3-MeO-PCP
3-methoxyphencyclidine
Viewing r1 — Apr 25, 2026 — CURRENT
Back to HistoryInteractions, related substances, and reports reflect the current entry and are not shown for historical revisions.
3-MeO-PCP (3-methoxyphencyclidine) is a synthetic dissociative of the arylcyclohexylamine class. It is a methoxy-substituted derivative of phencyclidine (PCP), distinguished by exceptional potency at the NMDA.[1] 3-MeO-PCP is an NMDA receptor antagonist, producing its effects by blocking glutamate signaling at one of the brain's primary excitatory channels.
Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
PCP, ketamine, MXE +3 morePCP, ketamine, MXE, 3-HO-PCP, DXM, nitrous oxide show less
First synthesized in 1979 during a structure-activity study of PCP derivatives,[2] 3-MeO-PCP remained an obscure laboratory compound for three decades before appearing on grey-market research chemical platforms around 2010.[3] It is now internationally controlled under UN Schedule II[4] and US DEA Schedule I.[5]
Subjective effects include dissociation, stimulation, mania-like disinhibition, visual hallucinations, and cognitive disconnection. The experience is marked by an unusual stimulant edge and a steep dose-response curve — the distance between a stimulating dissociative state and a full psychotic episode is narrow and unpredictable.[6] Amnesia, agitation, grandiosity, and prolonged aftereffects lasting up to 48 hours are characteristic unsought effects.safety citation needed
Dependence potential is uncharacterized in formal research; multiple fatalities are documented, with nearly all involving polysubstance use.[7][4] The combination of psychosis-prone pharmacology, stimulant-like behavioral disinhibition, and amnesia creates a risk profile in which users may be unable to recognize or recall dangerous behavior during the experience.[8] No controlled human studies have been conducted — the evidence base consists entirely of forensic case reports, in vitro receptor data, and computational modeling.[9]
History[edit]
Discovery
Phencyclidine (PCP), the parent compound of the arylcyclohexylamine class, was first synthesized in 1956 as a candidate surgical anesthetic. 3-MeO-PCP was synthesized two decades later, in 1979, by Geneste and colleagues at the Université de Montpellier as part of a structure-activity study of PCP derivatives.[2] The compound attracted no further pharmacological investigation. The first reported human use surfaced in 1999 from a pseudonymous chemist who described effects qualitatively similar to PCP at comparable doses.[10]
Market emergence and characterization
3-MeO-PCP entered the grey-market research chemical supply around 2010, with broad internet availability by 2011.[3][11] Forensic laboratories first identified it in European samples in 2012,[7] and by mid-decade fatal and non-fatal intoxications had been reported across Sweden, Italy, France, the Netherlands, the United Kingdom, and the United States.[3][12][13][14] The only comprehensive receptor binding study was published in 2013 by Roth and colleagues through the NIMH Psychoactive Drug Screening Program, establishing 3-MeO-PCP's high NMDA affinity and correcting the misconception that it acts at opioid receptors.[1]
Prohibition
Scheduling followed the accumulation of forensic cases. The United Kingdom added arylcyclohexylamines to the Misuse of Drugs Act in 2013, with 3-MeO-PCP explicitly listed as Class B in 2016.[15] Germany and Sweden scheduled it in 2015.[15] The WHO Expert Committee on Drug Dependence recommended international control in 2020,[9] the UN Commission on Narcotic Drugs placed it on Schedule II in 2021,[4] and the US DEA finalized Schedule I placement in March 2026.[5]
The name "3-MeO-PCP" follows standard chemical shorthand: "3-MeO" indicates a methoxy group at the third position of the phenyl ring, and "PCP" denotes the phencyclidine backbone. Within online research chemical communities, the compound is sometimes referred to simply as "3-MeO." Its reputation is shaped by its association with PCP — a substance carrying deep cultural stigma — and by its pronounced tendency to produce manic and psychotic presentations, which distinguish it from the more sedating dissociatives like ketamine that dominate the class in popular awareness.
Chemistry[edit]
Structural class
3-MeO-PCP belongs to the arylcyclohexylamine family, defined by a cyclohexane ring bonded to both an aromatic ring and an amine group. The parent compound is phencyclidine (PCP). 3-MeO-PCP differs from PCP by the addition of a methoxy group (-OCH₃) at the meta (3-) position of the phenyl ring — a substitution that dramatically increases NMDA potency relative to both PCP and the positional isomers 2-MeO-PCP and 4-MeO-PCP.[10]
Related compounds in this class include ketamine, methoxetamine, 3-HO-PCP, and 3-MeO-PCE. The systematic exploration of methoxy-substituted PCP derivatives began with Maddox, Godefroi, and Parcell in 1965,[16] with Geneste et al. completing the 3-methoxy isomer in 1979.[2]
Molecular properties
| Molecular formula | C₁₈H₂₇NO |
| Molecular weight (free base) | 273.4 g/mol |
| Molecular weight (HCl salt) | 309.9 g/mol |
The core structure is a cyclohexane ring bearing both a piperidine nitrogen and a 3-methoxyphenyl group at C-1. The methoxy group at the meta position is the critical pharmacophoric element — its placement is what gives 3-MeO-PCP its distinctive potency within the PCP derivative series.[17]
Stereochemistry
The C-1 carbon of the cyclohexane ring is a stereogenic center, making 3-MeO-PCP a chirality molecule. No published data exist on the individual enantiomers or their differential activity. By analogy with PCP, which circulates as a racemic mixture, 3-MeO-PCP is presumed to be encountered in racemic form.citation needed
Physical properties
The hydrochloride salt is a white crystalline solid with a melting point of 204–205 °C.[18] It is soluble in ethanol (~20 mg/mL), DMSO (~11 mg/mL), and phosphate-buffered saline (~10 mg/mL). No published characterization of the free base form exists.
Pharmacology[edit]
Mechanism of action
3-MeO-PCP blocks NMDA receptors — one of the brain's primary excitatory ion channels — by binding at the same site as PCP and dizocilpine (MK-801).[1][9] It binds with exceptional strength, ranking among the most potent NMDA antagonists characterized and exceeding PCP itself.[1] This blockade disrupts glutamate signaling, producing the dissociative, anesthetic, and psychosis-like effects that define the pharmacological class.
Secondary targets include the sigma-1 receptor, where 3-MeO-PCP acts as an agonist with high affinity — potentially contributing to its stimulant-like and psychotomimetic properties — and the SERT, where moderate inhibition introduces serotonergic activity relevant to both subjective effects and drug interaction risk.[1]
3-MeO-PCP shows no meaningful binding at opioid receptors, dopamine transporters, or dopamine receptors, correcting a persistent misclassification in secondary literature.[1] NMDA receptor inhibition has been independently confirmed using a high-throughput immunocytochemical assay.[19]
Pharmacokinetics
No human pharmacokinetic studies have been published for 3-MeO-PCP. Available data come entirely from computational modeling and laboratory experiments.
Computational models predict high oral absorption, ready passage into the brain, and extensive distribution into body tissues.[20] The compound is metabolized primarily in the liver, where enzymes remove the methoxy group and modify the ring structures.[21] Several of the enzymes responsible — CYP2D6 and CYP2C19 — vary significantly between individuals due to genetic differences, meaning some people may clear the drug much more slowly than others.[21]
No human half-life has been published. The parent compound PCP has a half-life of 7–46 hours depending on conditions; 3-MeO-PCP's elimination rate is unknown. Excretion is predicted to be primarily through the kidneys.[20]
Standard drug immunoassays do not reliably detect 3-MeO-PCP — laboratory confirmation requires specialized mass spectrometry techniques.[22]
Neuroscience[edit]
Where it acts
NMDA blockade disrupts glutamate signaling across cortical and subcortical brain regions, fragmenting the thalamocortical circuits that normally bind sensory input to higher-order processing. The result is the phenomenological disconnection characteristic of dissociatives — a sense of detachment from body, environment, and self.
In prefrontal cortex, the blockade preferentially silences inhibitory interneurons, paradoxically increasing excitatory activity and downstream dopamine release — a mechanism that accounts for both the psychosis-like symptoms and the stimulant quality that distinguish 3-MeO-PCP from more sedating dissociatives like ketamine.[1]
Why it matters
3-MeO-PCP's potent NMDA antagonism makes it directly relevant to the glutamate hypothesis of psychosis, which proposes that NMDA receptor dysfunction underlies both the hallucinations and the cognitive flattening seen in schizophrenia. The observation that 3-MeO-PCP can trigger persistent psychotic symptoms even after the drug has cleared[8] supports the idea that sustained NMDA disruption may cause lasting changes in brain circuit function — not merely transient chemical effects.
A single case of brain imaging during 3-MeO-PCP-induced psychosis has been published,[8] but no systematic neuroimaging, EEG, or electrophysiological studies exist.
Whether 3-MeO-PCP's individual mirror-image forms (enantiomers) differ in brain activity is unknown — PCP's do, and the same may hold here. Whether it promotes the rapid formation of new neural connections, as Ketamine does via different downstream pathways, has not been investigated.
Subjective Effects[edit]
The 3-MeO-PCP experience is defined by an unusual pairing of dissociation and stimulation — where most dissociatives produce sedation and withdrawal at deeper levels, 3-MeO-PCP maintains a driven, energized quality that can tip into mania-like grandiosity and frank psychosis as dose increases. The margin between a stimulating dissociative state and a psychiatric emergency is narrow, and set, setting, and dose precision exert outsized influence on the outcome.
Compared to ketamine, 3-MeO-PCP produces markedly less sedation and a far more psychosis-prone profile at equivalent dissociative depth. Compared to PCP, the effects are qualitatively similar — the same stimulant edge, the same psychotomimetic potential — but achieved at lower doses owing to 3-MeO-PCP's greater receptor potency.[1]
Effect Grid
At common oral doses (~4–8 mg), the full dissociative experience develops: pronounced derealization and depersonalization, cognitive disconnection from the body, and a distinctive manic or euphoric quality. Thought acceleration and grandiosity emerge. Mild visual distortions — drifting, brightening of colors — may occur, though visual effects are less prominent than with serotonergic psychedelics.
Physically, tachycardia and hypertension become clinically relevant. Psychomotor stimulation and disinhibition may impair judgment. Amnesia for portions of the experience is common at the upper end of this range.
The experience commits the user for 4–8 hours, with aftereffects potentially lasting 24–48 hours. Sleep is unlikely during peak effects.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Touch enhancement · Spatial disorientation · Visual haze / noise · Touch suppression · Music enhancement · Visual acuity enhancement · Perspective distortion · Dreaming enhancement · Internal hallucinations · External hallucinations · Auditory hallucinations · Visual processing suppression · Olfactory hallucination · Visual scenery slicing
Music enhancement · Visual acuity enhancement · Perspective distortion · Dreaming enhancement · Internal hallucinations · External hallucinations · Auditory hallucinations · Visual processing suppression · Olfactory hallucination · Visual scenery slicing
Tactile euphoria · Pain suppression · Appetite suppression · Restlessness · Excessive sweating · Dehydration sensation · Dizziness · Sexual arousal enhancement · Nausea suppression · Increased urination · Nausea · Motor control enhancement · Seizure threshold reduction
Restlessness · Excessive sweating · Dehydration sensation · Dizziness · Sexual arousal enhancement · Nausea suppression · Increased urination · Nausea · Motor control enhancement
Immersion enhancement · Thought deceleration · Thought acceleration · Creativity enhancement · Pattern recognition suppression · Conceptual thinking · Delusions
Creativity enhancement · Pattern recognition suppression · Conceptual thinking
Timeline
First alerts emerge 20-45 minutes after oral ingestion: subtle mood shift, mild cognitive brightening, faint stimulation. Effects are easily overlooked at lower doses.
Dissociative effects build over 30–60 minutes. Derealization and emerging cognitive disconnection become apparent. Stimulant-like qualities — increased confidence, mild disinhibition — intensify.
Maximum dissociation sustained for 30m-1 hour. Full depersonalization, cognitive euphoria or mania-like disinhibition, and psychotomimetic features at higher doses. Cardiovascular stress peaks: tachycardia, hypertension.
Effects plateau and begin gradual decline over 2-3 hours. Dissociation persists at reduced intensity. Cognitive impairment and disinhibition may remain significant.
Gradual return toward baseline over 1–2 hours. Residual cognitive fog, emotional blunting, and mild stimulation persist. Judgment remains impaired.
Residual effects persist for 4–48 hours: mood changes, cognitive fog, disrupted sleep architecture, and subtle perceptual shifts. The wide aftereffect window is characteristic of 3-MeO-PCP.
⚠ Do not drive or operate machinery until at least 48 hours after ingestion and a full night of normal sleep, as residual cognitive impairment may persist well beyond subjective baseline.
Safety[edit]
- Acute toxicity
- High
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- moderate
- Tolerance reset
- 10 days
- Physical
- Low
- Psychological
- Moderate
- Compulsive redosing
- Moderate
- Dose escalation
- Moderate
- Cross-tol.
- PCP · ketamine · MXE
Toxicity
Acute toxicity
The toxic dose of 3-MeO-PCP in humans is unknown. The WHO explicitly states that toxic dosage is not well characterized.[9]
Multiple fatalities are documented, with postmortem blood levels spanning a wide range (approximately 50–3,525 ng/mL).[7] Nearly all fatal cases involved other substances; a 2022 review of 16 published deaths concluded that blood levels associated with toxicity "remain unclear".[4] One published fatality has been attributed to 3-MeO-PCP alone, without co-substances.[6]
In overdose, consistent features include deep coma, agitation and delirium during recovery, respiratory depression, low body temperature, dilated pupils, hallucinations, and behavioral disinhibition.[12][6][23]
Cardiovascular toxicity
High blood pressure and rapid heart rate are consistent features of intoxication.[9] Computational modeling predicts risk of heart rhythm disruption (QT prolongation).[24] Physical exertion during intoxication — including dancing or vigorous activity — may worsen cardiovascular strain through additive effects on heart rate, body temperature, and blood pressure.[4]
Organ toxicity
Computational modeling predicts that lungs, liver, and blood are the primary organ targets.[24] No human autopsy data specifically characterize organ damage from 3-MeO-PCP.
Psychological risks
3-MeO-PCP carries substantial psychiatric risk. Persistent psychosis after cessation has been documented: one case described a 29-year-old who developed lasting psychotic symptoms with cognitive impairment after repeated use over two weeks.[8] Psychotic symptoms including paranoia, delusions, and hallucinations appear across multiple case reports.[6][8]
Mania-like presentations — grandiosity, agitation, pressured behavior, and disinhibition — occur at moderate-to-high doses.[6][8] Amnesia during the experience is reported,[6] impairing the ability to self-assess dose and recognize dangerous behavior.
The combination of psychosis-like effects, stimulant-driven disinhibition, and amnesia produces a behavioral risk profile distinct from ketamine, which more typically produces sedation and withdrawal at equivalent dissociative depth.
Tolerance and dependence
No animal or human studies on tolerance or dependence have been published.[9] The WHO explicitly states that no studies on dependence potential exist for this compound.[9]
Tolerance figures circulating in harm reduction resources — including a "5-day half-life" and "1.5-week full reset" — derive from user reports and inference from PCP/ketamine pharmacology, not primary research.safety citation needed
Dependence liability is inferred by analogy from PCP, which has documented dependence potential. Regulatory scheduling (DEA Schedule I;[5] UN Schedule II[9]) reflects high assessed abuse potential, but direct experimental evidence is absent.
Drug interactions
CNS depressant combinations
Alcohol appears in multiple fatal and non-fatal cases, with combined sedation and breathing suppression as the primary harm mechanism.[12][14]
Opioids present extreme risk: one documented fatality involved combined 3-MeO-PCP and an opioid metabolite (O-desmethyltramadol), with additive breathing suppression as the probable cause.[25]
Benzodiazepines appeared in one fatal polysubstance case.[13] While benzodiazepines are used medically to manage 3-MeO-PCP agitation, unsupervised combination carries breathing-suppression risk.
Serotonergic interactions
3-MeO-PCP's SERT inhibition creates a theoretical risk of serotonin syndrome when combined with SSRIs, SNRIs, MAOIs, or serotonergic psychedelics. No published cases document this outcome, but the mechanism is pharmacologically plausible.[1]
Metabolic interactions
3-MeO-PCP is broken down by liver enzymes (CYP2D6, CYP2C19, CYP2B6, CYP3A4).[21][20] Drugs that strongly inhibit these enzymes — including paroxetine, fluoxetine, bupropion, omeprazole, and fluvoxamine — may slow metabolism and raise blood levels. Paroxetine and bupropion were co-present in one fatal polysubstance case.[13]
Stimulant combinations
Multiple fatal cases involved amphetamine co-use.[14][11] The combination increases cardiovascular strain, psychosis risk, and overheating risk.
Contraindications
No formal contraindication studies exist. The following are inferred from pharmacology and clinical reports.
Heart conditions: High blood pressure and rapid heart rate are consistent features of intoxication,[9] and computational modeling predicts heart rhythm disruption risk.[24] Pre-existing cardiovascular disease, high blood pressure, irregular heart rhythms, or long QT syndrome are absolute contraindications.
Psychotic disorders and bipolar disorder: 3-MeO-PCP reliably produces psychosis-like effects and has triggered lasting substance-induced psychotic disorder.[8] Personal or family history of psychotic spectrum disorders or bipolar disorder is an absolute contraindication.
Liver impairment: Liver metabolism is the primary elimination pathway.[21] Impaired liver function may produce elevated and prolonged blood concentrations.
Pregnancy: No reproductive toxicity data exist. By analogy with PCP and other NMDA antagonists, which cause developmental brain damage in animal models, pregnancy is an absolute contraindication.safety citation needed
Harm Reduction[edit]
Forms & Identification
3-MeO-PCP is most commonly encountered as a white crystalline powder (hydrochloride salt) and is visually indistinguishable from many other research chemical dissociatives. The critical testing concern is distinguishing it from more potent or differently acting compounds — mislabeled products have been documented in the research chemical market. Quantitative testing through drug-checking services is the most reliable way to confirm identity and purity, since standard reagent panels have limited utility for differentiating arylcyclohexylamines from one another.
Because 3-MeO-PCP is active at very low doses, even small errors in substance identification or purity estimation can dramatically shift the effective dose and risk profile.
Guidelines
- Weigh doses with a milligram-precision scale — volumetric dosing errors with a compound this potent can be medically dangerous
- Start with a threshold dose and wait the full onset period before considering redosing — oral onset can be slow and the temptation to redose prematurely is a documented cause of overdose
- Have a sober, trusted sitter present who understands the compound's tendency toward mania and behavioral disinhibition
- Remove access to vehicles, keys, sharp objects, and anything that could facilitate harm during a disinhibited state
- Use in a private, calm environment — avoid public spaces, crowds, and settings involving physical exertion
- Prepare water and comfortable surroundings in advance; do not plan to leave the setting during the experience
- Set a hard rule against redosing — amnesia during the experience can make it impossible to remember what has already been taken
Set & Setting
The psychological and physical environment matters more for 3-MeO-PCP than for many other dissociatives. The compound's stimulant quality and tendency toward mania-like disinhibition mean that chaotic or public settings increase the risk of dangerous behavior. A calm, private, familiar environment with a sober sitter is strongly advisable.
Mental state at the time of use is equally important: anxiety, agitation, or pre-existing psychological distress may be amplified into paranoia or psychotic symptoms. The extended aftereffect window — potentially lasting up to 48 hours — means that responsibilities and obligations for the following day should be cleared.
Aftercare & integration. The aftereffect window following 3-MeO-PCP can persist up to 48 hours, during which cognitive function, emotional regulation, and sleep may remain disrupted. Rest, hydration, and light nutrition support physical recovery.
Dissociative experiences — particularly those involving mania, grandiosity, or psychotic features — may require active psychological processing. If the experience included frightening or confusing episodes, talking through them with a trusted person can help reintegrate the experience. Persistent symptoms beyond 72 hours — especially paranoia, hallucinations, or thought disorganization — warrant professional evaluation, as substance-induced psychotic disorder has been documented with this compound.[8]
Avoid using other substances during the aftereffect period, as altered brain chemistry may amplify interactions or adverse effects.
Recovery & Support
Compulsive use patterns with dissociatives can develop insidiously, particularly with compounds that produce stimulant-like effects and grandiosity. If use has become regular, escalating, or difficult to control, professional support is warranted.
Harm reduction services and addiction support organizations can provide confidential assessment and referral. For those experiencing persistent psychological effects after 3-MeO-PCP use — including lasting psychosis, cognitive impairment, or depersonalization — psychiatric evaluation is recommended rather than waiting for symptoms to resolve on their own.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Unresponsiveness or inability to be roused, seizure activity, extremely slow or irregular breathing, severe agitation with self-harm risk, rigid or overheated body, or psychotic behavior (paranoid delusions, complete detachment from reality) all require immediate medical help.
Immediate steps:
- Call emergency services immediately if the person is unresponsive, seizing, or breathing abnormally
- Place an unconscious but breathing person in the recovery position (on their side, airway clear)
- Do not restrain an agitated person unless there is immediate risk of self-harm or harm to others — restraint can escalate agitation
- Do not induce vomiting
- Stay with the person and monitor breathing continuously
What to tell the dispatcher: Name the substance (3-MeO-PCP, a dissociative), the approximate amount and time taken, the route of administration, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
No substance-specific antidote exists. Hospital treatment is supportive: airway management, benzodiazepines for agitation,[6] antipsychotics for persistent psychosis,[8] and continuous heart monitoring.[24] Standard drug tests will not detect 3-MeO-PCP — inform medical staff of the specific substance.[22]
Legal Status[edit]
As of April 2025, 3-MeO-PCP is internationally controlled under Schedule II of the 1971 Convention on Psychotropic Substances, following a 2021 decision by the UN Commission on Narcotic Drugs based on the WHO Expert Committee on Drug Dependence's 2020 recommendation.[4][9] In the United States, 3-MeO-PCP was placed in Schedule I of the Controlled Substances Act by DEA final rule in March 2026.[5]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| International (UN) | Schedule II, 1971 Convention on Psychotropic Substances | Placed April 2021 by UN Commission on Narcotic Drugs[4] |
| United States | Schedule I, Controlled Substances Act | DEA proposed June 2025; final rule March 2026[5] |
| United Kingdom | Class B (Misuse of Drugs Act) | Generic arylcyclohexylamine clause February 2013; explicitly listed May 2016[15] |
| Germany | Annex II (controlled narcotic) | Added May 2015[15] |
| Sweden | Controlled substance | Declared January 2015[15] |
| Czech Republic | Scheduled | Government Decree 243/2015, October 2015[15] |
| Canada | Schedule I (analogue provision) | Controlled under PCP analogue provisions of the Controlled Drugs and Substances Act[10] |
| Australia | Unconfirmed | Specific scheduling not verified in available literaturecitation needed |
references
- [1]
- [2]
- [3] ^abcJohansson A, Lindstedt D, Roman M, Thelander G, Nielsen EI, Lennborn U, Sandler H, Rubertsson S, Ahlner J, Kronstrand R, Kugelberg FC (2017) A non-fatal intoxication and seven deaths involving the dissociative drug 3-MeO-PCP — Forensic Science International doi:10.1016/j.forsciint.2017.02.034
- [4]
- [5]
- [6]