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3-Cl-PCP Facts

Dissociative; Arylcyclohexylamine; NMDA receptor antagonist

Description

3-Cl-PCP (3-chlorophencyclidine) is a synthetic dissociative of the arylcyclohexylamine class. It blocks glutamate signaling in the brain,[1] disrupting communication across memory, sensory, and motor circuits and producing a dissociative state.

Subjective effects include dissociation, depersonalization, motor impairment, perceptual distortion, and stimulant-like activation. The experience is expected to resemble PCP more closely than ketamine — longer-lasting,[2] more activating, and with greater potential to produce psychosis-like states.[3]

Both physical and psychological dependence are rated moderate,[4] and no toxic dose has been established in any species. The dominant risk is psychiatric: PCP-class compounds are among the most powerful psychotomimetics, and 3-Cl-PCP produced psychosis-like cognitive deficits in a rodent model.[3]

Dose and durationby route · individual sensitivity varies

Oral

No dose recorded for this route. The timings are not a dose guide.

Starts in 15 – 60 minLasts 4 – 10 hoursAfter-effects 6 – 48 hours

Body and dependence

Acute toxicity
Moderate
Chronic toxicity
Moderate
Physical dependence
Moderate
Psychological dependence
Moderate
Withdrawal
Moderate
Compulsive redosing
Moderate

Tolerance

Builds
Rapid
Fully resets after
10.5 days
Carries over to
ketamine; dextromethorphan; methoxetamine; 3-MeO-PCP; PCP; other NMDA antagonists; sigma agonists (SKF-10047)

Effectslikely at a common dose

Perception
Spatial disorientation; Perspective distortion; Vestibular distortion; +21 possible, including Double vision, Visual acuity suppression, Visual haze / noise
Body
Motor control impairment; +34 possible, including Dizziness, Nystagmus (eye wobbles), Dehydration sensation
Thinking
Memory suppression; Cognitive impairment; +30 possible, including Thought disorganization, Confusion, Decision impairment
Feeling
none likely · 12 possible, including Emotional lability, Empathy suppression, Anhedonia
Self
none likely · 9 possible, including Depersonalization, Derealization, Social disconnection
Time
Time alteration; +3 possible, including Temporal disorientation
Awareness
none likely · 1 possible

Who shouldn't take it

Absolute
Cardiovascular disease; Concurrent CNS depressant use; Psychotic disorders; Pregnancy and lactation; MAOI use
Relative
Concurrent stimulant use; Lithium use; Hepatic impairment; Renal impairment

Combinations61 recorded

Lethal (1)
GHB, GBL
Dangerous (32)
Benzodiazepines; Buprenorphine, Kratom; Naltrexone; NSAIDs; THC; Amphetamines; Anticholinergics; Antihistamines; Atypical antipsychotics; Benzodiazepines, Barbiturates; Buspirone; Clonidine, Guanfacine; Dopamine agonists; Gabapentin, Pregabalin; GHB, Baclofen; Ibogaine; Ketamine, DXM, PCP; Lithium; Local anesthetics; MAOIs; MDMA, Amphetamines; MDMA, MDA; NDRIs (Wellbutrin); NRIs; and 8 more, see full page
Caution (24)
See full page: psychedex.org/substances/3-cl-pcp
Not graded (4)
Not listed never means safe.

Seek help immediately if

  • Severe disorientation; unable to move or speak (deep dissociation / "k-hole")
  • Complete loss of coordination — cannot stand or walk safely
  • Vomiting while incapacitated (choking / aspiration risk)
  • Very high blood pressure; fast heart rate
  • Slow or shallow breathing at high doses (especially mixed with depressants)
  • Unconsciousness; rarely, seizures

What to do

  1. Move them somewhere safe, away from stairs, water, roads, and sharp edges — they cannot protect themselves
  2. Place in the recovery position if vomiting or unconscious (aspiration is a key risk)
  3. Stay with them and reassure calmly; keep the environment quiet
  4. If breathing is slow/shallow or they are unresponsive, call emergency services
  5. Do not let them wander; do not leave them alone
  6. Be ready to give rescue breaths / CPR

Effects wear off with time in a safe, monitored setting. The main dangers are physical injury and aspiration while incapacitated, and respiratory depression when combined with other depressants — not the dissociation itself.

988 Suicide & Crisis LifelineFireside Project: 62-FIRESIDE

Version r1 · Not medical advice

References

  1. [1]
    ^Jentsch JD, Roth RH (1999) The neuropsychopharmacology of phencyclidine: from NMDA receptor hypofunction to the dopamine hypothesis of schizophrenia. — Neuropsychopharmacology doi:10.1016/s0893-133x(98)00060-8
  2. [2]
    ^Bey T, Patel A (2007) Phencyclidine intoxication and adverse effects: a clinical and pharmacological review of an illicit drug — The California Journal of Emergency Medicine PMID:20440387
  3. [3]
    ^abShaw HE, Patel DR, Gannon BM, Fitzgerald LR, Carbonaro TM, Johnson CR, Fantegrossi WE (2024) Phencyclidine-Like Abuse Liability and Psychosis-Like Neurocognitive Effects of Novel Arylcyclohexylamine Drugs of Abuse in Rodents — The Journal of Pharmacology and Experimental Therapeutics doi:10.1124/jpet.123.001942
  4. [4]
    ^Spain JW, Klingman GI (1985) Continuous intravenous infusion of phencyclidine in unrestrained rats results in the rapid induction of tolerance and physical dependence — Journal of Pharmacology and Experimental Therapeutics PMID:4040569
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