4-MeO-PCP
4-methoxyphencyclidine
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4-MeO-PCP (4-methoxyphencyclidine) — methoxydine — is a synthetic dissociative of the arylcyclohexylamine class. It is a structural analog of PCP, distinguished by an exceptionally long duration of action. 4-MeO-PCP is an NMDA receptor antagonist, producing its effects by blocking glutamate signaling at the brain's primary excitatory ion channel.[1]
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PCP, 3-MeO-PCP, ketamine +2 morePCP, 3-MeO-PCP, ketamine, methoxetamine, dextromethorphan show less
First synthesized by Victor Maddox at Parke-Davis in 1965,[2] 4-MeO-PCP remained obscure for over four decades before becoming the first dissociative research chemical sold online in late 2008.[3] That event pioneered an online dissociative market that subsequently produced over a dozen additional compounds.[2] It remains unscheduled internationally despite being identified as the most common PCP-type substance reported by UN member states.[4]
Subjective effects include dissociation, visual disturbance, sedation, and depersonalization. The experience is described as deeply immobilizing — a heavy, slow-building disconnection closer in character to PCP than to the stimulant edge of 3-MeO-PCP.[5] Hypothermia, prolonged cognitive impairment, and premature redosing due to slow onset are characteristic unsought effects.
Dependence liability parallels the PCP class, and one fatality lists 4-MeO-PCP as the principal cause of death in a polysubstance context.[6] The primary risk is shaped by the extended duration — a slow onset invites premature redosing, while SERT affinity raises the potential for dangerous interactions with common antidepressants.[1] No clinical trials have been conducted; the current understanding rests on receptor screening data, a single fatality report, animal behavioral studies, and community-sourced estimates.
History[edit]
Discovery
4-MeO-PCP was synthesized in 1965 by Victor Maddox, a medicinal chemist at Parke-Davis — the same company that had originated phencyclidine in 1956.[2][3] It emerged from a program to find dissociative anesthetics with fewer emergence reactions than PCP, which was withdrawn from human clinical use that same year due to severe psychotomimetic adverse effects.[7] 4-MeO-PCP was never developed further for clinical application.
The First Online Dissociative
4-MeO-PCP holds the distinction of being the first dissociative research chemical sold online, introduced in late 2008 by a vendor trading as CBAY.[3][2] This event pioneered the online dissociative novel psychoactive substance market, which subsequently produced at least twelve additional compounds including methoxetamine and 3-MeO-PCP.[2]
Regulation and Forensic Detection
Forensic authorities first identified 4-MeO-PCP in Norway, Russia, and the United Kingdom in 2011.[4] The first confirmed fatality attributable principally to 4-MeO-PCP was published in 2015,[6] and comprehensive NPS legislation in the United Kingdom and Germany subsequently brought it under generic control. The UNODC identified 4-MeO-PCP as the most common PCP-type substance reported by member states, despite it never being placed under international control.[4]
The name methoxydine circulated alongside 4-MeO-PCP on the early research chemical market, though the compound is more commonly identified by its systematic abbreviation. At least 14 PCP derivatives had circulated for non-medical use from the late 1960s through the 1990s before the internet era,[2] but 4-MeO-PCP's online debut marked a new distribution model that reshaped the dissociative landscape entirely.
Chemistry[edit]
Structure
4-MeO-PCP belongs to the arylcyclohexylamine family, sharing the 1-(1-phenylcyclohexyl)piperidine scaffold with phencyclidine. It is distinguished by a methoxy group (–OCH₃) at the para (4-) position of the aromatic ring. Three positional isomers exist — 2-MeO-PCP, 3-MeO-PCP, and 4-MeO-PCP — each with distinct pharmacological profiles and distinguishable by mass spectrometry.[8][9]
| Molecular formula | C₁₈H₂₇NO |
| Molecular weight | 273.4 g/mol |
Stereochemistry
The cyclohexyl quaternary carbon constitutes a stereocenter, but 4-MeO-PCP is typically encountered as a racemate. No enantioselective pharmacology data specific to 4-MeO-PCP have been published, though related PCP analogs show significant differences in receptor affinity between enantiomers.citation needed
Structure-Activity Relationships
In the morpholine-ring analog series, para-methoxy substitution on the aromatic ring produces the lowest NMDA affinity in the series — below the meta-methoxy isomer.[10] This is consistent with the clinical impression that 4-MeO-PCP is less potent than 3-MeO-PCP. Whether this gradient fully translates from the morpholine to the piperidine series has not been confirmed, but is structurally consistent.
Analytical Considerations
The 4-MeO-PCP hydrochloride salt undergoes notable thermal degradation during gas chromatographic analysis — more so than the 3-MeO isomer — which can confound quantitative results.[8]
The HCl salt melts at 181–182 °C and is soluble in ethanol (20 mg/mL), DMSO (11 mg/mL), and phosphate-buffered saline (10 mg/mL).[11]
Pharmacology[edit]
Mechanism of Action
4-MeO-PCP acts primarily at the phencyclidine binding site on the NMDA glutamate receptor — the same molecular target responsible for the dissociative and anesthetic effects of PCP and ketamine.[1] The compound blocks the receptor in its open state, producing use-dependent inhibition of glutamate signaling.[12]
Beyond NMDA, 4-MeO-PCP shows appreciable affinity for sigma receptors and the serotonin transporter (SERT).[1] Dopamine reuptake inhibitor is plausible based on PCP's known DAT activity,[12] but has not been specifically measured for this compound.inferred The compound was inactive at mu, kappa, and delta opioid receptors in vitro.[13]
PCP-like drug discrimination in rodents confirms that 4-MeO-PCP produces PCP-like interoceptive effects, though with reduced locomotor stimulation compared to the parent compound.[5]
Pharmacokinetics
No human pharmacokinetic data have been published. Bioavailability, time to peak plasma concentration, plasma half-life, and volume of distribution are all unknown.
Metabolism is inferred from studies on the closely related 3-MeO-PCP.[14] O-demethylation would yield 4-hydroxyphencyclidine (4-OH-PCP), itself a known PCP metabolite, with additional pathways likely including hydroxylation of the cyclohexyl and piperidine rings and glucuronidation.inferred
The enzymes involved are all genetically variable across populations.[14] Individuals who metabolize drugs slowly through certain pathways may experience elevated drug exposure and prolonged effects, though this has not been clinically confirmed.
Community reports indicate a total duration of 12–20 hours by the oral route, placing 4-MeO-PCP among the longest-acting arylcyclohexylamines. No controlled clinical data confirm these durations.safety citation needed
Neuroscience[edit]
Where It Acts
No direct neuroimaging or electrophysiology data exist for 4-MeO-PCP. Its neural effects are inferred from the well-characterized neuroscience of NMDA antagonism. By blocking NMDA receptors on inhibitory interneurons in the prefrontal cortex, compounds like PCP and ketamine paradoxically increase cortical glutamate release.[12] This disinhibition disrupts communication between cortical regions and between the cortex and thalamus, producing the cognitive fragmentation, depersonalization, and reality distortion characteristic of dissociative states.[1]
The reduced locomotor stimulation of 4-MeO-PCP relative to PCP[5] may reflect lower dopaminergic activation in reward and motor circuits, though this has not been directly measured.
Why It Matters
PCP's pharmacology provided the experimental foundation for the glutamate hypothesis of schizophrenia — the theory that NMDA receptor dysfunction, particularly on cortical inhibitory neurons, produces the positive, negative, and cognitive symptoms of the disorder.[12][7] 4-MeO-PCP's confirmed PCP-like interoceptive profile[5] places it within this framework as a pharmacological model of NMDA hypofunction.
Within predictive processing theory, NMDA blockade degrades the brain's ability to distinguish expected from unexpected sensory input, producing derealization and depersonalization as perceptual predictions lose precision.
- Does 4-MeO-PCP produce neuroplastic changes? Ketamine's antidepressant mechanism involves downstream synapse formation — whether 4-MeO-PCP shares this pathway is unknown.
- What accounts for the exceptionally long duration? Lipophilicity, receptor residence time, and active metabolites are all plausible explanations, but none have been measured.
- Does the para-methoxy substitution alter cortical activation patterns relative to PCP or 3-MeO-PCP?
Subjective Effects[edit]
4-MeO-PCP produces a deeply sedating dissociative state — a heavy, enveloping disconnection from body and environment that builds slowly and persists for an uncommonly long period. At lower doses, the experience centers on mild perceptual distortion and emotional suppression; at higher doses, immobilization, full dissociation, and coma become possible. Set and setting strongly modulate the psychological character, particularly given the extended duration that can outlast the conditions in which use began.
Within the arylcyclohexylamine class, 4-MeO-PCP occupies a niche closer to PCP in duration but with a reportedly less agitated, more immobilizing character. It lacks the rapid onset and brief action of ketamine and the stimulant edge of 3-MeO-PCP.[5]
Effect Grid
At common doses, the full dissociative experience emerges: pronounced depersonalization and derealization, significant distortion of spatial and temporal perception, and a sense of detachment from the body. Visual disturbances include drifting, morphing of surfaces, and suppression of visual acuity. Thought processes become markedly fragmented, with difficulty maintaining linear trains of thought.
Physically, sedation is prominent — more so than with 3-MeO-PCP at equivalent subjective intensity. Nystagmus, ataxia, and slurred speech are typical. Nausea may occur during onset. The total experience extends 12–18 hours by community report, precluding normal activities for the full duration and requiring a clear schedule with no obligations.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Sensory deprivation · Touch suppression · Visual acuity suppression · Depth perception distortion · Dreaming enhancement · Music enhancement · Auditory distortion · Peripheral vision distortion · Visual haze / noise · Visual drifting · Auditory misinterpretation · Tinnitus · Tracers · Visual processing suppression · Internal hallucinations · Auditory hallucinations · External hallucinations · Environmental orbism / cubism · Visual scenery slicing · Perspective hallucinations
Dreaming enhancement · Music enhancement · Auditory distortion · Peripheral vision distortion · Visual haze / noise · Visual drifting · Auditory misinterpretation · Tinnitus · Tracers · Visual processing suppression · Internal hallucinations · Auditory hallucinations · External hallucinations · Environmental orbism / cubism · Visual scenery slicing · Perspective hallucinations
Body schema distortion · Physical fatigue · Body high · Insomnia · Nystagmus (eye wobbles) · Pain suppression · Pupil dilation · Tactile euphoria · Spontaneous body sensations · Headache · Laughter fits · Muscle relaxation · Nasal congestion · Nausea · Appetite suppression · Bodily heaviness · Dry mouth · Heart rate perception changes · Restlessness · Stimulation · Tingling / electric sensations · Vasoconstriction · Bruxism · Excessive sweating · Involuntary body movements · Muscle tension · Sexual arousal enhancement · Trembling · Vibrations / buzzing · Vomiting · Wakefulness · Motor control enhancement · Bodily dissociation · Tactile hallucination · Phantom limb sensations
Insomnia · Nystagmus (eye wobbles) · Pain suppression · Pupil dilation · Tactile euphoria · Spontaneous body sensations · Headache · Laughter fits · Muscle relaxation · Nasal congestion · Nausea · Appetite suppression · Bodily heaviness · Dry mouth · Heart rate perception changes · Restlessness · Stimulation · Tingling / electric sensations · Bruxism · Excessive sweating · Involuntary body movements · Muscle tension · Sexual arousal enhancement · Trembling · Vibrations / buzzing · Vomiting · Wakefulness · Motor control enhancement · Bodily dissociation · Tactile hallucination · Phantom limb sensations
Confusion · Focus suppression · Information processing suppression · Immersion enhancement · Thought deceleration · Cognitive fatigue · Memory fragmentation · Thought disorganization · Introspection enhancement · Pattern recognition suppression · Cognitive euphoria · Language suppression · Motivation suppression · Humor enhancement · Compulsive redosing urge · Conceptual thinking · Cognitive dysphoria · Delusions of sobriety · Novelty enhancement · Openness enhancement · Thought loops · Creativity enhancement · Aesthetic enhancement · Cognitive flexibility · Memory replays · Thought acceleration · Amnesia · Delirium · Delusions
Immersion enhancement · Thought deceleration · Cognitive fatigue · Memory fragmentation · Thought disorganization · Introspection enhancement · Pattern recognition suppression · Cognitive euphoria · Language suppression · Motivation suppression · Humor enhancement · Conceptual thinking · Cognitive dysphoria · Delusions of sobriety · Novelty enhancement · Openness enhancement · Thought loops · Creativity enhancement · Aesthetic enhancement · Cognitive flexibility · Memory replays · Thought acceleration · Amnesia · Delirium · Delusions
Emotional lability · Empathy suppression · Dysphoria · Emotional enhancement · Emotional suppression · Irritability · Mania · Anhedonia
Emotional enhancement · Emotional suppression · Irritability · Anhedonia
Social disconnection · Communication suppression · Sociability suppression · Automaticity · Craving · Ego inflation · Flow state · Sociability enhancement · Cognitive disconnection · Boundary dissolution · Identity alteration · Ego dissolution
Craving · Ego inflation · Flow state · Sociability enhancement · Cognitive disconnection · Boundary dissolution · Identity alteration · Ego dissolution
Non-dual awareness
Timeline
First alerts emerge gradually — a subtle shift in spatial awareness and mild cognitive blunting. Onset is slow and may be imperceptible for the first 30 minutes, encouraging premature redosing.
Dissociative effects build steadily over 1–2 hours. Depersonalization, spatial distortion, and sedation become clearly recognizable. Nausea may occur during this phase.
Maximum dissociative intensity: pronounced derealization, body detachment, fragmented cognition, and visual disturbances. The peak is broad and sustained, reflecting the compound's lipophilic CNS accumulation.
Effects remain perceptible but intensity diminishes gradually. Cognitive impairment, sedation, and mild dissociation persist. Motor coordination remains impaired.
Slow return toward baseline over several hours. Spatial perception normalises but cognitive fog, emotional blunting, and fatigue linger.
Residual cognitive slowing, emotional flatness, and mild perceptual oddities may persist for 4–12 hours beyond subjective resolution. Sleep quality is often poor.
⚠ Do not drive or operate machinery until after a full night's sleep following complete resolution of effects.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Moderate
- Withdrawal
- Mild
- Tolerance buildup
- moderate
- Tolerance reset
- 10 days
- Physical
- Low
- Psychological
- Moderate
- Compulsive redosing
- Low
- Dose escalation
- Moderate
- Cross-tol.
- PCP · 3-MeO-PCP · ketamine
Toxicity
Acute Toxicity
No formal lethal dose has been established for 4-MeO-PCP. Animal studies found lethal effects at tested doses, though the specific lethal dose was not reported.[5] No therapeutic index can be calculated.
One confirmed human fatality involved 4-MeO-PCP as the principal cause of death in a polysubstance context, with co-detected substances including an antidepressant, an antipsychotic, a benzodiazepine, and an antihistamine at therapeutic concentrations.[6] This single case does not establish a lethal threshold.
Expected Toxidrome
Based on PCP-class literature and case reports for the closely related 3-MeO-PCP, the expected presentation of overdose includes:
- Central nervous system: Dissociation, coma, delirium, psychosis, agitation
- Heart and circulation: Rapid heart rate, elevated blood pressure
- Breathing: respiratory depression at high doses, potentially requiring intubation[15]
- Eyes: Dilated pupils, involuntary eye movement (nystagmus)
- Temperature: Hypothermia documented in animal models;[13] overheating possible at high doses
- Muscles and kidneys: Muscle breakdown is a class risk for NMDA antagonists,[16] which can cause secondary kidney injury
- Seizures: Possible (class risk)
Organ Toxicity
Substantial liver accumulation was noted in the fatality case, though liver damage was not specifically described.[6] Chronic bladder damage — well documented with ketamine — is a recognized dissociative class risk but has not been studied for 4-MeO-PCP.
Detection
Standard urine drug screening for PCP may detect 4-MeO-PCP (1–143% cross-reactivity across commercial immunoassays)[17] but cannot confirm identity. Definitive identification requires laboratory mass spectrometry.[8][9] Thermal degradation of the compound during gas chromatography can confound quantitative results.[8]
Psychological Risks
PCP-like drug discrimination confirms that 4-MeO-PCP produces PCP-like subjective states,[5] supporting the inference that psychological risks parallel the PCP class:
- Acute psychosis: PCP is the prototypical pharmacological model of psychosis. Dissociative-induced psychotic episodes with paranoia, disorganized behavior, and agitation are well-documented.[12]
- Prolonged psychiatric disturbance: PCP can trigger psychotic episodes lasting days to weeks, particularly at high doses or with repeated use.[7] The extended duration of 4-MeO-PCP raises concern for correspondingly prolonged destabilization.
- Mania: Reported for 3-MeO-PCP; community reports suggest this is less prominent with 4-MeO-PCP, though published confirmation is lacking.[18]
Tolerance & Dependence
No controlled studies or systematic observational data exist for 4-MeO-PCP tolerance or dependence.
PCP produces established substance use disorder with tolerance and compulsive use patterns.[2][7] 4-MeO-PCP substitutes for PCP in drug discrimination, confirming shared interoceptive effects and supporting the inference that it carries a similar abuse liability.[5]
Tolerance develops through compensatory upregulation of NMDA receptors and downstream changes in glutamate signaling. Cross-tolerance among dissociatives sharing the PCP binding site is expected. Community estimates of tolerance half-life (~5 days) and full reset (~1.5 weeks) are unverified.safety citation needed
Drug Interactions
No controlled interaction studies exist. All interaction data are derived from the published fatality case, structural analog case reports, and class-level pharmacological inference.
CNS Depressants
Combination with alcohol, benzodiazepines, or opioids produces additive or synergistic depression of the central nervous system and breathing. All published fatalities in the MeO-PCP analog literature involve polysubstance exposure with at least one depressant.[9][19][20] The 4-MeO-PCP fatality case involved a benzodiazepine at therapeutic concentrations.[6]
Serotonergic Drugs
Serotonin transporter affinity raises concern for serotonin syndrome when combined with SSRIs, SNRIs, or MAOIs.[1] The fatality case involved an SNRI co-ingestion.[6] Interaction severity with serotonergic antidepressants remains uncharacterized.safety citation needed
Stimulants
One 3-MeO-PCP death involved co-ingestion with methamphetamine.[9] Stimulants may mask the sedative component of dissociative intoxication while cardiovascular strain compounds.
Metabolic Interactions
No enzyme inhibition data exist for 4-MeO-PCP. Given inferred metabolism via CYP2B6, CYP2C19, and CYP2D6,[14] inhibitors of these enzymes — including common antidepressants like fluoxetine and paroxetine — could theoretically elevate drug exposure.inferred
Emergency Management
No specific antidote exists. Management is supportive. Benzodiazepines are first-line for agitation in PCP-class intoxication; antipsychotics may be used but carry theoretical risks related to dopamine interactions.[21] The prolonged duration of action requires extended clinical monitoring after overdose presentation.
Contraindications
No substance-specific contraindication studies exist. The following are inferred from the pharmacological profile and class-level evidence:
- Serotonergic medications (SSRIs, SNRIs, MAOIs): serotonin transporter affinity raises the risk of serotonin syndrome[1]
- Heart conditions: sympathomimetic effects via dopaminergic and sigma receptor mechanisms[12]
- Seizure disorders: NMDA antagonists may lower seizure threshold
- Liver impairment: impaired metabolism may elevate drug exposure[14]
- Kidney impairment: impaired excretion of metabolites; muscle breakdown risk compounded
- Psychotic disorders or family history of psychosis: PCP-class compounds are the prototypical pharmacological model of psychosis[12]
- Pregnancy: no reproductive toxicity data; NMDA receptor involvement in brain development warrants precautionary contraindication
Harm Reduction[edit]
Forms & Identification
4-MeO-PCP is analytically difficult to distinguish from its positional isomer 3-MeO-PCP without laboratory mass spectrometry.[8][9] Standard PCP immunoassays show highly variable cross-reactivity (1–143%), meaning a positive PCP screening test is unreliable for confirming identity.[17]
Reagent testing can help exclude some substitutes but cannot definitively distinguish between MeO-PCP isomers. Given the substantial pharmacological differences between isomers — particularly in potency, duration, and stimulant character — laboratory analysis is the only reliable identification method.
Guidelines
- Verify substance identity with reagent testing at minimum; laboratory analysis is strongly recommended given isomer confusion risk.
- Start with the lowest suggested dose and wait the full onset window before assessing whether effects have been reached.
- Clear the full day and the following morning — effects can persist well beyond 12 hours and residual impairment may extend further.
- Arrange a sober companion for the full duration, particularly above threshold doses.
- Eat a light meal beforehand and keep water accessible throughout.
- Avoid redosing. The slow onset and extended duration mean additional doses compound unpredictably.
- Prepare for temperature changes — have blankets available, as hypothermia has been documented.[13]
Set & Setting
The exceptionally long duration makes environment planning critical. A session lasting the better part of a day requires a secure, comfortable location with access to food, water, and a bathroom for the entire period. A sober companion who can commit to the full duration is strongly recommended, particularly at higher doses where immobilization and loss of awareness become possible.
The slow onset creates a dangerous window for premature redosing. Effects may not be apparent for one to two hours after oral ingestion; taking additional material during this window is the most common source of accidental overdose with long-acting dissociatives.
Aftercare & integration. The extended duration means the aftereffect period may be correspondingly long. Allow at least a full day of rest after the experience subsides. Cognitive dulling, emotional flatness, and difficulty concentrating are commonly reported during recovery.
Reintegration into demanding tasks — driving, operating machinery, making important decisions — should be delayed until mental clarity has fully returned. If distressing psychological effects such as paranoia, depersonalization, or confusion persist beyond 48 hours after effects have otherwise resolved, seek professional evaluation.
Recovery & Support
PCP-class dissociatives carry established abuse liability.[2][7] If use has become compulsive or difficult to control, or if increasing doses are required to achieve desired effects, professional support is warranted.
Tolerance cross-generalizes across dissociatives sharing the NMDA mechanism, so switching compounds does not reset the cycle. Addiction counseling services, peer support groups, and crisis lines are available resources. A medical professional familiar with novel psychoactive substances can help develop a reduction strategy if dependence has developed.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Unresponsiveness or inability to be roused
- Slow, shallow, or stopped breathing
- Seizure activity
- Extreme agitation, paranoia, or self-harm risk
- Body temperature noticeably cold to the touch
Immediate steps:
- 1. Call emergency services if breathing is impaired, the person is unresponsive, or seizures occur.
- 2. Place an unresponsive but breathing person in the recovery position.
- 3. Monitor breathing continuously — respiratory depression is the primary acute danger.
- 4. Do not restrain an agitated person unless there is immediate risk of self-harm or harm to others.
- 5. Do not induce vomiting.
What to tell the dispatcher: Name the substance (4-MeO-PCP, a PCP-type dissociative), estimated amount and time of ingestion, and current symptoms. Many jurisdictions have Good Samaritan laws that protect callers from prosecution.
No reversal agent exists. Treatment is supportive. Benzodiazepines are standard for agitation in PCP-class intoxication.[21] The long duration requires extended monitoring — do not assume the situation is resolved because symptoms temporarily improve.
Legal Status[edit]
4-MeO-PCP is not under international control.[4] Unlike PCP itself and methoxetamine, both of which are Schedule II under the 1971 Convention on Psychotropic Substances, 4-MeO-PCP has no UN-level scheduling — despite being identified as the most common PCP-type substance reported by member states.[4]
National and regional control varies substantially, with most jurisdictions relying on generic NPS legislation or structural analog provisions rather than specific scheduling:
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States (federal) | Unscheduled | Not a named controlled substance. The Federal Analogue Act (21 USC §813) may apply as a structural and pharmacological analog of PCP (Schedule II) if intended for human consumption. Not formally adjudicated.[22] |
| Virginia (US state) | Temporary Schedule I | Scheduled June 26, 2019 through December 25, 2020.[22] |
| United Kingdom | Controlled (PSA 2016) | Covered under the Psychoactive Substances Act 2016, which bans production, supply, and possession with intent to supply of all psychoactive substances not otherwise exempt. Not specifically named in Misuse of Drugs Act schedules. |
| Germany | Controlled (NpSG) | Covered under the Neue-psychoaktive-Stoffe-Gesetz (NpSG) effective November 26, 2016; generic NPS legislation. |
| Sweden | Hazardous substance | Classified as a hazardous substance by the Swedish public health agency, November 10, 2014.[3] |
| Canada | Effectively controlled | The Controlled Drugs and Substances Act (CDSA) Schedule I covers PCP and its analogs/derivatives broadly, encompassing 4-MeO-PCP. |
| Australia | Presumed controlled | Expected to be controlled under the Standard for the Uniform Scheduling of Medicines and Poisons (SUSMP) Schedule 9 via PCP analogue provisions, but not confirmed from primary government source.citation needed |
references
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- [5] ^abcdefghShaw HE, Patel DR, Gannon BM, Fitzgerald LR, Carbonaro TM, Johnson CR, Fantegrossi WE (2024) Phencyclidine-Like Abuse Liability and Psychosis-Like Neurocognitive Effects of Novel Arylcyclohexylamine Drugs of Abuse in Rodents — The Journal of Pharmacology and Experimental Therapeutics doi:10.1124/jpet.123.001942
- [6]