3-HO-PCP (3-Hydroxyphencyclidine): Complete Toxicology, Dependence & Safety Monograph
What the evidence actually shows
Evidence Low direct human evidence; established dissociative/NMDA mechanism; WHO surveillance statusDirect answer
Reference-grade 3-HO-PCP monograph covering identity, PCP relationship, NMDA pharmacology, WHO review, analytically confirmed poisoning, metabolism, dissociative toxicity, tolerance, dependence uncertainty, testing, forensic interpretation, legal status, and evidence gaps. 3-HO-PCP (CAS 79787-43-2) is a phencyclidine analogue and NMDA-receptor antagonist with dissociative and psychotomimetic effects. Direct human evidence is limited: an analytically confirmed case involving 3-HO-PCP plus N-ethylhexedrone/clephedrone included hyperthermia, tachycardia, reduced consciousness, clonus and rhabdomyolysis, but the stimulant co-exposures prevent clean attribution. Human-hepatocyte and authentic-sample research identified hydroxylation, piperidine-ring-opening/N-dealkylation, glucuronidation and sulfation pathways, improving toxicology detection.
Research brief
Questions this page answers
- What is 3-HO-PCP?
- Is 3-HO-PCP the same as PCP?
- How does 3-HO-PCP work?
- Can 3-HO-PCP cause hyperthermia or rhabdomyolysis?
- Has 3-HO-PCP caused deaths?
- Can 3-HO-PCP cause tolerance or dependence?
- What does 3-HO-PCP withdrawal look like?
- How is 3-HO-PCP metabolized?
- Do routine drug tests detect 3-HO-PCP?
- Why did WHO keep 3-HO-PCP under surveillance rather than schedule it?
Signal
Scientific takeaways
- 3-HO-PCP (CAS 79787-43-2) is a phencyclidine analogue and NMDA-receptor antagonist with dissociative and psychotomimetic effects.
- Direct human evidence is limited: an analytically confirmed case involving 3-HO-PCP plus N-ethylhexedrone/clephedrone included hyperthermia, tachycardia, reduced consciousness, clonus and rhabdomyolysis, but the stimulant co-exposures prevent clean attribution.
- Human-hepatocyte and authentic-sample research identified hydroxylation, piperidine-ring-opening/N-dealkylation, glucuronidation and sulfation pathways, improving toxicology detection.
- WHO critically reviewed 3-HO-PCP in 2024 and concluded that its mechanism suggests abuse potential, but available evidence was insufficient to justify international scheduling; WHO recommended continued surveillance.
- WHO found no controlled human or animal dependence studies and only limited fatal/nonfatal intoxication reports, often with other substances and imperfect analytical confirmation.
- Repeated PCP-like dissociative use can plausibly produce tolerance and problematic use, but 3-HO-PCP-specific dependence incidence and withdrawal timelines are not established.
- Routine drug screens should not be assumed to identify 3-HO-PCP; definitive LC-MS/MS/HRMS methods and metabolite targets are more informative.
- As of October 2, 2026, 3-HO-PCP is not internationally scheduled. Exact U.S. federal/state legal treatment should be checked by molecule and jurisdiction rather than inferred from PCP.
3-HO-PCP (3-Hydroxyphencyclidine): Complete Toxicology, Dependence & Safety Monograph
Emergency dissociative toxicity: Severe unresponsiveness, seizure, dangerous overheating, collapse, severe agitation/confusion, chest pain, marked muscle rigidity/clonus, or serious injury after an unknown dissociative requires urgent medical care.
Quick answer
3-HO-PCP is 3-hydroxyphencyclidine, a PCP-related arylcyclohexylamine dissociative and NMDA-receptor antagonist.
Its name and chemical relationship make it tempting to describe it as “PCP with a hydroxy group.”
That is chemically true but clinically incomplete.
The direct human evidence base remains small.
WHO's 2024 critical review concluded:
- the drug's mechanism indicates likely abuse potential;
- limited fatal and nonfatal intoxications had been reported;
- many cases involved other psychoactive substances;
- causality was often unclear;
- evidence was insufficient to justify international scheduling;
- continued WHO surveillance was appropriate.
Identity
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| Field | Evidence-based answer |
|---|---|
| Canonical name | 3-Hydroxyphencyclidine |
| Common names | 3-HO-PCP, 3-OH-PCP |
| CAS | 79787-43-2 free base |
| Formula / molecular mass | C17H25NO / 259.39 g/mol |
| Class | PCP-type arylcyclohexylamine dissociative |
| Main mechanism | NMDA receptor antagonism |
| Approved medical use | None |
| International status | Not scheduled; WHO surveillance after 2024 critical review |
History
3-HO-PCP is a hydroxy analogue of phencyclidine.
PCP itself was developed as an anesthetic in the 1950s and later abandoned for routine human use because of severe emergence reactions and psychotomimetic effects.
3-HO-PCP later appeared in NPS/research-chemical markets as part of a broader resurgence of PCP/PCE analogues.
WHO reported clandestine manufacture, internet sales, seizures, and national controls in multiple countries.
Its market presence is therefore established even though large clinical datasets are not.
Relationship to PCP
3-HO-PCP and PCP are distinct molecules.
They share:
- arylcyclohexylamine structure;
- NMDA-antagonist mechanism;
- potential dissociative/psychotomimetic effects.
They do not necessarily share:
- human potency;
- half-life;
- metabolism;
- concentration–impairment relationship;
- dependence incidence.
PCP evidence is useful as class context—not as a dose conversion.
Pharmacology
WHO characterizes 3-HO-PCP as an NMDA receptor antagonist with a mechanism and effects similar to PCP.
NMDA blockade can produce:
- dissociation;
- altered perception;
- impaired coordination;
- analgesia;
- confusion;
- agitation;
- psychotomimetic effects.
Animal evidence suggests abuse potential similar to PCP.
What is not established
No controlled human trial defines:
- receptor occupancy at recreational exposure;
- a safe dose;
- human potency versus PCP;
- a therapeutic window.
Direct human poisoning evidence
A published analytically confirmed case involved a 56-year-old man with 3-HO-PCP plus N-ethylhexedrone and clephedrone.
Findings included:
- temperature 39.9°C;
- heart rate 150/min;
- reduced consciousness;
- ocular clonus;
- vertical nystagmus;
- subsequent rhabdomyolysis with CK peaking near 6000 IU/L.
He improved with supportive hospital treatment.
Why this case cannot define the 3-HO-PCP toxidrome
The cathinone co-exposures can independently produce:
- tachycardia;
- hyperthermia;
- clonus;
- sympathomimetic/serotonergic toxicity.
Thus the case proves real 3-HO-PCP exposure during severe intoxication, but not that every feature was caused by 3-HO-PCP alone.
Fatality evidence
WHO's 2024 review identified a limited number of fatal and nonfatal intoxication reports involving 3-HO-PCP.
Important limitations:
- other psychoactive substances were often present;
- in many reports, 3-HO-PCP use was not analytically confirmed;
- causality was uncertain.
Therefore this site does not publish a 3-HO-PCP fatal-concentration table.
Acute dissociative toxicity
Mechanistically plausible and reported effects include:
- dissociation;
- hallucinations;
- confusion;
- agitation;
- impaired consciousness;
- nystagmus;
- hypertension/tachycardia;
- loss of coordination;
- accidental injury.
Severe cases can become medically complicated by:
- hyperthermia;
- rhabdomyolysis;
- seizures;
- trauma;
- polysubstance exposure.
Hyperthermia and rhabdomyolysis
The confirmed mixed-intoxication case directly documents both hyperthermia and rhabdomyolysis.
The exact contribution of 3-HO-PCP cannot be isolated.
Still, in a severely agitated/dissociated person:
- muscular activity;
- impaired judgment;
- stimulant co-use;
- environmental heat;
- restraint/struggle
can compound physiologic stress.
Interactions
No controlled 3-HO-PCP interaction program exists.
Potentially high-risk contexts include:
- other dissociatives → deeper impairment/confusion;
- stimulants → more cardiovascular/hyperthermic stress;
- alcohol/benzodiazepines → more impaired consciousness/aspiration;
- opioids → opioid respiratory-depression risk;
- serotonergic stimulants → more complex mixed toxidromes.
No combination can be labeled safe from current evidence.
Metabolism
Human-hepatocyte and authentic-sample research identified multiple pathways.
Reported metabolites included:
- hydroxylated metabolites;
- piperidine-ring-opened/N-dealkylated carboxylic-acid metabolite;
- O-glucuronide conjugate;
- O-sulfate conjugate.
Metabolites can help laboratories document exposure when parent drug is low or absent.
Pharmacokinetics
The metabolism paper reported protein-binding information, but there is no robust controlled human PK program establishing:
- bioavailability;
- time to peak;
- half-life;
- clearance;
- accumulation;
- concentration-effect relationships.
Online duration estimates should not be presented as measured clinical PK.
Drug testing
Routine screens
Routine workplace/emergency immunoassays are not designed to reliably identify 3-HO-PCP.
A PCP screen may or may not cross-react depending on the assay; cross-reactivity cannot be assumed.
Definitive testing
Useful approaches include:
- LC-MS/MS;
- LC-HRMS;
- parent drug;
- metabolite targets.
Updated NPS libraries are important because PCP analogues can fall outside traditional panels.
Tolerance
Repeated NMDA-antagonist exposure can produce tolerance.
No controlled 3-HO-PCP human study defines:
- onset;
- magnitude;
- cross-tolerance with PCP/ketamine/PCE analogues.
Subjective tolerance does not prove tolerance to:
- impaired driving;
- delirium;
- accident risk;
- cardiovascular stress.
Dependence potential
WHO found no controlled studies in humans or animals directly measuring 3-HO-PCP dependence potential, although animal evidence from related effects suggests abuse potential.
No country responding to the 2024 WHO questionnaire reported treatment presentations specifically attributed to 3-HO-PCP dependence.
That is not proof dependence cannot occur.
It means population evidence is sparse.
Withdrawal
No validated 3-HO-PCP withdrawal syndrome or timeline exists.
With repeated PCP-like dissociative use, possible post-use problems can include:
- craving;
- low mood;
- irritability;
- sleep disturbance;
- anxiety;
- difficulty stopping.
These should be framed as class/repeated-use concerns, not a proven 3-HO-PCP withdrawal curve.
Treatment and support
There is no approved medication specifically for 3-HO-PCP use disorder.
Acute severe intoxication is managed according to clinical complications.
Problematic repeated use can be addressed through:
- substance-use assessment;
- behavioral treatment;
- management of co-occurring psychiatric illness;
- injury/medical evaluation.
U.S. readers can use FindTreatment.gov or SAMHSA 1-800-662-HELP (4357).
Forensic interpretation
A positive result establishes exposure, not causality
Interpretation requires:
- co-drugs;
- specimen type;
- timing;
- scene history;
- behavior;
- medical findings.
Concentration is not a dose or impairment threshold
No validated 3-HO-PCP concentration establishes:
- exact dose;
- degree of impairment;
- lethality.
Analytical confirmation matters
WHO specifically noted that many published cases were not analytically confirmed.
Chemically confirmed cases should therefore be weighted more heavily.
Special populations
No adequate controlled data exist for:
- pregnancy/breastfeeding;
- adolescents;
- older adults;
- cardiovascular disease;
- seizure disorders;
- severe psychiatric illness;
- liver/kidney disease.
PCP-like psychotomimetic effects are a particular concern in people vulnerable to psychosis or mania, but 3-HO-PCP-specific risk magnitude is unknown.
Legal and regulatory status — dated October 2, 2026
International
WHO critically reviewed 3-HO-PCP in 2024.
The ECDD concluded that the available public-health evidence was insufficient to warrant international control and recommended that it remain under WHO surveillance.
It is therefore not internationally scheduled under the drug-control conventions as of this review date.
United States
This review does not identify a current U.S. federal scheduling provision specifically naming 3-HO-PCP in the primary sources used here.
PCP itself is controlled, and federal analogue law or state-specific laws may apply depending on facts and jurisdiction.
Do not infer legal status from chemical similarity alone.
Myths and misconceptions
“3-HO-PCP is just weaker/stronger PCP.”
Too simplistic. There is no validated human conversion ratio.
“WHO did not schedule it, so WHO says it is safe.”
False. WHO identified abuse potential but judged the available population evidence insufficient for international scheduling.
“The severe 2019 case proves 3-HO-PCP alone causes serotonin syndrome.”
No. Cathinone co-exposures substantially confounded that case.
“A negative routine drug screen rules it out.”
False.
“No treatment admissions means no dependence risk.”
False. Sparse surveillance is not a dependence trial.
Evidence ledger
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| Status | Current conclusion |
|---|---|
| Established | 3-HO-PCP is a PCP-like NMDA antagonist; real drug-market exposure occurs; human metabolism and analytical targets are characterized; severe mixed intoxication is documented. |
| Strongly plausible / class-supported | Dissociation, psychotomimetic effects, tolerance, accidents and problematic repeated use are credible hazards. |
| Uncertain | Human PK, isolated-drug toxicity, dependence incidence, withdrawal, concentration–impairment relationships and long-term effects. |
| Not established | Safe dose, PCP-equivalent potency, fatal concentration, standardized withdrawal protocol or causal role in most reported deaths. |
Related evidence
- 3-MeO-PCE
- O-PCE
- DCK
- 2F-DCK
- FXE
- RC dissociatives evidence hub
- Substance Use, Dependence & Harm Reduction hub
Bottom line
3-HO-PCP has enough evidence to establish a real PCP-like dissociative mechanism and a genuine toxicology concern, but not enough to support the precision often claimed online.
WHO's decision to keep it under surveillance captures the evidence state well:
credible hazard, demonstrated abuse potential, limited human case data, and substantial uncertainty about population-level harm.
A useful reference should preserve all four of those facts at once.
Source ledger
References
7 sources
- 01Severe Toxicity to the New Psychoactive Substances 3-Hydroxyphencyclidine and N-Ethylhexedrone: an Analytically Confirmed Case Report Clinical toxicology case authors · 2019Human mixed-exposure toxicityAnalytically confirmed clinical case reportPMID 31482320 PubMed →
- 02In vitro and in vivo metabolism and detection of 3-HO-PCP, a synthetic phencyclidine, in human samples and pooled human hepatocytes using high resolution mass spectrometry Metabolism study authors · 2020Human hepatocytes + authentic human specimensHuman metabolism / analytical toxicologyPMID 32311838 PubMed →
- 033-Hydroxyphencyclidine — 47th ECDD Critical Review World Health Organization · 2024Authoritative evidence synthesisInternational expert critical review Source →
- 04WHO Expert Committee on Drug Dependence: Forty-seventh report World Health Organization · 2025Authoritative expert committee reportInternational scheduling recommendation Source →
- 05WHO Substances Under Surveillance — 3-Hydroxyphencyclidine World Health Organization · 2025Authoritative regulatory/scientific surveillanceInternational surveillance record Source →
- 063-Hydroxyphencyclidine WHO Expert Committee on Drug Dependence Information Repository · 2026Authoritative referenceWHO scheduling/review record Source →
- 07From PCP to MXE: a comprehensive review of the non-medical use of dissociative drugs Morris H, Wallach J · 2014Evidence synthesis / class contextDissociative pharmacology/history reviewPMID 24678061 PubMed →