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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.

Summary sheet: PCP
Molecular structure of Phencyclidine
Chemical Nomenclature
Common names PCP, "Angel Dust", "Sherman", Sernyl, "Wet"
Substitutive name Phencyclidine
Systematic name 1-(1-phenylcyclohexyl)piperidine
Class Membership
Psychoactive class Dissociative
Chemical class Arylcyclohexylamine
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.

Threshold 1 - 2 mg
Light 2 - 4 mg
Common 4 - 8 mg
Strong 8 - 12 mg
Heavy 12 mg+ Heavy doses may result in psychosis and mania.[3]
Total 4 - 6 hours
Onset 2 - 20 minutes
Come up 20 - 40 minutes
Peak 2 - 3 hours
Offset 1 - 2 hours
After effects 4 - 48 hours
Threshold 1 - 3 mg
Light 3 - 5 mg
Common 5 - 10 mg
Strong 10 - 15 mg
Heavy 15mg+ Heavy doses may result in psychosis and mania.[4]
Total 4 - 8 hours
Onset 30 - 90 minutes
Come up 40 - 120 minutes
Peak 2 - 3 hours
Offset 1 - 2 hours
After effects 4 - 48 hours

Threshold 1 - 2 mg
Light 2 - 4 mg
Common 4 - 8 mg
Strong 8 - 15 mg
Heavy 15mg+ Heavy doses may result in psychosis and mania.[5]
Total 4 - 6 hours
Onset 3 - 30 minutes
Come up 30 - 90 minutes
Peak 2 - 3 hours
Offset 1 - 2 hours
After effects 4 - 48 hours

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 synthetic dissociative substance of the arylcyclohexylamine chemical class that produces potent, long-lived dissociating, anesthetic, stimulating, disinhibiting and hallucinogenic effects when administered.

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.[7]

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 emerged as a recreational drug in mid-1967, under the name "The Peace Pill".[8][9] Since this time, a number of synthetic derivatives of PCP have been sold as dissociative drugs for both recreational and non-medical use.[10] As an established "street drug", PCP is associated with compulsive abuse.[11][10]

As a recreational substance, PCP may be ingested orally, smoked, insufflated or via injection.[12] 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 harm reduction practices if choosing to use this substance.


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.


Further information: NMDA receptor antagonist

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 also acts as a dopamine-reuptake inhibitor and a serotonin reuptake inhibitor with alleged µ-opioid affinity and typical dissociative effects. This provides an explanation for its euphoric and often stimulating properties.

Subjective effects

This subjective effect breakdown is a stub.

As such, it may contain incomplete or wrong information and is still in progress.

You can help by expanding it.

PCP is considerably more likely to induce psychosis and mania than other dissociatives and is therefore potentially dangerous even in a proper setting. The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances and are more likely to induce a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Visual effects

Disconnective effects

Cognitive effects

Experience reports

Anecdotal reports which describe the effects of this compound within our experience index include:

Additional experience reports can be found here:

Toxicity and harm potential

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).[15]

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.


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.[13] 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.[14]

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 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.[16][17] 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[18] 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.[19] It also induces symptoms in humans that mimic schizophrenia.[20]

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

Although many psychoactive substances are safe on their own, they can become dangerous and even life-threatening when combined with other substances. The list below contains some common potentially dangerous combinations, but may not include all of them. Certain combinations may be safe in low doses of each but still increase the potential risk of death. Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.

Prominent examples include PCP and its analogs 3-MeO-PCP, MXE, and the diarylethylamine dissociatives like diphenidine or ephenidine. There is also evidence that suggests that combining these two increases their neurotoxicity.[citation needed] Anecdotally, worsened comedowns are also commonly reported when these two classes of substances are combined.
  • Depressants - Because both depress the respiratory system, this combination can result in an increased risk of suddenly falling unconscious, vomiting and choking to death from the resulting suffocation. If nausea or vomiting occurs, users should attempt to fall asleep in the recovery position or have a friend move them into it.


  • Austria - PCP is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).
  • Canada - PCP is Schedule I in Canada.[citation needed]
  • New Zealand - PCP is Schedule I (class A) in New Zealand.[citation needed]
  • Poland - PCP is Schedule II (II-P group) in Poland.[citation needed]
  • Portugal - Effective July 2001, personal use of PCP was decriminalized by Law 30/2000. Possession of less than 100 mg is not regarded as a criminal offense, although the substance is liable to be seized and the possessor can be referred to mandatory treatment. Sale or possession of quantities greater than the personal possession limit are criminal offenses punishable by jail time.[citation needed]
  • United Kingdom - PCP is a class A in the U.K., making it illegal to buy or possess without a prescription.[citation needed]
  • United States - PCP is a Schedule II controlled substance.[citation needed]

See also

External links



  • 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


  1. http://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.
  2. Tasman, Allan, Jerald Kay, and Jeffrey A. Lieberman. Psychiatry. Chichester: John Wiley & Sons, 2003. Google Books. Wiley. Web. <https://books.google.com/books?id=l2KRBgAAQBAJ&pg=PT4957&lpg=PT4957&dq=Greifenstein+et+al.+1958%29.&source=bl&ots=s5CFdAfMzc&sig=GzsOq_N-V1qtahxyyHnKMJceEj0&hl=en&sa=X&ved=0ahUKEwji0pWTjNLKAhUBaD4KHTfqD0sQ6AEIHDAA#v=onepage&q=Greifenstein%20et%20al.%201958%29.&f=false>.
  3. PCP Psychosis (PsychonautWiki) | https://psychonautwiki.org/wiki/3-MeO-PCP#Toxicity_and_harm_potential
  4. PCP Psychosis (PsychonautWiki) | https://psychonautwiki.org/wiki/3-MeO-PCP#Toxicity_and_harm_potential
  5. 3-MeO-PCP Psychosis (PsychonautWiki) | https://psychonautwiki.org/wiki/3-MeO-PCP#Toxicity_and_harm_potential
  6. PCP Fast Facts | http://www.justice.gov/archive/ndic/pubs4/4440/
  7. 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
  8. "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
  9. "Sweet Streetfact's Lowdown on Low Dope Highs!". Berkeley Tribe, September 10-16, 1971. p12 (Independent Voices) | http://voices.revealdigital.com/cgi-bin/independentvoices?a=d&d=BFBJFGJ19710910.1.12
  10. 10.0 10.1 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
  11. 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.
  12. NIDA. (2016, January 11). Hallucinogens. Retrieved from https://www.drugabuse.gov/publications/drugfacts/hallucinogens on 2017, October 29 | http://drugabuse.gov/infofacts/hallucinogens.html
  13. 13.0 13.1 13.2 http://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.
  14. 14.0 14.1 14.2 Tasman, Allan, Jerald Kay, and Jeffrey A. Lieberman. Psychiatry. Chichester: John Wiley & Sons, 2003. Google Books. Wiley. Web. <https://books.google.com/books?id=l2KRBgAAQBAJ&pg=PT4957&lpg=PT4957&dq=Greifenstein+et+al.+1958%29.&source=bl&ots=s5CFdAfMzc&sig=GzsOq_N-V1qtahxyyHnKMJceEj0&hl=en&sa=X&ved=0ahUKEwji0pWTjNLKAhUBaD4KHTfqD0sQ6AEIHDAA#v=onepage&q=Greifenstein%20et%20al.%201958%29.&f=false>.
  15. PCP Effects by Erowid | https://www.erowid.org/chemicals/pcp/pcp_effects.shtml
  16. 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
  17. 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
  18. Jansen, Karl. Ketamine: Dreams and Realities. MAPS, 2004. ISBN 0-9660019-7-4
  19. 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
  20. 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