3-MeO-PCMo
3-methoxyphencyclomorpholine
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3-MeO-PCMo (4-[1-(3-methoxyphenyl)cyclohexyl]morpholine) is an emerging synthetic dissociative of the arylcyclohexylamine class. It is a morpholine-ring variant of 3-MeO-PCP, with weaker potency and shorter duration. 3-MeO-PCMo is an NMDA receptor antagonist, producing its effects by blocking glutamate-driven excitatory signaling in the brain.[1]
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ketamine, PCP, 3-MeO-PCP +2 moreketamine, PCP, 3-MeO-PCP, dextromethorphan, methoxetamine show less
3-MeO-PCMo first surfaced on research chemical markets in 2015, when the Netherlands notified the European Monitoring Centre for Drugs and Drug Addiction of its detection.[2] A single pharmacological study confirmed its NMDA activity and placed it within a potency series of related analogues.[1] It remains unscheduled in most jurisdictions and circulates in small quantities among research chemical users.
Subjective effects include depersonalization, derealization, cognitive disconnection, pain suppression, and amnesia. The experience is characterized by a warm, motionless body sensation with gradual cognitive detachment — slower-building and softer than most dissociatives at common doses.[2] Mania, compulsive redosing urge, and delusions of sobriety are characteristic unsought effects.
3-MeO-PCMo is rated as moderately addictive with moderate dependence potential.[2] The primary acute risk is respiratory depression when combined with CNS depressants — every documented fatality involving the closely related 3-MeO-PCP involved co-ingestion of alcohol or other depressants.[3][4] One pharmacological paper constitutes the entire published evidence base; no human toxicity, pharmacokinetic, or clinical data exist.[5]
History[edit]
History
Discovery
3-MeO-PCMo emerged on online research chemical markets in the mid-2010s as part of a wave of novel arylcyclohexylamine derivatives designed around the phencyclidine scaffold. It has no pharmaceutical origin, patent history, or clinical development program. The European Monitoring Centre for Drugs and Drug Addiction received formal notification of its detection from the Netherlands on August 7, 2015 — the earliest documented record of the compound on the drug market.[2]
Scientific characterization
The sole published study of 3-MeO-PCMo is Colestock et al. (2018), which synthesized the compound alongside five structural analogues, verified their identities by NMR and mass spectrometry, and screened all six across 46 CNS receptor targets.[1] This work established NMDA antagonism as 3-MeO-PCMo's primary pharmacological activity and produced the only published binding data for the compound. No further pharmacological, toxicological, or clinical research specific to 3-MeO-PCMo has appeared.[5]
Present status
3-MeO-PCMo remains in an early characterization state with no registered clinical trials and no published case reports of human intoxication. Its parent analogue 3-MeO-PCP, which had appeared on illicit markets around 2011,[3] was placed in US Schedule I effective April 2026[6] — increasing the likelihood of analogue-based prosecution for 3-MeO-PCMo in the United States.
Chemistry[edit]
Chemistry
Structural class
3-MeO-PCMo belongs to the arylcyclohexylamine family — compounds defined by an aryl ring bonded to a cyclohexane ring bearing an amine group. The class includes phencyclidine (PCP), ketamine, and methoxetamine (MXE).[1]
3-MeO-PCMo shares the 3-methoxyphenyl-cyclohexyl core of 3-MeO-PCP but replaces the piperidine ring with a morpholine ring, introducing an oxygen atom into the six-membered heterocycle. This oxygen substitution changes the compound's fat solubility, hydrogen-bonding behavior, and metabolic profile relative to the piperidine parent.
Molecular properties
| Molecular formula | C₁₇H₂₅NO₂ |
| Molecular weight | 275.4 g/mol |
The structure comprises three linked systems: a 3-methoxyphenyl aromatic ring, a cyclohexane ring, and a morpholine heterocycle. The methoxy group at the meta position of the phenyl ring is the key pharmacophoric element — its position drives the potency differences observed across the PCMo isomer series.[1]
Stereochemistry
3-MeO-PCMo is achiral — it has no asymmetric carbon centers and exists as a single stereoisomer.[2] This contrasts with Ketamine, which has a chirality center and exhibits stereoselective pharmacology.
Analytical distinction
Positional isomers within the PCMo series (2-MeO, 3-MeO, 4-MeO) share identical molecular formulae and similar fragmentation patterns, requiring careful chromatographic and spectroscopic methods to distinguish.[1] This complicates forensic identification and makes independent verification important for anyone handling material from unregulated sources.
Pharmacology[edit]
Pharmacology
Mechanism of action
3-MeO-PCMo is a non-competitive NMDA receptor antagonist. It binds to the phencyclidine (PCP) site inside the NMDA channel, blocking the flow of calcium and sodium ions that normally drive excitatory signaling.[1] This blockade is use-dependent — the channel must first be opened by glutamate before the compound can enter and occlude it.
Colestock et al. (2018) screened 3-MeO-PCMo across 46 CNS receptor targets and confirmed NMDA receptor antagonism as the primary activity.[1] The compound binds roughly 12 times more weakly than PCP and at comparable strength to ketamine at the same site.[1] Among the PCMo structural analog series, 3-MeO-PCMo falls in the middle of the potency rank order — stronger than the unsubstituted parent compound (PCMo) but weaker than the methyl analogue (3-Me-PCMo).[1]
Sigma receptor involvement is plausible but unconfirmed for 3-MeO-PCMo specifically. The closely related 3-MeO-PCP binds sigma receptors with high affinity,[7] and the structurally related methoxydine acts as a sigma receptor agonist.[8] Whether 3-MeO-PCMo shares this property has not been tested in a published binding study. inferred
NMDA receptor blockade in the prefrontal cortex also disinhibits dopamine release deeper in the brain — a mechanism shared across PCP-type compounds that contributes to their stimulating, mood-elevating, and potentially reinforcing qualities.[9]
Pharmacokinetics
No human pharmacokinetic data exist for 3-MeO-PCMo. Absorption rate, blood levels, half-life, and protein binding are all uncharacterized.
Metabolic pathways are inferred from 3-MeO-PCP, which shares the same core scaffold. Studies of 3-MeO-PCP metabolism found multiple breakdown routes: hydroxylation of the cyclohexyl and heterocyclic rings, removal of the methoxy group (O-demethylation), and glucuronide conjugation of the resulting metabolites.[10]
The liver enzymes responsible for 3-MeO-PCP metabolism are genetically variable across individuals, meaning some people metabolize the compound much faster or slower than others.[10] The morpholine ring in 3-MeO-PCMo would be expected to undergo similar breakdown reactions, though the specific enzymes involved have not been identified. inferred
The notably slow oral onset (1–2 hours) relative to oral Ketamine (roughly 20–30 minutes) may reflect slower absorption, greater first-pass metabolism, or slower distribution into the brain — the contributing factors have not been investigated.[2]
Neuroscience[edit]
Neuroscience
No neuroimaging or electrophysiological studies have been conducted with 3-MeO-PCMo. The following is inferred from its confirmed NMDA antagonism[1] and from established neuroscience of PCP-type dissociatives.
Where it acts
NMDA receptor blockade disrupts communication between cortical and subcortical brain regions — particularly the thalamus-to-cortex pathway that normally integrates sensory input with higher-order processing.[9] This disconnection is the proposed neural basis for depersonalization, derealization, and the sensation of being detached from one's own body and thoughts.
Simultaneously, blockade of NMDA receptors on inhibitory interneurons in the prefrontal cortex releases a brake on dopamine signaling, producing the stimulant and euphoric qualities characteristic of the PCP structural analog class.[9]
Why it matters
NMDA receptors are central to the brain's predictive processing — the continuous cycle of generating expectations about incoming sensory data and updating them against reality. Blocking these receptors disrupts the prediction machinery, producing the characteristic sense that the world has become unfamiliar, unreal, or fundamentally altered.
In the ketamine model, acute NMDA blockade triggers a compensatory surge of glutamate that activates alternative receptors and drives rapid formation of new synaptic connections — a neuroplasticity mechanism proposed to underlie ketamine's antidepressant effects. Whether 3-MeO-PCMo produces equivalent neuroplastic changes has not been investigated.
Key unknowns include whether the morpholine ring substitution alters brain connectivity differently from the piperidine parent (3-MeO-PCP), whether 3-MeO-PCMo produces ketamine-like neuroplasticity at any dose range, and what accounts for its substantially longer onset compared to oral ketamine — absorption kinetics, first-pass metabolism, or slower distribution into the brain.
Subjective Effects[edit]
The 3-MeO-PCMo experience unfolds gradually, with a creeping onset over one to two hours that distinguishes it from faster-acting dissociatives. Users describe a warm, motionless body sensation paired with progressive cognitive and sensory disconnection.[2] Set and setting substantially shape the emotional character — the same dose may produce serene detachment in quiet surroundings or disorienting confusion in a stimulating environment.
Within the arylcyclohexylamine class, 3-MeO-PCMo occupies a middle ground: less potent than 3-MeO-PCP and softer in character at common doses, with an experiential profile closer to oral ketamine but stretched across a slower timeline and without the same tendency toward deep dissociative immersion.
Effect Grid
At 200–300 mg oral, a full dissociative state develops. Depersonalization and derealization are clearly present — the body feels distant, the environment surreal. Cognitive disconnection is prominent: thought deceleration, analysis suppression, and impaired memory formation define the cognitive landscape. Music enhancement is often reported.
A warm, motionless body sensation with tactile euphoria is characteristic of this tier. Motor control impairment is moderate — walking is possible but unsteady. Touch suppression is noticeable. Spontaneous body sensations and bodily lightness contribute to the floating quality.
Time alteration distorts subjective duration. Euphoria and anxiety suppression are common. Immersion enhancement deepens engagement with music or visual media. Functional impairment is significant — plan for 6+ hours of commitment.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Vestibular distortion · Visual haze / noise · Touch suppression · Visual acuity suppression · Auditory distortion · Brightness alteration · Ganzfeld effect · Sensory deprivation · Sleep-transition hallucinations · Tracers · Visual drifting · Music enhancement · Dreaming enhancement · Auditory misinterpretation · Auditory suppression · Color alteration · Color suppression · Peripheral vision distortion · Tinnitus · Holotropic state · After-images · Auditory enhancement · Peripheral misidentification · Taste suppression · Visual morphing · Visual processing suppression · Internal hallucinations · Auditory hallucinations · External hallucinations · Perspective hallucinations
Auditory distortion · Brightness alteration · Ganzfeld effect · Sensory deprivation · Sleep-transition hallucinations · Tracers · Visual drifting · Music enhancement · Dreaming enhancement · Auditory misinterpretation · Auditory suppression · Color alteration · Color suppression · Peripheral vision distortion · Tinnitus · Holotropic state · After-images · Auditory enhancement · Peripheral misidentification · Taste suppression · Visual morphing · Visual processing suppression · Internal hallucinations · Auditory hallucinations · External hallucinations · Perspective hallucinations
Dizziness · Body high · Body schema distortion · Physical fatigue · Bodily lightness · Dry mouth · Appetite suppression · Insomnia · Restlessness · Wakefulness · Spontaneous body sensations · Bodily pressures · Headache · Heart rate perception changes · Involuntary body movements · Laughter fits · Muscle relaxation · Pupil dilation · Sedation · Tingling / electric sensations · Nausea · Tactile euphoria · Dehydration sensation · Breathing alteration · Bruxism · Excessive sweating · Muscle tension · Sexual arousal enhancement · Trembling · Vasoconstriction · Vibrations / buzzing · Yawning · Vomiting · Bodily dissociation · Tactile hallucination
Physical fatigue · Bodily lightness · Dry mouth · Appetite suppression · Insomnia · Restlessness · Wakefulness · Spontaneous body sensations · Bodily pressures · Headache · Heart rate perception changes · Involuntary body movements · Laughter fits · Muscle relaxation · Pupil dilation · Sedation · Tingling / electric sensations · Nausea · Tactile euphoria · Dehydration sensation · Breathing alteration · Bruxism · Excessive sweating · Muscle tension · Sexual arousal enhancement · Trembling · Vibrations / buzzing · Yawning · Vomiting · Bodily dissociation · Tactile hallucination
Cognitive euphoria · Confusion · Focus suppression · Information processing suppression · Memory fragmentation · Thought disorganization · Pattern recognition suppression · Introspection enhancement · Cognitive fatigue · Thought loops · Immersion enhancement · Thought deceleration · Conceptual thinking · Aesthetic enhancement · Cognitive flexibility · Delusions of sobriety · Language suppression · Multiple thought streams · Novelty enhancement · Openness enhancement · Suggestibility enhancement · Thought acceleration · Humor enhancement · Creativity enhancement · Cognitive dysphoria · Memory replays · Thought connectivity · Motivation enhancement · Amnesia · Delusions · Delirium
Information processing suppression · Memory fragmentation · Thought disorganization · Pattern recognition suppression · Introspection enhancement · Cognitive fatigue · Thought loops · Immersion enhancement · Thought deceleration · Conceptual thinking · Aesthetic enhancement · Cognitive flexibility · Language suppression · Multiple thought streams · Novelty enhancement · Openness enhancement · Suggestibility enhancement · Thought acceleration · Humor enhancement · Creativity enhancement · Cognitive dysphoria · Memory replays · Thought connectivity · Motivation enhancement · Amnesia · Delusions · Delirium
Emotional lability · Emotional suppression · Empathy suppression · Irritability · Anhedonia · Catharsis · Depression · Dysphoria · Emotional enhancement · Simultaneous emotions
Irritability · Anhedonia · Catharsis · Dysphoria · Emotional enhancement · Simultaneous emotions
Social disconnection · Disinhibition · Communication suppression · Automaticity · Craving · Sociability suppression · Sociability enhancement · Emotional susceptibility · Flow state · Cognitive disconnection · Identity alteration · Boundary dissolution · Ego dissolution
Craving · Sociability suppression · Sociability enhancement · Emotional susceptibility · Flow state · Cognitive disconnection · Identity alteration · Boundary dissolution · Ego dissolution
Time cessation
Near-death experience · Non-dual awareness · Transpersonal feelings
Timeline
Gradual, creeping emergence over 1–2 hours. Subtle bodily warmth and mild cognitive softening are the first signals. Effects may be imperceptible for the first 30–60 minutes.
Full dissociative plateau lasting 2–3 hours. Maximum depersonalization, cognitive disconnection, body warmth, and tactile euphoria. Euphoria and anxiety suppression most prominent here.
Gradual return of sensory integration over 1–2 hours. Residual cognitive fog and mild motor coordination impairment. Spatial awareness begins to normalize.
Mild residual cognitive effects lasting 2–3 hours. Possible dreaming enhancement if sleep follows. Generally non-impairing but cognitive sharpness not fully restored.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Low
- Withdrawal
- Mild
- Tolerance buildup
- moderate
- Tolerance reset
- 10.5 days
- Physical
- Moderate
- Psychological
- Moderate
- Compulsive redosing
- Moderate
- Dose escalation
- Moderate
- Cross-tol.
- ketamine · PCP · 3-MeO-PCP
Safety
Toxicity
No controlled toxicity data exist for 3-MeO-PCMo. No lethal dose has been established in any species, and no case reports of intoxication, adverse events, or death involving this specific compound have been published.[5]
All toxicity estimates derive from the closely related 3-MeO-PCP, which shares the same core structure but uses a piperidine ring where 3-MeO-PCMo has a morpholine ring. This structural difference may shift toxicity thresholds in unpredictable ways. inferred
Acute toxicity (class data)
Seven deaths involving 3-MeO-PCP were documented in Sweden between 2014 and 2016, all involving co-ingestion of alcohol and/or other drugs.[3] A fatal case in the Netherlands involved 3-MeO-PCP combined with amphetamine and alcohol; death was not attributed to 3-MeO-PCP alone.[4]
Non-fatal intoxications with 3-MeO-PCP have presented with coma, breathing difficulty, unequal pupils, and dangerously low body temperature requiring mechanical ventilation.[11] Delirium and agitation persisted up to 24 hours. Additional cases were documented by the STRIDA project in Sweden[12] and in a French case series.[13]
Potential organ risks
- Breathing: Dose-dependent respiratory depression is the primary lethal risk, especially in combination with other depressants.
- Heart and circulation: Increased heart rate and blood pressure at moderate-to-high doses, driven by dopamine release.
- Temperature regulation: Both dangerously high and dangerously low body temperatures have been documented in 3-MeO-PCP cases.
- Brain: Acute psychosis, severe agitation, and delirium are documented with 3-MeO-PCP.
- Seizures: High doses of PCP-type compounds may lower seizure threshold. safety citation needed
- Bladder (chronic use): ketamine causes direct bladder damage with chronic use.[14] Whether 3-MeO-PCMo produces similar damage is unknown.
All dose-toxicity thresholds for 3-MeO-PCMo are unverified. The margin between a strong dose and a dangerous dose has not been established. Community-sourced dose ranges have not been validated in any study.[2]
Psychological Risks
No controlled studies have assessed psychological risks specific to 3-MeO-PCMo. Risk inference comes from PCP-class pharmacology and 3-MeO-PCP case reports.
Dissociative states can trigger severe anxiety, panic, and acute psychotic episodes, particularly at higher doses or in unfamiliar settings. Mania is anecdotally reported.[2] PCP-class compounds are established psychosis-inducing agents, and both acute and persistent psychosis have been documented following 3-MeO-PCP use.[13][15]
Delusions of sobriety — feeling less impaired than one actually is — increase risky behavior during intoxication. This is particularly dangerous given 3-MeO-PCMo's 1–2 hour onset delay, which may prompt premature redosing. Compulsive redosing urge is separately reported,[2] compounding this risk.
Tolerance & Dependence
No published tolerance or dependence data exist for 3-MeO-PCMo specifically.
NMDA receptor antagonists produce tolerance through compensatory changes in glutamate signaling with repeated use. Community estimates suggest tolerance halves after roughly 5 days and resets after approximately 1.5 weeks.[2] These figures are unverified. safety citation needed
Cross-tolerance is expected across dissociatives sharing the PCP binding site, including Ketamine, PCP, 3-MeO-PCP, and dextromethorphan.
PCP analogues demonstrate reinforcing properties in animal studies, driven by dopamine release from NMDA blockade.[9] Community assessment rates 3-MeO-PCMo as moderately addictive with moderate physical and psychological dependence potential.[2] safety citation needed No specific withdrawal has been characterized.
Drug Interactions
No published interaction data exist for 3-MeO-PCMo. All risks are inferred from arylcyclohexylamine class pharmacology and the fatal case literature for 3-MeO-PCP. inferred
CNS depressants (alcohol, benzodiazepines, opioids, GHB): The most dangerous interaction class. These combinations produce additive or synergistic respiratory depression. Every documented 3-MeO-PCP fatality involved co-ingestion of CNS depressants.[3][4]
Stimulants (amphetamines, cocaine): Combination introduces unpredictable cardiovascular strain — additive stimulant effects layered on dopamine release from NMDA blockade, risking severe blood pressure elevation and cardiac events. Amphetamine was present in the fatal Netherlands case.[3]
Serotonergic agents (MAOIs, SSRIs): If 3-MeO-PCMo has meaningful SERT affinity — documented for related PCP analogues[7] — combination with serotonergic drugs could intensify serotonergic effects. Clinical risk is unquantified.
Tramadol: Combines serotonergic risk with seizure threshold reduction.
Lithium: May lower seizure threshold when combined with NMDA antagonists. safety citation needed
No specific antidote exists. Overdose management is supportive: airway protection, cardiovascular monitoring, and benzodiazepines for agitation and seizures.
Contraindications
No substance-specific contraindication data exist. The following are inferred from PCP-class pharmacology. inferred
Absolute:
- Psychotic disorders (personal or family history): PCP-class compounds reliably produce psychosis-like states and can trigger or worsen psychotic illness.[9]
- Concurrent CNS depressant use: Synergistic respiratory depression. Present in all documented 3-MeO-PCP fatalities.[3]
Relative:
- Heart conditions: Stimulant cardiovascular effects may trigger acute events.
- Seizure disorders: High-dose NMDA antagonists may lower seizure threshold. safety citation needed
- Liver impairment: metabolism relies on genetically variable liver enzymes;[10] impaired liver function could prolong drug exposure.
- Bipolar disorder: Risk of triggering manic episodes.
- Pregnancy and lactation: NMDA receptor antagonists disrupt brain development and are contraindicated during pregnancy as a class. safety citation needed
- CYP2D6 poor metabolizer status: Potential for substantially prolonged effects (inferred from 3-MeO-PCP data[10]).
Harm Reduction[edit]
Harm Reduction
Forms & Identification
3-MeO-PCMo circulates exclusively as a synthetic powder from unregulated research chemical vendors. No pharmaceutical-grade formulation exists, meaning purity and identity cannot be assumed from appearance alone.
Positional isomers in the PCMo series (2-MeO, 3-MeO, 4-MeO) are chemically near-identical and visually indistinguishable.[1] Reagent testing can confirm the arylcyclohexylamine class but cannot reliably distinguish between these isomers. Quantitative analysis through a drug-checking service is the only reliable method to verify identity and rule out more potent contaminants.
Guidelines
- Test all material with a reagent kit and, where available, a drug-checking service before use.
- Start with a low dose and wait a minimum of 2.5 hours before considering any redose — the slow onset is the most common trigger for accidental overdose through premature redosing.
- Pre-measure the dose with a milligram-precision scale. Do not estimate by eye.
- Eat a light meal 2–3 hours before dosing to reduce nausea without slowing absorption unpredictably.
- Remove access to vehicles, sharp objects, and balconies before onset.
- Have a sober sitter present, especially for unfamiliar doses.
- Keep water accessible. Avoid alcohol entirely.
- Set a phone timer at dosing to track elapsed time — time perception is unreliable under dissociation.
Set & Setting
The 1–2 hour onset window creates a distinct risk profile. Prepare the environment fully before dosing — once effects manifest, the ability to adjust surroundings or relocate is compromised.
A calm, familiar, low-stimulation environment is strongly recommended. Dissociative states amplify environmental input unpredictably: quiet settings tend toward serenity, while chaotic or unfamiliar ones can produce disorientation and anxiety. A sober companion who understands the compound's long onset and duration is valuable, particularly at higher doses where delusions of sobriety may impair self-assessment.
Aftercare & integration. Dissociative aftereffects may persist for 12–24 hours after the primary experience resolves. Residual cognitive fog, emotional flatness, or mild derealization are common and typically self-limiting.
Prioritize sleep, hydration, and light nutrition in the hours following the experience. Avoid driving or operating machinery until cognitive function feels fully restored. If the experience was intense or distressing, talking it through with a trusted person can help process unusual perceptual states. Persistent derealization, anxiety, or mood changes lasting more than a few days warrant professional evaluation.
Recovery & Support
For individuals who find themselves using 3-MeO-PCMo or other dissociatives compulsively, professional support is available. Dissociative dependence often develops gradually — escalating frequency and dose may not feel problematic until functional impairment becomes apparent.
SAMHSA's National Helpline (1-800-662-4357) provides free, confidential referrals. Online communities and harm reduction organizations can offer peer support and practical guidance for reducing or stopping use.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
Uncomfortable but manageable effects (nausea, confusion, anxiety) are distinct from medical emergencies. Seek immediate help if any of the following occur: slow or stopped breathing, blue or grey lips, unresponsiveness to voice and touch, seizure, severe chest pain, or body temperature that feels dangerously hot or cold through clothing.
Immediate steps:
- 1. Call emergency services immediately.
- 2. Place the person on their side in the recovery position if they are unconscious but breathing.
- 3. Do not leave them alone.
- 4. Do not induce vomiting.
- 5. Do not physically restrain them unless they pose immediate danger to themselves or others — agitated dissociation can escalate with restraint.
- 6. Monitor breathing continuously until help arrives.
What to tell the dispatcher:
State what substance was taken, how much, when it was taken, and what symptoms you observe. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency from prosecution.
No specific reversal agent exists for 3-MeO-PCMo. All treatment is supportive.
Legal Status[edit]
Legal Status
3-MeO-PCMo occupies a largely unscheduled legal position internationally. It is not controlled under any United Nations drug control treaty. The EMCDDA has monitored it via the European Early Warning System since notification by the Netherlands on August 7, 2015.[2] Where controls exist, they typically arise from structural analog legislation or blanket psychoactive substance bans rather than specific scheduling.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States (federal) | Not explicitly scheduled | Potential prosecution under the Federal Analogue Act (21 U.S.C. § 813) given structural and pharmacological similarity to PCP (Schedule II). The closely related 3-MeO-PCP was placed in Schedule I effective April 22, 2026,[6] strengthening the analogue argument for 3-MeO-PCMo.[2] |
| United States (Minnesota) | Schedule I (2016) | Explicitly scheduled at state level[2] |
| United Kingdom | Prohibited (Psychoactive Substances Act 2016) | Supply prohibited under blanket psychoactive substances legislation effective May 26, 2016. Not individually scheduled under the Misuse of Drugs Act 1971.[2] |
| Canada | Potentially controlled | PCP and its analogues are controlled under Schedule 1 of the Controlled Drugs and Substances Act. Whether the definition encompasses 3-MeO-PCMo has not been confirmed in published legal analysis.[2] citation needed |
| Australia | Not explicitly listed | Not named in the SUSMP. May be captured by analogue provisions. citation needed |
| European Union | Not scheduled (EU-level) | Monitored by EMCDDA since August 2015. Individual member states may have independent national controls.[2] |
Analogue considerations
The US Federal Analogue Act defines a controlled substance analogue as any substance "substantially similar" in chemical structure or pharmacological effect to a Schedule I or II substance. 3-MeO-PCMo is structurally analogous to PCP (Schedule II) — sharing the arylcyclohexylamine core — and pharmacologically analogous via confirmed NMDA antagonism.[1]
The 2026 federal scheduling of 3-MeO-PCP[6] provides an additional reference compound for analogue prosecution, as 3-MeO-PCMo differs from 3-MeO-PCP by a single oxygen atom in the heterocyclic ring.
references
- [1] ^abcdefghijklmColestock T, Wallach J, Mansi M, Filemban N, Morris H, Elliott SP, Westphal F, Brandt SD, Adejare A (2018) Syntheses, analytical and pharmacological characterizations of the 'legal high' 4-[1-(3-methoxyphenyl)cyclohexyl]morpholine (3-MeO-PCMo) and analogues — Drug Testing and Analysis doi:10.1002/dta.2213
- [2]
- [3] ^abcdefJohansson 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] ^abcde Jong LAA, Olyslager EJH, Duijst WLJM (2019) The risk of emerging new psychoactive substances: The first fatal 3-MeO-PCP intoxication in The Netherlands — Journal of Forensic and Legal Medicine doi:10.1016/j.jflm.2019.05.011
- [5] ^abcMohr ALA, Logan BK, Fogarty MF, Krotulski AJ, Papsun DM, et al. (2022) Reports of Adverse Events Associated with Use of Novel Psychoactive Substances, 2017–2020: A Review — Journal of Analytical Toxicology doi:10.1093/jat/bkac023
- [6]