PCP

1-(1-phenylcyclohexyl)piperidine

Overview

PCP belongs to Dissociatives / Arylcyclohexylamines.

Key safety note: PCP is one of the most behaviourally dangerous recreational drugs.^[3]^[4]

Effects

Subjective effects vary. What a substance feels like depends on dose, individual physiology, mindset, and setting. The points below describe commonly reported effects, not guaranteed, uniform, or desirable outcomes.

Dissociation and detachment from the body and surroundings, distorted perception of time and space, numbness, and, depending on dose and set, either euphoria and a feeling of strength/invulnerability or intense anxiety, confusion and dysphoria.
Physical signs: nystagmus (flicking eye movements), slurred speech, unsteady gait, sweating, raised heart rate and blood pressure, muscle rigidity and reduced pain sensation.
At higher doses or in sensitive users: agitation, paranoia, hallucinations, a schizophrenia-like psychosis, and the risk of violent or self-injurious behaviour. Very high doses can cause seizures, coma and dangerous hyperthermia. Confusion and low mood can persist for days.

Dosing & duration

Harm-reduction note: These are commonly cited reference ranges, not a recommendation or a “safe” dose. Potency, purity, body chemistry, tolerance, and drug combinations vary widely. Start low, go slow, wait for full effects before redosing, and never assume an unknown product matches these figures. Missing data is not evidence of safety.

Smoked, insufflated (snorted), oral, and (less commonly) injected. The ranges below are commonly cited reference figures, NOT a recommendation: PCP's dose–response is steep and unusually unpredictable.. PCP is exceptionally dose-sensitive: small increases in dose can turn a dissociative 'high' into severe agitation, psychosis, hyperthermia or unconsciousness, and street material is of unknown, often variable strength (frequently sold on plant matter or as liquid-dipped cigarettes with no way to gauge the dose). There is no safe dose and no antidote. Effects last many hours and, because the drug is stored in fat and slowly released, can recur or persist for days. Combining it with alcohol or other depressants sharply raises the risk of coma. Starting low cannot make it predictable.

Dose ranges

Threshold (oral)

≈1 mg

Light (oral)

≈1–5 mg

Common (oral)

≈5–10 mg

Strong (oral)

≈10–15 mg

Heavy (oral)

≈15 mg and above (rising risk of psychosis/overdose)

Duration

onset

Smoked ≈2–5 min, oral/insufflated ≈15–60 min

total

≈4–8 h (higher doses longer)

after effects

Confusion, low mood and cognitive impairment for hours to days. Effects can recur as the drug redistributes from fat

Chemical & Physical Properties

Formula	C17H25N
Molar mass	243.39 g/mol
State	Solid
Melting point	46.5 °C
Boiling point	136 °C at 1 mmHg
Density	Not reported
Vapor pressure	Not reported
pKa	8.29
LogP	4.69
Solubility	Soluble in ethanol
Refractive index	Not reported

Identifiers & Synonyms

CAS	77-10-1
CAS (enantiomer)
PubChem CID	6468
InChIKey	JTJMJGYZQZDUJJ-UHFFFAOYSA-N
InChI	InChI=1S/C17H25N/c1-4-10-16(11-5-1)17(12-6-2-7-13-17)18-14-8-3-9-15-18/h1,4-5,10-11H,2-3,6-9,12-15H2
SMILES	C1CCC(CC1)(C2=CC=CC=C2)N3CCCCC3

Synonyms

Phencyclidine
Angel dust
1-(1-phenylcyclohexyl)piperidine
Sherm

Pharmacodynamics & Biochemistry

Phencyclidine (PCP, 'angel dust') is an arylcyclohexylamine dissociative anaesthetic: the parent of the class that includes ketamine. Its primary action is non-competitive, open-channel block of the NMDA glutamate receptor: it enters and plugs the receptor's ion channel only while the channel is open, so it accumulates on active receptors and interrupts the excitatory glutamate signalling that supports perception, memory and the sense of a unified self, producing dissociation, analgesia and anaesthesia. It binds the NMDA (PCP) site with Kᵢ ≈59 nM. PCP is comparatively NMDA-selective but not clean: it has moderate affinity at the σ2 receptor (Kᵢ ≈136 nM) and weak activity at the serotonin transporter (Kᵢ ≈2.2 µM), while binding only weakly (>10 µM) at the dopamine and noradrenaline transporters, σ1 and the D2 receptor in its normal state. At higher concentrations it nonetheless raises synaptic dopamine (weak reuptake inhibition plus increased release) and it is a partial agonist at the high-affinity D2^High state: a likely contributor to its uniquely psychotomimetic, agitated and stimulant profile, which mimics schizophrenia more closely than ketamine does. It is highly lipophilic (logP ≈4.7), so it distributes into fat and brain and is released slowly, giving a long and variable half-life (≈7–46 h) and effects that can last many hours and recur. It is cleared mainly by hepatic oxidative hydroxylation (~90%) followed by glucuronidation, with about 9% excreted unchanged. Renal clearance rises in acidic urine, which has been used in managing intoxication. Because it redistributes slowly from fat, agitation and psychosis can wax and wane long after a single dose.

Biological targets

NMDA

Binding & functional measurements

Target	Measurement	Species
NMDA receptor	Ki 251 ± 29 nM	Human
NMDA receptor	Ki 99 ± 19 nM	Pig
NMDA receptor	Ki 22 ± 1.6 nM	Rat
Serotonin transporter	Ki 2,234 nM	Human
Sigma-2 receptor	Ki 136 nM	Rodent

Pharmacokinetics

Bioavailability	Smoked/insufflated high, oral variable
T_max	≈1–2 h oral
Half-life	≈7–46 h (lipophilic, wide range)
V_d	Not reported
Protein binding	Not reported
Metabolism	Hepatic hydroxylation
Excretion	Renal. Clearance increased by acidic urine

Toxicology & Safety

Harm-reduction note: Toxicity and risk depend on dose, route, purity, combinations, setting, and individual health factors. Missing harms should never be interpreted as evidence of safety.

10 mg/kg (rat, i.p.)

PCP is one of the most behaviourally dangerous recreational drugs. Beyond dissociation and anaesthesia it commonly causes agitation, confusion, paranoia and a psychosis that can closely mimic schizophrenia, and, because it is a potent analgesic that removes pain and normal fear, it is strongly associated with unpredictable, violent or self-injurious behaviour and severe accidental injury. Physical dangers include hypertension, tachycardia, dangerous hyperthermia, muscle rigidity and rhabdomyolysis (which can cause acute kidney failure), seizures, nystagmus, and, in overdose, coma and respiratory depression. Because PCP is highly lipophilic and slowly redistributes from fat, symptoms can be prolonged and can fluctuate or relapse over hours to days. Its dose–response is steep and unpredictable, so the gap between a recreational and a toxic dose is small. The danger is greatly increased by combining it with alcohol or other depressants. Regular use can produce psychological dependence and persistent cognitive and mood problems. There is no antidote: management is supportive (a calm low-stimulation environment, benzodiazepines for agitation, cooling, and treatment of rhabdomyolysis).^[3]^[4]

Legal Status

Legal note: Legal status can change over time and may vary by country, region, formulation, analogue status, prescription context, and enforcement practice. Always confirm with current official sources before relying on this section.

US: Schedule II. UK: Class A. DE: BtMG Anlage I

Interactions & Contraindications

Drug interactions

Alcohol, Benzodiazepines, Opioids Additive sedation with a sharply raised risk of coma and respiratory depression.^[3]

Stimulants (amphetamines, cocaine) Compounded hypertension, hyperthermia and agitation or psychosis.^[3]

Other dissociatives (NMDA antagonists) Unpredictable, potentiated dissociation and confusion.^[3]

Urinary acidifiers or alkalinisers Acidifying the urine accelerates PCP elimination and has been used to manage intoxication.^[3]^[4]

Contraindications

Personal or family history of psychosis, schizophrenia or bipolar disorder PCP reliably triggers or worsens psychosis.^[3]^[4]

Cardiovascular disease, hypertension or arrhythmia severe hypertension or cardiovascular disease.^[3]

Combining with alcohol or other CNS depressants any concurrent CNS depressant or heavy alcohol use.^[3]

Pregnancy or breastfeeding^[3]

Usage & Context

A recreational dissociative taken by smoking (often sprinkled on cannabis or a tobacco 'sherm'), insufflation, orally or, less commonly, by injection. Effects range from euphoric dissociation to severe agitation and psychosis.
Originally developed in the 1950s as the intravenous anaesthetic Sernyl, but abandoned for human use because of severe emergence delirium, agitation and hallucinations. Ketamine was later developed as a shorter-acting, less psychotomimetic successor.
Known on the street as 'angel dust', 'sherm', 'wet' or 'embalming fluid' (a slang term, not a literal ingredient).

Sources & Evidence

Further Information

More in this subclass