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'''Phencyclidine''' (also known as '''PCP''', '''Angel Dust''', '''Sherm''', and '''Sernyl''')<ref>PCP Fast Facts | http://www.justice.gov/archive/ndic/pubs4/4440/</ref> is a classical [[psychoactive class::dissociative]] substance of the [[chemical class::arylcyclohexylamine]] class. It is one of the oldest and most notorious dissociatives, known for its potent effects and reputation as an established "street drug" (along with [[cocaine]] and [[heroin]]).<ref>Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 374–375. ISBN 9780071481274. </ref> It produces its effects by [[NMDA receptor antagonist|blocking the NMDA receptor]].<ref>Kapur, S., & Seeman, P. (2002). NMDA receptor antagonists ketamine and PCP have direct effects on the dopamine D2 and serotonin 5-HT2receptors--implications for models of schizophrenia. Molecular psychiatry, 7(8), 837. | http://www.nature.com/mp/journal/v7/n8/full/4001093a.html</ref>
'''Phencyclidine''' (also known as '''PCP''', '''Angel Dust''', '''Sherm''', and '''Sernyl''')<ref>PCP Fast Facts | http://www.justice.gov/archive/ndic/pubs4/4440/</ref> is a synthetic [[psychoactive class::dissociative]] substance of the [[chemical class::arylcyclohexylamine]] chemical class that produces potent, long-lived [[dissociative|dissociating]], [[Pain relief|anesthetic]], [[stimulating]], [[disinhibition|disinhibiting]] and [[hallucinogenic]] effects when [[Routes of administration|administered]].
First marketed in the 1950s as an anesthetic pharmaceutical drug, PCP was taken off the market in 1965 due to the high rate of [[hallucinogenic]] side effects. It emerged as a recreational substance in mid-1967, under the name "The Peace Pill".<ref>"Peace Pill". Microgram. Bureau of Drug Abuse Control. Jan 1968. 1(3):p1 (Erowid.org) | https://erowid.org/library/periodicals/microgram/microgram_1968_01_v01n03.pdf</ref><ref>"Sweet Streetfact's Lowdown on Low Dope Highs!". Berkeley Tribe, September 10-16, 1971. p12 (Independent Voices) | https://www.jstor.org/stable/community.28033860?seq=12</ref> Since this time, a number of synthetic derivatives of PCP (e.g. [[3-MeO-PCP]], [[4-MeO-PCP]], [[MXE]]) have been sold as dissociative drugs for both recreational and non-medical use.<ref name="morris">From PCP to MXE: a comprehensive review of the non-medical use of dissociative drugs (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/24678061</ref>
PCP acts primarily as an [[NMDA receptor antagonist]], meaning it binds to and blocks the activity of the NMDA receptor, the receptor responsible for the transmission of neural impulses in the central nervous system.<ref>Kapur, S., & Seeman, P. (2002). NMDA receptor antagonists ketamine and PCP have direct effects on the dopamine D2 and serotonin 5-HT2receptors--implications for models of schizophrenia. Molecular psychiatry, 7(8), 837. | http://www.nature.com/mp/journal/v7/n8/full/4001093a.html</ref>
[[Subjective effects]] include [[motor control loss]], [[pain relief]], [[internal hallucinations]], [[memory suppression]], [[conceptual thinking]], [[euphoria]], and [[depersonalization]] / [[disconnective effects|dissociation]]. Routes of administration include [[oral]], [[Routes of administration#Smoking|smoking]], [[insufflation]] or [[Routes of administration#Injection|injection]].<ref>NIDA. (2016, January 11). Hallucinogens. Retrieved from https://www.drugabuse.gov/publications/drugfacts/hallucinogens on 2017, October 29 | http://drugabuse.gov/infofacts/hallucinogens.html</ref> The effects are among the most potent and long-lasting in the class. Additionally, PCP is reported to have strong [[stimulation|stimulating]] effects that can promote [[anxiety]] and motor activity.
It was marketed in the 1950s as an anesthetic pharmaceutical drug but was taken off the market in 1965 due to the high prevalence of dissociating and [[hallucinogenic]] side effects it produced. Afterward, a similar structurally related compound named [[ketamine]] was discovered by Parke-Davis researchers as a better-tolerated derivative for use as an anesthetic pharmaceutical drug.
PCP has high abuse potential. [[Compulsive redosing]] has been reported, as well as psychological dependence following chronic use (i.e. high dose, repeated administration). Additionally, it is suspected of producing neurotoxicity as well as bladder toxicity.{{citation needed}} It is highly advised to use [[harm reduction practices]] if using this substance.
PCP emerged as a recreational drug in mid-1967, under the name "The Peace Pill".<ref>"Peace Pill". Microgram. Bureau of Drug Abuse Control. Jan 1968. 1(3):p1 (Erowid.org) | https://erowid.org/library/periodicals/microgram/microgram_1968_01_v01n03.pdf</ref><ref>"Sweet Streetfact's Lowdown on Low Dope Highs!". Berkeley Tribe, September 10-16, 1971. p12 (Independent Voices) | https://www.jstor.org/stable/community.28033860?seq=12</ref> Since this time, a number of synthetic derivatives of PCP have been sold as dissociative drugs for both recreational and non-medical use.<ref name="morris">From PCP to MXE: a comprehensive review of the non-medical use of dissociative drugs (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/24678061</ref> As an established "street drug", PCP is associated with compulsive abuse.<ref>Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 374–375. ISBN 9780071481274. </ref><ref name="morris" />
==History and culture==
After being discovered in 1926, PCP was developed as a general anesthetic in the 1950s because it could achieve analgesia and anesthesia with minimal cardiovascular and respiratory suppression. It was marketed under the name Sernyl and began to be used in surgical procedures in 1963.<ref name="Journey>Journey JD, Bentley TP. Phencyclidine Toxicity. 2021 Sep 12. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. PMID: 29939642.</ref>
As a recreational substance, PCP may be ingested [[orally]], [[Routes of administration#Smoking|smoked]], [[insufflated]] or via [[Routes of administration#Injection|injection]].<ref>NIDA. (2016, January 11). Hallucinogens. Retrieved from https://www.drugabuse.gov/publications/drugfacts/hallucinogens on 2017, October 29 | http://drugabuse.gov/infofacts/hallucinogens.html</ref> Due to its potent dissociative and stimulant effects, known habit-forming properties as well as an established toxicity profile, it is strongly recommended that one use proper [[Responsible drug use|harm reduction practices]] if choosing to use this substance.
By 1967, it was discontinued due to postoperative dysphoria and hallucinations. After 1967, it was limited to veterinary use. Also in the 1960s, PCP began to be illegally manufactured in laboratories and emerged as a popular street drug in San Francisco. In the 1970s, PCP use became widespread.<ref name="Journey"/>
===Common names===
Common street names for PCP are the peace pill, angel dust, crystal joints, rocket fuel, sawgrass, zoom, the sheets, and elephant tranquilizer.<ref name="Journey"/>
==Chemistry==
==Chemistry==
Revision as of 19:41, 12 November 2021
PCP may cause psychosis and mania at a significantly higher rate than other dissociatives.[1][2]
It is strongly discouraged to use this substance in high doses or multiple days in a row. 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.
Phencyclidine (also known as PCP, Angel Dust, Sherm, and Sernyl)[6] is a classical dissociative substance of the arylcyclohexylamine class. It is one of the oldest and most notorious dissociatives, known for its potent effects and reputation as an established "street drug" (along with cocaine and heroin).[7] It produces its effects by blocking the NMDA receptor.[8]
First marketed in the 1950s as an anesthetic pharmaceutical drug, PCP was taken off the market in 1965 due to the high rate of hallucinogenic side effects. It emerged as a recreational substance in mid-1967, under the name "The Peace Pill".[9][10] Since this time, a number of synthetic derivatives of PCP (e.g. 3-MeO-PCP, 4-MeO-PCP, MXE) have been sold as dissociative drugs for both recreational and non-medical use.[11]
PCP has high abuse potential. Compulsive redosing has been reported, as well as psychological dependence following chronic use (i.e. high dose, repeated administration). Additionally, it is suspected of producing neurotoxicity as well as bladder toxicity.[citation needed] It is highly advised to use harm reduction practices if using this substance.
After being discovered in 1926, PCP was developed as a general anesthetic in the 1950s because it could achieve analgesia and anesthesia with minimal cardiovascular and respiratory suppression. It was marketed under the name Sernyl and began to be used in surgical procedures in 1963.[13]
By 1967, it was discontinued due to postoperative dysphoria and hallucinations. After 1967, it was limited to veterinary use. Also in the 1960s, PCP began to be illegally manufactured in laboratories and emerged as a popular street drug in San Francisco. In the 1970s, PCP use became widespread.[13]
Common names
Common street names for PCP are the peace pill, angel dust, crystal joints, rocket fuel, sawgrass, zoom, the sheets, and elephant tranquilizer.[13]
Chemistry
PCP, or phencyclidine, is a synthetic dissociative of the arylcyclohexylamine class. PCP contains cyclohexane, a six-member saturated ring, bonded to two additional rings at R1. One of these rings is a piperidine ring, a nitrogenous six member ring, bonded at its nitrogen group. The other ring is an aromatic phenyl ring. PCP is an initialism named from the first letters of the three constituent rings phenyl, cyclohexane and piperidine.
PCP acts as an NMDA receptor antagonist. NMDA receptors allow for electrical signals to pass between neurons in the brain and spinal column; for the signals to pass, the receptor must be open. Dissociatives close the NMDA receptors by blocking them. This disconnection of neurons leads to loss of feeling, difficulty moving, and eventually an almost identical equivalent of the notorious “k-hole.”
PCP is considerably more likely to induce psychosis and mania than other dissociatives and is therefore potentially dangerous even in a proper setting.
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 ☠.
At high doses, PCP can produce a full range of high-level hallucinatory states in a fashion that is less consistent and reproducible than that of many other commonly used hallucinogens. These effects include:
The general head space of PCP is often described as particularly stimulating, euphoric and clear-headed in comparison to that of DXM and ketamine. The specific cognitive effects can be broken down into several separate subcomponents which are listed and described below:
The long-term use of PCP may lead to schizophrenia-like psychotic episodes, severe lasting memory loss, disorganized thinking, depression, weight loss, liver abnormalities and rhabdomyolysis (skeletal muscle breakdown).[16]
It is strongly recommended that one use harm reduction practices, such as volumetric dosing, when using this substance to ensure the accurate administration of the intended dose.
Psychosis
PCP has been reported to cause psychosis and mania at a significantly higher rate than other dissociatives such as ketamine, diphenidine, or MXE. Multiple scientific papers describe states of psychosis, mania, and/or delirium occurring after moderate to large doses of the drug were ingested. In one initial human trial, it was reported that one-sixth of the patients who had received anesthetic doses experienced acute psychosis.[14] In some cases, it took up to a week or more to resolve. Similar results (although less severe) were reported during trials using subanesthetic doses of PCP for pain relief.[15]
It is very strongly recommended that one use extreme caution and harm reduction practices when using this drug. For example,
Users should avoid taking the drug multiple days in a row or becoming addicted to it as this increases the risk of severe adverse effects.
The recommended dosage range should not be exceeded as high doses can trigger adverse effects.
Users should start with extremely low doses and work their way up as slowly as possible. Volumetric liquid dosing should preferably be used due to the drug's potency; most standard milligram scales cannot accurately weigh out doses below 10-15mg.
Compulsive redosing before one has fully sobered up is not recommended and can result in too high of a dose.
Due to the risk of psychosis, it is not recommended to combine this drug with other substances, especially stimulants, psychedelics, or other dissociatives like MXE and DXM. Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.
Tolerance and addiction potential
The chronic use of PCP can be considered highly addictive with a high potential for adverse side effects such as psychosis. In comparison to other dissociatives, PCP has been reported to be more addictive than MXE, diphenidine, ephenidine, and ketamine. When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage. There have been multiple reports across the internet of people becoming seriously addicted daily users of this substance so serious precautions and considerations should be taken before trying this substance.
Tolerance to many of the effects of PCP develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). PCP presents cross-tolerance with [[Cross-tolerance::all dissociatives]], meaning that after the consumption of PCP, all dissociatives will have a reduced effect.
Neurological effects
Some studies found that, like other NMDA receptor antagonists, PCP can cause brain damage called Olney's lesions in rats.[17][18] Studies conducted on rats showed that high doses of the NMDA receptor antagonist dizocilpine caused reversible vacuoles to form in certain regions of the rats' brains. All studies of Olney's lesions have only been performed on non-human animals and may not apply to humans. One unpublished study by Frank Sharp reportedly showed no damage by the NMDA antagonist ketamine (a similar drug) far beyond recreational doses[19] but its validity is controversial since it was never published.
PCP has also been shown to cause schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate levels in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue.[20] It also induces symptoms in humans that mimic schizophrenia.[21]
Urinary tract effects
In terms of its long-term health effects when used repeatedly and excessively for extended periods of time, PCP seems to exhibit almost identical bladder and urinary tract problems to those produced by ketamine.
Urinary frequency - Urinary frequency is the need to empty the bladder every few minutes.
Urinary urgency - This can be described as a sudden, compelling need to urinate.
Urinary pressure - This is experienced as a constant sensation of fullness in the bladder that is unrelieved by urination.
Pelvic and bladder pain - Pain can develop suddenly and severely, particularly as the bladder fills with urine.
Hematuria - Hematuria is visible blood in the urine.
Incontinence - This is the uncontrolled leakage of urine.
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.
MXE - There are no reports available about this combination.
Caffeine - Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.
Opioids - PCP can reduce opioid tolerance, increasing the risk of overdose.
DOx - Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.
Amphetamines - This combination can easily lead to hypermanic states.
MDMA - This combination can easily lead to hypermanic states.
Cocaine - This combination can easily lead to hypermanic states.
Alcohol - Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.
Benzodiazepines - 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 - Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.
2C-T-x
ΑMT
5-MeO-xxT
DXM
GHB - Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.
GBL - Details of this combination are not well understood but PCP generally interacts in an unpredictable manner.
Tramadol
MAOIs - Little information exists about this combination.
Legal status
Internationally, PCP is a Schedule II substance under the Convention on Psychotropic Substances.[22]
Austria - PCP is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).[citation needed]
Canada - PCP is controlled under the Controlled Drugs and Substances Act as a Schedule I substance.[23]
Germany - PCP is controlled under BtMG Anlage I, making it illegal to manufacture, import, possess, sell, or transfer it without a license.[24]
New Zealand - PCP is Schedule I (class A) in New Zealand.[citation needed]
Poland - PCP is listed under "Wykaz środków odurzających i substancji psychotropowych[" (II-P group) in Poland, and is illegal to posses, sell and manufacture.[25]
Portugal - PCP is a Table-II-A substance under Decree-Law 15/93: Anti-Drug Legislation. PCP was decriminalized for personal use by Law 30/2000, but consumption or possession is still prohibited. The substance is liable to be seized and the possessor can be referred to mandatory treatment.[26][27]
Switzerland: - PCP is a controlled substance specifically named under Verzeichnis A. Medicinal use is permitted.[28]
United Kingdom - PCP is controlled under the Misuse of Drugs Act as a Schedule II Class A drug, making it illegal to possess without a prescription.[29]
United States - PCP is controlled under the Controlled Substances Act as a Schedule II controlled substance, making it illegal to possess without a prescription.[30][31]
Morris, H., & Wallach, J. (2014). From PCP to MXE: A comprehensive review of the non-medical use of dissociative drugs. Drug Testing and Analysis, 6(7–8), 614–632. https://doi.org/10.1002/dta.1620
↑Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 374–375. ISBN 9780071481274.
↑Kapur, S., & Seeman, P. (2002). NMDA receptor antagonists ketamine and PCP have direct effects on the dopamine D2 and serotonin 5-HT2receptors--implications for models of schizophrenia. Molecular psychiatry, 7(8), 837. | http://www.nature.com/mp/journal/v7/n8/full/4001093a.html
↑ 14.014.1http://archives.drugabuse.gov/pdf/monographs/21.pdf | Luisada, Paul V., M.D. "The Phencyclidine Psychosis: Phenomenology and Treatment." Phencyclidine (PCP) Abuse: An Appraisal. Rockville, Maryland: National Institute on Drug Abuse, 1978. pg. 241.
↑Olney, J. W., Labruyere, J., & Price, M. T. (1989). Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs. Science(Washington), 244(4910), 1360-1362. | https://www.ncbi.nlm.nih.gov/pubmed/2660263
↑Hargreaves, R. J., Hill, R. G., & Iversen, L. L. (1994). Neuroprotective NMDA antagonists: the controversy over their potential for adverse effects on cortical neuronal morphology. In Brain Edema IX (pp. 15-19). Springer, Vienna. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/7976530
↑Jansen, Karl. Ketamine: Dreams and Realities. MAPS, 2004. ISBN 0-9660019-7-4
↑Reynolds, L. M., Cochran, S. M., Morris, B. J., Pratt, J. A., & Reynolds, G. P. (2005). Chronic phencyclidine administration induces schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in rat brain. Schizophrenia research, 73(2), 147-152.(PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/15653257
↑Murray, J. B. (2002). Phencyclidine (PCP): a dangerous drug, but useful in schizophrenia research. The Journal of psychology, 136(3), 319-327. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/12206280
