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Severe neurotoxicity is associated with the use of 4-CA and can directly cause injury or death.
4-CA is strongly linked to neurotoxicity, severe injury, and death. Please see this section for more details.
|Summary sheet: 4-CA|
|Common names||4-CA, PCA, 4-CMP, P-CMP|
|Substitutive name||4-Chloroamphetamine, para-Chloroamphetamine|
|Psychoactive class||Stimulant / Entactogen|
|Routes of Administration|
4-Chloroamphetamine (also known as 4-CA, 4-CMP, para-Chloroamphetamine, PCA and P-CMP) is a novel, synthetic substituted amphetamine that induces a mixture of entactogenic and stimulant effects when administered. 4-CA is known for its severe neurotoxicity and was found to selectively destruct serotonergic neurons in animal study.
The use of this substance is strongly discouraged and it is recommended to use harm reduction practices if done anyway.
History and culture
In 1963, the effects of 4-CMA were described by the Swiss researchers Pletscher, Burkard, Bruderer and Gey. Because of their results, several other chlorinated analogs of amphetamine, including 4-CA had been synthesized by the American pharmaceutical company Eli Lilly and Company. They were examined as appetite suppressants. U.S. American biochemist Ray W. Fuller and collegues resynthesized these compounds and found that 4-CA was the most potent serotonin depletor. Van Praag and others conducted comprehensive clinical study on humans in 1971, and it has been found to have a potent antidepressant effect. It was well tolerated and having only few side effects. Yunger, McMaster, and Harvey described the related neurotoxicity in 1974. 4-CA became a common tool for selective modification of the serotonergic function in laboratory animals. The research of its promising medical effects was halted because the risks due to neurotoxicity were too high.
4-Chloroamphetamine is a synthetic compound of the substituted amphetamine class. Amphetamines contain a phenethylamine core featuring a phenyl ring bound to an amino (NH2) group through an ethyl chain with an additional methyl substitution at Rα. Amphetamines are alpha-methylated phenethylamines. 4-CA contains a chlorine atom at R4 of its phenyl ring and is a chlorinated analogue of amphetamine.
This pharmacology section is incomplete.
You can help by adding to it.
4-Chloroamphetamine acts as a releasing agent of the monoamine neurotransmitter serotonin. At higher doses, it can deplete brain serotonin.
A decreases in tryptophane hydroxylase activity could be observed.
|This subjective effects section is a stub.|
As such, it is still in progress and may contain incomplete or wrong information.
You can help by expanding or correcting it.
Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.
You may select physical effects to add below here.
- Abnormal heartbeat
- Appetite suppression
- Decreased blood pressure
- Decreased heart rate
- Difficulty urinating
- Dry mouth
- Frequent urination
- Increased blood pressure
- Increased bodily temperature
- Increased heart rate
- Increased perspiration
- Increased salivation
- Orgasm suppression
- Physical euphoria
- Pupil dilation
- Teeth grinding
- Temperature regulation suppression
- Temporary erectile dysfunction
- Vibrating vision
Not much ist known about the cognitive effects of 4-CA.
Not much ist known about the multisensory effects of 4-CA.
Not much ist known about the transpersonal effects of 4-CA.
There are currently 0 experience reports which describe the effects of this substance in our experience index.
Toxicity and harm potential
This toxicity and harm potential section is a stub.
As a result, it may contain incomplete or even dangerously wrong information! You can help by expanding upon or correcting it.
The use of this substance is strongly discouraged and it is recommended to use harm reduction practices if done anyway. 4-CA is known to induce heavy neurotoxicity
Tolerance and addiction potential
Not much is known about the tolerance and addiction potential.
Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).
Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.
- Alcohol - Drinking alcohol on stimulants is considered risky because it reduces the sedative effects of the alcohol that the body uses to gauge drunkenness. This often leads to excessive drinking with greatly reduced inhibitions, increasing the risk of liver damage and increased dehydration. The effects of stimulants will also allow one to drink past a point where they 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.
- GHB/GBL - Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the depressant effects of the GHB/GBL may overcome the user and cause respiratory arrest.
- Opioids - 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.
- Cocaine - The rewarding effects of cocaine are mediated by DAT inhibition, and an increase of exocytosis of dopamine through the cell membrane. Amphetamine reverses the direction of DAT and the direction vesicular transports within the cell by a pH mediated mechanism of displacement, thus excludes the regular mechanism of dopamine release through means of exocytosis because the effects Na+/K+ ATPase are inhibited. You will find cardiac effects with the combination of cocaine and amphetamine due to a SERT mediated mechanism from the subsequent activation of 5-HT2B, which is an effect of serotonin-related valvulopathy. Amphetamines generally cause hypertension in models of abuse, and this combination can increase the chances of syncope due to turbulent blood flow during valve operation. The rewarding mechanisms of cocaine are reversed by administration of amphetamine.
- Cannabis - Stimulants increase anxiety levels and the risk of thought loops and paranoia which can lead to negative experiences.
- Caffeine - This combination of stimulants is generally considered unnecessary and may increase strain on the heart, as well as potentially causing anxiety and physical discomfort.
- Tramadol - Tramadol and stimulants both increase the risk of seizures.
- DXM - Both substances raise heart rate, in extreme cases, panic attacks caused by these substances have led to more serious heart issues.
- Ketamine - Combining amphetamine and ketamine may result in psychoses that resemble schizophrenia, but not worse than the psychoses produced by either substance alone, but this is debatable. This is due to amphetamines ability to attenuated the disruption of working memory caused by ketamine. Amphetamine alone may result in grandiosity, paranoia, or somatic delusions with little to no effect on negative symptoms. Ketamine, however, will result in thought disorders, disruption of executive functioning, and delusions due to a modification of conception. These mechanisms are due to an increase of dopaminergic activity in the mesolimbic pathway caused by amphetamine due to its pharmacology effecting dopamine, and due to a disruption of dopaminergic functioning in the mesocortical pathways via NMDA antagonism effects of ketamine. Combining the two, you may expect mainly thought disorder along with positive symptoms.
- PCP - Increases risk of tachycardia, hypertension, and manic states.
- Methoxetamine - Increases risk of tachycardia, hypertension, and manic states.
- Psychedelics (e.g. LSD, mescaline, psilocybin) - Increases risk of anxiety, paranoia, and thought loops.
- 25x-NBOMe - Amphetamines and NBOMes both provide considerable stimulation that 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.
- 2C-T-x - Suspected of mild MAOI properties. May increase the risk of hypertensive crisis.
- 5-MeO-xxT - Suspected of mild MAOI properties. May increase the risk of hypertensive crisis.
- aMT - aMT has MAOI properties which may interact unfavorably with amphetamines.
- MAOIs - MAO-B inhibitors can increase the potency and duration of phenethylamines unpredictably. MAO-A inhibitors with amphetamine can lead to hypertensive crises.
This legality section is a stub.
As such, it may contain incomplete or wrong information. You can help by expanding it.
- Australia: 4-CA is a Schedule I controlled drug 
- Canada: 4-CA is not explicitly listed on the CSDA. However, as an analogue of amphetamine it is controlled as a Schedule I substance.
- China: 4-CA is a controlled substance in China.
- Germany: 4-CA is controlled under the NpSG (New Psychoactive Substances Act) as of November 26, 2016. Production and import with the aim to place it on the market, administration to another person and trading is punishable. Possession is illegal but not penalized.
- United Kingdom: 4-CA is treated as a Class A substance.
- United States: 4-CA remains unscheduled.
- ↑ Miller, Krys J.; Anderholm, David C.; Ames, Matthew M. (1986). "Metabolic activation of the serotonergic neurotoxin para-chloroamphetamine to chemically reactive intermediates by hepatic and brain microsomal preparations". Biochemical Pharmacology. 35 (10): 1737–1742. doi:10.1016/0006-2952(86)90332-1. ISSN 0006-2952.
- ↑ Pletscher, A.; Burkard, W.P.; Bruderer, H.; Gey, K.F. (1963). "Decrease of cerebral 5-hydroxytryptamine and 5-hydroxyindolacetic acid by an arylalkylamine". Life Sciences. 2 (11): 828–833. doi:10.1016/0024-3205(63)90094-8. ISSN 0024-3205.
- ↑ 3.0 3.1 3.2 Fuller, Ray W. (1992). "Effects of p-chloroamphetamine on brain serotonin neurons". Neurochemical Research. 17 (5): 449–456. doi:10.1007/BF00969891. ISSN 1573-6903.
- ↑ 4.0 4.1 Owen Jr., John E. (1963). "Psychopharmacological Studies of Some 1-(Chlorophenyl)-2-aminopropanes I: Effects on Appetitive-Controlled Behavior". Journal of Pharmaceutical Sciences. 52 (7): 679–683. doi:10.1002/jps.2600520716. ISSN 0022-3549.
- ↑ Fuller, Ray W.; Hines, C.W.; Mills, J. (1965). "Lowering of brain serotonin level by chloramphetamines". Biochemical Pharmacology. 14 (4): 483–488. doi:10.1016/0006-2952(65)90221-2. ISSN 0006-2952.
- ↑ van Praag, H.M.; Schut, T.; Bosma, E.; van den Bergh, R. (1971). "A comparative study of the therapeutic effects of some 4-chlorinated amphetamine derivatives in depressive patients". Psychopharmacologia. 20 (1): 66–76. doi:10.1007/BF00404060. ISSN 1432-2072.
- ↑ 7.0 7.1 7.2 Shulgin, Alexander T. (1978). "Chapter 6". In Iversen, Leslie L.; Iversen, Susan D.; Snyder, Solomon H. Handbook of Psychopharmacology. Volume 11: Stimulants. New York: Plenum Press,. p. 313 et seq. ISBN 978-1-4757-0512-6.
- ↑ Sanders-Bush, E.; Bushing, J.A.; Sulser, F. (1972). "p-Chloroamphetamine—inhibition of cerebral tryptophan hydroxylase". Biochemical Pharmacology. 21 (10): 1501–1510. doi:10.1016/0006-2952(72)90375-9. ISSN 0006-2952.
- ↑ 9.0 9.1 9.2 9.3 9.4 9.5 9.6 Stein, J.M.; Wayner, M.J.; Kantak, K.M. (1981). "Increased urination following p-chloroamphetamine". Pharmacology Biochemistry and Behavior. 15 (2): 297–301. doi:10.1016/0091-3057(81)90191-X. ISSN 0091-3057.
- ↑ 10.0 10.1 Stein, J.M.; Wayner, M.J.; Kantak, K.M.; Cook, R.C. (1978). "Short- and long-term effects of para-chloroamphetamine on ingestive behavior". Pharmacology Biochemistry and Behavior. 9 (1): 115–122. doi:10.1016/0091-3057(78)90021-7. ISSN 0091-3057.
- ↑ Quock, Raymond M.; Weick, Barton G. (1979). "p‐Chloroamphetamine‐induced hyperthermia pharmacologically distinct from fenfluramine‐induced hyperthermia". Journal of Pharmacy and Pharmacology. 31 (1): 27–32. doi:10.1111/j.2042-7158.1979.tb13416.x. ISSN 0022-3573.
- ↑ Greenwald, M. K., Lundahl, L. H., Steinmiller, C. L. (December 2010). "Sustained Release d-Amphetamine Reduces Cocaine but not 'Speedball'-Seeking in Buprenorphine-Maintained Volunteers: A Test of Dual-Agonist Pharmacotherapy for Cocaine/Heroin Polydrug Abusers". Neuropsychopharmacology. 35 (13): 2624–2637. doi:10.1038/npp.2010.175. ISSN 0893-133X.
- ↑ Siciliano, C. A., Saha, K., Calipari, E. S., Fordahl, S. C., Chen, R., Khoshbouei, H., Jones, S. R. (10 January 2018). "Amphetamine Reverses Escalated Cocaine Intake via Restoration of Dopamine Transporter Conformation". The Journal of Neuroscience. 38 (2): 484–497. doi:10.1523/JNEUROSCI.2604-17.2017. ISSN 0270-6474.
- ↑ Krystal, J. H., Perry, E. B., Gueorguieva, R., Belger, A., Madonick, S. H., Abi-Dargham, A., Cooper, T. B., MacDougall, L., Abi-Saab, W., D’Souza, D. C. (1 September 2005). "Comparative and Interactive Human Psychopharmacologic Effects of Ketamine and Amphetamine: Implications for Glutamatergic and Dopaminergic Model Psychoses and Cognitive Function". Archives of General Psychiatry. 62 (9): 985. doi:10.1001/archpsyc.62.9.985. ISSN 0003-990X.
- ↑ "Criminal Code Regulations 2019". Office of Parliamentary Counsel. Retrieved December 12, 2019.
- ↑ "Controlled Drugs and Substances Act - SCHEDULE I". Government of Canada. Retrieved December 12, 2019.
- ↑ "STATUS DECISION OF CONTROLLED AND NON-CONTROLLED SUBSTANCE - Chloroamphetamine" (PDF). Health Canada. Retrieved December 12, 2019.
- ↑ "关于印发《非药用类麻醉药品和精神药品列管办法》的通知" (in Chinese). China Food and Drug Administration. Archived from the original on February 10, 2017. Retrieved December 28, 2019.
- ↑ "Anlage NpSG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 23, 2019.
- ↑ "Gesetz zur Bekämpfung der Verbreitung neuer psychoaktiver Stoffe" (PDF). Bundesgesetzblatt Jahrgang 2016 Teil I Nr. 55 (in German). Bundesanzeiger Verlag. November 25, 2016. Retrieved December 23, 2019.
- ↑ "§ 4 NpSG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 23, 2019.