Phencyclidine (PCP)
PubChem records this structure as Phencyclidine.
Also known asPhencyclidine · 1-(1-Phenylcyclohexyl)piperidine · Angel dust · Fenciclidina · Phencyclidinum · Phencycline · Phenylcyclidine · Dust, Angel
1-(1-phenylcyclohexyl)piperidine
- PubChem CID
- 6468
- ChEMBL
- CHEMBL542581
- Measurements
- 28
- InChIKey
- JTJMJGYZQZDUJJ-UHFFFAOYSA-N
I · Summary
What is known
Published passages, each quoted whole and attributed to the database that published it. Two blocks are written here rather than quoted, and both say so where they stand: the synthesized summary at the top, which may draw only on the passages beneath it, and the history note, which cites the works it came from. Every claim in either carries a marker to its source.
No synthesized summary
24 passages, and enough of them are usable — but PCP's record leans heavily on the human toxicity literature, and a synthesis of it would be a paragraph about what phencyclidine does to people, at the top of the page, in this project's voice. That is the highest-stakes prose on the site and it should be written by someone who can be asked about it, not drafted here first.
What it is
Phencyclidine is a member of the class of piperidines that is piperidine in which the nitrogen is substituted with a 1-phenylcyclohexyl group. Formerly used as an anaesthetic agent, it exhibits both hallucinogenic and neurotoxic effects. It has a role as a psychotropic drug, an anaesthetic, a neurotoxin and a NMDA receptor antagonist. It is a member of benzenes and a member of piperidines. It derives from a hydride of a piperidine.
Phencyclidine is a DEA Schedule II controlled substance. Substances in the DEA Schedule II have a high potential for abuse which may lead to severe psychological or physical dependence. It is a Depressants substance.
A hallucinogen formerly used as a veterinary anesthetic, and briefly as a general anesthetic for humans. Phencyclidine is similar to ketamine in structure and in many of its effects. Like ketamine, it can produce a dissociative state. It exerts its pharmacological action through inhibition of NMDA receptors (receptors, N-methyl-D-aspartate). As a drug of abuse, it is known as PCP and Angel Dust.
Phencyclidine is an illegal, hallucinogenic drug that was initially used as an anesthetic agent in the 1950s and early 1960s, but was then withdrawn in 1965 because of dissociative hallucinogenic effects that were often disturbing and sometimes severe and prolonged. The “out-of-body” intense psychological and behavioral effects of low doses of phencyclidine led to its abuse. In the late 1960s and 1970s, phencyclidine (“angel dust”) became a widely used hallucinogenic drug. The effects were often extreme, marked by acute psychosis and aggressive and violent behaviors, and overdoses led to many emergency room visits and deaths from status epilepticus, hyperthermia, rhabdomyolysis and subsequen…
Recognized use
Enzyme Inhibitors; Hallucinogens; Excitatory Amino Acid Antagonists
Therapeutic Uses
Hazardous Substances Data Bank (HSDB)National Library of Medicine's Medical Subject Headings. Phencyclidine. Online file (MeSH, 2017). Available from, as of October 4, 2017: https://www.nlm.nih.gov/mesh/2017/mesh_browser/MBrowser.html
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations;…
Therapeutic Uses
Hazardous Substances Data Bank (HSDB)NIH/NLM; ClinicalTrials.Gov. Available from, as of October 4, 2017: https://clinicaltrials.gov/
Early clinical studies showed that phencyclidine (PCP) readily induced and maintained anesthesia, /however,/ the incidence of delirium, hallucinations, and disruptive reactions discouraged further use in surgical procedures.
Therapeutic Uses
Hazardous Substances Data Bank (HSDB)Domine EF; Int Rev Neurobiol 6: 303-47 (1964)
For more Therapeutic Uses (Complete) data for Phencyclidine (8 total), please visit the HSDB record page.
Therapeutic Uses
Phencyclidine (DEA Code Number: 7471) is a Schedule II controlled substance.
Use Classification
Hazardous Substances Data Bank (HSDB)21 CFR 1308.12(e) (USDEA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of October 19, 2017: https://www.ecfr.gov
Schedule II Controlled Substance: (A) The drug or other substance has a high potential for abuse; (B) The drug or other substance has a currently accepted medical use in treatment in the United States or a currently accepted medical use with severe restrictions; and (C) Abuse of the drug or other substances may lead to severe psychological or physical dependence.
Use Classification
Hazardous Substances Data Bank (HSDB)US Department of Justice/Office of Diversion Control; Schedule of Controlled Substances. Available from, as of October 19, 2017: https://www.deadiversion.usdoj.gov/21cfr/21usc/812.htm
Ethylamine analog of phencyclidine (DEA Code Number: 7455), pyrrolidine analog of phencyclidine (DEA Code Number: 7471)and the thiophene analog of phencyclidine (DEA Code Number: 7470) are Schedule 1 controlled substances. /Ethylamine analog of phencyclidine, pyrrolidine analog of phencyclidine, thiophene analog of phencyclidine/
Use Classification
Hazardous Substances Data Bank (HSDB)21 CFR 1308.11(d) (USDEA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of October 19, 2017: https://www.ecfr.gov
Schedule I Controlled Substance: (A) The drug or other substance has a high potential for abuse; (B) The drug or other substance has no currently accepted medical use in treatment in the United States; and (C) There is a lack of accepted safety for use of the drug or other substance under medical supervision.
Use Classification
Hazardous Substances Data Bank (HSDB)US Department of Justice/Office of Diversion Control; Schedule of Controlled Substances. Available from, as of October 19, 2017: https://www.deadiversion.usdoj.gov/21cfr/21usc/812.htm
How it acts
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.
Noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonists evoke a behavioral and neurobiological syndrome in experimental animals. We previously reported that phencyclidine (PCP), an NMDA receptor antagonist, increased locomotor activity in wildtype (WT) mice but not GluN2D subunit knockout mice. Thus, the aim of the present study was to determine whether the GluN2D subunit is involved in PCP-induced motor impairment. PCP or UBP141 (a GluN2D antagonist) induced potent motor impairment in WT mice but not GluN2D KO mice. By contrast, CIQ, a GluN2C/2D potentiator, induced severe motor impairment in GluN2D KO mice but not WT mice, suggesting that the GluN2D subunit plays an essential role…
Hazardous Substances Data Bank (HSDB)PMID 24330819Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3878647
Behavior carries the pharmacological classes and the acute-effect durations, with plasma half-life kept separate from duration of effect.
In the body
/Monkeys/ maintained a state of continuous intoxication which was sustained when the dose /of PCP/ was increased to 0.5 mg/kg. Substitution of saline after 58 days of exposure resulted in the appearance of numerous abstinence signs and symptoms including increased vocalizations, bruxism, oculomotor hyperactivity, diarrhea, refusal of preferred food, piloerection, and tremors. Less common signs included ear and facial twitches, priapism, abdominal contractions, emesis, and convulsions. The time course of withdrawal was characterized by an initial recovery from the PCP-induced intoxication at about 4 hr after saline substitution. Onset of hyper-responsive behaviors became evident at 8-12 hr, w…
Absorption, Distribution and Excretion
Hazardous Substances Data Bank (HSDB)Balster RL, Woolverton WL; Psychopharmacology 70: 5-10 (1980)
/Phencyclidine/ is rapidly absorbed from the respiratory and the gastrointestinal tracts; as such, it is typically self-administered by oral ingestion, nasal insufflation, smoking, or IV and subcutaneous injection.
Absorption, Distribution and Excretion
Hazardous Substances Data Bank (HSDB)Goldfrank, L.R., Goldfrank's Toxicologic Emergencies 9th Ed. 2011., McGraw-Hill, New York, N.Y., p. 1192
Urine pH is an important determinant of renal elimination of PCP. In acidic urine, PCP becomes ionized and then cannot be reabsorbed. Acidification of the urine increased renal clearance of PCP from 1.98 + or- 0.48 L/hr to 2.4 + or - 0.78 L/hr. Additional studies have found a much higher renal clearance (8.04 + or- 1.56 L/hr) if the urine pH was decreased to less than 5.0. Although this may account for a 23% increase in the renal clearance, it only represents a 1.2% increase of the total clearance.
Absorption, Distribution and Excretion
Hazardous Substances Data Bank (HSDB)Goldfrank, L.R., Goldfrank's Toxicologic Emergencies 9th Ed. 2011., McGraw-Hill, New York, N.Y., p. 1192
For more Absorption, Distribution and Excretion (Complete) data for Phencyclidine (8 total), please visit the HSDB record page.
Absorption, Distribution and Excretion
PCP is metabolized mainly in the liver. Oxidative hydroxylation to the inactive monohydroxypiperidine is followed by glucuronidation to a more water-soluble, conjugated derivative that is then excreted in the urine as the major form of metabolism. Significant first-pass liver metabolism also occurs when the drug is ingested orally, as opposed to being smoked or injected. Approximately 10% of drug is excreted unchanged un the urine.
Metabolism/Metabolites
Hazardous Substances Data Bank (HSDB)Haddad, L.M. (Ed). Clinical Management of Poisoning and Drug Overdose 3rd Edition. Saunders, Philadelphia, PA. 1998., p. 553
Abuse Liability: A bioassay procedure ... demonstrated that eight structurally related analogs of PCP were self administered by the dog. The thienyl-substituted analog was the most potent, followed by PCP, N-substituted alkyl analogs, monohydroxylated metabolites, and ketamine.
Metabolism/Metabolites
Hazardous Substances Data Bank (HSDB)Risner M; J Pharmacol Exp Ther 221: 637-44 (1982)
Phencyclidine has known human metabolites that include PCHP and c-PPC/t-PPC.
Metabolism/Metabolites
NORMAN Suspect List ExchangeS73 | METXBIODB | Metabolite Reaction Database from BioTransformer | DOI:10.5281/zenodo.4056560
History, discovery and cultural use
— Not in this archive. PubChem, ChEMBL and the Human Protein Atlas publish pharmacology, regulation and toxicology, and none of them publishes a heading for when Phencyclidine (PCP) was first made, by whom, or how it has been used. That is a gap in the databases this site reads and not a gap in the literature — the history of these compounds is written, at length and under peer review, in the works below. This site does not summarize them; it says where they are. Where a published passage above happens to touch origin or traditional use, it appears inside the entry that carries it.
Histories of this field
Scholarship on psychedelics generally, not on Phencyclidine (PCP) specifically. Whether any of these treats this compound is a question for the book, not for this page.
Mescaline: A Global History of the First Psychedelic
Traces mescaline and the peyote and San Pedro cacti from pre-Columbian ritual use through nineteenth-century chemistry to twentieth-century psychiatry and the counterculture.
Jay M. Mescaline: A Global History of the First Psychedelic. Yale University Press, New Haven and London; 2019. ISBN 9780300231076.
Expanding Mindscapes: A Global History of Psychedelicsopen access
Essays on the international and cross-cultural history of psychedelic science, deliberately decentring the standard North American and European account.
Dyck E, Elcock C, editors. Expanding Mindscapes: A Global History of Psychedelics. The MIT Press, Cambridge MA; 2023. ISBN 9780262546935 (paper), 9780262376891 (open access). doi:10.7551/mitpress/14417.001.0001.
Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers
Botany, ethnography and chemistry of the principal hallucinogenic plants, by the founder of modern ethnobotany and the chemist who first synthesized LSD.
Schultes RE, Hofmann A, Rätsch C. Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers. 2nd ed. Healing Arts Press, Rochester VT; 2001. ISBN 9780892819799.
Psychonauts: Drugs and the Making of the Modern Mind
The tradition of scientific self-experimentation with psychoactive drugs, and its part in the emergence of psychology and of modernism.
Jay M. Psychonauts: Drugs and the Making of the Modern Mind. Yale University Press, New Haven; 2023. ISBN 9780300257946.
Ancient Psychoactive Substances
Archaeological and bioarchaeological evidence for psychoactive plant use across the ancient world.
Fitzpatrick SM, editor. Ancient Psychoactive Substances. University Press of Florida, Gainesville; 2018. ISBN 9780813056708.
A chapter tracing psychedelic and entactogen research from earlier ritual use through the mid-century research period to current clinical trials.
Stroud C, Posey Norris SM, Matney C, editors. History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders. In: Exploring Psychedelics and Entactogens as Treatments for Psychiatric Disorders: Proceedings of a Workshop. National Academies Press, Washington DC; 2022. NBK587225.
Workshop proceedings record what participants said; they are not a consensus statement of the National Academies.
Peer-reviewed review covering the isolation, synthesis, pharmacology and ritual use of peyote and mescaline.
Dinis-Oliveira RJ, Pereira CL, da Silva DD. Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions. Current Molecular Pharmacology 12(3):184–194; 2019. doi:10.2174/1874467211666181010154139.
Institutional archives
- Heffter Research Institute Funds and coordinates clinical research on psilocybin, and keeps records of the studies it has supported since 1993. Sponsors the research it archives.
- Multidisciplinary Association for Psychedelic Studies (MAPS) Sponsors clinical research, chiefly on MDMA-assisted therapy, and publishes an archive of historical and contemporary documents. A sponsor and an advocacy organization, not a disinterested archive; its clinical programme has a commercial arm.
The rest of this dossier
- Affinity — 28 measurements in this archive, equilibrium constants kept apart from functional readouts.
- Toxicology — 9 published passages, plus any assay in this archive bearing on toxicity.
- Legal — DEA Schedule II, with the passage it was read from.
- Systems — where this compound’s targets are transcribed, by brain region and tissue.
Passages via PubChem descriptive sections, aggregating DrugBank, LiverTox, FDA, DEA, HSDB, EPA. Each is quoted whole and attributed to the database that published it. The only prose written here about Phencyclidine (PCP) is the history note, which says so on its face and carries a reference for every claim in it.
II · Identity
Structure and descriptors
Descriptors are computed here with RDKit from the structure PubChem returns — not from the archive's stored copy, so an edited local structure cannot reach this table.
- Formula
- C17H25NR
- Molecular weight
- 243.39g/molR
- Exact mass
- 243.1987DaR
- cLogP
- 4.33R
- TPSA
- 3.2ŲR
- H-bond donors
- 0R
- H-bond acceptors
- 1R
- Rotatable bonds
- 2R
- Aromatic rings
- 1R
- Heavy atoms
- 18R
- Fraction sp³
- 0.647R
- Formal charge
- 0R
Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.
Bemis–Murcko scaffold
c1ccc(C2(N3CCCCC3)CCCCC2)cc1
Shared with 3-Chloro-PCP, 3-Fluoro-PCP, 3-HO-PCP, 3-MeO-PCP, 3-Methyl-PCP, 4-MeO-PCP. All families
III · Behavior
Behavioral summary
Class, mechanism, and the duration of acute effects — each quoted from the record or trial that publishes it. Duration of effects and plasma half-life are shown separately, because they are different quantities and diverge by a factor of three or four.
Classification
Duration of acute subjective effects
—
No controlled human trial reporting a duration for this compound is cited here. The archive does hold onset and duration ranges for it, inherited from an earlier build, but their source column is empty and so they cannot be shown. A duration is not inferred from a chemical relative.
Plasma elimination half-life
How fast the body clears the drug — not how long the effects last. The two diverge sharply: LSD is cleared with a half-life of about 2.6 h while its subjective effects run 8–12 h.
PCP elimination from plasma is consistent with first-order kinetics with a half life of 7 to 26 hours.
Hazardous Substances Data Bank (HSDB)Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1107 The terminal phase serum half-life of PCP is 21 to 24 hours.
Hazardous Substances Data Bank (HSDB)Haddad, L.M. (Ed). Clinical Management of Poisoning and Drug Overdose 3rd Edition. Saunders, Philadelphia, PA. 1998., p. 553 /PCP/ has an apparent terminal half life of 21 + or - 3 hours under both control and overdose settings.
Hazardous Substances Data Bank (HSDB)Goldfrank, L.R., Goldfrank's Toxicologic Emergencies 9th Ed. 2011., McGraw-Hill, New York, N.Y., p. 1192 Harmonic mean elimination half-lives of 14 hr (iv administration), 24 hr (oral administration), and 17 hr (administration via smoking) have been reported ...
Hazardous Substances Data Bank (HSDB)Young, L.Y., M.A. Koda-Kimble (eds.). Applied Therapeutics. The Clinical Use of Drugs. 6th ed. Vancouver, WA., Applied Therapeutics, Inc. 1995., p. 86-8
Primary pharmacological drivers
ChEMBL holds no curated mechanism-of-action record for this compound. The measured affinities below are the evidence this archive has for what it binds.
Mechanism, as published
Quoted verbatim from the database named after each passage, never summarized.
Noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonists evoke a behavioral and neurobiological syndrome in experimental animals. We previously reported that phencyclidine (PCP), an NMDA receptor antagonist, increased locomotor activity in wildtype (WT) mice but not GluN2D subunit knockout mice. Thus, the aim of the present study w…
Hazardous Substances Data Bank (HSDB)PMID 24330819Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3878647 Prepulse inhibition (PPI) is an example of sensorimotor gating and deficits in PPI have been demonstrated in schizophrenia patients. Phencyclidine (PCP) suppression of PPI in animals has been studied to elucidate the pathological elements of schizophrenia. However, the molecular mechanisms underlying PCP treatment or PPI in the brain are…
Hazardous Substances Data Bank (HSDB)PMID 25869802Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4605830 Phencyclidine (PCP), a noncompetitive N-methyl-D-aspartate receptor antagonist, induces psychotomimetic effects in humans and animals. Administration of PCP to rodents is used as a preclinical model for schizophrenia; however, the molecular mechanisms underlying the symptoms remain largely unknown. Acute PCP treatment rapidly induces beha…
Hazardous Substances Data Bank (HSDB)PMID 24564430Palmowski P et al; J Proteome Res 13 (3): 1578-92 (2014) 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 recepto…
DrugBank Phencyclidine works primarily as an NMDA receptor antagonist, which blocks the activity of the NMDA Receptor.
DrugBank
IV · Clinical
Clinical description
Where this compound's substance class sits in ICD-11 and DSM-5-TR, and how much of the recorded literature speaks to each domain of a mental status examination.
Filed under Hallucinogens
- 6C49Disorders due to use of hallucinogens
Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR): Hallucinogen-Related Disorders. Category names only — the manual is in copyright and no diagnostic criterion is reproduced here.
How much has been written about each domain
The clinical domains, and how many of the records this archive holds for this compound say something under each. What the terms mean, and the word list behind every spoke, are set out in the method.
- Mood 1
- matched on “mood” · in Toxicology: Hazardous Substances Data Bank (HSDB)
- Perception 2
- matched on “hallucinogen” · in Toxicology: Hazardous Substances Data Bank (HSDB); Toxicology: LiverTox
- Cognition 2
- matched on “cognitiv” · in Pharmacology: Mechanism of Action; PMID 24564430
- Thought content 1
- matched on “delusion” · in Toxicology: Hazardous Substances Data Bank (HSDB)
- Psychomotor activity 1
- matched on “stupor” · in Toxicology: Hazardous Substances Data Bank (HSDB)
V · Systems
Systems physiology
Where the targets this compound binds are transcribed — brain regions on the left, peripheral and autonomic tissues on the right. A join of two measurements, not a claim about what the compound does to either.
Brain
basal ganglia: drawn as the caudate nucleus, putamen and globus pallidus.
Measured but not drawn — this anatomogram has no outline for them: retina 0.9, midbrain 0.6, pituitary gland 0.3, spinal cord 0.2.
Body
Square-root ramp · shared scale across both plates
Shading is transcript level — not affinity, and not affinity combined with expression. Outlined but unshaded organs hold none of this compound’s resolved targets above the atlas’s detection threshold. Anatomy from EMBL-EBI Anatomogram (Apache License 2.0); regions identified by Uberon (uberon.org), CC BY 3.0.
Brain regions
Regions where this compound's measured targets are transcribed. Linked from the plate above.
cerebellum
4.4 nTPMbasal ganglia
3.8 nTPMcerebral cortex
2.7 nTPMhypothalamus
2.6 nTPMamygdala
1.9 nTPMretina
0.9 nTPMhippocampal formation
0.9 nTPMmidbrain
0.6 nTPMpituitary gland
0.3 nTPMspinal cord
0.2 nTPM
Peripheral & autonomic
Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.
small intestine
38.0 nTPMlung
27.2 nTPMduodenum
9.7 nTPMpancreas
1.3 nTPMskeletal muscle
1.0 nTPMheart muscle
0.9 nTPMstomach 1
0.8 nTPMadrenal gland
0.8 nTPMsalivary gland
0.6 nTPMcolon
0.4 nTPMthyroid gland
0.4 nTPMspleen
0.4 nTPMkidney
0.2 nTPMsmooth muscle
0.2 nTPM- MOROPRM15.3 pX0.2
liver
0.2 nTPM- MOROPRM15.3 pX0.2
urinary bladder
0.1 nTPM- MOROPRM15.3 pX0.1
Each row joins two published measurements and nothing else: the affinity this archive holds for the compound at that target, and the transcript level the Human Protein Atlas reports for that target’s gene in that region. Bars scale with expression only. Expression is not activation — a receptor transcribed in a region is a receptor available to be bound there, which is a weaker and more defensible claim than saying the region is affected.
3 of this compound’s targets could not be resolved to a gene and are absent from both columns: 5-HT3, NMDA, Sigma 2.
Expression data from Human Protein Atlas (CC BY-SA 3.0), RNA expression, nTPM (normalized transcripts per million), consensus tissue dataset. Uhlén M, et al. Tissue-based map of the human proteome. Science. 2015;347(6220):1260419.
VI · Profile
Affinity rosette
The strongest measurement at each of 7 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.
VII · Toxicology
Toxicological profile
What has been measured, and what has been published — kept apart, and neither scored. There is no risk rating on this page; the archive once carried one, identical for every compound, produced by a stub.
Measured in this archive
Assays that bear on toxicity, drawn from the same ChEMBL records as everything else on this page. They are measurements of what a compound binds or does to cells — not verdicts about what it does to a person.
No hERG, cytochrome, cytotoxicity or transport measurement exists for Phencyclidine (PCP) in this archive.
Lethal-dose values — animal studies
These are not human doses. An LD50 is the dose killing half of a group of animals of one species by one route, and it is a poor predictor of human risk for these compounds. Each value is printed whole, with the species and route it was measured in, because a lethal dose separated from those two facts is worse than no figure at all. Nothing here supports inferring a safe dose for anyone.
LD50 Mouse oral 76.5 mg/kg
Hazardous Substances Data Bank (HSDB)O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1343
LD50 Mouse ip 2800 ug/kg
Hazardous Substances Data Bank (HSDB)Lewis, R.J. Sr. (ed) Sax's Dangerous Properties of Industrial Materials. 11th Edition. Wiley-Interscience, Wiley & Sons, Inc. Hoboken, NJ. 2004., p. 2878
As published
Quoted verbatim from the database named after each passage, never summarized — a summary of a toxicology statement is a new claim.
Toxicity Summary
IDENTIFICATION AND USE: Phencyclidine (PCP) is a white, crystalline powder. It is a Schedule II Controlled Substance. PCP was formerly used as a preinduction anesthetic and as an animal tranquilizer. It has no current medical indications, although it is still used illegally as a hallucinogen. HUMAN STUDIES: PCP causes distortion of perception and produces a feeling of detachment of dissociation from the user's surrou…
Hepatotoxicity
Phencyclidine is no longer used medically and its production is outlawed. Nevertheless, phencyclidine remains an agent of abuse, used for its hallucinogenic effects. At low doses, phencyclidine appears to have little effect on the liver. However, high doses of phencyclidine have been associated with malignant hyperthermia which can trigger acute hepatitis necrosis and liver failure. Patients generally present with se…
Human Toxicity Excerpts
/HUMAN EXPOSURE STUDIES/ After swallowing a 7.5 mg tablet, /normal volunteers were given a/ battery of /seven/ tests /that were/ repeated every 15 minutes for 2 hr. Phencyclidine produced a general impairment in sensory function as evidenced by the elevated thresholds on all seven tests. Two-point discrimination, aesthesiometry, and perimetry thresholds showed the greatest increase, while taste was the least affected…
Hazardous Substances Data Bank (HSDB)Morganstern FS et al; Psychopharmacologia 3: 193-201 (1962)
/SIGNS AND SYMPTOMS/ Nervous system effects include seizures, stupor, coma, cerebral ischemia, subarachnoid hemorrhage, amaurosis fugax, and muscle rigidity. The muscle rigidity, along with agitation, can result in acute rhabdomyolysis and myoglobin-induced renal failure. Myoclonic, choreoathetoid, and dystonic movements, including opisthotonus and torticollis, may be seen.
Hazardous Substances Data Bank (HSDB)Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1108
/SIGNS AND SYMPTOMS/ PCP causes distortion of perception and produces a feeling of detachment of dissociation from the user's surroundings and self. It is not a classic hallucinogen but better described as a dissociative agent or anesthetic. The most common physical findings are nystagmus and hypertension.
Hazardous Substances Data Bank (HSDB)Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1107
/SIGNS AND SYMPTOMS/ Most deaths in PCP-intoxicated patients occur because of its behavioral toxicity. The bizarre and violent behavior induced by PCP, along with analgesic effects and lack of muscular coordination, may cause drowning or significant trauma. Nontraumatic causes of death include cardiopulmonary arrest after status epilepticus, primary respiratory arrest, and intracranial hemorrhage.
Hazardous Substances Data Bank (HSDB)Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1108
For more Human Toxicity Excerpts (Complete) data for Phencyclidine (25 total), please visit the HSDB record page.
Published passages via PubChem toxicology sections, aggregating Hazardous Substances Data Bank (HSDB), RTECS, LiverTox. No figure on this page is scored, ranked or combined into a risk level.
VIII · Evidence
Every measurement
One row per published value. The identifier in the last column resolves to the ChEMBL assay record it was read from.
Equilibrium binding constants 25
Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.
| Target | Class | Type | Value (nM) | pX | Organism | Assay |
|---|---|---|---|---|---|---|
| NMDA | Glutamate receptors | Ki | 22.00 | 7.66 | RAT | PMID 28513099 |
| NMDA | Glutamate receptors | Ki | 22.10 | 7.66 | RAT | PMID 31152702 |
| NMDA | Glutamate receptors | Ki | 28.00 | 7.55 | PIG | PMID 26430967 |
| NMDA | Glutamate receptors | Ki | 42.20 | 7.37 | RAT | PMID 7566488 |
| NMDA | Glutamate receptors | Ki | 48.00 | 7.32 | RAT | PMID 3016248 |
| NMDA | Glutamate receptors | Ki | 57.90 | 7.24 | RAT | PMID 27314670 |
| NMDA | Glutamate receptors | Ki | 57.90 | 7.24 | RAT | PMID 31152702 |
| NMDA | Glutamate receptors | Ki | 58.00 | 7.24 | RAT | PMID 27314670 |
| NMDA | Glutamate receptors | Ki | 59.00 | 7.23 | HUMAN | PMID 23527166 |
| NMDA | Glutamate receptors | Ki | 66.00 | 7.18 | RAT | PMID 3016248 |
| NMDA | Glutamate receptors | Ki | 75.86 | 7.12 | Rattus norvegicus | PMID 42332075 |
| Sigma 2 | Sigma receptors | Ki | 136 | 6.87 | RAT | PMID 23527166 |
| NMDA | Glutamate receptors | Ki | 180 | 6.74 | RAT | PMID 7566488 |
| 5-HT3 | Serotonin receptors | Ki | 273 | 6.56 | GUINEA PIG | PMID 8246171 |
| NMDA | Glutamate receptors | Ki | 311 | 6.51 | RAT | PMID 3016248 |
| NMDA | Glutamate receptors | Ki | 625 | 6.20 | RAT | PMID 3016248 |
| NMDA | Glutamate receptors | Ki | 758 | 6.12 | RAT | PMID 3016248 |
| SERT | Monoamine transporters | Ki | 2,234 | 5.65 | HUMAN | PMID 23527166 |
| 5-HT3 | Serotonin receptors | Ki | 2,671 | 5.57 | GUINEA PIG | PMID 8246171 |
| MOR | Opioid receptors | Ki | 4,786 | 5.32 | Homo sapiens | PMID 42332075 |
| KOR | Opioid receptors | Ki | 7,586 | 5.12 | Homo sapiens | PMID 42332075 |
| MOR | Opioid receptors | Ki | 8,710 | 5.06 | Rattus norvegicus | PMID 42332075 |
| KOR | Opioid receptors | Ki | 8,795 | 5.06 | RAT | PDSP |
| DOR | Opioid receptors | Ki | 25,119 | 4.60 | Rattus norvegicus | PMID 42332075 |
| DOR | Opioid receptors | Ki | 60,256 | 4.22 | Homo sapiens | PMID 42332075 |
Functional readouts 3
IC₅₀, EC₅₀, AC₅₀ and potency. Assay-dependent, and not interchangeable with a binding constant.
| Target | Class | Type | Value (nM) | pX | Organism | Assay |
|---|---|---|---|---|---|---|
| MOR | Opioid receptors | EC50 | 4,266 | 5.37 | Homo sapiens | PMID 42332075 |
| KOR | Opioid receptors | EC50 | 11,220 | 4.95 | Homo sapiens | PMID 42332075 |
| DOR | Opioid receptors | EC50 | 38,019 | 4.42 | Homo sapiens | PMID 42332075 |
- P
- PubChem
- C
- ChEMBL
- R
- Computed here with RDKit
- D
- Derived here from the stored measurement
IX · Trials
Registered clinical trials
Studies filed with ClinicalTrials.gov that name this compound as an intervention. A registered trial is a protocol, not a result — status and enrollment are printed beside every row, and withdrawn studies are counted rather than hidden.
— No registered study names Phencyclidine (PCP) as an intervention. That is an absence of registered research, not evidence about the compound. Most of this archive has never been the subject of a registered trial.
Records from ClinicalTrials.gov (U.S. National Library of Medicine, NIH), API v2. A study is listed against a compound only when a verified name for that compound appears as a whole word in one of the study's own intervention names. A short code must appear as written, and a name the registry uses for something else (Aleph, a vaccine maker) is not matched. Title matches are not accepted. The matched name and the intervention text it matched are shown with every row.
Searched as Phencyclidine · 1-(1-Phenylcyclohexyl)piperidine · Angel dust. Run this search at the registry.
A registered trial is a protocol somebody filed with the registry. It is not a result, and nothing on this plate says whether Phencyclidine (PCP) worked.
X · Legal
Controlled-substance status
United States federal scheduling, read from the DEA records this archive holds and shown with the passage each was read from. Not legal advice, and not necessarily current.
- DEA class
- Depressants and Tranquilizers
- Added
- October 1998
As the DEA states it
Quoted whole. The badge above is a reading of these passages and adds nothing to them.
PCP (Class: Depressants and Tranquilizers, Added Date: 10-1998)
Schedule II - Substances in the DEA Schedule II have a high potential for abuse which may lead to severe psychological or physical dependence.
Other regulatory records
Registers outside the DEA that hold an entry for Phencyclidine (PCP) — chemical-safety and national inventories, each naming itself. They are not scheduling decisions.
Piperidine, 1-(1-phenylcyclohexyl)-: Does not have an individual approval but may be used under an appropriate group standard
Schedule II shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. ... Unless specifically excepted or unless listed in another schedule, any material, compound, mixture, or preparation which contains any quantity of the following substances having a depressant effect on the central nervous system, including its salts, isomers, and salts of isomers whenever the existence of such salts, isomers, and salts of isomers is possible within the specific chemical designation. Phencyclidine…
Hazardous Substances Data Bank (HSDB)21 CFR 1308.12(e) (USDEA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of October 19, 2017: https://www.ecfr.gov
Schedule I shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. ... Unless specifically excepted or unless listed in another schedule, any material, compound, mixture, or preparation, which contains any quantity of the following hallucinogenic substances, or which contains any of its salts, isomers, and salts of isomers whenever the existence of such salts, isomers, and salts of isomers is possible within the specific chemical designation (for purposes of this paragraph only, the…
Hazardous Substances Data Bank (HSDB)21 CFR 1308.11(d) (USDEA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of October 19, 2017: https://www.ecfr.gov
United States federal status only. State law differs, and so does the law of every other country — none of it is represented here. Scheduling changes, and this reflects the DEA records held by PubChem descriptive sections when the monograph was last harvested, not necessarily today. This is a record of what a database publishes, not legal advice.
XI · Literature
Sources behind this dossier
The papers this compound's values were read from, ranked by what each contributed. Not a review of the field.
Every paper below is one some value on this page came from — a binding constant, a passage of pharmacology or toxicology, or a measured duration. Each entry says what this archive took from it. Nothing else is claimed about any of them: the title is the study’s own account of itself, and a summary written here would be an assertion with no source behind it.
- 01
Structural basis of opioid receptor activation by PCP and ketamine
Jiang Q, Han J, Fine EJ et al. · Nature structural & molecular biology 2026
- · 9 measurements at 4 targets (EC50, Ki), strongest NMDA at 7.12 pX
- 02
Largent BL, Gundlach AL, Snyder SH · The Journal of pharmacology and experimental therapeutics 1986
- · 5 measurements at 1 target (Ki), strongest NMDA at 7.32 pX
- 03
Roth BL, Gibbons S, Arunotayanun W et al. · PloS one 2013
- · 3 measurements at 3 targets (Ki), strongest NMDA at 7.23 pX
- 04
Pharmacological characterizations of the 'legal high' fluorolintane and isomers
Wallach J, Colestock T, Agramunt J et al. · European journal of pharmacology 2019
- · 2 measurements at 1 target (Ki), strongest NMDA at 7.66 pX
- 05
Wallach J, Kang H, Colestock T et al. · PloS one 2016
- · 2 measurements at 1 target (Ki), strongest NMDA at 7.24 pX
- 06
Bresink I, Danysz W, Parsons CG et al. · Neuropharmacology 1995
- · 2 measurements at 1 target (Ki), strongest NMDA at 7.37 pX
- 07
Bonhaus DW, Loury DN, Jakeman LB et al. · The Journal of pharmacology and experimental therapeutics 1993
- · 2 measurements at 1 target (Ki), strongest 5-HT3 at 6.56 pX
- 08
Colestock T, Wallach J, Mansi M et al. · Drug testing and analysis 2018
- · 1 measurement at 1 target (Ki), strongest NMDA at 7.66 pX
- 09
Bonifazi A, Del Bello F, Mammoli V et al. · Journal of medicinal chemistry 2015
- · 1 measurement at 1 target (Ki), strongest NMDA at 7.55 pX
- 10
McClatchy DB, Savas JN, Martínez-Bartolomé S et al. · Molecular psychiatry 2016
- · Mechanism of Action
- 11
Palmowski P, Rogowska-Wrzesinska A, Williamson J et al. · Journal of proteome research 2014
- · Mechanism of Action
- 12
Yamamoto H, Kamegaya E, Sawada W et al. · Molecular brain 2013
- · Mechanism of Action