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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kiran Singh, M.D. [2]


Phencyclidine (a contraction of the chemical name phenylcyclohexylpiperidine), abbreviated PCP, is a dissociative drug formerly used as an anesthetic agent, exhibiting hallucinogenic and neurotoxic effects.[citation needed]

It was first patented in 1952 by the Parke-Davis pharmaceutical company and marketed under the brand name Sernyl. PCP is listed as a Schedule II drug in the United States under the Convention on Psychotropic Substances.[1]

In chemical structure, PCP is an arylcyclohexylamine derivative, and, in pharmacology, it is a member of the family of dissociative anesthetics. PCP works primarily as an NMDA receptor antagonist, which blocks the activity of the NMDA Receptor.[2] Other NMDA receptor antagonists include ketamine, tiletamine, and dextromethorphan. Although the primary psychoactive effects of the drug last only hours, total elimination from the body is prolonged, typically extending over weeks.

More than 30 different analogues of PCP were reported as being used on the street during the 1970s and 1980s, mainly in the USA. The best known of these are PCPy (Rolicyclidine, 1-(1-phenylcyclohexyl)pyrrolidine); PCE (Eticyclidine, N-ethyl-1-phenylcyclohexylamine); and TCP (Tenocyclidine, 1-(1-(2-Thienyl)cyclohexyl)piperidine). These compounds were never widely-used and did not seem to be as well-accepted by users as PCP itself, however they were all added onto Schedule I of the Controlled Substance Act because of their putative similar effects.[3]

The generalised structural motif required for PCP-like activity is derived from structure-activity relationship studies of PCP analogues, and summarised below. All of these analogues would have somewhat similar effects to PCP itself, although, with a range of potencies and varying mixtures of anaesthetic, dissociative and stimulant effects depending on the particular substituents used. In some countries such as the USA, Australia, and New Zealand, all of these compounds would be considered controlled substance analogues of PCP, and are hence illegal drugs, even though many of them have never been made or tested.[4][5]


Like other NMDA receptor antagonists, it is postulated that phencyclidine can cause a certain kind of brain damage called Olney's Lesions.[6][7] Studies conducted on rats showed that high doses of the NMDA receptor antagonist MK-801 caused reversible vacuoles to form in certain regions of the rats' brains, and experts say that it is possible that similar brain damage can occur in humans.[8]

All studies on Olney's lesions were performed only on animals and may not apply to humans. Critics have cited poorly-performed studies and differences in animal metabolism to suggest that Olney's lesions may not occur in humans.[9][10]

Medical Use

PCP was first tested after World War I as a surgical anesthetic. Because of its adverse side-effects, such as hallucinations, mania, delirium, and disorientation, it was shelved until the 1950s. In 1963, it was patented by Parke-Davis and named Sernyl (referring to serenity), but was withdrawn from the market two years later because of side-effects. It was renamed Sernylan in 1967, and marketed as a veterinary anaesthetic, but again discontinued. Its side-effects and long half-life in the human body made it unsuitable for medical applications.

PCP is retained in fatty tissue and is broken down by the human metabolism into PCHP, PPC and PCAA. When smoked, some of it is broken down by heat into 1-phenyl-1-cyclohexene (PC) and piperidine.

Recreational use

PCP is consumed in a recreational manner by drug users. Compton (near Los Angeles) remains the primary source of PCP throughout the United States. Los Angeles street gangs continue to control both production and distribution of PCP.[11] It comes in both powder and liquid forms (PCP base dissolved most often in ether), but typically it is sprayed onto leafy material such as marijuana, mint, oregano, parsley, or ginger leaves, then smoked. Common street names for the drug vary from locale to locale, but include "angel dust," "illy," "wet," "fry," "amp," "Nature Boy," and "supergrass" (when combined with marijuana).

PCP is a Schedule II substance in the United States and a Class A substance in the United Kingdom.

Biochemical action

The N-methyl-D-Aspartate (NMDA) receptor, a type of ionotropic receptor, is found on the dendrites of neurons and receives signals in the form of neurotransmitters. It is a major excitatory receptor in the brain. Normal physiological function requires that the activated receptor fluxes positive ions through the channel part of the receptor. PCP enters the ion channel from the outside of the neuron and binds, reversibly, to a site in the channel pore, blocking the flux of positive ions into the cell. PCP therefore inhibits depolarization of neurons and interferes with cognitive and other functions of the nervous system.

In a similar manner, PCP and analogues also inhibit nicotinic acetylcholine receptor channels (nAChR). Some analogues have greater potency at nAChR than at NMDAR. In some brain regions, these effects act synergistically to inhibit excitatory activity.

Method of absorption

The term "embalming fluid" is often used to refer to the liquid PCP in which a cigarette or joint is dipped (a "sherm" or "dippy"), to be ingested through smoking. Smoking PCP is known as "getting wet." There is much confusion over the practice of dipping cigarettes in "embalming fluid" leading some to think that real embalming fluid may actually be used. This is a misconception that may cause serious health consequences beyond those of consuming PCP.

In its powder form, PCP can be insufflated.

In Canada, particularly in the provinces of Quebec and New Brunswick, PCP is mostly encountered as "mescaline" (often locally called "mess" or "mesc"), although most local users are aware that the drug is not, in fact, mescaline, but is actually a mixture of quinine or lactose and PCP freebase. The most common form of ingesting PCP is through smoking; however, the drug may also be insufflated.

In its pure form, PCP is a white crystalline powder that readily dissolves in water. However, most PCP on the illicit market contains a number of contaminants as a result of makeshift manufacturing, causing the color to range from tan to brown, and the consistency to range from powder to a gummy mass.


PCP gives a feeling of being disconnected to one's body and environment. PCP has potent effects on the nervous system, altering perceptual functions (hallucinations, delusional ideas, delirium or confused thinking), motor functions (unsteady gait, loss of coordination, and disrupted eye movement or nystagmus), and autonomic nervous system regulation (rapid heart rate, altered temperature regulation). The drug has been known to alter mood states in an unpredictable fashion, causing some individuals to become detached, and others to become animated. Intoxicated individuals may act in an unpredictable fashion, driven by their delusions or hallucinations. Included in the portfolio of behavioral disturbances are acts of self-injury including suicide, and attacks on others or destruction of property. The analgesic properties of the drug can cause users to feel less pain, and persist in violent or injurious acts as a result. Recreational doses of the drug can also induce a psychotic state that resembles schizophrenic episodes.

Phencyclidine Intoxication

DSM-V Diagnostic Criteria for Phencyclidine[12]

  • A.Recent use of phencyclidine (or a pharmacologically similar substance).


  • B.Clinically significant problematic behavioral changes (e.g., belligerence, assaultiveness, impulsiveness, unpredictability, psychomotor agitation, impaired judgment) that developed during, or shortly after, phencyclidine use.


  • C.Within 1 hour, two (or more) of the following signs or symptoms:

Note:When the drug is smoked, “snorted,” or used intravenously, the onset may be particularly rapid .


  • D.The signs or symptoms are not attributable to another medical condition and are not better explained by another mental disorder, including Intoxication with another substance.

Epidemiology and Demographics


The prevalence of phencyclidine intoxication is 2,500 per 100,000 (2.5%) of the overall population.[12]

Differential Diagnosis

  • Other substance intoxication
  • Other conditions
  • Vascular insults[12]

Phencyclidine Use Disorder

DSM-V Diagnostic Criteria for Phencyclidine Use Disorder[12]

  • A.A pattern of phencyclidine (or a pharmacologically similar substance) use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:
  • 1.Phencyclidine is often taken in larger amounts or over a longer period than was intended.
  • 2.There is a persistent desire or unsuccessful efforts to cut down or control phencyclidine use.
  • 3.A great deal of time is spent in activities necessary to obtain phencyclidine, use the phencyclidine, or recover from its effects.
  • 4.Craving, or a strong desire or urge to use phencyclidine.
  • 5.Recurrent phencyclidine use resulting in a failure to fulfill major role obligations at work, school, or home (e.g., repeated absences from work or poor work performance

related to phencyclidine use; phencyclidine-related absences, suspensions, or expulsions from school; neglect of children or household).

  • 6.Continued phencyclidine use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the phencyclidine (e.g.,arguments with a spouse about consequences of intoxication; physical fights).
  • 7.Important social, occupational, or recreational activities are given up or reduced because of phencyclidine use.
  • 8.Recurrent phencyclidine use in situations in which it is physically hazardous (e.g., driving an automobile or operating a machine when impaired by a phencyclidine).
  • 9.Phencyclidine use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the phencyclidine.
  • 10.Tolerance, as defined by either of the following:
  • a.A need for markedly increased amounts of the phencyclidine to achieve intoxication or desired effect.
  • b.A markedly diminished effect with continued use of the same amount of the phencyclidine.

Note:Withdrawal symptoms and signs are not established for phencyclidines, and so this criterion does not apply. (Withdrawal from phencyclidines has been reported in animals but not documented in human users.) .

Specify if:

  • In early remission: After full criteria for phencyclidine use disorder were previously met, none of the criteria for phencyclidine use disorder have been met for at least

3 months but for less than 12 months (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the phencyclidine,” may be met).

  • In sustained remission: After full criteria for phencyclidine use disorder were previously met, none of the criteria for phencyclidine use disorder have been met at any time

during a period of 12 months or longer (with the exception that Criterion A4, “Craving, or a strong desire or urge to use the phencyclidine,” may be met).

Specify if:

  • In a controlled environment: This additional specifier is used if the individual is in an environment where access to phencyclidines is restricted.

Specify current severity:

  • Mild: Presence of 2-3 symptoms.
  • Moderate: Presence of 4-5 symptoms.
  • Severe: Presence of 6 or more symptoms.

Epidemiology and Demographics


The prevalence of phencyclidine use disorder is unknown.[12]

Risk Factors

  • Age
  • Lower educational levels
  • Geographical
  • West &
  • Northeast regions of the United States[12]

Differential Diagnosis

  • Other substance use disorders

See also


  1. "List of psychotropic substances under control, in accordance with the Convention on Psychotropic Substances of 1971": Report from 2003 (pdf)
  2. Kapur, S. and P. Seeman. "NMDA receptor antagonists ketamine and PCP have direct effects on the dopamine D2 and serotonin 5-HT2receptors¾implications for models of schizophrenia" Molecular Psychiatry. 7(8): 837–844 (2002)
  4. Itzhak Y, Kalir A, Weissman BA, Cohen S. New analgesic drugs derived from phencyclidine. Journal of Medicinal Chemistry. 1981; 24(5):496–499
  5. Chaudieu I, Vignon J, Chicheportiche M, Kamenka JM, Trouiller G, Chicheportiche R. Role of the aromatic group in the inhibition of phencyclidine binding and dopamine uptake by PCP analogs. Pharmacology Biochemistry and Behaviour. 1989 Mar;32(3):699–705.
  6. Olney J, Labruyere J, Price M (1989). "Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs". Science. 244 (4910): 1360–2. PMID 2660263.
  7. Hargreaves R, Hill R, Iversen L. "Neuroprotective NMDA antagonists: the controversy over their potential for adverse effects on cortical neuronal morphology". Acta Neurochir Suppl (Wien). 60: 15–9. PMID 7976530.
  9. Jansen, Karl. Ketamine: Dreams and Realities. MAPS, 2004. ISBN 0966001974
  12. 12.0 12.1 12.2 12.3 12.4 12.5 12.6 Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.

External links

Template:Dissociative hallucinogens


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