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PCE Facts

Dissociative; Arylcyclohexylamine; NMDA receptor antagonist

Description

PCE (eticyclidine) is a synthetic dissociative of the arylcyclohexylamine class. It blocks glutamate signaling in the brain,[1][2] producing deep dissociation from body and environment.

Subjective effects include bodily dissociation, cognitive disconnection, amnesia, perceptual distortion, and emotional numbness. The experience is heavier and more sedating than PCP — lower doses bring detached numbness, higher doses push toward complete mental disconnection and memory loss.

PCE carries high abuse liability — both physical and psychological — and no lethal dose has been established in any species.safety citation needed The substance clears the body slowly, sustaining prolonged glutamate blockade; compulsive redosing prolongs this further and sharply raises the risk of psychosis.[3]

Dose and durationby route · individual sensitivity varies

Oral(mg)
Threshold< 1 mgLight3 – 5 mgCommon5 – 10 mgStrong10 – 15 mgHeavynot recorded

Starts in 30 – 90 minLasts 4 – 8 hoursAfter-effects 4 – 48 hours

Body and dependence

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

Tolerance

Builds
Moderate
Fully resets after
10.5 days
Carries over to
dissociatives

Effectslikely at a common dose

Perception
Spatial disorientation; +19 possible, including Vestibular distortion, Visual acuity suppression, Visual haze / noise
Body
Motor control impairment; Nystagmus (eye wobbles); Pain suppression; +29 possible, including Dizziness, Heart rate perception changes, Insomnia
Thinking
Cognitive impairment; +20 possible, including Confusion, Decision impairment, Information processing suppression
Feeling
none likely · 8 possible, including Anxiety, Dysphoria, Emotional lability
Self
none likely · 9 possible, including Depersonalization, Derealization, Communication suppression
Time
none likely · 4 possible, including Temporal disorientation

Who shouldn't take it

Absolute
History of psychotic disorders; Concurrent MAOI use
Relative
Cardiovascular disease; Seizure disorders; Hepatic impairment; Renal impairment; Pregnancy; History of rhabdomyolysis

Combinations61 recorded

Lethal (2)
GHB, GBL; Ibogaine
Dangerous (36)
Amphetamines; Benzodiazepines; Buprenorphine, Kratom; Ephedrine, Pseudoephedrine; MDMA, Amphetamines; Naltrexone; NDRIs (Wellbutrin); NRIs; NSAIDs; Opioids; THC; Anticholinergics; Antihistamines; Atypical antipsychotics; Benzodiazepines, Barbiturates; Buspirone; Caffeine; Clonidine, Guanfacine; Dopamine agonists; DXM; Gabapentin, Pregabalin; GHB, Baclofen; Ketamine, DXM, PCP; Lithium; and 12 more, see full page
Caution (20)
See full page: psychedex.org/substances/pce
Not graded (3)
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]
    ^Maragos WF, Penney JB, Young AB (1988) Anatomic correlation of NMDA and 3H-TCP-labeled receptors in rat brain — Journal of Neuroscience doi:10.1523/jneurosci.08-02-00493.1988
  2. [2]
    ^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
  3. [3]
    ^Chakrabarti S, Law FC (1983) The dispositional kinetics of phencyclidine and its N-ethylamine analogue in rats. — European Journal of Drug Metabolism and Pharmacokinetics PMID:6673975
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