enkephalin - Opioid Growth Factor (OGF), Endogenous opioid peptide. Primary ligand of the δ receptor along with Leu-enkephalin (high potency and selectivity at δ). Low BA & is metabolised rapidly.
:Opiorphin - Endogenous opioid isolated from human saliva.

== Others ==

:3-HO-TCP - PCP analogue. More glutamergic than the PCP analogue.
:3-HO-BCP - Substitutes for both cocaine and morphine at ~5mg (made-up).
:AD-1211 - Structure looks unrelated to /most/ other opioid drugs. Mixed Agonist-antagonist at opioid recepts similar to pentazocine. Little to no developement of tolerance/dependence in animal studies.
:AH-7921 - Selective μ agonist, with 80% potency of Morphine. distributed as an RC, TRs show that it has very little euphoria, indicating euphoria comes from somewhere else. Perhaps sigma? Other opioids are heavily potentiated by it. Perhaps μ agonism is purely analgesic and high comes from a combination of μ & δ with each multiplying the affect of the other. This indicates ultimate opioid high would be moderately selective δ agonist.
:Azaprocin - Azaprocin - ~10x potency of Morphine. Faster onset and short duration of actin. Discoved in 1963, never been marketed. The derivative subbed on the phenyl ring with a p-nitro group would be more potent by roughly 2.5. (So 25x potency of M) The open ringed 2,6-dimethylpiperazine analouges would also be active.
:BRL-52537 - Highly potent and selective κ agonist. Neuroprotective.
:Bromadol (BDPC) - 500-10,000x potency of Morphine. Similar to PCP analogues & -HO bonds within theMorphine.
:C-8813 (Thiobromadol) - 591x potency of Morphine. μ agonist & δ antagonist to reduce repiratory depression. Making the drug safer.
:Ciramadol - Opioid related to PCP, Tramadol & Tapentadol. mixed agonist-antagonist for μ, low abuse potential and ceiling on respiratory depression.
:Enadoline - Highly selective κ agonist. Produces visual distortions, dissociation and of course dysphoria similar to Salvia.
:Herkinorin - Analogue of Salvinorin A but the complete opposite. 100x higher μ affinity and 50x lower κ affinity. Also; "does not promote the recruitment of β-arrestin-2 to the intracellular domain of the μ-opioid receptor, or induce receptor internalization". This means Herkinorin may not produce tolerance or dependance.
:HZ-2 - κ-opioid agonist, same potency as morphine, long duration, high oral BA.
:ICI-199,441 - High potency, highly selective κ agonist with analgesic effects.
:Methopholine - Isoquinilone derivative with same efficacy as codeine. Could produces corneal opacity. Analogues are more potent with 4'-nitromethopholine at 20x codeine.
:MT-45 - 80% of Morphine. mixed agonist-antagonist and mild NMDA antagonist.
:Nortilidine - Equipotency of Morphine. Opioid activity is in (1S,2R) iso, NMDA antagonism is in (1R,2S) iso. Also acts as a DRI.
:O-Desmethyltramadol - Metabolite of Tramadol. Considerably more potent than Tramadol. Both (+) & (-) isomers lose SRI function but (-) retains NRI functionality. RC.
:Salvinorin A - Highly potent κ agonist and even more potent D2 partial agonist. Use in therapy for addiction.
:Salvinorin B ethoxymethyl ether - Semi-synthetic analogue of Salv. A. Longer duration @ ~3hrs, active at 50ug & 3000x (!) selectivity over μ & δ.
:Salvinorin B methoxymethyl ether - Similar to ^^ but less selective. 5x potency as Salvinorin A. Deacetylised from Salvinorin A.
:SC-17599 - Selective μ agonist with little or no affinity for δ & κ. Potency in between pethidine & morphine.
:RWJ-394674 - Potent and selective δ agonist, however once inside body it is dealkylated to its monodesethyl metabolite RWJ-413216 which is a potent μ agonist with less affinity for δ. δ activity counteracts the respiratory depression the μ causes. Only prominent side effect is sedation (and euphoria!).
:TAN-67 - Potent and selective δ1 agonist. Has analgesic properties & releases dopamine in the brain. Neuro & cardiac protective properties.
:Tapentadol - μ & σ agonist & SNRI. Potency in between M & TraMorphine.
:Tifluadom - Benzo derivative but without GABAa agonisMorphine. Instead selective κ agonisMorphine.
:U-47700 - Overlays betaprodine, 7.5x morphine.
:U-50488 - Highly selective κ agonist with analgesic effects.
:U-69,593 - Potent and selective κ1 agonist. Produces; antinociception, anti-inflammation, anxiolysis (low doses), respiratory depression & diuresis. Also inhibits periphery oxytocin secretion. Not sure if Hallucinogenic.
:W-15 - 5.4x Morphine. RC.
:W-18 - 10,000x potency of M, structure abstract from any other drug. These super potent opioids are used in vetenarian practice for tranquilising elephants.

== Opioid Antagonists and Inverse Agonists ==
(selective δ antagonists may reduce physical addiction without causing w/d if attatched to an opioid).
:Chlornaltrexamine - Irreversible mixed agonist-antagonist at μ opioid. 22x more potent than Morphine.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors.
:Diprenorphine - Strongest opioid antagonist available. 100x potency of Nalorphine. Used to reverse effects of super-potent opioids.
:Levallorphan - μ opioid antagonist, when used with opioids, it potentiates it and removes addiction potential or induces withdrawal in addicts.
:Nalbuphine - Mixed agonist-antagonist as is common with this class, there occurs analgesia with no addictive properties.
:Naloxazone - Irreversible μ opioid receptor antagonist.
:Naloxonazine - Very Potent Irreversible μ opioid antagonist. Dimerizes from Naloxazone under acidic conditions.
:Naltrexone - Competitive antagonist at μ & κ receptors, and to a lesser extent, δ. Modulation of the dopaminergic mesolimbic pathway makes it good for countering alcohol dependance as well as opioid addiction. Blocks the euphoric effects of opioids and is used in rapid detoxification and attenuation of withdrawal. If opioids are used simultaneously, oD may occur.
:Samidorphan - Selective μ antagonist. potential for addiction treatment.

== Uncategorised Opioids ==

:FE 200665 - Is an all D-Amino acid peptide that acts as a restucted K-opioid receptor agnoist. Was dosed at 0.36mg/kg IV. Was compared to 15mg oxycodone. Slightly less than hydrocodone. Caused Hyperalgesic response in a skin pinch test. Also known as CR665.
:SoRI-9409 - Mixed μ agonist & δ antagonist. moderate analgesia without development of tolerance. Anti-addictive effects for all dopaminergic drugs.
:Synthetic Conotoxin - Snail toxin derived painkiller 1000x potency of morphine. Non-addictive.

==RELATED COMPOUNDS==
:Amiphenazole - Treatment for OD. counteracts respiratory depression. If Morphine-N-oxide is taken on this, M's potency will increase.
:Chitosan - Linear polysaccharide that can give Morphine up to 60% BA intranasally. Powdered & the ratio is 1.3g : 6.7g (morphine : chitosan).
:BIMU-8 - Nootropic.

:NMDA antagonists - Inhibit development of tolerance to morphine.
:Tezampanel - Anxiolytic.
:Ibudilast - Nootropic.
:Nuciferine
:Tetrahydropalmatine - Anxiolytic.
:Lofexidine - Anxiolytic.
:d & l Phenylalanine (DLPA) - Increases dopamine and endorphin levels, reducing opioid tolerance and even providing an analgesic effect of it's own.

== CCK Antagonists ==

:Proglumide - Acts as a d opioid agonist and non selective CCK antagonist.Enhances analgesia produced by opioids and can prevent or even reverse the development of tolerance
:Devazepide - No affinity for GABAa, selective CCKa antagonist.
:Lorglumide - Selective CCKa antagonist for treatment of gastrointestinal problems and some forms of cancer as well as opioid interacting properties.

== Nocieceptinergic drugs ==
(ORL-1 ant. & ag.'s)
:J-113,397 - Highly selective ORL-1 antagonist. Prevents development of opioid tolerance, stimulates dopamine release, cognitive enhancer
:SB-612,111 - Selective ORL-1 antagonist but several times ^^
:MCOPPB - Potent, selective ORL-1 agonist with only moderate affinity for μ, even less for δ & κ. Anxiolytic with no inhibition of memory, motor function or sedation.
:NNC 63-0532 - Potent, selective ORL-1 agonist.
:Ro64-6198 - Potent, selective ORL-1 agonist with 100x selectivity over others. In rats produced anxiolytic but no anticonvulsant effects. Impairs short term memory & increases appetite. Reduces analgesic effects of Morphine but does not prevent tolerance. In primates it showed analgesic behaviour without respiratory depression.
:Menabitan - Potent cannabinoid receptor agonist with anti-nociceptive effects.

== Enkephalin Potease Inhibitors ==

:RB-101*** - Inhibits enzymes responsible for breaking down enkephalin (regulates nociceptin). Weak μ & δ affinity and slight σ1. Potentiates opioids, stops withdrawal symptoms, no addiction potential, produces no respiratory depression. Also exerts very potent antidepressant and anxiolytic effects. Not orally active so analogues vv were developed.
:RB-120 - Orally active version of the above.
:RB-3007 - Another Enkeph. PI & Nociceptin antagonist.

Opioid Notes

2014-10-17T18:51:00Z

Roi: spelling and shit

=== Opium Derivatives ===

== Opium Alkaloids ==
:Thebaine - 6,14 Dimethoxy version of Oxymorphone. Stimulant rather than an analgesic.
:Narceine - Bitter, Crystalline, formerly used as a substitute for Morphine.
:Noscapine - Acts on the Sigma receptor. Non painkilling. Used commonly in Antitussives. Blocks Bradykinine B-2 receptors in Stroke patients.

== Alkaloid Salt Mixtures ==
:Pantopon - Preparation of all alkaloids present in opium without plant matter. Injectable and slightly less potent than Morphine.

== Morphine Family ==
:6-MDDM - 80x Morphine, has a faster onset and less body load then the prior.
:Azidomorphine - 40x Morphine, has a high affinity for μ.
:Hydromorphinol - Derivative of Morphine, yet more potent, with a steeper-dose-response curve and a longer half life. Scripted in Sweden.
:Methyldesorphin - 15x Morphine. Is found in some mixtures of Krokodil.
:MR-2096 - Oxymorphone analogue that is roughly the same potency.
:N-Phenethylnormorphine - 8-14x Morphine.
:RAM-378 - N-Phenethyl analogue of Hydromorphinol. It is probably more potent as a result.

== 3,6 Morphine Diesters ==
:Diacetyldihydromorphine - Occasionally used as an alternative to diamorphine, of which it is faster acting, longer lasting and has less side effects such as euphoria and addiction. However it is equipotent with Morphine.
:Dipropanoylmorphine - Ester of Morphine used to treat severe pain. Rarely used but considered to be safer and less addictive than Morphine. As such carries less side effects, such as euphoria. Slower acting, longer lasting and slightly more potent than Morphine.
:Nicomorphone - 2-3x Morphine and commonly prescribed in German speaking countries.

== Codeine-Dionine Family ==
:Heterocodeine - Reverse isomer of codeine. 6x Morphine, while Codeine is a prodrug, Heterocodeine is a direct agonist.
:Myrophine - Acts as a prodrug to Morphine. Has a slow onset and longer duration, but reduced potency. Does NOT produce addiction or dependence regardless of dose.
:Acetyldihydrocodeine - Used in Germany. Close relative of Thebacon, where only the 6-7 cond is unsaturated. 6-Acetyl derivative of Dihydrocodeine. Metabolizes into Dihydromorphine. Higher lipophilicity than codeine. Would probably be more potent and longer lasting as a result. Higher oral BA than Codeine.
== Morphinones and Morphols ==
:14-Cinnamoyloxycodeinone - 100x Morphine.
:14-Methoxymetopon - 500x Morphine. Can be up to one million times Morphine if injected into the spine.
:14-Phenylpropoxymetopon - 2000x potency of Morphine. When injected into the spine up to one million times Morphine. 14-Methoxymetopon has a ceiling effect on respiratory depression, but the above has been left untested.
:3-Acetyloxymorphone - Acetylated analogue of Oxymorphone.
:7-Spiroindanyloxymorphone - Odd Oxymorphone analogue that is selective at dopamine.
:Acetylmorphone - Acetoxy version of Hydromorphone, has a higher bioavailability as a result.
:Chloroxymorphamine - Derivative of Oxymorphone and irreversible full agonist.
:Methyldihydromorphone - Related to Heterocodieine not dihydrocodeine. Is 6-9x Morphine.
:Metopon - Methylated Hydromorphone, less potent. More than likely would have more euphoria as a result.
:N-Phenethyl - 14-Ethoxymetopon - 60x Morphine, but produces less constipation. d & u agonist.
:Oxymorphol - 6-Hydrogenated Oxymorphone.
:Pentamorphone - Few times more potent than Fentanyl. Short duration, yet low respiratory depression.
:Semorphone - 2x Morphine. Partial u agonist and has a ceiling effect on both analgesia and respiratory depression.
:Thebacon - Thebaine analogue, that is fairly uninteresting. 6-8x Codeine.

== Hydrazones ==
:Oxymorphazone - Half Oxymorphone, yet higher doses last up to 48 hours.

== Morphians ==
:Butorphanol - Partial agonist-antagonist at μ opioid and competitive antagonist/partial agonist at κ opioid. dysphoria is common at normal dose.
:Drotebanol - Morphinan derivative synthesised from Thebaine with analgesic effects several times more potent than codeine but weaker than morphine. Moderately addictive but limited physical dependance. Under Metabanyl when available as a script.
:Dextromethorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, (very weak) μ, δ & κ opioid agonist, SERT & NET inhibitor, NADPH Oxidase inhibitor. (Race)Methorphan = racemic
:Dextrorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, L-Type voltage-gated calcium channel (LVGCC) blocker, SRI.
:Cyclorphan - Mixed antagonist-agonist with affinity for κ.
:Levophenacylmorphan - 10x potency of Morphine.
:Levofurethylnormorphanol (Ro4-1539) - potent μ opioid agonist 30-60x potency of Levorphanol.
:Levomethorphan (+) - NDMA antagonist, σ1 & σ2 sigma agonist, μ, δ & κ opioid agonist.
:Levorphanol (+) - μ, κ & δ agonist, 4-8x potency of M, long duration, no cross tolerance with morphine.
:Norlevorphanol - Opioid analgesic, uninteresting.
:Phenomorphan - 10x potency of Levorphanol. :└--> N-(2-(2-furyl)ethyl) analogue - 60x Levorphanol :└--> N-(2-(2-thienyl)ethyl) analogue - 45x Levorphanol.
:Proxorphan - Partial κ agonist, lesser partial μ agonist.
:Ro4-1539 (Furethylnorlevorphanol) - 30-60x Morphine. One of the more potent u agonists from the Morphans.

:(Race)Methorphan: L(eft) (+) Levomethorphan >< Dextromethorphan (-) D(exter) --> l = Opioid >< d = Hallucinogenic opioid.
└--> Racemic mix of both isomers, embodying their properties.

:Morphinan (Racemorphan): l (+) Levorphanol >< Dextrorphan (-) d --> l = Opioid >< :d = Hallucinogenic opioid.
:└--> Racemic mix of both isomers, embodying their properties.

:(Race)Allorphan: l (+) Levallorphan >< Dextrallorphan (-) d --> l = Opioid antagonist >< d = NMDA antagonist.
: └--> Racemic mix of both isomers, embodying their properties.

:3-Hydroxymorphinan: l (+) Norlevorphanol >< Nordextrorphan (-) d --> l = Opioid >< d = Nootropic.
└--> Racemic mix of both isomers, embodying their properties.

:Oxilorphan: μ antagonist & weak partial κ agonist.
:Dimemorfan - Sigmaergic drug.
:Xorphanol - Mixed agonist-antagonist produces convulsions at highest dose tested.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors.
:Samidorphan - selective μ antagonist. potential for addiction treatment.

== Benzomorphans ==

:Butinazocine - Benzomorphan opioid that was never marketed.
:Carbazocine - Benzomorphan opioid that was never marketed.
:Etazocine - Partial opioid agonist with mixed agonist-antagonist effects. low potency.
:Ethylketocyclozocine - Partial opioid agonist with mixed agonist-antagonist effects.
:Ibazocine - Benzomorphan opioid that was never marketed.
:Moxazocine - 10x potency of Morphine, partial/mixed agonist-antagonist.
:Tonazocine - Partial agonist at μ & δ, no adverse effects on breathing.
:Volazocine - Benzomorphan opioid that was never marketed.
:Fluorophen - Radioligand, full μ agonist (6x M) & lower affinity for δ.
:Zenazocine - Partial agonist at μ & δ.
:Eptazocine - Japanese κ agonist & μ antagonist.
:Pentazocine - Mixed agonist-antagonist (-) is the κ agonist side, the (+) displays 10x the affinity for sigma receptors. NO μ agonism.
:Phenazocine - Related to ^ but stronger analgesic, 4x potency of Morphine.
:Cyclazocine - Mixed agonist-antagonist.
:Dezocine - Mixed agonist-antagonist with high κ antagonisMorphine. Low dose=euphoria (μ) High dose=dysphoria (κ). Weird structure.
:8-Carboxamidocyclazocine (8-CAC) - κ & μ agonist, long duration.
:Bremazocine - κ agonist related to Pentazocine.
:Metazocine - Analgesic; mixed agonist-antagonist at μ, activity also at κ and sigma.
:Alazocine - σ1 agonist, κ opioid agonist & slight NMDA antagonist.

== 4-Phenylpiperidines ==
:4-Fluoropethidine - In comparison to pethidine, it is 50% less potent as an analgesic but 50% more potent as a DRI. (4-iodo & 3, 4-dichloro only increase these differences)
:Anileridine - Another banned pethidine analogue, probably abused. Higher analgesia than Meperidine due to n-aminophenyl group and acts withing 15 mins orally, lasting 2-3 hours.
:Benzethidine - 4-phenylpiperidine analogue of pethidine. Probably somewhat more potent and euphoric. Never scripted.
:Carperidine - Fairly normal opioid but unused in medicine and currently legal (08/06/2013).
:Furethidine - 4-Phenylpiperidine analogue of pethidine. Probably a lot more potent and abuse prone. Never prescribed.
:Morpheridine - Related to meperidine but 4x the potency and does not cause convulsions.
:Phenoperidine - 20-200x Pethidine. Less hypnotic and than morphine but more emetic (nausea). This can be cured by Haloperidol.
:Piminodine - Similar dose to Morphine, used in 60's and 70's but was banned. It was probably abused widely.
.
== Prodines ==
:Alphaprodine - 1.5x Morphine.
:Allylprodine - Prodine analogue 23x potency of Morphine.
:Betaprodine - 7.5x Morphine.
:Prosidol - Russian Prodine analogue.

== Ketobemidones ==
:Acetoxyketobemidone - Unschedualed analogue of Ketobemidone.
:Bemidone - Analogue of Pethidine but significantly less potent, however it has NMDA antagonism like Ketobemidone.
:Ketobemidone - μ opioid antagonist & NMDA antagonist. More addictive than Morphine.

== Others ==
:Loperamide - Peripheral opioid so it cannot cross BBB. useful anti-Diarrhoea med. When used in conjuction with Quinine or Omerprazole can cross BBB and opioid effects are seen.
:Picenadol - R isomer (or Levopicenadol) is pure μ agonist while S is antagonist. Racemic is mixed that casues low abuse potential but has low κ activity.

=== Open Chain Opioids ===
== Amidones ==
:Dipipadone - Lost Ark of the Covenant.
:Phenadoxone - Methadone analogue, similar dose to M, lasts 1-4 hours.
:Levacetylmethadol - Methadone analogue with u agonism and noncompetitive a3b4 NACh antagonisMorphine. Brand name Orlaam, prescribed to those unresponsive to methadone or subutex. Long half life (3 days) and heavier affect.
:Norpipanone - Was not under international control until case reports of addiction arose.
:Isomethadone - Previously used in medicine. μ- δ- agonisMorphine. S-isomer more potent.

==Methadols ==
:Dimepheptanol - Related to Methadone, has two isomers which also have two isomers so 6 possible isomers including racemic.

== Moramides ==
:Palfium (Dextomoramide) - 3x potency of M but shorter acting. High BA & fast acting, oral feels like shooting. Low LD50 & inconsistent potency (one day you may need 5mg, next day 3mg)

== Thiambutens ==
:Thiambutenes - Dimethyl-TAB, Diethyl-TAB, Ethylmethyl-TAB. Used in vetinary medicine in Japan. Banned in virtually all countried due to high abuse potential. Anticholinergic and antihistamine properties!

== Phenalkoxams ==
:Dextropropoxyphene - Low potency opioid not absorbed by CYP2D6. Also is a potent, noncompetitive α3β4 NACh antagonist and a weak SRI.
:Dimenoxadol - Benzillic Acid derivative related to methadone. Banned due to high abuse potential it seems.
:Dioxaphetyl butyrate - Banned opioid similar to methadone. Possibly in use or previously in use as a med under the names Amidalgon & Spasmoxal.

== Ampromides ==
:Diampromide - Banned Analgesic related to PropiraMorphine. Similar potency to Morphine.
:Propiram - Slightly more potent than codeine, 3-6hr duration. mixed μ agonist-antagonist favouring agonisMorphine. affinity for κ & δ, sigma and nmda. 97% oral BA!

== Others ==
:IC-26 Methadone analogue with similar potency, but unscheduled.
:Lefetamine - Weak opioid on the same scale as codeine but has DRI properties.
:R-4066 - Methadone analogue with 212x the potency, but a much shorter duration. (3 hours)

== Amilidopiperidines ==

:3-Methylfentanyl - 400-6000x potency of M depending on isomer (cis-iso more potent).
:Alfentanil - 1/4 the potency and 1/3 the duration of fent but 4x quicker onset. The businessman's lunch of opioids.
:Betahydroxythiofentanyl - One of the more favoured fentanyl analogues by addicts, implying euphoria.
:Carfentanil - 100x potency of fent., 10000x Morphine. Used in spetznaz hostage crisis. 10,000x potency of Morphine. Activity in humans starts at 1μg.
:Lofentanil - More potent and with a longer duration than carfentanil.
:Mirfentanil - Fentanyl analogue with strong selevtivity over μ. Lower doses it antagonises effects caused by lesser opioids but at higher doses is resistant to antagonists, suggesting it has non-opioid mechanisms.
:Ohmefentanyl - 6300x morphine at it's most active isomer. Analogues of this are even stronger with one possessing 30,000x Morphine.
:Parofluorofentanyl - 150-200x morphine. Sold breifly in 1980.
:R-30490 - Analogue of carfentanil. Most selective μ agonist of all fentanyl analogues.
:Remifentanil - Potent ultra short acting fent. analogue. Potency from between 20 and 100ug. Used in medicine as an anaesthetic under Ultiva.
:Sufentanil - 5-10x potency of fent

== Opipavine Derivatives ==
:7-PET - 300x potency of M, 3-OH derivative is 2200x potency of Morphine. Unscheduled.
:Acetorphine - 8700x potency of Morphine.
:BU-48 - Etorphine derivative. Selective δ agonist and produces only convulsions with slight antidepression.
:Buprenorphin - Subutex.
:Cyprenorphine - Buprenorphine analogue, agonist-antagonist effects but with higher affinity towards κ.
:Dihydroetorphine -1000-12000x potency of M depending on RoA. Less addictive than other opioids and is used in a similar fashion to Subutex in China.
:Etorphine - 1000-3000x potency of Morphine. μ, κ & δ opioid agonist. weak affinity for ORL1 nociceptin/orphanin FQ receptor.

== Indoles ==
:18-Methoxycoronaridine - Ibogaine derivative, selective α3β4 nicotinic antagonist, however no affinity for α4β2, NMDA or seretonin. Retains modest affinity at μ & κ opioid.
:7-Hydroxymitragynine - Alkaloid in KratoMorphine. Some 17x potency of Morphine. 30x potency of Mitragynine.
:Eseroline - Metabolite of the ACh inhibitor physostigmine but potent μ agonist.
:Hodgkinsine - Alkaloid found in Psychotria colorata plants. Has antiviral, antibacterial and antifungal properties. Also μ opioid agonist & NMDA antagonist.
:Ibogaine - Addiction CURE. HT2a agonist, κ opioid agonist, NMDA antagonist.
:Mitragynine - Alkaloid in KratoMorphine. Fairly selective μ agonist but little affinity for δ & κ.
:Noribogaine - Metabolite of Ibogaine. Potent SRI, κ antagonist, weak μ full agonist.
:Voacangine - Precursor to Ibogine used by iboga plant. Displays similar effects towards addiction as Ibogaine.

== Diphenylmethylpiperazines ==
:BW373U86 - Selective δ agonist at 15x stronger affinity. Analgesic and anti-depressant properties along with BDNF release. Produces convulsions at high doses and reverses respiratory depression produced by μ agonisMorphine. Also protects heart muscle cells from death during oxygen deprivation, a result of heart attacks.
:DPI-227 - Highly selective δ agonist with antidepressant effects but produces fewer convulsions than most other dugs in it's family.
:DPI-3290 - Potent δ & μ agonist but produces little respiratory depression.

== Opioid Peptides ==

:Biphalin - Endogenous eptide with high affinity for δ & μ receptors. Potency almost 7x greater than Etorphine and 7000x Morphine. Low side effects; no dependancy caused.
:Casomorphins - Opioids found in Cow's milk.
:DAMGO - Synthetic opioid peptide with high μ selectivity. When administered alongside M for 7 days, M had the same effect at the same dose as the first day. I.e. removes tolerance.
:Deltorphin - High affinity and selectivity, naturally occuring δ opioid agonist.
:Dermorphin - South American Tree frog skin. Natural opioid peptide. High potency (30-40x M) and selectivity to μ but may be less likely to cause tolerance and addiction.
:Dynorphins - Endogenous opioid peptides, primarily k agonists. Useful in the analysis of addiction.
:Leu-enkephalin - Endogeneous opioid petide that acts as a δ & μ agonist with strong selectivity for δ.
:Met-enkephalin - Opioid Growth Factor (OGF), Endogenous opioid peptide. Primary ligand of the δ receptor along with Leu-enkephalin (high potency and selectivity at δ). Low BA & is metabolised rapidly.
:Opiorphin - Endogenous opioid isolated from human saliva.

== Others ==

:3-HO-TCP - PCP analogue. More glutamergic than the PCP analogue.
:3-HO-BCP - Substitutes for both cocaine and morphine at ~5mg (made-up).
:AD-1211 - Structure looks unrelated to /most/ other opioid drugs. Mixed Agonist-antagonist at opioid recepts similar to pentazocine. Little to no developement of tolerance/dependence in animal studies.
:AH-7921 - Selective μ agonist, with 80% potency of Morphine. distributed as an RC, TRs show that it has very little euphoria, indicating euphoria comes from somewhere else. Perhaps sigma? Other opioids are heavily potentiated by it. Perhaps μ agonism is purely analgesic and high comes from a combination of μ & δ with each multiplying the affect of the other. This indicates ultimate opioid high would be moderately selective δ agonist.
:Azaprocin - Azaprocin - ~10x potency of Morphine. Faster onset and short duration of actin. Discoved in 1963, never been marketed. The derivative subbed on the phenyl ring with a p-nitro group would be more potent by roughly 2.5. (So 25x potency of M) The open ringed 2,6-dimethylpiperazine analouges would also be active.
:BRL-52537 - Highly potent and selective κ agonist. Neuroprotective.
:Bromadol (BDPC) - 500-10,000x potency of Morphine. Similar to PCP analogues & -HO bonds within theMorphine.
:C-8813 (Thiobromadol) - 591x potency of Morphine. μ agonist & δ antagonist to reduce repiratory depression. Making the drug safer.
:Ciramadol - Opioid related to PCP, Tramadol & Tapentadol. mixed agonist-antagonist for μ, low abuse potential and ceiling on respiratory depression.
:Enadoline - Highly selective κ agonist. Produces visual distortions, dissociation and of course dysphoria similar to Salvia.
:Herkinorin - Analogue of Salvinorin A but the complete opposite. 100x higher μ affinity and 50x lower κ affinity. Also; "does not promote the recruitment of β-arrestin-2 to the intracellular domain of the μ-opioid receptor, or induce receptor internalization". This means Herkinorin may not produce tolerance or dependance.
:HZ-2 - κ-opioid agonist, same potency as morphine, long duration, high oral BA.
:ICI-199,441 - High potency, highly selective κ agonist with analgesic effects.
:Methopholine - Isoquinilone derivative with same efficacy as codeine. Could produces corneal opacity. Analogues are more potent with 4'-nitromethopholine at 20x codeine.
:MT-45 - 80% of Morphine. mixed agonist-antagonist and mild NMDA antagonist.
:Nortilidine - Equipotency of Morphine. Opioid activity is in (1S,2R) iso, NMDA antagonism is in (1R,2S) iso. Also acts as a DRI.
:O-Desmethyltramadol - Metabolite of Tramadol. Considerably more potent than Tramadol. Both (+) & (-) isomers lose SRI function but (-) retains NRI functionality. RC.
:Salvinorin A - Highly potent κ agonist and even more potent D2 partial agonist. Use in therapy for addiction.
:Salvinorin B ethoxymethyl ether - Semi-synthetic analogue of Salv. A. Longer duration @ ~3hrs, active at 50ug & 3000x (!) selectivity over μ & δ.
:Salvinorin B methoxymethyl ether - Similar to ^^ but less selective. 5x potency as Salvinorin A. Deacetylised from Salvinorin A.
:SC-17599 - Selective μ agonist with little or no affinity for δ & κ. Potency in between pethidine & morphine.
:RWJ-394674 - Potent and selective δ agonist, however once inside body it is dealkylated to its monodesethyl metabolite RWJ-413216 which is a potent μ agonist with less affinity for δ. δ activity counteracts the respiratory depression the μ causes. Only prominent side effect is sedation (and euphoria!).
:TAN-67 - Potent and selective δ1 agonist. Has analgesic properties & releases dopamine in the brain. Neuro & cardiac protective properties.
:Tapentadol - μ & σ agonist & SNRI. Potency in between M & TraMorphine.
:Tifluadom - Benzo derivative but without GABAa agonisMorphine. Instead selective κ agonisMorphine.
:U-47700 - Overlays betaprodine, 7.5x morphine.
:U-50488 - Highly selective κ agonist with analgesic effects.
:U-69,593 - Potent and selective κ1 agonist. Produces; antinociception, anti-inflammation, anxiolysis (low doses), respiratory depression & diuresis. Also inhibits periphery oxytocin secretion. Not sure if Hallucinogenic.
:W-15 - 5.4x Morphine. RC.
:W-18 - 10,000x potency of M, structure abstract from any other drug. These super potent opioids are used in vetenarian practice for tranquilising elephants.

== Opioid Antagonists and Inverse Agonists ==
(selective δ antagonists may reduce physical addiction without causing w/d if attatched to an opioid).
:Chlornaltrexamine - Irreversible mixed agonist-antagonist at μ opioid. 22x more potent than Morphine.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors.
:Diprenorphine - Strongest opioid antagonist available. 100x potency of Nalorphine. Used to reverse effects of super-potent opioids.
:Levallorphan - μ opioid antagonist, when used with opioids, it potentiates it and removes addiction potential or induces withdrawal in addicts.
:Nalbuphine - Mixed agonist-antagonist as is common with this class, there occurs analgesia with no addictive properties.
:Naloxazone - Irreversible μ opioid receptor antagonist.
:Naloxonazine - Very Potent Irreversible μ opioid antagonist. Dimerizes from Naloxazone under acidic conditions.
:Naltrexone - Competitive antagonist at μ & κ receptors, and to a lesser extent, δ. Modulation of the dopaminergic mesolimbic pathway makes it good for countering alcohol dependance as well as opioid addiction. Blocks the euphoric effects of opioids and is used in rapid detoxification and attenuation of withdrawal. If opioids are used simultaneously, oD may occur.
:Samidorphan - Selective μ antagonist. potential for addiction treatment.

== Uncategorised Opioids ==

:FE 200665 - Is an all D-Amino acid peptide that acts as a restucted K-opioid receptor agnoist. Was dosed at 0.36mg/kg IV. Was compared to 15mg oxycodone. Slightly less than hydrocodone. Caused Hyperalgesic response in a skin pinch test. Also known as CR665.
:SoRI-9409 - Mixed μ agonist & δ antagonist. moderate analgesia without development of tolerance. Anti-addictive effects for all dopaminergic drugs.
:Synthetic Conotoxin - Snail toxin derived painkiller 1000x potency of morphine. Non-addictive.

==RELATED COMPOUNDS==
:Amiphenazole - Treatment for OD. counteracts respiratory depression. If Morphine-N-oxide is taken on this, M's potency will increase.
:Chitosan - Linear polysaccharide that can give Morphine up to 60% BA intranasally. Powdered & the ratio is 1.3g : 6.7g (morphine : chitosan).
:BIMU-8 - Nootropic.

:NMDA antagonists - Inhibit development of tolerance to morphine.
:Tezampanel - Anxiolytic.
:Ibudilast - Nootropic.
:Nuciferine
:Tetrahydropalmatine - Anxiolytic.
:Lofexidine - Anxiolytic.
:d & l Phenylalanine (DLPA) - Increases dopamine and endorphin levels, reducing opioid tolerance and even providing an analgesic effect of it's own.

== CCK Antagonists ==

:Proglumide - Acts as a d opioid agonist and non selective CCK antagonist.Enhances analgesia produced by opioids and can prevent or even reverse the development of tolerance
:Devazepide - No affinity for GABAa, selective CCKa antagonist.
:Lorglumide - Selective CCKa antagonist for treatment of gastrointestinal problems and some forms of cancer as well as opioid interacting properties.

== Nocieceptinergic drugs ==
(ORL-1 ant. & ag.'s)
:J-113,397 - Highly selective ORL-1 antagonist. Prevents development of opioid tolerance, stimulates dopamine release, cognitive enhancer
:SB-612,111 - Selective ORL-1 antagonist but several times ^^
:MCOPPB - Potent, selective ORL-1 agonist with only moderate affinity for μ, even less for δ & κ. Anxiolytic with no inhibition of memory, motor function or sedation.
:NNC 63-0532 - Potent, selective ORL-1 agonist.
:Ro64-6198 - Potent, selective ORL-1 agonist with 100x selectivity over others. In rats produced anxiolytic but no anticonvulsant effects. Impairs short term memory & increases appetite. Reduces analgesic effects of Morphine but does not prevent tolerance. In primates it showed analgesic behaviour without respiratory depression.
:Menabitan - Potent cannabinoid receptor agonist with anti-nociceptive effects.

== Enkephalin Potease Inhibitors ==

:RB-101*** - Inhibits enzymes responsible for breaking down enkephalin (regulates nociceptin). Weak μ & δ affinity and slight σ1. Potentiates opioids, stops withdrawal symptoms, no addiction potential, produces no respiratory depression. Also exerts very potent antidepressant and anxiolytic effects. Not orally active so analogues vv were developed.
:RB-120 - Orally active version of the above.
:RB-3007 - Another Enkeph. PI & Nociceptin antagonist.

Opioid Notes

2014-10-17T15:42:25Z

Roi: /* Others */

=== Opium Derivatives ===

== Opium Alkaloids ==
:Thebaine - 6,14 Dimethoxy version of Oxymorphone. Stimulant rather than an analgesic.
:Narceine - Bitter, Crystalline, formerly used as a substitute for Morphine.
:Noscapine - Acts on the Sigma receptor. Non painkilling. Used commonly in Antitussives. Blocks Bradykinine B-2 receptors in Stroke patients.

== Alkaloid Salt Mixtures ==
:Pantopon - Preparation of all alkaloids present in opium without plant matter. Injectable and slightly less potent than Morphine.

== Morphine Family ==
:6-MDDM - 80x the potency of Morphine, has a faster onset and less body load then the prior.
:Azidomorphine - 40x the potency of Morphine, has a high affinity for μ.
:Hydromorphinol - Derivative of Morphine, yet more potent, with a steeper-dose-response curve and a longer half life. Scripted in Sweden.
:Methyldesorphin - 15x the potency of Morphine. Is found in some mixtures of Krokodil.
:MR-2096 - Oxymorphone analogue that is roughly the same potency.
:N-Phenethylnormorphine - 8-14x the potency of Morphine.
:RAM-378 - N-Phenethyl analogue of Hydromorphinol. It is probably more potent as a result.

== 3,6 Morphine Diesters ==
:Diacetyldihydromorphine - Occasionally used as an alternative to diamorphine, of which it is faster acting, longer lasting and has less side effects such as euphoria and addiction. However it is equipotent with Morphine.
:Dipropanoylmorphine - Ester of Morphine used to treat severe pain. Rarely used but considered to be safer and less addictive than Morphine. As such carries less side effects, such as euphoria. Slower acting, longer lasting and slightly more potent than Morphine.
:Nicomorphone - 2-3x the potency of Morphine and commonly prescribed in German speaking countries.

== Codeine-Dionine Family ==
:Heterocodeine - Reverse isomer of codeine. 6x the potency of Morphine, while Codeine is a prodrug, Heterocodeine is a direct agonist.
:Myrophine - Acts as a prodrug to Morphine. Has a slow onset and longer duration, but reduced potency. Does NOT produce addiction or dependence regardless of dose.
:Acetyldihydrocodeine - Used in Germany. Close relative of Thebacon, where only the 6-7 cond is unsaturated. 6-Acetyl derivative of Dihydrocodeine. Metabolizes into Dihydromorphine. Higher lipophilicity than codeine. Would probably be more potent and longer lasting as a result. Higher oral BA than Codeine.
== Morphinones and Morphols ==
:14-Cinnamoyloxycodeinone - 100x the potency of Morphine.
:14-Methoxymetopon - 500x the potency of Morphine. Can be up to one million times the potency of Morphine if injected into the spine.
:14-Phenylpropoxymetopon - 2000x potency of Morphine. When injected into the spine up to one million times the potency of Morphine. 14-Methoxymetopon has a ceiling effect on respiratory depression, but the above has been left untested.
:3-Acetyloxymorphone - Acetylated analogue of Oxymorphone.
:7-Spiroindanyloxymorphone - Odd Oxymorphone analogue that is selective at dopamine.
:Acetylmorphone - Acetoxy version of Hydromorphone, has a higher bioavailability as a result.
:Chloroxymorphamine - Derivative of Oxymorphone and irreversible full agonist.
:Methyldihydromorphone - Related to Heterocodieine not dihydrocodeine. Is 6-9x the potency of Morphine.
:Metopon - Methylated Hydromorphone, less potent. More than likely would have more euphoria as a result.
:N-Phenethyl-14-Ethoxymetopon - 60x the potency of Morphine, but produces less constipation. d & u agonist.
:Oxymorphol - 6-Hydrogenated Oxymorphone.
:Pentamorphone - Few times more potent than Fentanyl. Short duration, yet low respiratory depression.
:Semorphone - 2 times the potency of Morphine. Partial u agonist and has a ceiling effect on both analgesia and respiratory depression.
:Thebacon - Thebaine analogue, that is fairly uninteresting. 6-8x the potency of Codeine.

== Hydrazones ==
:Oxymorphazone - Half the potency of Oxymorphone, yet higher doses last up to 48 hours.

== Morphians ==
:Butorphanol - partial ant.-ag. at μ opioid and competitive antagonist/partial agonist at κ opioid. dysphoria is common at normal dose.
:Drotebanol - Morphinan derivative synthesised from Thebaine with analgesic effects several times more potent than codeine but weaker than morphine. Moderately addictive but limited physical dependance. Under Metabanyl when available as a script.
:Dextromethorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, (very weak) μ, δ & κ opioid agonist, SERT & NET inhibitor, NADPH Oxidase inhibitor. (Race)Methorphan = racemic
:Dextrorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, L-Type voltage-gated calcium channel (LVGCC) blocker, SRI.
:Cyclorphan - mixed antagonist-agonist with affinity for κ
:Levophenacylmorphan - 10x potency of M
:Levofurethylnormorphanol (Ro4-1539) - potent μ opioid agonist 30-60x potency of Levorphanol.
:Levomethorphan (+) - NDMA antagonist, σ1 & σ2 sigma agonist, μ, δ & κ opioid agonist.
:Levorphanol (+) - μ, κ & δ agonist, 4-8x potency of M, long duration, no cross tolerance with morphine
:Norlevorphanol - Opioid analgesic, uninteresting.
:Phenomorphan - 10x potency of Levorphanol. :└--> N-(2-(2-furyl)ethyl) analogue - 60x Levorphanol :└--> N-(2-(2-thienyl)ethyl) analogue - 45x Levorphanol
:Proxorphan - partial κ agonist, lesser partial μ agonist
:Ro4-1539 (Furethylnorlevorphanol) - 30-60x the potency of M. One of the more potent u agonists from the Morphans.

:(Race)Methorphan: L(eft) (+) Levomethorphan >< Dextromethorphan (-) D(exter) --> l=OPIATE >< d=HALLUCINOGENIC OPIATE
└--> Racemic mix of both isomers, embodying their properties.

:Morphinan (Racemorphan): l (+) Levorphanol >< Dextrorphan (-) d --> l=OPIATE >< :d=HALLUCINOGENIC OPIATE
:└--> Racemic mix of both isomers, embodying their properties.

:(Race)Allorphan: l (+) Levallorphan >< Dextrallorphan (-) d --> l= ANTI-OPIOID >< d=NMDA :ANTAGONISTS
: └--> Racemic mix of both isomers, embodying their properties.

:3-Hydroxymorphinan: l (+) Norlevorphanol >< Nordextrorphan (-) d --> l=OPIATE >< d=NOOTROPIC
└--> Racemic mix of both isomers, embodying their properties.

:Oxilorphan: μ antagonist & weak partial κ agonist
:Dimemorfan - SIGMAERGIC DRUG
:Xorphanol - mixed ant.-ag. produces convulsions at highest dose tested.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors
:Samidorphan - selective μ antagonist. potential for addiction treatment.

== 4-Phenylpiperidines ==
:4-Fluoropethidine - In comparison to pethidine, it is 50% less potent as an analgesic but 50% more potent as a DRI. (4-iodo & 3, 4-dichloro only increase these differences)
:Anileridine - Another banned pethidine analogue, probably abused. Higher analgesia than Meperidine due to n-aminophenyl group and acts withing 15 mins orally, lasting 2-3 hours.
:Benzethidine - 4-phenylpiperidine analogue of pethidine. Probably somewhat more potent and euphoric. Never scripted.
:Carperidine - fairly normal opiate but unused in medicine and currently LEGAL (08/06/2013)
:Furethidine - 4-Phenylpiperidine analogue of pethidine. Probably a lot more potent and abuse prone. Never prescribed.
:Morpheridine - related to meperidine but 4x the potency and does not cause convulsions
:Phenoperidine - 20-200x the potency of Pethidine. Less hypnotic and than morphine but more emetic (nausea). This can be cured by Haloperidol.
:Piminodine - similar dose to M, used in 60's and 70's but was banned. It was probably abused widely
.
== Prodines ==
:Alphaprodine - 1.5x Morphine
:Allylprodine - Prodine analogue 23x potency of Morphine
:Betaprodine - 7.5x Morphine
:Prosidol - Russian Prodine analogue

== Ketobemidones ==
:Acetoxyketobemidone - Unschedualed analogue of ketobemidone
:Bemidone - Analogue of Pethidine but significantly less potent, however it has NMDA antagonism like KetoB.
:Ketobemidone - μ opioid antagonist & NMDA antagonist. More addictive than M

== Others ==
:Loperamide - Peripheral opioid so it cannot cross BBB. useful anti-Diarrhoea med. When used in conjuction with Quinine or Omerprazole can cross BBB and opioid effects are seen.
:Picenadol - R isomer (or Levopicenadol) is pure μ agonist while S is antagonist. Racemic is mixed that casues low abuse potential but has low κ activity

=== Open Chain Opioids ===
== Amidones ==
:Dipipadone - Lost Ark of the Covenant.
:Phenadoxone - methadone analogue, similar dose to M, lasts 1-4 hours
:Levacetylmethadol - Methadone analogue with u agonism and noncompetitive a3b4 NACh antagonism. Brand name Orlaam, prescribed to those unresponsive to methadone or subutex. Long half life (3 days) and heavier affect.
:Norpipanone - Was not under international control until case reports of addiction arose.
:Isomethadone - Previously used in medicine. μ- δ- agonism. S-isomer more potent.

==Methadols ==
:Dimepheptanol - Related to Methadone, has two isomers which also have two isomers so 6 possible isomers including racemic.

== Moramides ==
:Palfium (Dextomoramide) - 3x potency of M but shorter acting. High BA & fast acting, oral feels like shooting. Low LD50 & inconsistent potency (one day you may need 5mg, next day 3mg)

== Thiambutens ==
:Thiambutenes - Dimethyl-TAB, Diethyl-TAB, Ethylmethyl-TAB. Used in vetinary medicine in Japan. Banned in virtually all countried due to high abuse potential. Anticholinergic and antihistamine properties!

== Phenalkoxams ==
:Dextropropoxyphene - Low potency opiate not absorbed by CYP2D6. Also is a potent, noncompetitive α3β4 NACh antagonist and a weak SRI.
:Dimenoxadol - Benzillic Acid derivative related to methadone. Banned due to high abuse potential it seems.
:Dioxaphetyl butyrate - Banned opioid similar to methadone. Possibly in use or previously in use as a med under the names Amidalgon & Spasmoxal.

== Ampromides ==
:Diampromide - Banned Analgesic related to Propiram. Similar potency to M.
:Propiram - Slightly more potent than codeine, 3-6hr duration. mixed μ ant.-ag. favouring agonism. affinity for κ & δ, sigma and nmda. 97% oral BA!

== Others ==
:IC-26 Methadone analogue with similar potency, but unscheduled.
:Lefetamine - Weak opiate on the same scale as codeine but has DRI properties
:R-4066 - Methadone analogue with 212x the potency, but a much shorter duration. (3 hours)

== Amilidopiperidines ==

:3-Methylfentanyl - 400-6000x potency of M depending on isomer (cis-iso more potent)
:Alfentanil - 1/4 the potency and 1/3 the duration of fent but 4x quicker onset. The businessman's lunch of opiates.
:Betahydroxythiofentanyl - one of the more favoured fent. analogues by addicts, implying euphoria.
:Carfentanil - 100x potency of fent., 10000x the potency of M. Used in spetznaz hostage crisis. 10,000x potency of M. Activity in humans starts at 1μg.
:Lofentanil - more potent and with a longer duration than carfentanil.
:Mirfentanil - fent. analogue with strong selevtivity over μ. Lower doses it antagonises effects caused by lesser opioids but at higher doses is resistant to antagonists, suggesting it has non-opioid mechanisms.
:Ohmefentanyl - 6300x morphine at it's most active isomer. Analogues of this are even stronger with one possessing 30,000x the potency of M.
:Parofluorofentanyl - 150-200x morphine. Sold breifly in 1980.
:R-30490 - analogue of carfentanil. Most selective μ agonist of all fentanyl analogues
:Remifentanil - Potent ultra short acting fent. analogue. Potency from between 20 and 100ug. Used in medicine as an anaesthetic under Ultiva.
:Sufentanil - 5-10x potency of fent

== Opipavine Derivatives ==
:7-PET - 300x potency of M, 3-OH derivative is 2200x potency of M. Unscheduled.
:Acetorphine - 8700x potency of M
:BU-48 - Etorphine derivative. Selective δ agonist and produces only convulsions with slight antidepression.
:Buprenorphin - Subutex
:Cyprenorphine - Buprenorphine analogue, ant.-ag. effects but with higher affinity towards κ.
:Dihydroetorphine -1000-12000x potency of M depending on RoA. Less addictive than other opiates and is used in a similar fashion to Subutex in China.
:Etorphine - 1000-3000x potency of M. μ, κ & δ opioid agonist. weak affinity for ORL1 nociceptin/orphanin FQ receptor.

== Indoles ==
:18-Methoxycoronaridine - Ibogaine derivative, selective α3β4 nicotinic antagonist, however no affinity for α4β2, NMDA or seretonin. Retains modest affinity at μ & κ opioid.
:7-Hydroxymitragynine - Alkaloid in Kratom. Some 17x potency of M. 30x potency of Mitragynine
:Eseroline - Metabolite of the ACh inhibitor physostigmine but potent μ agonist
:Hodgkinsine - alkaloid found in Psychotria colorata plants. Has antiviral, antibacterial and antifungal properties. Also μ opioid agonist & NMDA antagonist.
:Ibogaine - Addiction CURE. HT2a agonist, κ opioid agonist, NMDA antagonist
:Mitragynine - Alkaloid in Kratom. Fairly selective μ agonist but little affinity for δ & κ.
:Noribogaine - Metabolite of Ibogaine. Potent SRI, κ antagonist, weak μ full agonist
:Voacangine - precursor to Ibogine used by iboga plant. Displays similar effects towards addiction as Ibogaine.

== Diphenylmethylpiperazines ==
:BW373U86 - Selective δ agonist at 15x stronger affinity. Analgesic and anti-depressant properties along with BDNF release. Produces convulsions at high doses and reverses respiratory depression produced by μ agonism. Also protects heart muscle cells from death during oxygen deprivation, a result of heart attacks.
:DPI-227 - highly selective δ agonist with antidepressant effects but produces fewer convulsions than most other dugs in it's family.
:DPI-3290 - Potent δ & μ agonist but produces little respiratory depression.

== Opioid Peptides ==

:Biphalin - endogenous eptide with high affinity for δ & μ receptors. Potency almost 7x greater than Etorphine and 7000x M. Low side effects; no dependancy caused.
:Casomorphins - opiates found in Cow's milk.
:DAMGO - synthetic opiate peptide with high μ selectivity. When administered alongside M for 7 days, M had the same effect at the same dose as the first day. I.e. removes tolerance.
:Deltorphin - High affinity and selectivity, naturally occuring δ opioid agonist.
:Dermorphin - South American Tree frog skin. Natural opioid peptide. High potency (30-40x M) and selectivity to μ but may be less likely to cause tolerance and addiction.
:Dynorphins - endogenous opioid peptides, primarily k agonists. Useful in the analysis of addiction.
:Leu-enkephalin - Endogeneous opioid petide that acts as a δ & μ agonist with strong selectivity for δ.
:Met-enkephalin - Opioid Growth Factor (OGF), Endogenous opioid peptide. Primary ligand of the δ receptor along with Leu-enkephalin (high potency and selectivity at δ). Low BA & is metabolised rapidly.
:Opiorphin - Endogenous opioid isolated from human saliva.

== Others ==

:3-HO-TCP - PCP analogue. More glutamergic than the PCP analogue.

:3-HO-BCP - substitutes for both cocaine and morphine at ~5mg (made-up)

:AD-1211 - Structure looks unrelated to /most/ other opioid drugs. Mixed Agonist-antagonist at opioid recepts similar to pentazocine. Little to no developement of tolerance/dependence in animal studies.

:AH-7921 - Selective μ agonist, with 80% potency of M. distributed as an RC, TRs show that it has very little euphoria, indicating euphoria comes from somewhere else. Perhaps sigma? Other opioids are heavily potentiated by it. Perhaps μ agonism is purely analgesic and high comes from a combination of μ & δ with each multiplying the affect of the other. This indicates ultimate opiate high would be moderately selective δ agonist

:Azaprocin - Azaprocin - ~10x potency of M. Faster onset and short duration of actin. Discoved in 1963, never been marketed. The derivative subbed on the phenyl ring with a p-nitro group would be more potent by roughly 2.5. (So 25x potency of M) The open ringed 2,6-dimethylpiperazine analouges would also be active.

:BRL-52537 - Highly potent and selective κ agonist. Neuroprotective.

:Bromadol (BDPC) - 500-10,000x potency of M. Similar to PCP analogues & -HO bonds within them.

:C-8813 (Thiobromadol) - 591x potency of M. μ agonist & δ antagonist to reduce repiratory depression. Making the drug safer.

:Ciramadol - Opioid related to PCP, Tramadol & Tapentadol. mixed ant.-ag. for μ, low abuse potential and ceiling on respiratory depression.

:Enadoline - Highly selective κ agonist. Produces visual distortions, dissociation and of course dysphoria similar to Salvia.

:Herkinorin - Analogue of Salvinorin A but the complete opposite. 100x higher μ affinity and 50x lower κ affinity. Also; "does not promote the recruitment of β-arrestin-2 to the intracellular domain of the μ-opioid receptor, or induce receptor internalization". This means Herkinorin may not produce tolerance or dependance.

:HZ-2 - κ-opioid agonist, same potency as morphine, long duration, high oral BA

:ICI-199,441 - high potency, highly selective κ agonist with analgesic effects

:Methopholine - Isoquinilone derivative with same efficacy as codeine. Could produces corneal opacity. Analogues are more potent with 4'-nitromethopholine at 20x codeine.

:MT-45 - 80% of M. mixed ant.-ag. and mild NMDA antagonist

:Nortilidine - Equipotency of M. Opioid activity is in (1S,2R) iso, NMDA antagonism is in (1R,2S) iso. Also acts as a DRI.

:O-Desmethyltramadol - metabolite of Tramadol. Considerably more potent than Tramadol. Both (+) & (-) isomers lose SRI function but (-) retains NRI functionality. RC.

:Salvinorin A - Highly potent κ agonist and even more potent D2 partial agonist. Use in therapy for addiction.

:Salvinorin B ethoxymethyl ether - semi-synthetic analogue of Salv. A. Longer duration @ ~3hrs, active at 50ug & 3000x (!) selectivity over μ & δ

:Salvinorin B methoxymethyl ether - Similar to ^^ but less selective. 5x potency as Salvinorin A. Deacetylised from Salvinorin A.

:SC-17599 - selective μ agonist with little or no affinity for δ & κ. Potency in between pethidine & morphine.

:RWJ-394674 - potent and selective δ agonist, however once inside body it is dealkylated to its monodesethyl metabolite RWJ-413216 which is a potent μ agonist with less affinity for δ. δ activity counteracts the respiratory depression the μ causes. Only prominent side effect is sedation (and euphoria!)

:TAN-67 - potent and selective δ1 agonist. Has analgesic properties & releases dopamine in the brain. Neuro & cardiac protective properties.

:Tapentadol - μ & σ agonist & SNRI. Potency in between M & Tram.

:Tifluadom - Benzo derivative but without GABAa agonism. Instead selective κ agonism.

:U-47700 - Overlays betaprodine, 7.5x morphine.

:U-50488 - highly selective κ agonist with analgesic effects

:U-69,593 - Potent and selective κ1 agonist. Produces; antinociception, anti-inflammation, anxiolysis (low doses), respiratory depression & diuresis. Also inhibits periphery oxytocin secretion. Not sure if hallucinogenic.

:W-15 - 5.4x Morphine. RC.

:W-18 - 10,000x potency of M, structure abstract from any other drug. These super potent opioids are used in vetenarian practice for tranquilising elephants.

== Opioid Antagonists and Inverse Agonists ==

(selective δ antagonists may reduce physical addiction without causing w/d if attatched to an opioid)

:Chlornaltrexamine - Irreversible mixed ant.-ag. at μ opioid. 22x more potent than M

:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors

:Diprenorphine - Strongest opiate antagonist available. 100x potency of Nalorphine. Used to reverse effects of super-potent opioids.

:Levallorphan - μ opioid antagonist, when used with opiate, it potentiates it and removes addiction potential or induces withdrawal in addicts.

:Nalbuphine - mixed ant.-ag. as is common with this class, there occurs analgesia with no addictive properties.

:Naloxazone - Irreversible μ opioid receptor antagonist

:Naloxonazine - Very Potent Irreversible μ opioid antagonist. dimerizes from Naloxazone under acidic conditions

:Naltrexone - Competitive antagonist at μ & κ receptors, and to a lesser extent, δ. Modulation of the dopaminergic mesolimbic pathway makes it good for countering alcohol dependance as well as Opiate addiction. Blocks the euphoric effects of opioids and is used in rapid detoxification and attenuation of withdrawal. If opiates are used simultaneously, oD may occur.

:Samidorphan - selective μ antagonist. potential for addiction treatment.

== Uncategorised Opioids ==

:FE 200665 - Is an all D-Amino acid peptide that acts as a restucted K-opioid receptor agnoist. Was dosed at 0.36mg/kg IV. Was compared to 15mg oxycodone. Slightly less than the potency of hydrocodone. Caused Hyperalgesic response in a skin pinch test. Also known as CR665.

:SoRI-9409 - mixed μ agonist & δ antagonist. moderate analgesia without development of tolerance. Anti-addictive effects for all dopaminergic drugs.

:Synthetic Conotoxin - Snail toxin derived painkiller 1000x potency of morphine. Non-addictive

==RELATED COMPOUNDS==
:Amiphenazole - treatment for OD. counteracts respiratory depression. If Morphine-N-oxide is taken on this, M's potency will increase.

:Chitosan - linear polysaccharide that can give Morphine up to 60% BA intranasally. Powdered & the ratio is 1.3g : 6.7g (morpine : chitosan)

:BIMU-8 - NOOTROPIC

:NMDA antagonists - Inhibit development of tolerance to morphine

:Tezampanel - ANXIOLYTIC

:Ibudilast - NOOTROPIC

:Nuciferine

:Tetrahydropalmatine - ANXIOLYTIC

:Lofexidine - ANXIOLYTIC

:d & l Phenylalanine (DLPA) - Increases dopamine and endorphin levels, reducing opiate tolerance and even providing an analgesic effect of it's own.

== CCK Antagonists ==

:Proglumide - Acts as a d opioid agonist and non selective CCK antagonist. Enhances analgesia produced by opioids and can prevent or even reverse the development of tolerance

:Devazepide - No affinity for GABAa, selective CCKa antagonist.

:Lorglumide - Selective CCKa antagonist for treatment of gastrointestinal problems and some forms of cancer as well as Opioid interacting properties.

== Nocieceptinergic Drugs ==

(ORL-1 ant. & ag.'s)

:J-113,397 - Highly selective ORL-1 antagonist. Prevents development of opiate tolerance, stimulates dopamine release, cognitive enhancer

:SB-612,111 - Selective ORL-1 antagonist but several times the potency of ^^

:MCOPPB - Potent, selective ORL-1 agonist with only moderate affinity for μ, even less for δ & κ. Anxiolytic with no inhibition of memory, motor function or sedation

:NNC 63-0532 - Potent, selective ORL-1 agonist.

:Ro64-6198 - Potent, selective ORL-1 agonist with 100x selectivity over others. In rats produced anxiolytic but no anticonvulsant effects. Impairs Short term memory & increases appetite. Reduces analgesic effects of M but no preventing tolerance. In primates it showed analgesic behaviour without respiratory depression.

:Menabitan - potent cannabinoid receptor agonist with anti-nociceptive effects

== Enkephalin Potease Inhibitors ==

:RB-101*** - Inhibits enzymes responsible for breaking down enkephalin (regulates nociceptin). Weak μ & δ affinity and slight σ1. Potentiates opiates, stops withdrawal symptoms, no addiction potential, produces no respiratory depression. Also exerts very potent antidepressant and anxiolytic effects. Not orally active so analogues vv were developed.

:RB-120 - Orally active version of the above.

:RB-3007 - Another Enkeph. PI & Nociceptin antagonist

Opioid Notes

2014-10-17T15:41:05Z

Roi: /* Prodines */

=== Opium Derivatives ===

== Opium Alkaloids ==
:Thebaine - 6,14 Dimethoxy version of Oxymorphone. Stimulant rather than an analgesic.
:Narceine - Bitter, Crystalline, formerly used as a substitute for Morphine.
:Noscapine - Acts on the Sigma receptor. Non painkilling. Used commonly in Antitussives. Blocks Bradykinine B-2 receptors in Stroke patients.

== Alkaloid Salt Mixtures ==
:Pantopon - Preparation of all alkaloids present in opium without plant matter. Injectable and slightly less potent than Morphine.

== Morphine Family ==
:6-MDDM - 80x the potency of Morphine, has a faster onset and less body load then the prior.
:Azidomorphine - 40x the potency of Morphine, has a high affinity for μ.
:Hydromorphinol - Derivative of Morphine, yet more potent, with a steeper-dose-response curve and a longer half life. Scripted in Sweden.
:Methyldesorphin - 15x the potency of Morphine. Is found in some mixtures of Krokodil.
:MR-2096 - Oxymorphone analogue that is roughly the same potency.
:N-Phenethylnormorphine - 8-14x the potency of Morphine.
:RAM-378 - N-Phenethyl analogue of Hydromorphinol. It is probably more potent as a result.

== 3,6 Morphine Diesters ==
:Diacetyldihydromorphine - Occasionally used as an alternative to diamorphine, of which it is faster acting, longer lasting and has less side effects such as euphoria and addiction. However it is equipotent with Morphine.
:Dipropanoylmorphine - Ester of Morphine used to treat severe pain. Rarely used but considered to be safer and less addictive than Morphine. As such carries less side effects, such as euphoria. Slower acting, longer lasting and slightly more potent than Morphine.
:Nicomorphone - 2-3x the potency of Morphine and commonly prescribed in German speaking countries.

== Codeine-Dionine Family ==
:Heterocodeine - Reverse isomer of codeine. 6x the potency of Morphine, while Codeine is a prodrug, Heterocodeine is a direct agonist.
:Myrophine - Acts as a prodrug to Morphine. Has a slow onset and longer duration, but reduced potency. Does NOT produce addiction or dependence regardless of dose.
:Acetyldihydrocodeine - Used in Germany. Close relative of Thebacon, where only the 6-7 cond is unsaturated. 6-Acetyl derivative of Dihydrocodeine. Metabolizes into Dihydromorphine. Higher lipophilicity than codeine. Would probably be more potent and longer lasting as a result. Higher oral BA than Codeine.
== Morphinones and Morphols ==
:14-Cinnamoyloxycodeinone - 100x the potency of Morphine.
:14-Methoxymetopon - 500x the potency of Morphine. Can be up to one million times the potency of Morphine if injected into the spine.
:14-Phenylpropoxymetopon - 2000x potency of Morphine. When injected into the spine up to one million times the potency of Morphine. 14-Methoxymetopon has a ceiling effect on respiratory depression, but the above has been left untested.
:3-Acetyloxymorphone - Acetylated analogue of Oxymorphone.
:7-Spiroindanyloxymorphone - Odd Oxymorphone analogue that is selective at dopamine.
:Acetylmorphone - Acetoxy version of Hydromorphone, has a higher bioavailability as a result.
:Chloroxymorphamine - Derivative of Oxymorphone and irreversible full agonist.
:Methyldihydromorphone - Related to Heterocodieine not dihydrocodeine. Is 6-9x the potency of Morphine.
:Metopon - Methylated Hydromorphone, less potent. More than likely would have more euphoria as a result.
:N-Phenethyl-14-Ethoxymetopon - 60x the potency of Morphine, but produces less constipation. d & u agonist.
:Oxymorphol - 6-Hydrogenated Oxymorphone.
:Pentamorphone - Few times more potent than Fentanyl. Short duration, yet low respiratory depression.
:Semorphone - 2 times the potency of Morphine. Partial u agonist and has a ceiling effect on both analgesia and respiratory depression.
:Thebacon - Thebaine analogue, that is fairly uninteresting. 6-8x the potency of Codeine.

== Hydrazones ==
:Oxymorphazone - Half the potency of Oxymorphone, yet higher doses last up to 48 hours.

== Morphians ==
:Butorphanol - partial ant.-ag. at μ opioid and competitive antagonist/partial agonist at κ opioid. dysphoria is common at normal dose.
:Drotebanol - Morphinan derivative synthesised from Thebaine with analgesic effects several times more potent than codeine but weaker than morphine. Moderately addictive but limited physical dependance. Under Metabanyl when available as a script.
:Dextromethorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, (very weak) μ, δ & κ opioid agonist, SERT & NET inhibitor, NADPH Oxidase inhibitor. (Race)Methorphan = racemic
:Dextrorphan (-) - NMDA antagonist / σ1 & σ2 sigma agonist / a3b4, a4b2, a7 nACH antagonist, L-Type voltage-gated calcium channel (LVGCC) blocker, SRI.
:Cyclorphan - mixed antagonist-agonist with affinity for κ
:Levophenacylmorphan - 10x potency of M
:Levofurethylnormorphanol (Ro4-1539) - potent μ opioid agonist 30-60x potency of Levorphanol.
:Levomethorphan (+) - NDMA antagonist, σ1 & σ2 sigma agonist, μ, δ & κ opioid agonist.
:Levorphanol (+) - μ, κ & δ agonist, 4-8x potency of M, long duration, no cross tolerance with morphine
:Norlevorphanol - Opioid analgesic, uninteresting.
:Phenomorphan - 10x potency of Levorphanol. :└--> N-(2-(2-furyl)ethyl) analogue - 60x Levorphanol :└--> N-(2-(2-thienyl)ethyl) analogue - 45x Levorphanol
:Proxorphan - partial κ agonist, lesser partial μ agonist
:Ro4-1539 (Furethylnorlevorphanol) - 30-60x the potency of M. One of the more potent u agonists from the Morphans.

:(Race)Methorphan: L(eft) (+) Levomethorphan >< Dextromethorphan (-) D(exter) --> l=OPIATE >< d=HALLUCINOGENIC OPIATE
└--> Racemic mix of both isomers, embodying their properties.

:Morphinan (Racemorphan): l (+) Levorphanol >< Dextrorphan (-) d --> l=OPIATE >< :d=HALLUCINOGENIC OPIATE
:└--> Racemic mix of both isomers, embodying their properties.

:(Race)Allorphan: l (+) Levallorphan >< Dextrallorphan (-) d --> l= ANTI-OPIOID >< d=NMDA :ANTAGONISTS
: └--> Racemic mix of both isomers, embodying their properties.

:3-Hydroxymorphinan: l (+) Norlevorphanol >< Nordextrorphan (-) d --> l=OPIATE >< d=NOOTROPIC
└--> Racemic mix of both isomers, embodying their properties.

:Oxilorphan: μ antagonist & weak partial κ agonist
:Dimemorfan - SIGMAERGIC DRUG
:Xorphanol - mixed ant.-ag. produces convulsions at highest dose tested.
:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors
:Samidorphan - selective μ antagonist. potential for addiction treatment.

== 4-Phenylpiperidines ==
:4-Fluoropethidine - In comparison to pethidine, it is 50% less potent as an analgesic but 50% more potent as a DRI. (4-iodo & 3, 4-dichloro only increase these differences)
:Anileridine - Another banned pethidine analogue, probably abused. Higher analgesia than Meperidine due to n-aminophenyl group and acts withing 15 mins orally, lasting 2-3 hours.
:Benzethidine - 4-phenylpiperidine analogue of pethidine. Probably somewhat more potent and euphoric. Never scripted.
:Carperidine - fairly normal opiate but unused in medicine and currently LEGAL (08/06/2013)
:Furethidine - 4-Phenylpiperidine analogue of pethidine. Probably a lot more potent and abuse prone. Never prescribed.
:Morpheridine - related to meperidine but 4x the potency and does not cause convulsions
:Phenoperidine - 20-200x the potency of Pethidine. Less hypnotic and than morphine but more emetic (nausea). This can be cured by Haloperidol.
:Piminodine - similar dose to M, used in 60's and 70's but was banned. It was probably abused widely
.
== Prodines ==
:Alphaprodine - 1.5x Morphine
:Allylprodine - Prodine analogue 23x potency of Morphine
:Betaprodine - 7.5x Morphine
:Prosidol - Russian Prodine analogue

== Ketobemidones ==
:Acetoxyketobemidone - Unschedualed analogue of ketobemidone
:Bemidone - Analogue of Pethidine but significantly less potent, however it has NMDA antagonism like KetoB.
:Ketobemidone - μ opioid antagonist & NMDA antagonist. More addictive than M

== Others ==
:Loperamide - Peripheral opioid so it cannot cross BBB. useful anti-Diarrhoea med. When used in conjuction with Quinine or Omerprazole can cross BBB and opioid effects are seen.
:Picenadol - R isomer (or Levopicenadol) is pure μ agonist while S is antagonist. Racemic is mixed that casues low abuse potential but has low κ activity

=== Open Chain Opioids ===
== Amidones ==
:Dipipadone - Lost Ark of the Covenant.
:Phenadoxone - methadone analogue, similar dose to M, lasts 1-4 hours
:Levacetylmethadol - Methadone analogue with u agonism and noncompetitive a3b4 NACh antagonism. Brand name Orlaam, prescribed to those unresponsive to methadone or subutex. Long half life (3 days) and heavier affect.
:Norpipanone - Was not under international control until case reports of addiction arose.
:Isomethadone - Previously used in medicine. μ- δ- agonism. S-isomer more potent.

==Methadols ==
:Dimepheptanol - Related to Methadone, has two isomers which also have two isomers so 6 possible isomers including racemic.

== Moramides ==
:Palfium (Dextomoramide) - 3x potency of M but shorter acting. High BA & fast acting, oral feels like shooting. Low LD50 & inconsistent potency (one day you may need 5mg, next day 3mg)

== Thiambutens ==
:Thiambutenes - Dimethyl-TAB, Diethyl-TAB, Ethylmethyl-TAB. Used in vetinary medicine in Japan. Banned in virtually all countried due to high abuse potential. Anticholinergic and antihistamine properties!

== Phenalkoxams ==
:Dextropropoxyphene - Low potency opiate not absorbed by CYP2D6. Also is a potent, noncompetitive α3β4 NACh antagonist and a weak SRI.
:Dimenoxadol - Benzillic Acid derivative related to methadone. Banned due to high abuse potential it seems.
:Dioxaphetyl butyrate - Banned opioid similar to methadone. Possibly in use or previously in use as a med under the names Amidalgon & Spasmoxal.

== Ampromides ==
:Diampromide - Banned Analgesic related to Propiram. Similar potency to M.
:Propiram - Slightly more potent than codeine, 3-6hr duration. mixed μ ant.-ag. favouring agonism. affinity for κ & δ, sigma and nmda. 97% oral BA!

== Others ==
:IC-26 Methadone analogue with similar potency, but unscheduled.
:Lefetamine - Weak opiate on the same scale as codeine but has DRI properties
:R-4066 - Methadone analogue with 212x the potency, but a much shorter duration. (3 hours)

== Amilidopiperidines ==

:3-Methylfentanyl - 400-6000x potency of M depending on isomer (cis-iso more potent)
:Alfentanil - 1/4 the potency and 1/3 the duration of fent but 4x quicker onset. The businessman's lunch of opiates.
:Betahydroxythiofentanyl - one of the more favoured fent. analogues by addicts, implying euphoria.
:Carfentanil - 100x potency of fent., 10000x the potency of M. Used in spetznaz hostage crisis. 10,000x potency of M. Activity in humans starts at 1μg.
:Lofentanil - more potent and with a longer duration than carfentanil.
:Mirfentanil - fent. analogue with strong selevtivity over μ. Lower doses it antagonises effects caused by lesser opioids but at higher doses is resistant to antagonists, suggesting it has non-opioid mechanisms.
:Ohmefentanyl - 6300x morphine at it's most active isomer. Analogues of this are even stronger with one possessing 30,000x the potency of M.
:Parofluorofentanyl - 150-200x morphine. Sold breifly in 1980.
:R-30490 - analogue of carfentanil. Most selective μ agonist of all fentanyl analogues
:Remifentanil - Potent ultra short acting fent. analogue. Potency from between 20 and 100ug. Used in medicine as an anaesthetic under Ultiva.
:Sufentanil - 5-10x potency of fent

== Opipavine Derivatives ==
:7-PET - 300x potency of M, 3-OH derivative is 2200x potency of M. Unscheduled.
:Acetorphine - 8700x potency of M
:BU-48 - Etorphine derivative. Selective δ agonist and produces only convulsions with slight antidepression.
:Buprenorphin - Subutex
:Cyprenorphine - Buprenorphine analogue, ant.-ag. effects but with higher affinity towards κ.
:Dihydroetorphine -1000-12000x potency of M depending on RoA. Less addictive than other opiates and is used in a similar fashion to Subutex in China.
:Etorphine - 1000-3000x potency of M. μ, κ & δ opioid agonist. weak affinity for ORL1 nociceptin/orphanin FQ receptor.

== Indoles ==
:18-Methoxycoronaridine - Ibogaine derivative, selective α3β4 nicotinic antagonist, however no affinity for α4β2, NMDA or seretonin. Retains modest affinity at μ & κ opioid.
:7-Hydroxymitragynine - Alkaloid in Kratom. Some 17x potency of M. 30x potency of Mitragynine
:Eseroline - Metabolite of the ACh inhibitor physostigmine but potent μ agonist
:Hodgkinsine - alkaloid found in Psychotria colorata plants. Has antiviral, antibacterial and antifungal properties. Also μ opioid agonist & NMDA antagonist.
:Ibogaine - Addiction CURE. HT2a agonist, κ opioid agonist, NMDA antagonist
:Mitragynine - Alkaloid in Kratom. Fairly selective μ agonist but little affinity for δ & κ.
:Noribogaine - Metabolite of Ibogaine. Potent SRI, κ antagonist, weak μ full agonist
:Voacangine - precursor to Ibogine used by iboga plant. Displays similar effects towards addiction as Ibogaine.

== Diphenylmethylpiperazines ==
:BW373U86 - Selective δ agonist at 15x stronger affinity. Analgesic and anti-depressant properties along with BDNF release. Produces convulsions at high doses and reverses respiratory depression produced by μ agonism. Also protects heart muscle cells from death during oxygen deprivation, a result of heart attacks.
:DPI-227 - highly selective δ agonist with antidepressant effects but produces fewer convulsions than most other dugs in it's family.
:DPI-3290 - Potent δ & μ agonist but produces little respiratory depression.

== Opioid Peptides ==

:Biphalin - endogenous eptide with high affinity for δ & μ receptors. Potency almost 7x greater than Etorphine and 7000x M. Low side effects; no dependancy caused.
:Casomorphins - opiates found in Cow's milk.
:DAMGO - synthetic opiate peptide with high μ selectivity. When administered alongside M for 7 days, M had the same effect at the same dose as the first day. I.e. removes tolerance.
:Deltorphin - High affinity and selectivity, naturally occuring δ opioid agonist.
:Dermorphin - South American Tree frog skin. Natural opioid peptide. High potency (30-40x M) and selectivity to μ but may be less likely to cause tolerance and addiction.
:Dynorphins - endogenous opioid peptides, primarily k agonists. Useful in the analysis of addiction.
:Leu-enkephalin - Endogeneous opioid petide that acts as a δ & μ agonist with strong selectivity for δ.
:Met-enkephalin - Opioid Growth Factor (OGF), Endogenous opioid peptide. Primary ligand of the δ receptor along with Leu-enkephalin (high potency and selectivity at δ). Low BA & is metabolised rapidly.
:Opiorphin - Endogenous opioid isolated from human saliva.

== Others ==

:3-HO-TCP - PCP analogue. More glutamergic than the PCP analogue.

:3-HO-BCP - substitutes for both cocaine and morphine at ~5mg (made-up)

:AD-1211 - Structure looks unrelated to /most/ other opioid drugs. Mixed Agonist-antagonist at opioid recepts similar to pentazocine. Little to no developement of tolerance/dependence in animal studies.

:AH-7921 - Selective μ agonist, with 80% potency of M. distributed as an RC, TRs show that it has very little euphoria, indicating euphoria comes from somewhere else. Perhaps sigma? Other opioids are heavily potentiated by it. Perhaps μ agonism is purely analgesic and high comes from a combination of μ & δ with each multiplying the affect of the other. This indicates ultimate opiate high would be moderately selective δ agonist

:Azaprocin - Azaprocin - ~10x potency of M. Faster onset and short duration of actin. Discoved in 1963, never been marketed. The derivative subbed on the phenyl ring with a p-nitro group would be more potent by roughly 2.5. (So 25x potency of M) The open ringed 2,6-dimethylpiperazine analouges would also be active.

:BRL-52537 - Highly potent and selective κ agonist. Neuroprotective.

:Bromadol (BDPC) - 500-10,000x potency of M. Similar to PCP analogues & -HO bonds within them.

:C-8813 (Thiobromadol) - 591x potency of M. μ agonist & δ antagonist to reduce repiratory depression. Making the drug safer.

:Ciramadol - Opioid related to PCP, Tramadol & Tapentadol. mixed ant.-ag. for μ, low abuse potential and ceiling on respiratory depression.

:Enadoline - Highly selective κ agonist. Produces visual distortions, dissociation and of course dysphoria similar to Salvia.

:Herkinorin - Analogue of Salvinorin A but the complete opposite. 100x higher μ affinity and 50x lower κ affinity. Also; "does not promote the recruitment of β-arrestin-2 to the intracellular domain of the μ-opioid receptor, or induce receptor internalization". This means Herkinorin may not produce tolerance or dependance.

:HZ-2 - κ-opioid agonist, same potency as morphine, long duration, high oral BA

:ICI-199,441 - high potency, highly selective κ agonist with analgesic effects

:Methopholine - Isoquinilone derivative with same efficacy as codeine. Could produces corneal opacity. Analogues are more potent with 4'-nitromethopholine at 20x codeine.

:MT-45 - 80% of M. mixed ant.-ag. and mild NMDA antagonist

:Nortilidine - Equipotency of M. Opioid activity is in (1S,2R) iso, NMDA antagonism is in (1R,2S) iso. Also acts as a DRI.

:O-Desmethyltramadol - metabolite of Tramadol. Considerably more potent than Tramadol. Both (+) & (-) isomers lose SRI function but (-) retains NRI functionality. RC.

:Salvinorin A - Highly potent κ agonist and even more potent D2 partial agonist. Use in therapy for addiction.

:Salvinorin B ethoxymethyl ether - semi-synthetic analogue of Salv. A. Longer duration @ ~3hrs, active at 50ug & 3000x (!) selectivity over μ & δ

:Salvinorin B methoxymethyl ether - Similar to ^^ but less selective. 5x potency as Salvinorin A. Deacetylised from Salvinorin A.

:SC-17599 - selective μ agonist with little or no affinity for δ & κ. Potency in between pethidine & morphine.

:RWJ-394674 - potent and selective δ agonist, however once inside body it is dealkylated to its monodesethyl metabolite RWJ-413216 which is a potent μ agonist with less affinity for δ. δ activity counteracts the respiratory depression the μ causes. Only prominent side effect is sedation (and euphoria!)

:TAN-67 - potent and selective δ1 agonist. Has analgesic properties & releases dopamine in the brain. Neuro & cardiac protective properties.

:Tapentadol - μ & σ agonist & SNRI. Potency in between M & Tram.

:Tifluadom - Benzo derivative but without GABAa agonism. Instead selective κ agonism.

:U-50488 - highly selective κ agonist with analgesic effects

:U-69,593 - Potent and selective κ1 agonist. Produces; antinociception, anti-inflammation, anxiolysis (low doses), respiratory depression & diuresis. Also inhibits periphery oxytocin secretion. Not sure if hallucinogenic.

:W-15 - 5.4x Morphine. RC.

:W-18 - 10,000x potency of M, structure abstract from any other drug. These super potent opioids are used in vetenarian practice for tranquilising elephants.

== Opioid Antagonists and Inverse Agonists ==

(selective δ antagonists may reduce physical addiction without causing w/d if attatched to an opioid)

:Chlornaltrexamine - Irreversible mixed ant.-ag. at μ opioid. 22x more potent than M

:Cyprodime - Selective μ opioid antagonist with no affinity for κ or δ receptors

:Diprenorphine - Strongest opiate antagonist available. 100x potency of Nalorphine. Used to reverse effects of super-potent opioids.

:Levallorphan - μ opioid antagonist, when used with opiate, it potentiates it and removes addiction potential or induces withdrawal in addicts.

:Nalbuphine - mixed ant.-ag. as is common with this class, there occurs analgesia with no addictive properties.

:Naloxazone - Irreversible μ opioid receptor antagonist

:Naloxonazine - Very Potent Irreversible μ opioid antagonist. dimerizes from Naloxazone under acidic conditions

:Naltrexone - Competitive antagonist at μ & κ receptors, and to a lesser extent, δ. Modulation of the dopaminergic mesolimbic pathway makes it good for countering alcohol dependance as well as Opiate addiction. Blocks the euphoric effects of opioids and is used in rapid detoxification and attenuation of withdrawal. If opiates are used simultaneously, oD may occur.

:Samidorphan - selective μ antagonist. potential for addiction treatment.

== Uncategorised Opioids ==

:FE 200665 - Is an all D-Amino acid peptide that acts as a restucted K-opioid receptor agnoist. Was dosed at 0.36mg/kg IV. Was compared to 15mg oxycodone. Slightly less than the potency of hydrocodone. Caused Hyperalgesic response in a skin pinch test. Also known as CR665.

:SoRI-9409 - mixed μ agonist & δ antagonist. moderate analgesia without development of tolerance. Anti-addictive effects for all dopaminergic drugs.

:Synthetic Conotoxin - Snail toxin derived painkiller 1000x potency of morphine. Non-addictive

==RELATED COMPOUNDS==
:Amiphenazole - treatment for OD. counteracts respiratory depression. If Morphine-N-oxide is taken on this, M's potency will increase.

:Chitosan - linear polysaccharide that can give Morphine up to 60% BA intranasally. Powdered & the ratio is 1.3g : 6.7g (morpine : chitosan)

:BIMU-8 - NOOTROPIC

:NMDA antagonists - Inhibit development of tolerance to morphine

:Tezampanel - ANXIOLYTIC

:Ibudilast - NOOTROPIC

:Nuciferine

:Tetrahydropalmatine - ANXIOLYTIC

:Lofexidine - ANXIOLYTIC

:d & l Phenylalanine (DLPA) - Increases dopamine and endorphin levels, reducing opiate tolerance and even providing an analgesic effect of it's own.

== CCK Antagonists ==

:Proglumide - Acts as a d opioid agonist and non selective CCK antagonist. Enhances analgesia produced by opioids and can prevent or even reverse the development of tolerance

:Devazepide - No affinity for GABAa, selective CCKa antagonist.

:Lorglumide - Selective CCKa antagonist for treatment of gastrointestinal problems and some forms of cancer as well as Opioid interacting properties.

== Nocieceptinergic Drugs ==

(ORL-1 ant. & ag.'s)

:J-113,397 - Highly selective ORL-1 antagonist. Prevents development of opiate tolerance, stimulates dopamine release, cognitive enhancer

:SB-612,111 - Selective ORL-1 antagonist but several times the potency of ^^

:MCOPPB - Potent, selective ORL-1 agonist with only moderate affinity for μ, even less for δ & κ. Anxiolytic with no inhibition of memory, motor function or sedation

:NNC 63-0532 - Potent, selective ORL-1 agonist.

:Ro64-6198 - Potent, selective ORL-1 agonist with 100x selectivity over others. In rats produced anxiolytic but no anticonvulsant effects. Impairs Short term memory & increases appetite. Reduces analgesic effects of M but no preventing tolerance. In primates it showed analgesic behaviour without respiratory depression.

:Menabitan - potent cannabinoid receptor agonist with anti-nociceptive effects

== Enkephalin Potease Inhibitors ==

:RB-101*** - Inhibits enzymes responsible for breaking down enkephalin (regulates nociceptin). Weak μ & δ affinity and slight σ1. Potentiates opiates, stops withdrawal symptoms, no addiction potential, produces no respiratory depression. Also exerts very potent antidepressant and anxiolytic effects. Not orally active so analogues vv were developed.

:RB-120 - Orally active version of the above.

:RB-3007 - Another Enkeph. PI & Nociceptin antagonist

2C-X

2014-10-17T14:59:34Z

Roi: /* 2C Family */

[[File:2cc.jpg|thumb|250px|2C-C vial and powder]]

The 2C family is a group of psychedelic phenethylamines that share the same basic 2C structure. The name '2C' is an acronym for the two carbons between the benzene ring and the amino group in all 2C chemicals. There are also two methoxy groups on the the 2 and 5 positions of the benzene ring. The -x denotes a number of different varieties of 2C's that differ in their substituents on the 3 and 4 positions of the benzene ring.

= History =
Alexander Shulgin coined this term and also synthesized the majority of the 2C's, publishing detailed information about their synthesis in his book PiHKAL (Phenethylamines i Have Known And Loved).

= 2C Family =

* [[2C-B]] (Dimethoxybromophenethylamine)
* [[2C-B-FLY]] (Dihydrodifuran-2C-B)
* [[2C-BZ]] (Dimethoxybenzylolicphenethylamine)
* [[2C-C]] (Dimethoxychlorophenethylamine)
* [[2C-CN]] (Dimethoxycyanidephenethylamine)
* [[2C-D]] (Dimethoxymethylphenethylamine)
* [[2C-E]] (Dimethoxyethylphenethylamine)
* [[2C-EF]] (Fluoroethylmethoxyphenethylamine)
* [[2C-G]] (Dimethyldimethoxyphenethylamine)
* [[2C-I]] (Dimethoxyiodophenethylamine)
* [[2C-N]] (Dimethoxynitrophenethylamine)
* [[2C-P]] (Dimethoxypropylphenethylamine)
* [[2C-PYN]] (Dimethoxypropnylphenethylamine)
* [[2C-iP]] (Dimethoxyisopropylphenethylamine)
* [[2C-T]] (Dimethoxymethylthiophenethylamine)
* [[2C-T-2]] (Dimethoxyethylthiophenethylamine)
* [[2C-T-4]] (Dimethoxyisopropylthiophenethylamine)
* [[2C-T-7]] (Dimethoxypropylthiophenethylamine)
* [[2C-T-13]] (Dimethoxy-(β-methoxyethylthio)phenethylamine)
* [[2C-T-17]] (Dimethoxy-(β-secbutylthio)phenethylamine)
* [[2C-T-21]] (Dimethoxyfluoroethylthiophenethylamine)
* [[2C-TFM]] (Dimethoxytrifluorophenethylamine)
* [[2C-YN]] (Dimethoxyethynylphenethylamine)

=Images=

<gallery mode="packed-hover" heights="200px">
Image:2cb.jpg|''2C-B''
Image:2cc.jpg|''2C-C''
Image:2ce.jpg|''2C-E''
</gallery>

[[Category:Psychedelic]]
[[Category:Drugs]]

2C-E

2014-10-17T14:54:54Z

Roi:

[[File:2ce.jpg|thumb|200px|Vial of 2C-E with powder]]

2C-E is a chemical of the [[2C-X]] series which is characterised by its particularly intense visuals and higher potency when compared with other members of the family.

= History =

2C-E, like many of its close analogues, was first synthesized by Alexander Shulgin and published in PiHKAL. He was quite fond of it, granting it a place in his "Magical Half Dozen" alongside of [[DOM]], [[2C-B]], [[2C-T-2]] & 7 and [[mescaline]].

= Uses =

2C-E is mainly a recreational entheogen. It can be quite introspective in appropriate doses and settings. It doesn't lend itself well to intense party-like surroundings, much like LSD or similarly intense psychedelics.

= Dosage =

{| class="wikitable"

|+ Oral

|-

| Light || 5-10mg

|-

| Common || 10-15mg

|-

| Strong || 15-30mg

|-

| Heavy || 25-40mg+

|}

{| class="wikitable"

|+ Insulated

|-

| Light || 1-3mg

|-

| Common || 3-7mg

|-

| Strong || 6-10mg

|-

| Heavy || 10mg+

|}

= Duration =

Note: Duration can be significantly longer with higher doses.

Anecdotal evidence has shown the oral onset of 2C-E may vary wildly for some users, taking up to three hours before first effects in some cases.

{| class="wikitable"

|+ Oral

| Onset || 60-90 minutes

|-

| Total || 9-14 hours

|}

{| class="wikitable"

|+ Insufflated

| Onset || 20-40 minutes

|-

| Total || 6-9 hours

|}

= Effects =

2C-E is a psychedelic phenethylamine and as such has psychedelic and stimulant effects. As with all psychedelics, different users are likely to experience different sets of effects, which usually include some however very rarely would include all of the following effects.

Compared to other members of the 2C-X family, 2C-E is generally considered to have a heavier body load and to be more visual than its counterparts.

Note: The prevalence of negative effects increases with higher doses.

== Positive ==

* Mood lift, euphoria, sense of well-being

* Enhanced sensory perception

* Increase in associative & creative thinking; introspection

* Life-changing 'spiritual' experiences

* Closed and Open eye visuals, patterning, tracers, color-enhancement, etc.

* Enhanced appreciation of music

* Increase in energy

== Neutral ==

* Time dilation

* Slight increase in heart-rate and body temperature

* Inability to focus or difficulty focusing

== Negative ==

* Tension

* Anxiety, restlessness, confusion

* Dizziness

* Nausea, gastrointestinal discomfort, possible vomiting

* Over-sensitivity to music or other sensory stimuli

* Unwanted 'spiritual' experiences

* Racing thoughts

= Harm Reduction =

* As with all psychedelic drugs 2C-E carries with it the potential for a very powerful experience, and as such has the potential to create a very difficult experience ('bad' trip). Mindset and setting play important roles in governing the nature of a psychedelic experience, among other things.

See [[Psychedelics#Harm_Reduction|Psychedelic Harm Reduction]] for more information.

* As with all stimulants, care should be taken when dosing via different ROAs. The oral route has a much lower bioavailabity than those that bypass first pass metabolism i.e. Insulated, rectal, intramuscular, intravenous and subcutaneous.

See [[Stimulants#Harm Reduction|Stimulant Harm Reduction]] for more information.

==Interactions==

See the [[Drug combinations]] chart for more information.

= Chemistry and Pharmacology =

==Chemistry==

2,5-Dimethoxy-4-ethylphenethylamine is a colorless oil and analogue of mescaline. Similarly it is classified as a psychedelic phenethylamine. It shares the substituted amphetamine core found in the structure of many entactogens. Crystalline forms are obtained as the amine salt by reacting the free base with a mineral acid, typically HCl. It is soluble in both water and ethanol. Maximum concentration in H2O is reported at ~50mg/ml and it is said to be relatively stable in solution. A drop below normal ambient temperatures can cause particles to crystalize out.

Shulgin does not report an exact boiling point for the free base, stating only that during one synthesis the fraction boiling between 90-100 °C at 0.25 mmHg pressure was collected and converted to the hydrochloride salt. Shulgin reports the melting point of the hydrochloride salt as 208.5-210.5 °C. Similarly it is classified as a psychedelic phenethylamine. It shares the substituted amphetamine core found in the structure of many entactogens.

A full write up on Shulgin's synthesis for 2C-E can be found [https://www.erowid.org/library/books_online/pihkal/pihkal024.shtml here].

==Pharmacology==

Like most psychedelic drugs, 2C-E is a 5-HT2a Agonist; from that, we can presume the concurrent or pre-administration of SSRIs may reduce the effects of 2C-E. 2C-E is one of the most potent of the 2C-X family, behind only 2C-P and 2C-T-4. The 2C-X family, specifically, 2C-E, 2C-I, and 2C-C all stimulated G protein binding, suggesting more of an activity similar to tryptamines such as 5-MeO-DMT and, interestingly, DPT. G Proteins are membrane proteins that effectively mediate interaction between hormone receptors and enzymes responsible for changes of metabolism as a result of hormonal changes.

In rats, Stage I metabolism involved deamination and O-Demthylation, which are related to the Monoamine oxidase (MAO) and cytochrome P450 (CYP) enzymes. For virtually all the 2C’s, (B,I,D,E,T-2, and T-7), MAO-A and MAO-B were reacted upon; interestingly, ½ of the molecules in Shulgin’s Magical Half Dozen (2C-E, 2C-T-2, 2C-T-7, with the addition of 2C-D) also act to a small extent on the CYP2D6 enzyme. Because of the commonality of these receptors, the 2C-X family is likely to be more reactive with other concurrently administered chemicals.

== LD50 ==

The LD50 in humans is not currently known. Use caution when exploring high doses of this compound.

= Legal status =

* In Australia, 2C-E was added to the 'Dangerous Drugs' list of the 'Drugs Misuse Amendment Act 2008.

* In Denmark, 2C-E has been added to the list of Schedule B controlled substances.

* In New Zealand, 2C-E is illegal under the Analogues section of Schedule 3 / Class C, along with 2C-I, DOI, ephedrine and pseudoephedrine.

* In Sweden, 2C-E has been made illegal to sell or possess under their Act on the Prohibition of Certain Goods Dangerous to Health (''lagen om förbud mot vissa hälsofarliga varor'').

* In the UK, 2C-E is a Class A controlled Substance under the Misuse of Drugs Act's 2002 amendments and as such is illegal to possess to supply.

* In Germany, 2C-E is a Schedule I drug as of late 2014.

* In the USA, 2C-E is a Schedule I substance under the FDA Safety and Innovation act of 2012, and is illegal to possess, distribute or manufacture.

= Links =

* [https://www.erowid.org/chemicals/2ce/ Erowid]

* [https://www.erowid.org/library/books_online/pihkal/pihkal024.shtml PiHKAL Entry]

* [https://www.wikipedia.org/wiki/2C-E/ Wikipedia]

[[Category:Stimulant]]

[[Category:Psychedelic]]

[[Category:Drugs]]

2C-E

2014-10-16T05:29:29Z

Roi:

[[File:2ce.jpg|thumb|200px|Vial of 2C-E with powder]]

2C-E is a chemical of the [[2C-X]] series which is characterised by its particularly intense visuals and higher potency when compared with other members of the family.

= History =

2C-E, like many of its close analogues, was first synthesized by Alexander Shulgin and published in PiHKAL. He was quite fond of it, granting it a place in his "Magical Half Dozen" alongside of [[DOM]], [[2C-B]], [[2C-T-2]] & 7 and [[mescaline]].

= Uses =

2C-E is mainly a recreational entheogen. It can be quite introspective in appropriate doses and settings. It doesn't lend itself well to intense party-like surroundings, much like LSD or similarly intense psychedelics.

= Dosage =

{| class="wikitable"

|+ Oral

|-

| Light || 5-10mg

|-

| Common || 10-15mg

|-

| Strong || 15-30mg

|-

| Heavy || 25-40mg+

|}

{| class="wikitable"

|+ Insulated

|-

| Light || 1-3mg

|-

| Common || 3-7mg

|-

| Strong || 6-10mg

|-

| Heavy || 10mg+

|}

= Duration =

Note: Duration can be significantly longer with higher doses.

Anecdotal evidence has shown the oral onset of 2C-E may vary wildly for some users, taking up to three hours before first effects in some cases.

{| class="wikitable"

|+ Oral

| Onset || 60-90 minutes

|-

| Total || 9-14 hours

|}

{| class="wikitable"

|+ Insufflated

| Onset || 20-40 minutes

|-

| Total || 6-9 hours

|}

= Effects =

2C-E is a psychedelic phenethylamine and as such has psychedelic and stimulant effects. As with all psychedelics, different users are likely to experience different sets of effects, which usually include some however very rarely would include all of the following effects.

Compared to other members of the 2C-X family, 2C-E is generally considered to have a heavier body load and to be more visual than its counterparts.

Note: The prevalence of negative effects increases with higher doses.

== Positive ==

* Mood lift, euphoria, sense of well-being

* Enhanced sensory perception

* Increase in associative & creative thinking; introspection

* Life-changing 'spiritual' experiences

* Closed and Open eye visuals, patterning, tracers, color-enhancement, etc.

* Enhanced appreciation of music

* Increase in energy

== Neutral ==

* Time dilation

* Slight increase in heart-rate and body temperature

* Inability to focus or difficulty focusing

== Negative ==

* Tension

* Anxiety, restlessness, confusion

* Dizziness

* Nausea, gastrointestinal discomfort, possible vomiting

* Over-sensitivity to music or other sensory stimuli

* Unwanted 'spiritual' experiences

* Racing thoughts

= Harm Reduction =

* As with all psychedelic drugs 2C-E carries with it the potential for a very powerful experience, and as such has the potential to create a very difficult experience ('bad' trip). Mindset and setting play important roles in governing the nature of a psychedelic experience, among other things.

See [[Psychedelics#Harm_Reduction|Psychedelic Harm Reduction]] for more information.

* As with all stimulants, care should be taken when dosing via different ROAs. The oral route has a much lower bioavailabity than those that bypass first pass metabolism i.e. Insulated, rectal, intramuscular, intravenous and subcutaneous.

See [[Stimulants#Harm Reduction|Stimulant Harm Reduction]] for more information.

==Interactions==

* As with all psychedelic phenethylamines caution must be exercised when used in conjunction with other drugs. In particular 2C-E is thought to carry risk of causing potentially life-threatening psychological and/or physiological problems when used in conjunction with certain types of medication, including MAOIs and possibly Lithium.<ref>http://mentalmana.blogspot.com/2013/05/2c-e-europa-eternity.html</ref>

Note: This information is based on unconfirmed anecdotal reports and logical deduction based on pharmacological properties when compared with other potent psychedelics. We strongly suggest erring on the side of caution considering the lack of concrete evidence either way.

See the [[Drug combinations]] chart for more information.

= Chemistry and Pharmacology =

==Chemistry==

2,5-Dimethoxy-4-ethylphenethylamine is a colorless oil and analogue of mescaline. Similarly it is classified as a psychedelic phenethylamine. It shares the substituted amphetamine core found in the structure of many entactogens. Crystalline forms are obtained as the amine salt by reacting the free base with a mineral acid, typically HCl. It is soluble in both water and ethanol. Maximum concentration in H2O is reported at ~50mg/ml and it is said to be relatively stable in solution. A drop below normal ambient temperatures can cause particles to crystalize out.

Shulgin does not report an exact boiling point for the free base, stating only that during one synthesis the fraction boiling between 90-100 °C at 0.25 mmHg pressure was collected and converted to the hydrochloride salt. Shulgin reports the melting point of the hydrochloride salt as 208.5-210.5 °C. Similarly it is classified as a psychedelic phenethylamine. It shares the substituted amphetamine core found in the structure of many entactogens.

A full write up on Shulgin's synthesis for 2C-E can be found [https://www.erowid.org/library/books_online/pihkal/pihkal024.shtml here].

==Pharmacology==

Like most psychedelic drugs, 2C-E is a 5-HT2a Agonist; from that, we can presume the concurrent or pre-administration of SSRIs may reduce the effects of 2C-E. 2C-E is one of the most potent of the 2C-X family, behind only 2C-P and 2C-T-4. The 2C-X family, specifically, 2C-E, 2C-I, and 2C-C all stimulated G protein binding, suggesting more of an activity similar to tryptamines such as 5-MeO-DMT and, interestingly, DPT. G Proteins are membrane proteins that effectively mediate interaction between hormone receptors and enzymes responsible for changes of metabolism as a result of hormonal changes.

In rats, Stage I metabolism involved deamination and O-Demthylation, which are related to the Monoamine oxidase (MAO) and cytochrome P450 (CYP) enzymes. For virtually all the 2C’s, (B,I,D,E,T-2, and T-7), MAO-A and MAO-B were reacted upon; interestingly, ½ of the molecules in Shulgin’s Magical Half Dozen (2C-E, 2C-T-2, 2C-T-7, with the addition of 2C-D) also act to a small extent on the CYP2D6 enzyme. Because of the commonality of these receptors, the 2C-X family is likely to be more reactive with other concurrently administered chemicals.

== LD50 ==

The LD50 in humans is not currently known. Use caution when exploring high doses of this compound.

= Legal status =

* In Australia, 2C-E was added to the 'Dangerous Drugs' list of the 'Drugs Misuse Amendment Act 2008.

* In Denmark, 2C-E has been added to the list of Schedule B controlled substances.

* In New Zealand, 2C-E is illegal under the Analogues section of Schedule 3 / Class C, along with 2C-I, DOI, ephedrine and pseudoephedrine.

* In Sweden, 2C-E has been made illegal to sell or possess under their Act on the Prohibition of Certain Goods Dangerous to Health (''lagen om förbud mot vissa hälsofarliga varor'').

* In the UK, 2C-E is a Class A controlled Substance under the Misuse of Drugs Act's 2002 amendments and as such is illegal to possess to supply.

* In Germany, 2C-E is a Schedule I drug as of late 2014.

* In the USA, 2C-E is a Schedule I substance under the FDA Safety and Innovation act of 2012, and is illegal to possess, distribute or manufacture.

= Links =

* [https://www.erowid.org/chemicals/2ce/ Erowid]

* [https://www.erowid.org/library/books_online/pihkal/pihkal024.shtml PiHKAL Entry]

* [https://www.wikipedia.org/wiki/2C-E/ Wikipedia]

= Notes =

<references />

[[Category:Stimulant]]

[[Category:Psychedelic]]

[[Category:Drugs]]

2C-E

2014-10-16T05:28:07Z

Roi: /* Chemistry */

[[File:2ce.jpg|thumb|200px|Vial of 2C-E with powder]]

2C-E is a chemical of the [[2C-X]] series which is characterised by its particularly intense visuals and higher potency when compared with other members of the family.

= History =

2C-E, like many of its close analogues, was first synthesized by Alexander Shulgin and published in PiHKAL. He was quite fond of it, granting it a place in his "Magical Half Dozen" alongside of [[DOM]], [[2C-B]], [[2C-T-2]] & 7 and [[mescaline]].

= Uses =

2C-E is mainly a recreational entheogen. It can be quite introspective in appropriate doses and settings. It doesn't lend itself well to intense party-like surroundings, much like LSD or similarly intense psychedelics.

= Dosage =

{| class="wikitable"

|+ Oral

|-

| Light || 5-10mg

|-

| Common || 10-15mg

|-

| Strong || 15-30mg

|-

| Heavy || 25-40mg+

|}

{| class="wikitable"

|+ Insulated

|-

| Light || 1-3mg

|-

| Common || 3-7mg

|-

| Strong || 6-10mg

|-

| Heavy || 10mg+

|}

= Duration =

Note: Duration can be significantly longer with higher doses.

Anecdotal evidence has shown the oral onset of 2C-E may vary wildly for some users, taking up to three hours before first effects in some cases.

{| class="wikitable"

|+ Oral

| Onset || 60-90 minutes

|-

| Total || 9-14 hours

|}

{| class="wikitable"

|+ Insufflated

| Onset || 20-40 minutes

|-

| Total || 6-9 hours

|}

= Effects =

2C-E is a psychedelic phenethylamine and as such has psychedelic and stimulant effects. As with all psychedelics, different users are likely to experience different sets of effects, which usually include some however very rarely would include all of the following effects.

Compared to other members of the 2C-X family, 2C-E is generally considered to have a heavier body load and to be more visual than its counterparts.

Note: The prevalence of negative effects increases with higher doses.

== Positive ==

* Mood lift, euphoria, sense of well-being

* Enhanced sensory perception

* Increase in associative & creative thinking; introspection

* Life-changing 'spiritual' experiences

* Closed and Open eye visuals, patterning, tracers, color-enhancement, etc.

* Enhanced appreciation of music

* Increase in energy

== Neutral ==

* Time dilation

* Slight increase in heart-rate and body temperature

* Inability to focus or difficulty focusing

== Negative ==

* Tension

* Anxiety, restlessness, confusion

* Dizziness

* Nausea, gastrointestinal discomfort, possible vomiting

* Over-sensitivity to music or other sensory stimuli

* Unwanted 'spiritual' experiences

* Racing thoughts

= Harm Reduction =

* As with all psychedelic drugs 2C-E carries with it the potential for a very powerful experience, and as such has the potential to create a very difficult experience ('bad' trip). Mindset and setting play important roles in governing the nature of a psychedelic experience, among other things.

See [[Psychedelics#Harm_Reduction|Psychedelic Harm Reduction]] for more information.

* As with all stimulants, care should be taken when dosing via different ROAs. The oral route has a much lower bioavailabity than those that bypass first pass metabolism i.e. Insulated, rectal, intramuscular, intravenous and subcutaneous.

See [[Stimulants#Harm Reduction|Stimulant Harm Reduction]] for more information.

==Interactions==

* As with all psychedelic phenethylamines caution must be exercised when used in conjunction with other drugs. In particular 2C-E is thought to carry risk of causing potentially life-threatening psychological and/or physiological problems when used in conjunction with certain types of medication, including MAOIs and possibly Lithium.<ref>http://mentalmana.blogspot.com/2013/05/2c-e-europa-eternity.html</ref>

Note: This information is based on unconfirmed anecdotal reports and logical deduction based on pharmacological properties when compared with other potent psychedelics. We strongly suggest erring on the side of caution considering the lack of concrete evidence either way.

See the [[Drug combinations]] chart for more information.

= Chemistry and Pharmacology =

==Chemistry==

2,5-Dimethoxy-4-ethylphenethylamine is a colorless oil and analogue of mescaline. Similarly it is classified as a psychedelic phenethylamine. It shares the substituted amphetamine core found in the structure of many entactogens. Crystalline forms are obtained as the amine salt by reacting the free base with a mineral acid, typically HCl. It is soluble in both water and ethanol. Maximum concentration in H2O is reported at ~50mg/ml and it is said to be relatively stable in solution. A drop below normal ambient temperatures can cause particles to crystalize out.

Shulgin does not report an exact boiling point for the free base, stating only that during one synthesis the fraction boiling between 90-100 °C at 0.25 mmHg pressure was collected and converted to the hydrochloride salt. Shulgin reports the melting point of the hydrochloride salt as 208.5-210.5 °C. Similarly it is classified as a psychedelic phenethylamine. It shares the substituted amphetamine core found in the structure of many entactogens.

A full write up on Shulgin's synthesis for 2C-E can be found [https://www.erowid.org/library/books_online/pihkal/pihkal024.shtml here].

==Pharmacology==

Like most psychedelic drugs, 2C-E is a 5-HT2a Agonist; from that, we can presume the concurrent or pre-administration of SSRIs may reduce the effects of 2C-E. 2C-E is one of the most potent of the 2C-X family, behind only 2C-P and 2C-T-4. The 2C-X family, specifically, 2C-E, 2C-I, and 2C-C all stimulated G protein binding, suggesting more of an activity similar to tryptamines such as 5-MeO-DMT and, interestingly, DPT. G Proteins are membrane proteins that effectively mediate interaction between hormone receptors and enzymes responsible for changes of metabolism as a result of hormonal changes.

In rats, Stage I metabolism involved deamination and O-Demthylation, which are related to the Monoamine oxidase (MAO) and cytochrome P450 (CYP) enzymes. For virtually all the 2C’s, (B,I,D,E,T-2, and T-7), MAO-A and MAO-B were reacted upon; interestingly, ½ of the molecules in Shulgin’s Magical Half Dozen (2C-E, 2C-T-2, 2C-T-7, with the addition of 2C-D) also act to a small extent on the CYP2D6 enzyme. Because of the commonality of these receptors, the 2C-X family is likely to be more reactive with other concurrently administered chemicals.

== LD50 ==

The LD50 in humans is not currently known. Use caution when exploring high doses of this compound.

= Legal status =

* In Australia, 2C-E was added to the 'Dangerous Drugs' list of the 'Drugs Misuse Amendment Act 2008.

* In Denmark, 2C-E has been added to the list of Schedule B controlled substances.

* In New Zealand, 2C-E is illegal under the Analogues section of Schedule 3 / Class C, along with 2C-I, DOI, ephedrine and pseudoephedrine.

* In Sweden, 2C-E has been made illegal to sell or possess under their Act on the Prohibition of Certain Goods Dangerous to Health (''lagen om förbud mot vissa hälsofarliga varor'').

* In the UK, 2C-E is a Class A controlled Substance under the Misuse of Drugs Act's 2002 amendments and as such is illegal to possess to supply.

* In Germany, 2C-E is a Schedule I drug as of late 2014.

* In the USA, 2C-E is a Schedule I substance under the FDA Safety and Innovation act of 2012, and is illegal to possess, distribute or manufacture.

= Links =

* [https://www.erowid.org/chemicals/2ce/ Erowid]

* [https://www.erowid.org/library/books_online/pihkal/pihkal024.shtml PiHKAL Entry]

* [https://www.wikipedia.org/wiki/2C-E/ Wikipedia]

[[Category:Stimulant]]

[[Category:Psychedelic]]

[[Category:Drugs]]

2C-E

2014-10-16T05:27:30Z

Roi: /* Pharmacology */

[[File:2ce.jpg|thumb|200px|Vial of 2C-E with powder]]

2C-E is a chemical of the [[2C-X]] series which is characterised by its particularly intense visuals and higher potency when compared with other members of the family.

= History =

2C-E, like many of its close analogues, was first synthesized by Alexander Shulgin and published in PiHKAL. He was quite fond of it, granting it a place in his "Magical Half Dozen" alongside of [[DOM]], [[2C-B]], [[2C-T-2]] & 7 and [[mescaline]].

= Uses =

2C-E is mainly a recreational entheogen. It can be quite introspective in appropriate doses and settings. It doesn't lend itself well to intense party-like surroundings, much like LSD or similarly intense psychedelics.

= Dosage =

{| class="wikitable"

|+ Oral

|-

| Light || 5-10mg

|-

| Common || 10-15mg

|-

| Strong || 15-30mg

|-

| Heavy || 25-40mg+

|}

{| class="wikitable"

|+ Insulated

|-

| Light || 1-3mg

|-

| Common || 3-7mg

|-

| Strong || 6-10mg

|-

| Heavy || 10mg+

|}

= Duration =

Note: Duration can be significantly longer with higher doses.

Anecdotal evidence has shown the oral onset of 2C-E may vary wildly for some users, taking up to three hours before first effects in some cases.

{| class="wikitable"

|+ Oral

| Onset || 60-90 minutes

|-

| Total || 9-14 hours

|}

{| class="wikitable"

|+ Insufflated

| Onset || 20-40 minutes

|-

| Total || 6-9 hours

|}

= Effects =

2C-E is a psychedelic phenethylamine and as such has psychedelic and stimulant effects. As with all psychedelics, different users are likely to experience different sets of effects, which usually include some however very rarely would include all of the following effects.

Compared to other members of the 2C-X family, 2C-E is generally considered to have a heavier body load and to be more visual than its counterparts.

Note: The prevalence of negative effects increases with higher doses.

== Positive ==

* Mood lift, euphoria, sense of well-being

* Enhanced sensory perception

* Increase in associative & creative thinking; introspection

* Life-changing 'spiritual' experiences

* Closed and Open eye visuals, patterning, tracers, color-enhancement, etc.

* Enhanced appreciation of music

* Increase in energy

== Neutral ==

* Time dilation

* Slight increase in heart-rate and body temperature

* Inability to focus or difficulty focusing

== Negative ==

* Tension

* Anxiety, restlessness, confusion

* Dizziness

* Nausea, gastrointestinal discomfort, possible vomiting

* Over-sensitivity to music or other sensory stimuli

* Unwanted 'spiritual' experiences

* Racing thoughts

= Harm Reduction =

* As with all psychedelic drugs 2C-E carries with it the potential for a very powerful experience, and as such has the potential to create a very difficult experience ('bad' trip). Mindset and setting play important roles in governing the nature of a psychedelic experience, among other things.

See [[Psychedelics#Harm_Reduction|Psychedelic Harm Reduction]] for more information.

* As with all stimulants, care should be taken when dosing via different ROAs. The oral route has a much lower bioavailabity than those that bypass first pass metabolism i.e. Insulated, rectal, intramuscular, intravenous and subcutaneous.

See [[Stimulants#Harm Reduction|Stimulant Harm Reduction]] for more information.

==Interactions==

* As with all psychedelic phenethylamines caution must be exercised when used in conjunction with other drugs. In particular 2C-E is thought to carry risk of causing potentially life-threatening psychological and/or physiological problems when used in conjunction with certain types of medication, including MAOIs and possibly Lithium.<ref>http://mentalmana.blogspot.com/2013/05/2c-e-europa-eternity.html</ref>

Note: This information is based on unconfirmed anecdotal reports and logical deduction based on pharmacological properties when compared with other potent psychedelics. We strongly suggest erring on the side of caution considering the lack of concrete evidence either way.

See the [[Drug combinations]] chart for more information.

= Chemistry and Pharmacology =

==Chemistry==

2,5-Dimethoxy-4-ethylphenethylamine is a colorless oil and analogue of mescaline. Similarly it is classified as a psychedelic phenethylamine. It shares the substituted amphetamine core found in the structure of many entactogens. Crystalline forms are obtained as the amine salt by reacting the free base with a mineral acid, typically HCl. It is soluble in both water and ethanol. Maximum concentration in H2O is reported at ~50mg/ml and it is said to be relatively stable in solution. A drop below normal ambient temperatures can cause particles to crystalize out.

Shulgin does not report an exact boiling point for the free base, stating only that during one synthesis the fraction boiling between 90-100 °C at 0.25 mmHg pressure was collected and converted to the hydrochloride salt. Shulgin reports the melting point of the hydrochloride salt as 208.5-210.5 °C. Similarly it is classified as a psychedelic phenethylamine. It shares the substituted amphetamine core found in the structure of many entactogens.

A full write up on Shulgin's synthesis for 2C-E can be found [https://www.erowid.org/library/books_online/pihkal/pihkal024.shtml here]

==Pharmacology==

Like most psychedelic drugs, 2C-E is a 5-HT2a Agonist; from that, we can presume the concurrent or pre-administration of SSRIs may reduce the effects of 2C-E. 2C-E is one of the most potent of the 2C-X family, behind only 2C-P and 2C-T-4. The 2C-X family, specifically, 2C-E, 2C-I, and 2C-C all stimulated G protein binding, suggesting more of an activity similar to tryptamines such as 5-MeO-DMT and, interestingly, DPT. G Proteins are membrane proteins that effectively mediate interaction between hormone receptors and enzymes responsible for changes of metabolism as a result of hormonal changes.

In rats, Stage I metabolism involved deamination and O-Demthylation, which are related to the Monoamine oxidase (MAO) and cytochrome P450 (CYP) enzymes. For virtually all the 2C’s, (B,I,D,E,T-2, and T-7), MAO-A and MAO-B were reacted upon; interestingly, ½ of the molecules in Shulgin’s Magical Half Dozen (2C-E, 2C-T-2, 2C-T-7, with the addition of 2C-D) also act to a small extent on the CYP2D6 enzyme. Because of the commonality of these receptors, the 2C-X family is likely to be more reactive with other concurrently administered chemicals.

== LD50 ==

The LD50 in humans is not currently known. Use caution when exploring high doses of this compound.

= Legal status =

* In Australia, 2C-E was added to the 'Dangerous Drugs' list of the 'Drugs Misuse Amendment Act 2008.

* In Denmark, 2C-E has been added to the list of Schedule B controlled substances.

* In New Zealand, 2C-E is illegal under the Analogues section of Schedule 3 / Class C, along with 2C-I, DOI, ephedrine and pseudoephedrine.

* In Sweden, 2C-E has been made illegal to sell or possess under their Act on the Prohibition of Certain Goods Dangerous to Health (''lagen om förbud mot vissa hälsofarliga varor'').

* In the UK, 2C-E is a Class A controlled Substance under the Misuse of Drugs Act's 2002 amendments and as such is illegal to possess to supply.

* In Germany, 2C-E is a Schedule I drug as of late 2014.

* In the USA, 2C-E is a Schedule I substance under the FDA Safety and Innovation act of 2012, and is illegal to possess, distribute or manufacture.

= Links =

* [https://www.erowid.org/chemicals/2ce/ Erowid]

* [https://www.erowid.org/library/books_online/pihkal/pihkal024.shtml PiHKAL Entry]

* [https://www.wikipedia.org/wiki/2C-E/ Wikipedia]

[[Category:Stimulant]]

[[Category:Psychedelic]]

[[Category:Drugs]]

2C-E

2014-10-16T05:27:03Z

Roi: /* Interactions */

[[File:2ce.jpg|thumb|200px|Vial of 2C-E with powder]]

2C-E is a chemical of the [[2C-X]] series which is characterised by its particularly intense visuals and higher potency when compared with other members of the family.

= History =

2C-E, like many of its close analogues, was first synthesized by Alexander Shulgin and published in PiHKAL. He was quite fond of it, granting it a place in his "Magical Half Dozen" alongside of [[DOM]], [[2C-B]], [[2C-T-2]] & 7 and [[mescaline]].

= Uses =

2C-E is mainly a recreational entheogen. It can be quite introspective in appropriate doses and settings. It doesn't lend itself well to intense party-like surroundings, much like LSD or similarly intense psychedelics.

= Dosage =

{| class="wikitable"

|+ Oral

|-

| Light || 5-10mg

|-

| Common || 10-15mg

|-

| Strong || 15-30mg

|-

| Heavy || 25-40mg+

|}

{| class="wikitable"

|+ Insulated

|-

| Light || 1-3mg

|-

| Common || 3-7mg

|-

| Strong || 6-10mg

|-

| Heavy || 10mg+

|}

= Duration =

Note: Duration can be significantly longer with higher doses.

Anecdotal evidence has shown the oral onset of 2C-E may vary wildly for some users, taking up to three hours before first effects in some cases.

{| class="wikitable"

|+ Oral

| Onset || 60-90 minutes

|-

| Total || 9-14 hours

|}

{| class="wikitable"

|+ Insufflated

| Onset || 20-40 minutes

|-

| Total || 6-9 hours

|}

= Effects =

2C-E is a psychedelic phenethylamine and as such has psychedelic and stimulant effects. As with all psychedelics, different users are likely to experience different sets of effects, which usually include some however very rarely would include all of the following effects.

Compared to other members of the 2C-X family, 2C-E is generally considered to have a heavier body load and to be more visual than its counterparts.

Note: The prevalence of negative effects increases with higher doses.

== Positive ==

* Mood lift, euphoria, sense of well-being

* Enhanced sensory perception

* Increase in associative & creative thinking; introspection

* Life-changing 'spiritual' experiences

* Closed and Open eye visuals, patterning, tracers, color-enhancement, etc.

* Enhanced appreciation of music

* Increase in energy

== Neutral ==

* Time dilation

* Slight increase in heart-rate and body temperature

* Inability to focus or difficulty focusing

== Negative ==

* Tension

* Anxiety, restlessness, confusion

* Dizziness

* Nausea, gastrointestinal discomfort, possible vomiting

* Over-sensitivity to music or other sensory stimuli

* Unwanted 'spiritual' experiences

* Racing thoughts

= Harm Reduction =

* As with all psychedelic drugs 2C-E carries with it the potential for a very powerful experience, and as such has the potential to create a very difficult experience ('bad' trip). Mindset and setting play important roles in governing the nature of a psychedelic experience, among other things.

See [[Psychedelics#Harm_Reduction|Psychedelic Harm Reduction]] for more information.

* As with all stimulants, care should be taken when dosing via different ROAs. The oral route has a much lower bioavailabity than those that bypass first pass metabolism i.e. Insulated, rectal, intramuscular, intravenous and subcutaneous.

See [[Stimulants#Harm Reduction|Stimulant Harm Reduction]] for more information.

==Interactions==

* As with all psychedelic phenethylamines caution must be exercised when used in conjunction with other drugs. In particular 2C-E is thought to carry risk of causing potentially life-threatening psychological and/or physiological problems when used in conjunction with certain types of medication, including MAOIs and possibly Lithium.<ref>http://mentalmana.blogspot.com/2013/05/2c-e-europa-eternity.html</ref>

Note: This information is based on unconfirmed anecdotal reports and logical deduction based on pharmacological properties when compared with other potent psychedelics. We strongly suggest erring on the side of caution considering the lack of concrete evidence either way.

See the [[Drug combinations]] chart for more information.

= Chemistry and Pharmacology =

==Chemistry==

2,5-Dimethoxy-4-ethylphenethylamine is a colorless oil and analogue of mescaline. Similarly it is classified as a psychedelic phenethylamine. It shares the substituted amphetamine core found in the structure of many entactogens. Crystalline forms are obtained as the amine salt by reacting the free base with a mineral acid, typically HCl. It is soluble in both water and ethanol. Maximum concentration in H2O is reported at ~50mg/ml and it is said to be relatively stable in solution. A drop below normal ambient temperatures can cause particles to crystalize out.

Shulgin does not report an exact boiling point for the free base, stating only that during one synthesis the fraction boiling between 90-100 °C at 0.25 mmHg pressure was collected and converted to the hydrochloride salt. Shulgin reports the melting point of the hydrochloride salt as 208.5-210.5 °C. Similarly it is classified as a psychedelic phenethylamine. It shares the substituted amphetamine core found in the structure of many entactogens.

A full write up on Shulgin's synthesis for 2C-E can be found [https://www.erowid.org/library/books_online/pihkal/pihkal024.shtml here]

==Pharmacology==

Like most psychedelic drugs, 2C-E is a 5-HT2a Agonist; from that, we can presume the concurrent or pre-administration of SSRI’s may reduce the effects of 2C-E. 2C-E is one of the most potent of the 2C-X family, behind only 2C-P and 2C-T-4. The 2C-X family, specifically, 2C-E, 2C-I, and 2C-C all stimulated G protein binding, suggesting more of an activity similar to tryptamines such as 5-MeO-DMT and, interestingly, DPT. G Proteins are membrane proteins that effectively mediate interaction between hormone receptors and enzymes responsible for changes of metabolism as a result of hormonal changes.

In rats, Stage I metabolism involved deamination and O-Demthylation, which are related to the Monoamine oxidase (MAO) and cytochrome P450 (CYP) enzymes. For virtually all the 2C’s, (B,I,D,E,T-2, and T-7), MAO-A and MAO-B were reacted upon; interestingly, ½ of the molecules in Shulgin’s Magical Half Dozen (2C-E, 2C-T-2, 2C-T-7, with the addition of 2C-D) also act to a small extent on the CYP2D6 enzyme. Because of the commonality of these receptors, the 2C-X family is likely to be more reactive with other concurrently administered chemicals.

== LD50 ==

The LD50 in humans is not currently known. Use caution when exploring high doses of this compound.

= Legal status =

* In Australia, 2C-E was added to the 'Dangerous Drugs' list of the 'Drugs Misuse Amendment Act 2008.

* In Denmark, 2C-E has been added to the list of Schedule B controlled substances.

* In New Zealand, 2C-E is illegal under the Analogues section of Schedule 3 / Class C, along with 2C-I, DOI, ephedrine and pseudoephedrine.

* In Sweden, 2C-E has been made illegal to sell or possess under their Act on the Prohibition of Certain Goods Dangerous to Health (''lagen om förbud mot vissa hälsofarliga varor'').

* In the UK, 2C-E is a Class A controlled Substance under the Misuse of Drugs Act's 2002 amendments and as such is illegal to possess to supply.

* In Germany, 2C-E is a Schedule I drug as of late 2014.

* In the USA, 2C-E is a Schedule I substance under the FDA Safety and Innovation act of 2012, and is illegal to possess, distribute or manufacture.

= Links =

* [https://www.erowid.org/chemicals/2ce/ Erowid]

* [https://www.erowid.org/library/books_online/pihkal/pihkal024.shtml PiHKAL Entry]

* [https://www.wikipedia.org/wiki/2C-E/ Wikipedia]

[[Category:Stimulant]]

[[Category:Psychedelic]]

[[Category:Drugs]]

2C-E

2014-10-16T05:26:18Z

Roi: fixing this madness

[[File:2ce.jpg|thumb|200px|Vial of 2C-E with powder]]

2C-E is a chemical of the [[2C-X]] series which is characterised by its particularly intense visuals and higher potency when compared with other members of the family.

= History =

2C-E, like many of its close analogues, was first synthesized by Alexander Shulgin and published in PiHKAL. He was quite fond of it, granting it a place in his "Magical Half Dozen" alongside of [[DOM]], [[2C-B]], [[2C-T-2]] & 7 and [[mescaline]].

= Uses =

2C-E is mainly a recreational entheogen. It can be quite introspective in appropriate doses and settings. It doesn't lend itself well to intense party-like surroundings, much like LSD or similarly intense psychedelics.

= Dosage =

{| class="wikitable"

|+ Oral

|-

| Light || 5-10mg

|-

| Common || 10-15mg

|-

| Strong || 15-30mg

|-

| Heavy || 25-40mg+

|}

{| class="wikitable"

|+ Insulated

|-

| Light || 1-3mg

|-

| Common || 3-7mg

|-

| Strong || 6-10mg

|-

| Heavy || 10mg+

|}

= Duration =

Note: Duration can be significantly longer with higher doses.

Anecdotal evidence has shown the oral onset of 2C-E may vary wildly for some users, taking up to three hours before first effects in some cases.

{| class="wikitable"

|+ Oral

| Onset || 60-90 minutes

|-

| Total || 9-14 hours

|}

{| class="wikitable"

|+ Insufflated

| Onset || 20-40 minutes

|-

| Total || 6-9 hours

|}

= Effects =

2C-E is a psychedelic phenethylamine and as such has psychedelic and stimulant effects. As with all psychedelics, different users are likely to experience different sets of effects, which usually include some however very rarely would include all of the following effects.

Compared to other members of the 2C-X family, 2C-E is generally considered to have a heavier body load and to be more visual than its counterparts.

Note: The prevalence of negative effects increases with higher doses.

== Positive ==

* Mood lift, euphoria, sense of well-being

* Enhanced sensory perception

* Increase in associative & creative thinking; introspection

* Life-changing 'spiritual' experiences

* Closed and Open eye visuals, patterning, tracers, color-enhancement, etc.

* Enhanced appreciation of music

* Increase in energy

== Neutral ==

* Time dilation

* Slight increase in heart-rate and body temperature

* Inability to focus or difficulty focusing

== Negative ==

* Tension

* Anxiety, restlessness, confusion

* Dizziness

* Nausea, gastrointestinal discomfort, possible vomiting

* Over-sensitivity to music or other sensory stimuli

* Unwanted 'spiritual' experiences

* Racing thoughts

= Harm Reduction =

* As with all psychedelic drugs 2C-E carries with it the potential for a very powerful experience, and as such has the potential to create a very difficult experience ('bad' trip). Mindset and setting play important roles in governing the nature of a psychedelic experience, among other things.

See [[Psychedelics#Harm_Reduction|Psychedelic Harm Reduction]] for more information.

* As with all stimulants, care should be taken when dosing via different ROAs. The oral route has a much lower bioavailabity than those that bypass first pass metabolism i.e. Insulated, rectal, intramuscular, intravenous and subcutaneous.

See [[Stimulants#Harm Reduction|Stimulant Harm Reduction]] for more information.

==Interactions==

* As with all psychedelic phenethylamines caution must be exercised when used in conjunction with other drugs. In particular 2C-E is thought to carry risk of causing potentially life-threatening psychological and/or physiological problems when used in conjunction with certain types of medication, including MAOIs, SSRIs, NDRIs and possibly Lithium.<ref>http://mentalmana.blogspot.com/2013/05/2c-e-europa-eternity.html</ref>

Note: This information is based on unconfirmed anecdotal reports and logical deduction based on pharmacological properties when compared with other potent psychedelics. We strongly suggest erring on the side of caution considering the lack of concrete evidence either way.

See the [[Drug combinations]] chart for more information.

= Chemistry and Pharmacology =

==Chemistry==

2,5-Dimethoxy-4-ethylphenethylamine is a colorless oil and analogue of mescaline. Similarly it is classified as a psychedelic phenethylamine. It shares the substituted amphetamine core found in the structure of many entactogens. Crystalline forms are obtained as the amine salt by reacting the free base with a mineral acid, typically HCl. It is soluble in both water and ethanol. Maximum concentration in H2O is reported at ~50mg/ml and it is said to be relatively stable in solution. A drop below normal ambient temperatures can cause particles to crystalize out.

Shulgin does not report an exact boiling point for the free base, stating only that during one synthesis the fraction boiling between 90-100 °C at 0.25 mmHg pressure was collected and converted to the hydrochloride salt. Shulgin reports the melting point of the hydrochloride salt as 208.5-210.5 °C. Similarly it is classified as a psychedelic phenethylamine. It shares the substituted amphetamine core found in the structure of many entactogens.

A full write up on Shulgin's synthesis for 2C-E can be found [https://www.erowid.org/library/books_online/pihkal/pihkal024.shtml here]

==Pharmacology==

Like most psychedelic drugs, 2C-E is a 5-HT2a Agonist; from that, we can presume the concurrent or pre-administration of SSRI’s may reduce the effects of 2C-E. 2C-E is one of the most potent of the 2C-X family, behind only 2C-P and 2C-T-4. The 2C-X family, specifically, 2C-E, 2C-I, and 2C-C all stimulated G protein binding, suggesting more of an activity similar to tryptamines such as 5-MeO-DMT and, interestingly, DPT. G Proteins are membrane proteins that effectively mediate interaction between hormone receptors and enzymes responsible for changes of metabolism as a result of hormonal changes.

In rats, Stage I metabolism involved deamination and O-Demthylation, which are related to the Monoamine oxidase (MAO) and cytochrome P450 (CYP) enzymes. For virtually all the 2C’s, (B,I,D,E,T-2, and T-7), MAO-A and MAO-B were reacted upon; interestingly, ½ of the molecules in Shulgin’s Magical Half Dozen (2C-E, 2C-T-2, 2C-T-7, with the addition of 2C-D) also act to a small extent on the CYP2D6 enzyme. Because of the commonality of these receptors, the 2C-X family is likely to be more reactive with other concurrently administered chemicals.

== LD50 ==

The LD50 in humans is not currently known. Use caution when exploring high doses of this compound.

= Legal status =

* In Australia, 2C-E was added to the 'Dangerous Drugs' list of the 'Drugs Misuse Amendment Act 2008.

* In Denmark, 2C-E has been added to the list of Schedule B controlled substances.

* In New Zealand, 2C-E is illegal under the Analogues section of Schedule 3 / Class C, along with 2C-I, DOI, ephedrine and pseudoephedrine.

* In Sweden, 2C-E has been made illegal to sell or possess under their Act on the Prohibition of Certain Goods Dangerous to Health (''lagen om förbud mot vissa hälsofarliga varor'').

* In the UK, 2C-E is a Class A controlled Substance under the Misuse of Drugs Act's 2002 amendments and as such is illegal to possess to supply.

* In Germany, 2C-E is a Schedule I drug as of late 2014.

* In the USA, 2C-E is a Schedule I substance under the FDA Safety and Innovation act of 2012, and is illegal to possess, distribute or manufacture.

= Links =

* [https://www.erowid.org/chemicals/2ce/ Erowid]

* [https://www.erowid.org/library/books_online/pihkal/pihkal024.shtml PiHKAL Entry]

* [https://www.wikipedia.org/wiki/2C-E/ Wikipedia]

[[Category:Stimulant]]

[[Category:Psychedelic]]

[[Category:Drugs]]

Medikinet

2014-10-14T23:51:06Z