3-MeO-PCMo
3-methoxyphencyclomorpholine
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3-MeO-PCMo (4-[1-(3-methoxyphenyl)cyclohexyl]morpholine) is a synthetic dissociative of the arylcyclohexylamine class. It is a morpholine-ring variant of 3-MeO-PCP, with weaker potency and a softer character. It blocks glutamate signaling in the brain,[1] producing the disconnection from body and surroundings that defines the dissociative experience.
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ketamine, PCP, 3-MeO-PCP +2 moreketamine, PCP, 3-MeO-PCP, dextromethorphan, methoxetamine show less
3-MeO-PCMo first appeared on research chemical markets in 2015, when the Netherlands reported its detection to European drug monitoring authorities.[2] A single 2018 pharmacological study confirmed its mechanism and placed it in a potency ranking alongside related analogues.[1] It remains unscheduled in most countries and circulates in small quantities among research chemical users.
Subjective effects include depersonalization, derealization, cognitive disconnection, pain suppression, and amnesia. The experience builds slowly — a warm, motionless body sensation with gradual mental detachment, softer and more drawn out than most dissociatives.[2] Mania, compulsive redosing urge, and delusions of sobriety — feeling less impaired than one actually is — are characteristic unsought effects.
3-MeO-PCMo carries moderate addiction and dependence potential.[2] The dominant risk is combining it with alcohol or other depressants — every documented death involving the closely related 3-MeO-PCP involved that combination, through additive respiratory depression.[3][4] One pharmacological study constitutes the entire published evidence base; no human toxicity or clinical data exist.[5]
History[edit]
History
Discovery
3-MeO-PCMo emerged on research chemical markets in the mid-2010s as part of a wave of arylcyclohexylamine analogues built around the phencyclidine scaffold. It has no pharmaceutical origin or clinical history. The Netherlands notified European drug monitoring authorities of its detection on August 7, 2015 — the first documented record of the compound.[2]
Scientific characterization
The only published study is Colestock et al. (2018), which synthesized 3-MeO-PCMo alongside five related compounds and screened all six across 46 brain receptor targets.[1] This confirmed NMDA antagonism as the primary mechanism and produced the only published binding data for the compound. No further research has followed.[5]
Present status
3-MeO-PCMo has no clinical trials, no published intoxication case reports, and no scheduled legal status in most countries. Its close analogue 3-MeO-PCP appeared on illicit markets around 2011[3] and was placed in US Schedule I effective April 2026[6] — increasing the likelihood of analogue prosecution for 3-MeO-PCMo in the United States.
Chemistry[edit]
Chemistry
Structural class
3-MeO-PCMo belongs to the arylcyclohexylamine family — the same chemical class as phencyclidine (PCP), ketamine, and methoxetamine.[1] It is a close structural relative of 3-MeO-PCP, differing by a single substitution: the piperidine ring is replaced with a morpholine ring, which adds an oxygen atom into the six-membered heterocycle.[1]
Molecular properties
| Molecular formula | C₁₇H₂₅NO₂ |
| Molecular weight | 275.4 g/mol |
The methoxy group's position on the phenyl ring drives the potency differences observed across the PCMo isomer series.[1] Positional isomers (2-MeO, 3-MeO, 4-MeO) share identical molecular formulae and are visually indistinguishable — reliable identification requires specialized laboratory analysis.[1]
Pharmacology[edit]
Pharmacology
Mechanism of action
3-MeO-PCMo is a non-competitive NMDA receptor antagonist — it blocks glutamate-driven signaling by entering the NMDA channel and stopping ion flow.[1] The channel must first be opened by glutamate before the compound can enter. A 2018 study screened it across 46 brain targets and confirmed NMDA antagonism as the dominant activity.[1]
It binds roughly 12 times more weakly than PCP and at comparable strength to ketamine at the same site.[1] NMDA blockade in the prefrontal cortex also releases a brake on dopamine signaling, contributing to the stimulating and mood-elevating qualities shared by PCP-type compounds.[7]
Pharmacokinetics
No human pharmacokinetic data exist. The oral onset is notably slow — 1 to 2 hours — compared to roughly 20–30 minutes for oral Ketamine; the reason has not been investigated.[2] Metabolic pathways are inferred from 3-MeO-PCP, where the liver processes the compound through multiple breakdown routes that vary substantially between individuals.[8]
Neuroscience[edit]
Neuroscience
No neuroimaging or brain activity 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 the thalamus and cortex — the pathway that normally integrates sensory input with higher-level processing.[7] This disconnection is the proposed basis for depersonalization, derealization, and the sensation of detachment from body and thoughts.
Why it matters
NMDA receptors help the brain constantly predict incoming sensory data and update those predictions against reality. Block them, and the world starts to feel unfamiliar, unreal, or fundamentally altered.
Key unknowns include whether the morpholine ring changes brain connectivity differently from 3-MeO-PCP, whether 3-MeO-PCMo produces ketamine-like neuroplasticity at any dose range, and what causes its unusually slow oral onset compared to Ketamine.
Subjective Effects[edit]
The 3-MeO-PCMo experience builds gradually over one to two hours, settling into a warm, motionless body sensation paired with progressive mental and sensory detachment.[2] Quiet environments tend toward serene disconnection; stimulating ones can produce confusion and anxiety.
Within the arylcyclohexylamine class, it sits below 3-MeO-PCP in potency and softer in character. The experience is closest to oral ketamine — but stretched across a much slower timeline and less prone to deep dissociative immersion at common doses.
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 published case reports of intoxication with this specific compound exist.[5] All risk estimates derive from the closely related 3-MeO-PCP, which shares the same core structure. inferred
Acute toxicity (class data)
Seven deaths involving 3-MeO-PCP were recorded in Sweden between 2014 and 2016; all involved co-ingestion of alcohol or other drugs.[3] A fatal Dutch case combined 3-MeO-PCP with amphetamine and alcohol.[4] Non-fatal intoxications presented with coma, breathing difficulty, and dangerously low body temperature requiring mechanical ventilation;[9] delirium lasted up to 24 hours. Additional cases were documented in Sweden[10] and France.[11]
Potential organ risks
- Breathing: Dose-dependent respiratory depression is the primary lethal risk, especially combined with other depressants.
- Heart and circulation: Increased heart rate and blood pressure at moderate-to-high doses.
- 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.[12] 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
Dissociative states can produce severe anxiety, panic, and acute psychosis — particularly at higher doses or in unfamiliar settings. Mania is anecdotally reported,[2] and both acute and persistent psychosis have been documented with 3-MeO-PCP.[11][13]
Delusions of sobriety — feeling less impaired than one actually is — increase risky behavior during intoxication. This is especially dangerous given the 1–2 hour onset delay, which can prompt premature redosing. Compulsive redosing urge is separately reported,[2] compounding this risk.
Tolerance & Dependence
NMDA 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 with other dissociatives sharing the same site: Ketamine, PCP, 3-MeO-PCP, and dextromethorphan. 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 3-MeO-PCP fatality data. inferred
CNS depressants (alcohol, benzodiazepines, opioids, GHB): These combinations amplify respiratory depression. Every documented 3-MeO-PCP fatality involved co-ingestion of CNS depressants.[3][4]
Stimulants (amphetamines, cocaine): Combining stimulant effects with dopamine release from NMDA blockade risks severe blood pressure elevation and cardiac events. Amphetamine was present in the fatal Netherlands case.[3]
Serotonergic agents (MAOIs, SSRIs): If 3-MeO-PCMo affects serotonin transport — as documented for related PCP analogues[14] — combining it with serotonergic drugs could intensify serotonin activity dangerously. 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 treatment is supportive: airway protection, cardiovascular monitoring, and benzodiazepines for agitation and seizures.
Contraindications
No substance-specific 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.[7]
- 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;[8] 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[8]).
Harm Reduction[edit]
Forms & Identification
3-MeO-PCMo circulates only as a synthetic powder from unregulated research chemical vendors. No pharmaceutical-grade formulation exists — purity and identity cannot be assumed from appearance.
Positional isomers in the PCMo series (2-MeO, 3-MeO, 4-MeO) are visually indistinguishable and chemically near-identical.[1] Reagent tests confirm the arylcyclohexylamine class but cannot reliably distinguish between isomers. A drug-checking service is the only reliable way 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 creates a specific risk: prepare the environment fully before dosing. Once effects manifest, the ability to adjust surroundings or relocate is compromised.
A calm, familiar, low-stimulation environment reduces the risk of disorientation and anxiety. Dissociative states amplify environmental input unpredictably. A sober companion who understands the compound's long onset is valuable, especially 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 is unscheduled in most jurisdictions and not controlled under any United Nations drug treaty. The EMCDDA has monitored it since August 2015.[2] Where controls exist, they arise from structural analog legislation or blanket psychoactive substance bans.
| 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 covers substances "substantially similar" in structure or pharmacological effect to a Schedule I or II drug. 3-MeO-PCMo shares the arylcyclohexylamine core of PCP (Schedule II) and confirmed NMDA antagonism.[1] The 2026 federal scheduling of 3-MeO-PCP[6] strengthens the analogue argument — 3-MeO-PCMo differs from 3-MeO-PCP by a single oxygen atom.
Legal status changes frequently and varies by jurisdiction. The information above may be out of date. This is not legal advice.
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]