3-MeO-PCP

3-Methoxyphencyclidine

3-MeO

Psychoactive Class

Chemical Class

3-MeO-PCP is a dissociative hallucinogen of the arylcyclohexylamine class and a derivative of phencyclidine (PCP).¹² First synthesized in 1979 during an investigation of PCP derivatives, it emerged as a widely used novel psychoactive substance in the 2010s. Compared to other dissociatives, it is notably more physically stimulating and prone to producing hypomanic-type effects that, while potentially euphoric at lower doses, can become dangerous at higher amounts. It is considered habit-forming.

Dosage & Duration

Dosage

Threshold1-2 mg

Light2-5 mg

Moderate5-8 mg

Strong8-12 mg

Heavy12-15 mg

Strong and heavy doses can produce deliriant-like effects in which users may not recognize that their perceptions and thoughts are hallucinatory; psychosis-like symptoms and mania are reported in this range.

Duration

Onset30-90 minutes

Come Up45-120 minutes

Peak2-3 hours

Offset1-2 hours

After Effects4-48 hours

Total4-8 hours

Subjective Effects

Effects vary widely by individual, dose, and context.

Physical

Increased heart rate Tactile disconnection Spontaneous tactile sensations Tactile enhancement Tactile suppression Bodily control enhancement Motor control lossPhysical autonomy Physical euphoria Perception of decreased weight Dizziness Nausea

Visual

Forked from Subjective Effect Documentation work

by Josie KinsAugust 2016.

Reagent Testing

Loading reagent data

Expected colorimetric results are being prepared.

Pharmacology

Pharmacodynamics

3-MeO-PCP acts primarily as an NMDA receptor antagonist, binding to the dizocilpine (MK-801) site with a Ki of 20 nM.³ This represents higher NMDA receptor affinity than PCP and the highest among the three isomeric methoxy-substituted PCP analogs.⁴ Beyond NMDA receptor antagonism, 3-MeO-PCP shows appreciable affinity for the sigma-1 receptor (Ki = 42 nM) and the serotonin transporter (Ki = 216 nM)⁵, functioning as a serotonin reuptake inhibitor, with additional low-affinity binding at the histamine H1 receptor (Ki = 2,960 nM). Findings at secondary targets including the κ-opioid receptor, sigma-2 receptor, norepinephrine transporter, and dopamine transporter are conflicting between studies, with one reporting negligible binding (Ki >10,000 nM) and another reporting moderate affinities at these sites.

Pharmacokinetics

3-MeO-PCP has an estimated elimination half-life of 10 to 11 hours based on limited clinical case data.⁵ It undergoes hepatic metabolism through hydroxylation of the cyclohexyl and piperidine rings and O-demethylation, with these reactions primarily catalyzed by CYP2B6 and with contributions from CYP2C19 and CYP2D6.⁶ O-demethylation yields 3-HO-PCP (O-demethyl-3-MeO-PCP), which appears to be a major metabolite⁷ and is itself a similarly potent dissociative that may contribute to the overall effects. Phase II metabolism involves glucuronidation.⁶

Interactions

Dangerous

Highest risk

These combinations are considered extremely harmful and should always be avoided. Reactions to these drugs taken in combination are highly unpredictable and have a potential to cause death.

DepressantsStimulants

TripSit

Tolerance

Full Tolerance

Tolerance to the effects of 3-MeO-PCP develops rapidly with repeated use, often within a few days of consecutive dosing. At lighter doses, similar effects may persist for several days, particularly for non-dissociative effects such as stimulation, mood enhancement, and anxiolysis. However, the full dissociative effects associated with moderate to strong doses become progressively more difficult to achieve within just a few days of use. With substantial use patterns, such as daily dosing at low to moderate levels or weekly use of higher doses over weeks to months, some degree of tolerance may persist for weeks to months after complete cessation.

Baseline Reset

1-2 weeks under normal use patterns. However, following extended heavy use, residual tolerance may persist for weeks to months according to subjective reports.

Half Tolerance

3-7 days

Cross Tolerance

Dissociatives

Harm Potential

Addiction & Dependence

Psychological

High

High abuse potential with significant risk of psychological dependence, reported as more likely to produce dependence than other dissociatives.⁵ Compulsive redosing is a notable problem, particularly with intranasal and vaporized routes of administration due to faster onset and offset. Multiple reports document users becoming seriously dependent on this substance.

Physical

Low

Physical dependence can develop with chronic use. Cravings and withdrawal effects may occur upon sudden cessation.

Toxicity

Urinary System

Repeated and excessive use over extended periods may cause bladder and urinary tract problems similar to those seen with ketamine, though potentially to a lesser extent due to lower quantities needed for effect; symptoms can include urinary frequency, urgency, pelvic pain, hematuria, and incontinence.⁸

Cardiovascular

Acute cardiovascular effects include increased blood pressure and heart rate during intoxication,² reported as more pronounced than with other dissociatives; abnormal heartbeat has also been reported.¹

Central Nervous System

Frequent use or high doses may cause neurotoxicity, as reported for arylcyclohexylamine class dissociatives generally; acute effects include confusion, disorientation, and cognitive impairment.²⁸

Respiratory

Respiratory depression has been reported at heavier dosage levels.¹⁹

Psychosis Risk

Reported to cause psychosis, delusions, and mania at significantly higher rates than other dissociatives such as ketamine, MXE, or diphenidine.⁸ A large number of experience reports describe psychotic delirium, amnesia, mania, and other serious consequences. Episodes typically occur during the offset but can emerge during onset. Hospitalization is sometimes required, with resolution occasionally taking a week or more. Risk factors include high doses, multi-day use, compulsive redosing, sleep deprivation, and chronic daily use even at low doses over weeks or months.

Seizure Risk

The extent to which seizures can occur is unknown, but they may happen in predisposed individuals, particularly under physically taxing conditions such as dehydration, fatigue, or undernourishment.⁵

History & Culture

Synthesis and Early Research

3-MeO-PCP was first synthesized in 1979 by Geneste and colleagues during an investigation into phencyclidine derivatives.¹ This work followed earlier research by Maddox et al. in 1965, which had produced the related compounds 2-MeO-PCP and 4-MeO-PCP as part of an…

Trip Reports

Legality

International

1961 Single Convention: 3-MeO-PCP is not individually scheduled.

1971 Convention on Psychotropic Substances: 3-MeO-PCP is not individually scheduled.

1988 Convention: 3-MeO-PCP is not listed in precursor Tables I or II.

By Country

United StatesIllegalSchedule I

Federal Register final rule, 91 FR (March 23, 2026)²⁰

Current official national law expressly controls 3-MeO-PCP in United States; unauthorized possession, supply, or manufacture is prohibited.

AustriaIllegal (NPSG)Citation needed

Controlled under the Neue-Psychoaktive-Substanzen-Gesetz (New Psychoactive Substances Act). Possession, production, and sale are prohibited.

CanadaIllegalSchedule I controlled substance

Controlled Drugs and Substances Act, Schedule I arylcyclohexylamine provision¹⁴

Current official national law expressly controls 3-MeO-PCP in Canada; unauthorized possession, supply, or manufacture is prohibited.

Czech RepublicSchedule ICitation needed

Became a scheduled substance effective October 1, 2015 under Government Decree no. 243/2015 Coll.,¹⁵ which amended Government Regulation no. 463/2013 Coll.

GermanyIllegalAnlage II controlled substance

Betäubungsmittelgesetz, Anlage II¹⁶

Current official national law expressly controls 3-MeO-PCP in Germany; unauthorized possession, supply, or manufacture is prohibited.

NetherlandsSchedule I (Opiumwet)Citation needed

Listed as a Schedule I controlled substance under the Dutch Opium Act.¹⁸ Possession, production, and distribution are prohibited.

SwedenControlled substanceCitation needed

The Swedish public health agency recommended classification as a hazardous substance on November 10, 2014. On January 16, 2015, 3-MeO-PCP was officially declared a controlled substance.

TurkeyIllegalCitation needed

Classified as a controlled drug. Possession, production, supply, and importation are prohibited.

AustraliaProhibited (Schedule 9 analogue)Citation needed

Captured under broad drug analogue laws at both federal and state levels. As PCP is a Schedule 9 prohibited substance, 3-MeO-PCP is similarly prohibited as a structural analogue.¹²

BrazilControlled substanceCitation needed

Added to Portaria SVS/MS nº 344 on May 17, 2018.¹³ Possession, distribution, and use are prohibited.

ChileIllegalCitation needed

Controlled under Ley 20000 (Ley de drogas). As an ether of PCP, 3-MeO-PCP falls under the prohibition of all PCP esters and ethers specified in Chilean drug law.

DenmarkIllegalCitation needed

As of August 25, 2015, all MeO-PCP isomers including 3-MeO-PCP were added to the list of controlled substances.

ItalySchedule ICitation needed

Listed as a Schedule I controlled substance under Italian drug legislation.¹⁷ Possession, production, and distribution are prohibited.

PortugalUncontrolledCitation needed

Not specifically controlled as 3-MeO-PCP is neither a salt nor an isomer of PCP under Portuguese drug legislation. Standard decriminalization policies for personal drug use may apply.

SwitzerlandControlled (Verzeichnis E)Citation needed

Specifically named as a controlled substance under Verzeichnis E of Swiss narcotics legislation.

United KingdomIllegalClass B · Schedule 1

Misuse of Drugs Act 1971; Misuse of Drugs Regulations 2001¹⁹

Current official national law expressly controls 3-MeO-PCP in United Kingdom; unauthorized possession, supply, or manufacture is prohibited.

References

Source Pages

Citations

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3-MeO-PCP

3-Methoxyphencyclidine

3-MeO

Psychoactive Class

Dissociative Hallucinogen

Chemical Class

Arylcyclohexylamine