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Talk:4-CA
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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.
WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.
DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.
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.[1]
The use of this substance is strongly discouraged and it is recommended to use harm reduction practices if done anyway.
In 1963, the effects of 4-CMA were described by the Swiss researchers Pletscher, Burkard, Bruderer and Gey.[2] 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.[3][4] U.S. American biochemist Ray W. Fuller and collegues resynthesized these compounds and found that 4-CA was the most potent serotonin depletor.[5] 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.[6][7] Yunger, McMaster, and Harvey described the related neurotoxicity in 1974.[7] 4-CA became a common tool for selective modification of the serotonergic function in laboratory animals.[3] The research of its promising medical effects was halted because the risks due to neurotoxicity were too high.[7]
Chemistry
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.
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 PsychonautWikicontributors. 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 ☠.
Physical effects
You may select physical effects to add below here.
Not much ist known about the transpersonal effects of 4-CA.
Experience reports
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. Note: Always conduct independent research and use harm reduction practices if using this substance.
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.
Dangerous interactions
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 over come the user and cause respiratory arrest.
Benzodiazepines - These substances can strongly mitigate the comedown of Stimulants and allow higher doses of them, which is a dangerous combination. And through the habit-forming properties, these substances should be consumed with extreme caution.
Opioids - Opioids combined with amphetamines have been found to potentially synergize unpredictably, increasing the chance of overdose.[12] Stimulants also increase respiration rate allowing a higher dose of opioids. 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.[13][14]
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 psychosis that resembles schizophrenia, but not worse than the psychosis 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.[15]
PCP - Increases risk of tachycardia, hypertension, and manic states.
Methoxetamine - Increases risk of tachycardia, hypertension, and manic states.
Gabapentinoids - Gabapentinoids like Pregabalin or Gabapentin can mitigate the comedown of Stimulants, but through the very fast tolerance development the effects will become less after a few days
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.
DOx
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.
Acetazolamide - Administration may increase serum concentration of amphetamine.
Ascorbic acid - Lowers urinary pH; may enhance amphetamine excretion.
Furazolidone - Amphetamines may induce a hypertensive response in patients taking furazolidone.
Guanethidine - Amphetamine inhibits the antihypertensive response to guanethidine.
Haloperidol - Limited evidence indicates that haloperidol may inhibit the effects of amphetamine but the clinical importance of this interaction is not established.
Lithium carbonate - Isolated case reports indicate that lithium may inhibit the effects of amphetamine.
Norepinephrine - Amphetamine abuse may enhance the pressor response to norepinephrine.
Phenothiazines - Amphetamine may inhibit the antipsychotic effect of phenothiazines, and phenothiazines may inhibit the anorectic effect of amphetamines.
Sodium bicarbonate - Large doses of sodium bicarbonate inhibit the elimination of amphetamine, thus increasing the amphetamine effect.
TCAs - Theoretically increases the effect of amphetamine, but clinical evidence is lacking.
As such, it may contain incomplete or wrong information. You can help by expanding it.
Australia: 4-CA is a Schedule I controlled drug [16]
Canada: 4-CA is not explicitly listed on the CSDA.[17] However, as an analogue of amphetamine it is controlled as a Schedule I substance.[18]
China: 4-CA is a controlled substance in China.[19]
Germany: 4-CA is controlled under the NpSG (New Psychoactive Substances Act)[20] as of November 26, 2016.[21] 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.[22]
United Kingdom: 4-CA is treated as a Class A substance.[citation needed]
↑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. ISSN0006-2952.
↑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. ISSN0024-3205.
↑ 3.03.13.2Fuller, Ray W. (1992). "Effects of p-chloroamphetamine on brain serotonin neurons". Neurochemical Research. 17 (5): 449–456. doi:10.1007/BF00969891. ISSN1573-6903.
↑ 4.04.1Owen 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. ISSN0022-3549.
↑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. ISSN0006-2952.
↑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. ISSN1432-2072.
↑ 10.010.1Stein, 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. ISSN0091-3057.
↑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. ISSN0022-3573.
↑Greenwald, M. K., Lundahl, L. H., & Steinmiller, C. L. (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: 2624–2637. doi:10.1038/npp.2010.175.
