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Serotonin receptor ligandpsilocybin, psilocin, LSD +5 morepsilocybin, psilocin, LSD, mescaline, DMT, 4-AcO-DMT, 4-HO-DET, 4-HO-DiPT show less
4-HO-MET
4-hydroxy-N-methyl-N-ethyltryptamine
4-HO-MET (4-hydroxy-N-methyl-N-ethyltryptamine) — metocin, methylcybin — is a synthetic psychedelic of the tryptamine class. It is a close structural analog of psilocin, the compound responsible for psilocybin mushroom effects. It activates serotonin receptors in the brain, producing the visual distortions and altered thinking characteristic of classical psychedelics.[1]
4-HO-MET (4-hydroxy-N-methyl-N-ethyltryptamine) — metocin, methylcybin — is a synthetic psychedelic of the tryptamine class. It is a close structural analog of psilocin, distinguished by an asymmetric N-methyl-N-ethyl substitution. 4-HO-MET is a 5-HT₂A receptor agonist, producing its effects by disrupting serotonin-mediated sensory filtering and default cognitive processing.[1]
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Serotonin receptor ligandpsilocybin, psilocin, LSD +5 morepsilocybin, psilocin, LSD, mescaline, DMT, 4-AcO-DMT, 4-HO-DET, 4-HO-DiPT show less
First synthesized in 1981 as part of a systematic study of psilocin analogs,[2] it was characterized by Alexander Shulgin in TiHKAL in 1997.[3] Research chemical vendors began selling it around 2008, and it spread through online communities as a lighter alternative to psilocybin mushrooms.[4] It has no approved medical use and continues to circulate in unregulated markets, including in commercially sold tablets confirmed as recently as 2026.[5]
Subjective effects include brightened colors, rippling surfaces, geometric visual patterns, synesthesia, mood elevation, and euphoria. The experience is lighter than psilocybin — visually rich and playful, with less introspective weight — though higher doses can produce ego dissolution and unusual thought patterns.[4] Nausea, restlessness, and rapid swings between euphoria and anxiety are common unsought effects.
4-HO-MET does not produce physical dependence,[6] and no human death has been attributed to the compound alone. The primary risks are psychological — panic, confusion, or acute psychosis[7] — and combining it with serotonin-raising drugs can trigger life-threatening overheating and seizures.[8] Research is extremely limited, and preclinical data flag unquantified heart rhythm effects[9] — most of what is known comes from user reports and analogy to psilocin.
History[edit]
Discovery
4-HO-MET was first synthesized in 1981 by Repke, Ferguson, and Bates as part of a systematic exploration of psilocin analogs.[2] Alexander Shulgin later documented it as entry #21 in TiHKAL (1997), reporting that at 20 mg orally the effects were "qualitatively a lot like psilocin" and speculating it would be indistinguishable from Psilocin in a blind study.[3]
Market emergence and scheduling
The compound appeared on recreational research chemical markets around 2008. Swedish internet forums documented established use patterns by 2011,[4] and Sweden's Medical Products Agency scheduled it in May 2012.[10] No clinical trials have been registered.
Present day
As of 2026, 4-HO-MET continues to circulate globally in unregulated markets. Barovic et al. confirmed its presence in tablets marketed as "Party Duck" in the United States, demonstrating that regulatory gaps in jurisdictions without specific scheduling allow continued manufacture and distribution.[5]
The compound carries several informal names. Metocin and methylcybin derive from its structural relationship to psilocin (4-HO-DMT) — methylcybin referencing psilocybin with a methyl-ethyl substitution, metocin a condensed form. The street name Colour reflects its reputation for vivid chromatic visual effects.[4][11]
Chemistry[edit]
Structural class
4-HO-MET belongs to the 4-substituted tryptamine family — the same structural group as psilocin.[12] The hydroxyl group at position 4 of the indole ring is what activates serotonin receptors and drives psychedelic effects.
4-HO-MET differs from psilocin by a single nitrogen substitution — one methyl group replaced by an ethyl group — placing it between psilocin and 4-HO-DET in the structural series.[1]
Molecular properties
| Molecular formula | C₁₃H₁₈N₂O |
| Molecular weight | 218.29 g/mol |
Pharmacology[edit]
Mechanism of action
4-HO-MET activates serotonin receptors in the brain,[13][14] with its strongest binding at the receptor type most responsible for psychedelic effects.[1][15] Animal studies confirmed it acts through the same serotonin pathway as established classical psychedelics.[16] It does not activate dopamine reward circuits,[15][17][16] which accounts for its negligible dependence potential.
Pharmacokinetics
The body breaks 4-HO-MET down extensively through the liver, producing at least 12 identified metabolites.[18] Standard toxicology screening does not detect it in blood; specialized laboratory analysis is required.[11] People who process certain drugs slowly — through the CYP2D6 enzyme pathway — may experience altered or prolonged effects.[19]
Neuroscience[edit]
Where it acts
No brain imaging studies have been conducted with 4-HO-MET. As a potent serotonin receptor activator,[1] it likely triggers neurons in the prefrontal cortex — the same mechanism responsible for the psychedelic state in related compounds like psilocybin and LSD. This disrupts the brain's normal sensory filtering, loosens boundaries between inputs, and increases communication between brain regions that do not normally interact.
Why it matters
The visual distortions, ego boundary dissolution, and emotional swings reported with 4-HO-MET[4] match a well-established model of psychedelic brain action: the brain's hierarchy of perception loosens, letting raw sensory input overwhelm established mental frameworks. At higher doses, a secondary serotonin receptor may dampen this disruption — potentially placing a ceiling on intensity.[17]
Key unknowns include whether 4-HO-MET promotes structural brain changes comparable to psilocin, how its asymmetric N-methyl-N-ethyl substitution affects brain activation relative to psilocin's symmetric structure, and whether secondary serotonin receptor activity creates a measurable ceiling on neural disruption at higher doses.
Subjective Effects[edit]
The 4-HO-MET experience is defined by the visual and the playful. Color and form shift dramatically, sounds can trigger visual impressions or physical sensations, and the emotional tone tends toward lightness. Mood is unstable, though — euphoria and sharp anxiety can arrive within the same session.[4]
The closest comparison is psilocin[3] — similar in duration and perceptual character — but with more pronounced visuals and less introspective weight. Community reports consistently describe it as lighter in cognitive character than psilocybin mushrooms. This distinction has not been confirmed in controlled research, but the pattern is consistent across reports.[4]
First synthesized by Repke, Ferguson, and Bates in 1981 as part of a psilocin analog series,[2] 4-HO-MET received brief characterization by Alexander Shulgin in TiHKAL (1997).[3] The compound appeared on research chemical markets around 2008, prompting scheduling in Sweden by 2012.[4] It continues to circulate in unregulated markets, including in commercially sold tablets confirmed as recently as 2026.[5]
Subjective effects include color enhancement, geometric visual patterns, synesthesia, lateral cognition, and ego dissolution. The experience is often described as visually rich and playful — a lighter, more recreational variant of the psilocin state where perceptual shifts dominate over deep introspection.[4] Anxiety, paranoia, and rapid swings between euphoria and acute distress are characteristic unsought effects.
4-HO-MET produces no physical dependence, and rapid tolerance makes compulsive redosing self-limiting.[6] The primary risks are psychological — acute psychosis has been documented in a first-time adolescent user[7] — and preclinical data indicate potential heart rhythm effects that remain unquantified in humans.[8] No clinical trials have been conducted; the current understanding rests on one phenomenological study, scattered case reports, and animal data.
History[edit]
Discovery
4-HO-MET was first synthesized by Repke, Ferguson, and Bates in 1981 as part of a systematic exploration of psilocin analogs with varied N,N-dialkyl substitutions.[2] Alexander Shulgin later documented the compound as entry #21 in TiHKAL (1997), reporting that at 20 mg orally the effects were "qualitatively a lot like psilocin" — with alterations of color and form and synesthetic sound perception — and speculated it would be indistinguishable from Psilocin in a blind study.[3]
Market emergence and scheduling
The compound appeared on recreational research chemical markets around 2008. By 2011, Swedish internet forums documented established use patterns among users aged 18–30,[4] and Sweden's Medical Products Agency responded by scheduling 4-HO-MET in May 2012.[9] No clinical trials have been registered, and the compound has not entered pharmaceutical development.
Present day
As of 2026, 4-HO-MET continues to circulate in unregulated markets globally. Barovic et al. confirmed its presence in commercially available tablets marketed as "Party Duck" in the United States, demonstrating ongoing exploitation of regulatory gaps in jurisdictions without specific scheduling.[5]
The compound is known by several informal names: metocin and methylcybin derive from its structural relationship to psilocin (4-HO-DMT) — methylcybin referencing psilocybin with the methyl-ethyl substitution, metocin a condensed form. The street name Colour reflects the compound's reputation for producing vivid chromatic visual effects.[4][10]
Chemistry[edit]
Structural class
4-HO-MET belongs to the 4-substituted tryptamine family — a series of psilocin analogs sharing the indol-4-ol core. Where psilocin (4-HO-DMT) carries symmetric N,N-dimethyl substitution, 4-HO-MET replaces one methyl group with an ethyl group, yielding an asymmetric N-methyl-N-ethyl pattern. This places it between psilocin and 4-HO-DET (N,N-diethyl) in the homologous series.
The 4-hydroxyl group on the indole ring is the pharmacophore responsible for serotonin receptor agonism in this class.[11] Increasing the bulk of N-alkyl substituents modulates potency and duration across the 4-hydroxytryptamine series — the methyl-to-ethyl swap in 4-HO-MET represents the smallest asymmetric departure from psilocin's structure.
Molecular properties
| Molecular formula | C₁₃H₁₈N₂O |
| Molecular weight | 218.29 g/mol |
The molecule consists of an indole bicyclic ring system hydroxylated at the 4-position, with a 2-aminoethyl side chain carrying the N-methyl-N-ethyl substitution.[1]
Stereochemistry
4-HO-MET is achiral, possessing no stereocenters.[1] Enantiomeric considerations do not apply.
Physical properties
Shulgin reported a melting point of 118–119 °C for the free base.[3] No published data on aqueous solubility, logP, pKa, or long-term stability exist. Like other 4-hydroxytryptamines, the compound is presumed susceptible to oxidative degradation at the 4-hydroxy position, though specific degradation kinetics have not been characterized.
Pharmacology[edit]
Mechanism of action
4-HO-MET acts as a direct agonist at the serotonin 5-HT₂A receptor, the primary molecular target responsible for classical psychedelic effects.[12][13] It binds strongly to 5-HT₂A, with secondary activity at 5-HT₂C and 5-HT₁A receptors.[1][14] This receptor profile is consistent with other 4-substituted tryptamines.[15]
The 5-HT₁A activity may partially dampen 5-HT₂A-driven effects at higher doses, potentially producing a ceiling on intensity observed with other 4-hydroxytryptamines.[15] In animal studies, 4-HO-MET fully substituted for the hallucinogen DOM in rats trained to discriminate psychedelic from non-psychedelic drugs, confirming its psychedelic action operates through the 5-HT₂A pathway.[16]
No dopaminergic activity has been identified at relevant concentrations,[14][15][16] which is significant for the compound's low dependence potential.
Pharmacokinetics
No formal human pharmacokinetic parameters — peak concentration time, bioavailability, or half-life — have been published. The oral duration of 4–6 hours and onset within 30 minutes[3] provide indirect timing estimates but do not constitute formal characterization.
Metabolism is substantial. Studies using human liver microsomes identified 12 phase I metabolites, predominantly through hydroxylation of the indole core, demethylation, and deethylation.[17] In actual human urine samples, monohydroxylation and glucuronidation were the dominant pathways.[17] Compatible metabolic pathways were confirmed using a microbial model.[18]
The only published human blood measurement is a plasma concentration of 193 ng/mL from a non-fatal intoxication case, detected by LC-HRMS/MS.[10] Standard GC-MS failed to detect the compound in the same sample, meaning specialized testing is required for clinical identification. Class-level evidence identifies CYP2D6 as the predominant enzyme for tryptamine metabolism,[19] suggesting that individuals who metabolize drugs poorly through this pathway may experience altered effects.
Neuroscience[edit]
Where it acts
No neuroimaging studies have been conducted with 4-HO-MET specifically. As a potent serotonin 2A receptor agonist,[1] it is expected to activate neurons in the prefrontal cortex — the cellular trigger for the psychedelic state observed with related compounds like psilocybin and LSD. This activation disrupts the brain's default mode network, reduces sensory filtering by the thalamus, and increases communication between brain regions that do not normally interact.
At higher doses, 5-HT₁A receptor activity may impose a ceiling on these effects, dampening the cortical disruption produced by 5-HT₂A activation alone.[15]
Why it matters
The perceptual distortions, ego boundary dissolution, and bidirectional emotional shifts reported for 4-HO-MET[4] are consistent with the REBUS model of psychedelic action — the brain's predictive processing hierarchy loosens, allowing raw sensory information to overwhelm established mental frameworks. Class-level evidence suggests serotonergic psychedelics promote structural brain changes through neuroplasticity pathways, though whether 4-HO-MET specifically induces such changes remains untested.
Key unknowns include whether 4-HO-MET promotes structural neuroplasticity comparable to psilocin, how the asymmetric N-methyl-N-ethyl substitution affects brain activation relative to psilocin's symmetric structure, and whether the 5-HT₁A activity creates a measurable ceiling on neural disruption intensity at higher doses.
Subjective Effects[edit]
The 4-HO-MET experience leans toward the visual and playful end of the tryptamine spectrum. Color perception shifts dramatically, geometry overlay the visual field, and sounds may trigger visual impressions or physical sensations. Set and setting powerfully modulate the experience — intensely positive and intensely negative states frequently occur within the same session, with most users encountering both extremes.[4]
Shulgin described 4-HO-MET as "qualitatively a lot like psilocin",[3] and the experiential overlap is substantial — similar dose ranges, durations, and perceptual character. Community reports suggest 4-HO-MET tends toward more pronounced visual effects and a lighter cognitive footprint than Psilocin, with less of the deep introspective weight that defines a psilocin experience. This distinction has not been confirmed in any controlled comparison.
Effect Grid
At common doses (15–25 mg oral), the full psychedelic experience manifests. Pronounced color enhancement and color shifting dominate the visual field. Geometric patterns overlay surfaces and fill closed-eye space. Visual drifting, morphing of objects, and tracers behind moving objects are typical. Auditory distortion and synesthesia — particularly sound-to-color translations — emerge. Time distortion becomes significant, with minutes feeling substantially longer.
Thought acceleration and lateral cognition produce novel associative chains. Emotional intensification amplifies responses to music, social interactions, and environmental stimuli. Ego boundary softening may begin at the upper end of this range.
Physically, nausea during the come-up is common. Body load manifests as temperature dysregulation, mild stimulation, and pupil dilation. Sleep is not possible during the 4–6 hour active window.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Environmental patterning · Music enhancement · Auditory enhancement · Visual breathing · Tracers · Symmetrical texture repetition · Brightness alteration · Depth perception distortion · Perspective distortion · Touch enhancement · Visual morphing · Holotropic state · After-images · Auditory distortion · Synesthesia · Light sensitivity · Peripheral vision distortion · Proprioceptive distortion · Sound sensitivity · Spatial disorientation · Visual diffraction · Visual melting · Visual acuity enhancement · Sleep-transition hallucinations · Vestibular distortion · Visual haze / noise · Olfactory enhancement · Visual processing acceleration · Dreaming enhancement · Peripheral misidentification · Visual magnification · Taste enhancement · Ganzfeld effect · Tinnitus · Object transformations · Internal hallucinations · Visual recursion · Flashbacks · External hallucinations · Object activation · Visual scenery slicing · Auditory hallucinations · Environmental orbism / cubism · Perspective hallucinations · Visual flipping · Olfactory hallucination · Shadow people · Persisting hallucinations
Tracers · Symmetrical texture repetition · Brightness alteration · Depth perception distortion · Perspective distortion · Touch enhancement · Visual morphing · Holotropic state · After-images · Auditory distortion · Synesthesia · Light sensitivity · Peripheral vision distortion · Proprioceptive distortion · Sound sensitivity · Spatial disorientation · Visual diffraction · Visual melting · Visual acuity enhancement · Sleep-transition hallucinations · Vestibular distortion · Visual haze / noise · Olfactory enhancement · Visual processing acceleration · Dreaming enhancement · Peripheral misidentification · Visual magnification · Taste enhancement · Ganzfeld effect · Tinnitus · Object transformations · Internal hallucinations · Visual recursion · Flashbacks · External hallucinations · Object activation · Visual scenery slicing · Auditory hallucinations · Environmental orbism / cubism · Perspective hallucinations · Visual flipping · Olfactory hallucination · Shadow people · Persisting hallucinations
Body high · Appetite suppression · Stimulation · Body schema distortion · Wakefulness · Tactile euphoria · Heart rate perception changes · Laughter fits · Tingling / electric sensations · Vibrations / buzzing · Muscle tension · Nausea · Dizziness · Dry mouth · Insomnia · Physical fatigue · Restlessness · Bodily heaviness · Bodily lightness · Bodily pressures · Breathing alteration · Excessive sweating · Muscle relaxation · Sexual arousal enhancement · Vasoconstriction · Yawning · Abnormal heartbeat · Watery eyes · Brain zaps · Salivation · Bruxism · Dehydration sensation · Headache · Involuntary body movements · Nystagmus (eye wobbles) · Pain suppression · Sedation · Trembling · Diarrhea · Vomiting · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Body schema distortion · Wakefulness · Tactile euphoria · Heart rate perception changes · Laughter fits · Tingling / electric sensations · Vibrations / buzzing · Muscle tension · Nausea · Dizziness · Dry mouth · Insomnia · Physical fatigue · Restlessness · Bodily heaviness · Bodily lightness · Bodily pressures · Breathing alteration · Excessive sweating · Muscle relaxation · Sexual arousal enhancement · Yawning · Abnormal heartbeat · Watery eyes · Brain zaps · Salivation · Bruxism · Dehydration sensation · Headache · Involuntary body movements · Nystagmus (eye wobbles) · Pain suppression · Sedation · Trembling · Diarrhea · Vomiting · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Cognitive euphoria · Pattern recognition enhancement · Immersion enhancement · Cognitive flexibility · Introspection enhancement · Multiple thought streams · Openness enhancement · Conceptual thinking · Thought acceleration · Cognitive impairment · Increased nature relatedness · Creativity enhancement · Humor enhancement · Analysis enhancement · Cognitive fatigue · Focus suppression · Information processing suppression · Synchronicity · Thought disorganization · Confusion · Memory fragmentation · Information processing enhancement · Language enhancement · Motivation enhancement · Memory suppression · Thought loops · Cognitive dysphoria · Memory replays · Motivation suppression · Thought deceleration · Focus enhancement · Delusions of sobriety · Delusions
Cognitive flexibility · Introspection enhancement · Multiple thought streams · Openness enhancement · Conceptual thinking · Thought acceleration · Cognitive impairment · Increased nature relatedness · Creativity enhancement · Humor enhancement · Analysis enhancement · Cognitive fatigue · Focus suppression · Information processing suppression · Synchronicity · Thought disorganization · Confusion · Memory fragmentation · Information processing enhancement · Language enhancement · Motivation enhancement · Memory suppression · Thought loops · Cognitive dysphoria · Memory replays · Motivation suppression · Thought deceleration · Focus enhancement · Delusions
Simultaneous emotions · Empathy enhancement · Catharsis · Anxiety · Anxiety suppression · Dysphoria · Irritability
Anxiety suppression · Dysphoria · Irritability
Disinhibition · Sociability enhancement · Communication enhancement · Flow state · Automaticity · Depersonalization · Ego inflation · Social disconnection · Boundary dissolution · Identity alteration · Ego dissolution · Cognitive disconnection · Telepathic feelings
Automaticity · Depersonalization · Ego inflation · Social disconnection · Boundary dissolution · Identity alteration · Ego dissolution · Cognitive disconnection · Telepathic feelings
Time cessation
Transpersonal memory access · Transpersonal visions · Entity contact · Cessation
Mindfulness enhancement · Recursive awareness
Timeline
First alerts emerge as subtle shifts in color brightness and a gentle internal awareness. Physical cues include mild pupil dilation and faint stomach awareness.
Effects build steadily — color enhancement deepens, geometric patterning begins to emerge, and body load (nausea, restlessness) peaks during this phase. Anticipatory anxiety is common.
Maximum intensity. Visual geometry, color shifting, and object morphing dominate the perceptual field. Synesthesia, time distortion, and lateral cognition are fully active.
Perceptual effects recede gradually — visual geometry simplifies and emotional intensity softens. Cognitive function returns progressively. A sense of gentle mental fatigue or reflective calm is common.
Residual mood elevation or contemplative fatigue may persist. Mild visual brightness and enhanced color perception can linger. Sleep may remain difficult for 1–2 hours beyond the subjective resolution.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- psilo · psilocin · LSD
Toxicity
Acute toxicity
No lethal dose has been determined in any species, and no death has been solely attributed to 4-HO-MET.[11] One polydrug death involved 4-HO-MET alongside designer benzodiazepines and opiates in a 21-year-old male; death was attributed to the benzodiazepines and opiates, not the tryptamines.[20]
Heart rhythm effects
Laboratory and animal studies show that 4-HO-MET disrupts the electrical signals that regulate heartbeat — blocking potassium channels in heart cells and lengthening the recovery time between beats.[9] What this means for human risk at typical recreational doses remains unquantified.safety citation needed
Analytical detection
Standard GC-MS screening does not detect 4-HO-MET in blood; specialized LC-HRMS/MS testing is required.[11] A metabolite of the Parkinson's drug ropinirole can appear identical to 4-HO-MET on standard tests, creating a false-positive identification risk that requires full spectral review and clinical context to resolve.[21]
Psychological risks
One published case documents an adolescent first-time user developing acute psychosis after taking 4-HO-MET.[7] In a study of experience reports, roughly half described intensely negative states — anxiety, paranoia, and acute distress — yet most participants reported overall satisfaction with the experience.[4]
Challenging experiences are statistically linked to set and setting variables across the psychedelic class.[22] No data on persistent visual disturbances (HPPD), long-term psychotic episodes, or psychiatric destabilization beyond acute psychosis have been published for 4-HO-MET.
Tolerance and dependence
Tolerance builds rapidly — detectable within 24 hours of a single dose, with progressive buildup after repeated use.[6] Cross-tolerance with other serotonergic psychedelics is expected. The tolerance is self-limiting: repeated daily use produces diminishing effects rather than escalating reinforcement.[6]
Physical and psychological dependence is negligible. 4-HO-MET does not activate dopamine reward circuits,[15][17][16] and the rapid tolerance makes compulsive use self-limiting.
Drug Interactions
Serotonergic agents (dangerous)
Combining 4-HO-MET with drugs that raise serotonin — including SSRIs, SNRIs, tramadol, and MAOIs — creates risk of serotonin syndrome: a dangerous overheating and seizure response.[23][19]
MAOIs are the highest-risk combination. They block the body's main pathway for clearing tryptamines, dramatically increasing exposure while amplifying serotonin signaling. Deaths have been documented for MAOI combinations with related tryptamines,[8] and the same mechanism applies to 4-HO-MET. Tramadol adds seizure threshold lowering to serotonin reuptake inhibitor, compounding the risk further.
Lithium (caution)
Lithium is significantly associated with both increased difficulty during psychedelic experiences and overall risk of harm.[22][24]
Cannabis (unpredictable)
Cannabis produces dose-dependent, unpredictable changes to the psychedelic experience.[25][24]
QT-prolonging medications (absolute contraindication)
4-HO-MET disrupts the heart's electrical timing.[9] Combining it with other QT-prolonging medications — including certain heart rhythm drugs, macrolide antibiotics, fluoroquinolones, and some antipsychotics — creates additive risk of dangerous irregular heartbeat.
Contraindications
7 knownHeart rhythm conditions and QT prolongation: Demonstrated disruption of heart electrical signals[9] supports absolute contraindication with pre-existing long QT syndrome, congenital heart rhythm conditions, or concurrent QT-prolonging medication use.
Psychotic disorders and high-risk psychiatric conditions: The documented acute psychosis case[7] and class-level evidence support avoiding use with a personal or family history of psychotic disorders. The lithium interaction data further support avoidance during lithium therapy.[22]
Liver impairment: Extensive liver processing of 4-HO-MET[18] means severe impairment could significantly alter drug handling and increase exposure.
Adolescence: The sole published adverse event involved a first-time adolescent user.[7]
Pregnancy: No reproductive or developmental safety data exist. Theoretical serotonergic risk supports absolute contraindication.safety citation needed
Harm Reduction[edit]
Forms & Identification
4-HO-MET circulates primarily as powder and pressed tablets. Tablets marketed as "Party Duck" in the United States averaged only 1.45 mg per tablet — far below typical active doses — confirming that commercially available products are unreliable.[5]
Standard GC-MS testing does not detect 4-HO-MET in biological samples.[11] A metabolite of the Parkinson's drug ropinirole mimics 4-HO-MET on standard tests.[21] Use multiple reagent tests to distinguish 4-HO-MET from other tryptamines in the 4-substituted series. Quantitative laboratory analysis is the only reliable way to confirm both identity and dose.
Guidelines
- Test all material with reagent kits before use; send a sample for laboratory analysis when possible
- Start with a low dose and wait at least 90 minutes before considering redosing — onset can be delayed
- Use a scale accurate to the milligram; never estimate doses by eye with powder
- Have a sober, trusted person present, especially for first experiences or higher doses
- Choose a safe, comfortable environment with no driving or responsibilities for 8+ hours
- Eat lightly several hours beforehand; stay hydrated throughout
- Prepare mentally: set a positive intention, but accept that the experience may include challenging moments
- Keep the environment controllable — have options to change lighting, music, or room
Set & Setting
Roughly half of analyzed experience reports described intensely negative states, yet most participants reported overall satisfaction — suggesting a supportive environment helps manage difficult moments rather than preventing them.[4]
A calm, familiar, private space with no obligations for the following day provides the strongest foundation. A sober, trusted companion who understands the substance is strongly recommended, particularly for anyone without prior psychedelic experience. The sole published psychosis case involved a first-time adolescent user in an unsupported setting[7] — inexperience, youth, and unsupported settings compound psychological risk.
Aftercare & integration. The days following a 4-HO-MET experience may include subtle emotional openness or sensitivity. Allow time for rest and reflection before returning to demanding routines.
Journaling within 24 hours helps capture insights while they remain accessible. If the experience included challenging moments — anxiety, paranoia, or ego dissolution — processing these with a trusted person or integration-trained therapist can help extract meaning rather than leaving them as unresolved distress. Persistent anxiety, depersonalization, or visual disturbances lasting more than a week warrant professional consultation.
Recovery & Support
4-HO-MET carries negligible abuse liability — compulsive use patterns are rare due to rapid tolerance and the absence of dopamine mesolimbic pathway activation. Psychological attachment to psychedelic experiences can develop in some individuals, particularly when used to escape rather than explore.
If psychedelic use is causing distress, interfering with daily functioning, or escalating in frequency despite negative consequences, support resources include the Fireside Project (62-FIRESIDE / 623-473-7433), the MAPS Integration List for finding integration-trained therapists, and local harm reduction organizations.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Most difficult 4-HO-MET experiences resolve on their own within 4–6 hours. The line between uncomfortable and dangerous:
Uncomfortable but manageable: anxiety, paranoia, confusion, nausea, rapid heartbeat, emotional distress. These are common and typically pass. Reassurance, calm surroundings, and patient companionship are usually sufficient.
Seek immediate help if:
- The person is at risk of harming themselves or others
- Chest pain, irregular heartbeat, or fainting occurs
- The person becomes completely unresponsive to verbal communication
- Severe overheating or seizure activity develops
- Psychotic symptoms (fixed delusions, command hallucinations) persist and escalate
While waiting for help:
- Call emergency services
- Keep the person in a safe, quiet space — do not restrain unless there is immediate danger of self-harm
- Do not leave them alone
- Do not induce vomiting
Tell the dispatcher: the substance name (4-HO-MET or metocin), approximate amount taken, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
4-HO-MET is not internationally scheduled and is not specifically controlled at the federal level in the United States, though its legal status varies widely by jurisdiction.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Federally unscheduled | Potential Schedule I analog of psilocin under the Federal Analogue Act; no documented prosecutions. South Dakota and West Virginia have state-level scheduling[10][26] |
| United Kingdom | Class A controlled drug | Caught under tryptamine catch-all clause of the Misuse of Drugs Act 1971[10] |
| Australia | Schedule 9 Prohibited Substance | Prohibited for all non-research purposes[26] |
| Canada | Not a controlled substance (as of 2025) | No specific scheduling identified[26] |
| Sweden | Schedule I (LVFS 2012:6) | Controlled since May 2012 following documented recreational use[10][4] |
| Germany | Controlled (NpSG) | Neue-psychoaktive-Stoffe-Gesetz effective July 18, 2019; production, import for market placement, and trading prohibited. Possession not separately punishable[26] |
Legal status changes frequently. This information is not legal advice. Verify current laws in the relevant jurisdiction before acting on it.
Legal status information relies primarily on Erowid (last updated 2015) and secondary web sources.[10][26] Independent verification is recommended. Finland has been reported as controlled but the specific regulation was not confirmed.citation needed
The ongoing availability of 4-HO-MET in commercial products[5] demonstrates that the patchwork regulatory landscape allows continued manufacture and distribution through jurisdictions lacking specific controls.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- psilo · psilocin · LSD
Toxicity
Acute toxicity
No lethal dose has been determined for 4-HO-MET in any species. The only published human exposure measurement is a plasma concentration of 193 ng/mL from a non-fatal intoxication case.[10] No death has been solely attributed to 4-HO-MET.
One polydrug fatality involved 4-HO-MET alongside other tryptamines, designer benzodiazepines, and opiates in a 21-year-old male; death was attributed to the benzodiazepines and opiates, not the tryptamines.[20]
Heart rhythm effects
Preclinical studies demonstrated that 4-HO-MET inhibits hERG potassium channels in cell cultures and prolongs the QT interval in rats.[8] These findings indicate a potential cardiac risk signal, though human heart risk at typical doses remains unquantified.safety citation needed
The broader psychedelic class carries theoretical cardiovascular concern through 5-HT₂A/2B receptor activity, which is associated with blood clot formation and irregular heart rhythm potential.[21]
Analytical detection
Standard GC-MS fails to detect 4-HO-MET in blood samples; specialized LC-HRMS/MS testing is required.[10] A clinically significant interference exists: a metabolite of the Parkinson's drug ropinirole mimics 4-HO-MET on standard laboratory testing,[22] requiring full spectral review and clinical context to avoid false-positive identification.
Psychological risks
One case of drug-induced acute psychosis has been published in a first-time adolescent user.[7] This remains the only published psychiatric adverse event for the compound.
In Kjellgren and Soussan's phenomenological study, roughly half of analyzed experience reports described intensely negative states — anxiety, paranoia, and acute distress — sometimes occurring within the same session as positive experiences.[4] Despite encountering these states, most participants reported overall satisfaction.
Challenging psychedelic experiences are statistically associated with set and setting variables across the psychedelic class.[23] No data on HPPD (HPPD), long-term psychotic episodes, or psychiatric destabilization beyond acute psychosis have been published for 4-HO-MET.
Tolerance and dependence
Tolerance develops rapidly through 5-HT₂A downregulation — class-level mouse data show detectable tolerance within 24 hours of a single dose, with progressive tolerance after repeated dosing.[6] Cross-tolerance between serotonergic psychedelics is expected. The commonly cited 3-day half-life and 7-day full reset is a class-level inference, not a measured parameter for 4-HO-MET.
Physical and psychological dependence liability is negligible. 4-HO-MET does not engage dopamine reward pathways,[14][15][16] and the rapid tolerance buildup is self-limiting — repeated daily use produces diminishing returns rather than escalating reinforcement.[6]
Drug Interactions
Serotonergic agents (dangerous)
Combining 4-HO-MET with drugs that increase serotonin levels — including SSRIs, SNRIs, tramadol, and MAOIs — carries serotonin syndrome risk.[24][19]
MAOIs block the primary metabolic clearance pathway for tryptamines, dramatically increasing exposure while potentiating serotonin signaling. Fatalities have been documented for MAOI combinations with related tryptamines including DMT and 5-MeO-DMT.[25] By mechanism, MAOI + 4-HO-MET carries equivalent risk.
Tramadol combines serotonin reuptake inhibitor with seizure threshold lowering, creating compounded risk with serotonergic psychedelics.
Lithium (caution)
Lithium use is significantly associated with both increased difficulty during psychedelic experiences and overall risk of harm.[23][26]
Cannabis (unpredictable)
Cannabis produces dose-dependent modulation of the psychedelic experience, though the clinical significance remains unclear.[27][26]
QT-prolonging medications (absolute contraindication)
Based on 4-HO-MET's demonstrated hERG channel inhibition and QT prolongation,[8] concurrent use of QT-prolonging medications creates additive irregular heart rhythm risk. This is the best-evidenced drug interaction for 4-HO-MET, supported by substance-specific experimental data. Relevant medication classes include certain heart rhythm drugs, macrolide antibiotics, fluoroquinolones, and some antipsychotics.
Contraindications
7 knownHeart rhythm conditions and QT prolongation: The demonstrated hERG inhibition and QT prolongation[8] support absolute contraindication in individuals with pre-existing long QT syndrome, congenital irregular heart rhythms, or concurrent QT-prolonging medication use.
Psychotic disorders and high-risk psychiatric conditions: The documented case of acute psychosis in an adolescent[7] and class-level risk support contraindication in individuals with personal or family history of psychotic disorders. The lithium interaction data further support avoidance in individuals on lithium therapy.[23]
Liver impairment: The 12 phase I metabolites identified indicate substantial liver processing.[17] Severe liver impairment could significantly alter how the body handles the drug and increase exposure.
Adolescence: The sole published adverse event involves an adolescent first-time user experiencing acute psychosis,[7] supporting caution for this age group.
Pregnancy: No reproductive or developmental safety data exist. The absence of data combined with theoretical serotonergic risk supports absolute contraindication.safety citation needed
Harm Reduction[edit]
Forms & Identification
4-HO-MET circulates primarily as powder and pressed tablets — Barovic et al. confirmed its presence in tablets marketed as "Party Duck" in the United States.[5] Tablet dosages in that analysis averaged 1.45 mg per tablet, well below typical active doses, underscoring the unreliability of commercially marketed products.
Reagent testing is essential but limited with this compound. Standard GC-MS fails to detect 4-HO-MET in biological samples,[10] and a clinically significant analytical confusion exists: a metabolite of the Parkinson's drug ropinirole mimics 4-HO-MET on standard laboratory testing.[22] Multiple reagent tests should be used to distinguish 4-HO-MET from other tryptamines in the 4-substituted series. Quantitative laboratory analysis is the only reliable way to confirm both identity and dose.
Guidelines
- Test all material with reagent kits before use; send a sample for laboratory analysis when possible
- Start with a low dose and wait at least 90 minutes before considering redosing — onset can be delayed
- Use a scale accurate to the milligram; never estimate doses by eye with powder
- Have a sober, trusted person present, especially for first experiences or higher doses
- Choose a safe, comfortable environment with no driving or responsibilities for 8+ hours
- Eat lightly several hours beforehand; stay hydrated throughout
- Prepare mentally: set a positive intention, but accept that the experience may include challenging moments
- Keep the environment controllable — have options to change lighting, music, or room
Set & Setting
The phenomenological evidence for 4-HO-MET underscores the role of context. Roughly half of analyzed experience reports included intensely negative states, yet most users reported overall satisfaction — suggesting that a supportive environment helps manage difficult moments rather than preventing them.[4]
A calm, familiar, private space with minimal obligations for the following day provides the strongest foundation. A trusted, sober companion who understands the substance's effects and duration is strongly recommended, particularly for those without prior psychedelic experience. The adolescent psychosis case involved a first-time user[7] — inexperience, youth, and unsupported settings compound psychological risk.
Aftercare & integration. The days following a 4-HO-MET experience may include subtle emotional openness or sensitivity. Allow time for rest and reflection before returning to demanding routines.
Journaling within 24 hours helps capture insights while they remain accessible. If the experience included challenging moments — anxiety, paranoia, or ego dissolution — processing these with a trusted person or integration-trained therapist can help extract meaning rather than leaving them as unresolved distress. Persistent anxiety, depersonalization, or visual disturbances lasting more than a week warrant professional consultation.
Recovery & Support
4-HO-MET carries negligible abuse liability — compulsive use patterns are rare due to rapid tolerance and the absence of dopamine mesolimbic pathway activation. However, psychological attachment to psychedelic experiences can develop in some individuals, particularly when used to escape rather than explore.
If psychedelic use is causing distress, interfering with daily functioning, or escalating in frequency despite negative consequences, support resources include the Fireside Project (62-FIRESIDE / 623-473-7433), the MAPS Integration List for finding integration-trained therapists, and local harm reduction organizations.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Most difficult 4-HO-MET experiences resolve on their own within 4–6 hours. The line between uncomfortable and dangerous:
Uncomfortable but manageable: anxiety, paranoia, confusion, nausea, rapid heartbeat, emotional distress. These are common and typically pass. Reassurance, calm surroundings, and patient companionship are usually sufficient.
Seek immediate help if:
- The person is at risk of harming themselves or others
- Chest pain, irregular heartbeat, or fainting occurs
- The person becomes completely unresponsive to verbal communication
- Severe overheating or seizure activity develops
- Psychotic symptoms (fixed delusions, command hallucinations) persist and escalate
While waiting for help:
- Call emergency services
- Keep the person in a safe, quiet space — do not restrain unless there is immediate danger of self-harm
- Do not leave them alone
- Do not induce vomiting
Tell the dispatcher: the substance name (4-HO-MET or metocin), approximate amount taken, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
4-HO-MET occupies a fragmented regulatory position globally. It is not internationally scheduled under United Nations conventions and is not specifically controlled at the federal level in the United States, though the Federal Analogue Act creates prosecution risk when intended for human consumption. Several jurisdictions have enacted specific or blanket controls.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Federally unscheduled | Potential Schedule I analog of psilocin under the Federal Analogue Act; no documented prosecutions. South Dakota and West Virginia have state-level scheduling[9][28] |
| United Kingdom | Class A controlled drug | Caught under tryptamine catch-all clause of the Misuse of Drugs Act 1971[9] |
| Australia | Schedule 9 Prohibited Substance | Prohibited for all non-research purposes[28] |
| Canada | Not a controlled substance (as of 2025) | No specific scheduling identified[28] |
| Sweden | Schedule I (LVFS 2012:6) | Controlled since May 2012 following documented recreational use[9][4] |
| Germany | Controlled (NpSG) | Neue-psychoaktive-Stoffe-Gesetz effective July 18, 2019; production, import for market placement, and trading prohibited. Possession not separately punishable[28] |
Legal status information relies primarily on Erowid (last updated 2015) and secondary web sources.[9][28] Independent verification of current statutes is recommended. Finland has been reported as controlled by web sources but the specific regulation was not confirmed.citation needed
The ongoing availability of 4-HO-MET in commercial products — confirmed by Barovic et al.[5] — demonstrates that the patchwork regulatory landscape allows continued manufacture and distribution through jurisdictions lacking specific controls.
Frequently asked questions
How long does 4-HO-MET last?
Total duration by route of administration — Oral: 4 – 6 hours; Smoked: 25 – 45 min. Ranges vary with dose and individual factors; see the duration table for onset, peak, and after-effect phases.
Where can I find dosage information for 4-HO-MET?
Psychedex publishes a dosage table for 4-HO-MET on this page covering these routes of administration: oral, smoked. Dose values are presented only in that table, always alongside their route of administration.
What are dangerous combinations with 4-HO-MET?
The highest-severity documented interactions for 4-HO-MET: MAOIs (Lethal), Dopamine agonists (Dangerous), GHB, Baclofen (Dangerous), GHB, GBL (Dangerous), Ibogaine (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is 4-HO-MET addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 4-HO-MET: tolerance builds rapid; full reset takes 7 days; cross-tolerance develops with psilocybin, psilocin, LSD, mescaline, DMT, 4-AcO-DMT, 4-HO-DET, 4-HO-DiPT. See the article's dependence and safety sections for recorded dependence data.
experience reports
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1]
- [2] ^abRepke D, Ferguson W, Bates D (1981) Psilocin analogs II. Synthesis of 3-[2-(dialkylamino)ethyl]-, 3-[2-(N-methyl-N-alkylamino)ethyl]-, and 3-[2-(cycloalkylamino)ethyl]indol-4-ols — Journal of Heterocyclic Chemistry doi:10.1002/jhet.5570180131
- [3]
- [4]
- [5] ^abcdBarovic A, Pittiglio M, Barrett J, Aretz C, Tesfatsion T, Ramirez G, Cruces W (2026) Presence of 4-Hydroxy-N-methyl-N-ethyltryptamine in Commercially Available Products — ACS Omega doi:10.1021/acsomega.5c10889
- [6] ^abcde la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J (2022) Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice — ACS Chemical Neuroscience doi:10.1021/acschemneuro.2c00170
references
- [1]
- [2] ^abRepke D, Ferguson W, Bates D (1981) Psilocin analogs II. Synthesis of 3-[2-(dialkylamino)ethyl]-, 3-[2-(N-methyl-N-alkylamino)ethyl]-, and 3-[2-(cycloalkylamino)ethyl]indol-4-ols — Journal of Heterocyclic Chemistry doi:10.1002/jhet.5570180131
- [3]
- [4]
- [5] ^abcdBarovic A, Pittiglio M, Barrett J, Aretz C, Tesfatsion T, Ramirez G, Cruces W (2026) Presence of 4-Hydroxy-N-methyl-N-ethyltryptamine in Commercially Available Products — ACS Omega doi:10.1021/acsomega.5c10889
- [6] ^abcde la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J (2022) Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice — ACS Chemical Neuroscience doi:10.1021/acschemneuro.2c00170