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5-MeO-MiPT
5-methoxy-N-methyl-N-isopropyltryptamine
5-MeO-MiPT (5-methoxy-N-methyl-N-isopropyltryptamine) — Moxy — is a synthetic psychedelic of the tryptamine class. It is a close structural relative of 5-MeO-DiPT, sharing a similar base with a distinct nitrogen arrangement. It activates serotonin receptors in the brain, producing psychedelic effects defined by unusual physical intensity.[1]
5-MeO-MiPT (5-methoxy-N-methyl-N-isopropyltryptamine) — Moxy — is a synthetic psychedelic of the tryptamine class. It is a close structural relative of 5-MeO-DiPT, distinguished by pronounced somatic stimulation alongside its psychedelic action. 5-MeO-MiPT is a full agonist at the serotonin 5-HT₂A receptor, producing its effects by activating G-protein signaling cascades that alter sensory processing and cognition.[1]
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Repke, Grotjahn, and Shulgin first synthesized it in 1985,[2] and Shulgin documented it in depth in his 1997 book TiHKAL.[3] Recreational use emerged through online research chemical markets in the early 2000s, where it acquired the name "Moxy." It remains unscheduled at the US federal level, though a 2022 DEA scheduling proposal was withdrawn pending further review.[4]
Subjective effects include physical stimulation, tactile enhancement, aphrodisiac warmth, empathogenic openness, and mild visual changes. The experience is defined by its body emphasis — a buzzing physical activation and emotional openness that sets it apart from the visually dominant character of most classical tryptamines. At higher doses, intense body load, vasoconstriction, and overwhelming stimulation are characteristic unsought effects.
5-MeO-MiPT does not produce physical dependence; tolerance builds rapidly after a single dose, limiting compulsive use.[5] The main acute danger is cardiovascular stress — documented as rapid heart rate and elevated blood pressure;[6] serotonergic drugs and stimulants sharply compound this risk. The evidence base is sparse — no clinical trials exist, and knowledge rests on self-experiments, forensic reports, and animal studies.
History[edit]
Discovery
5-MeO-MiPT was first synthesized by David Repke, David Grotjahn, and Alexander Shulgin, with results published in 1985.[2] Among eight related compounds tested for hallucinogenic activity, the 5-methoxy version stood out for its potency and oral activity.[2] Shulgin expanded the account in TiHKAL (1997), adding synthesis details, dosage guidance, and self-experiment notes.[3]
Recreational emergence
5-MeO-MiPT entered recreational use through online research chemical vendors in the early 2000s. Forensic traces appeared in Italy in 2014,[7] Germany and Switzerland by 2016,[8] and Japanese monitoring databases by 2007.[9] No institutional research program has ever been established; its entire pharmacological profile derives from self-experiments, forensic cases, and animal studies.
Regulatory history
The DEA classified 5-MeO-MiPT as an structural analog of 5-MeO-DiPT in 2005, making it potentially prosecutable under the Federal Analogue Act when intended for human consumption. A formal Schedule I proposal came in January 2022 and was withdrawn in July 2022 pending updated scientific review.[4] Federal scheduling remains unresolved as of April 2026.
The name "Moxy" emerged in online communities during the compound's early circulation through research chemical markets. 5-MeO-MiPT is frequently discussed alongside 5-MeO-DiPT ("Foxy") and 4-HO-MiPT, forming a trio of asymmetrically N-alkylated tryptamines with overlapping but distinct experiential profiles. Its reputation for unusually body-focused psychedelia and aphrodisiac effects sets it apart from most classical tryptamines in user discussions.
Chemistry[edit]
Structural class
5-MeO-MiPT belongs to the substituted tryptamine family, sharing the indole-ethylamine backbone common to DMT, psilocin, and 5-MeO-DMT.
The methoxy group at the 5-position of the indole ring is critical for activity — positional isomers placed elsewhere on the ring lack significant psychoactivity.[3] The compound has no chirality center, so no stereoisomer considerations apply.[10]
Molecular properties
| Molecular formula | C₁₅H₂₂N₂O |
| Molecular weight | 246.35 g/mol |
Pharmacology[edit]
Mechanism of action
5-MeO-MiPT activates serotonin receptors in the brain — the same pathway used by psilocybin and LSD.[1] It does not work by flooding the brain with serotonin the way MDMA does; it directly stimulates the receptor.[1][11][12] Whether it also engages a second serotonin receptor pathway — which might soften the experience — remains unresolved.[1][13] citation needed
Pharmacokinetics
No human pharmacokinetic studies exist. Metabolism has been characterized using human liver tissue and forensic samples[8]: the compound is broken down primarily by removal of the N-methyl group and modification of the methoxy group, yielding four metabolites detectable in blood and seven in urine.[8]
Route-dependent potency
5-MeO-MiPT is several times more potent when taken orally than when smoked — the inverse of 5-MeO-DMT.[3] The reason is unknown — it may reflect better oral absorption or conversion to a more active compound during liver processing. Neither mechanism has been formally investigated.
Neuroscience[edit]
Where it acts
No brain imaging studies have been conducted with 5-MeO-MiPT. As a serotonin receptor activator,[1] it is expected to act on neurons in the prefrontal cortex — where other serotonergic psychedelics disrupt the brain's filtering of sensory input and alter thought patterns.
Why it matters
The experience skews toward body and cognition rather than visual effects. This suggests the compound engages body-sensing and conceptual processing networks more than visual cortex — though this remains speculative without imaging data.
Zebrafish studies show that sustained 5-MeO-MiPT exposure causes liver-brain signaling disruption and tissue damage;[14][15] whether this translates to human use is unknown. The greater oral than smoked potency raises the question of whether liver metabolism produces an active metabolite. Conflicting data on a second serotonin receptor pathway[1][13] cannot be resolved without direct receptor occupancy studies.
Subjective Effects[edit]
5-MeO-MiPT centers on the body. Physical stimulation, tactile enhancement, and a warm empathogenic openness dominate the common dose range. Visual changes are subtle — altered depth perception and mild pattern enhancement — rather than the rich geometric hallucinations of classical tryptamines. The balance between sociable warmth and introspective withdrawal shifts with environment and mood.
The experience sits between 5-MeO-DMT and 4-HO-MiPT. It lacks the ego-dissolving intensity of 5-MeO-DMT and the visual richness of 4-HO-MiPT. What it offers instead is physical activation and conceptual fluidity — a body-forward psychedelia closer to an empathogen than a classical visionary tryptamine.
Synthesized by Repke, Grotjahn, and Shulgin in 1985,[2] 5-MeO-MiPT was documented in detail in Shulgin's 1997 TiHKAL monograph.[3] Recreational use emerged through online research chemical markets in the early 2000s, where the compound acquired the name "Moxy." It remains unscheduled at the US federal level — a 2022 DEA proposal to place it in Schedule I was withdrawn pending further review.[4]
Subjective effects include physical stimulation, tactile enhancement, enhanced conceptual thinking, and aphrodisiac warmth. The experience is defined by its somatic emphasis — a buzzing physical activation with empathogenic openness and cognitive fluidity that distinguishes it from the visually dominant character of most classical tryptamines. Intense body load, vasoconstriction, and overwhelming stimulation at higher doses are characteristic unsought effects.
No physical dependence has been documented, and rapid tolerance development via 5-HT₂A downregulation provides an inherent brake on compulsive redosing.[5] The primary acute risk is cardiovascular stress — rapid heart rate and elevated blood pressure observed in the single documented human poisoning case[6] — compounded by unpredictable dose-response at single-digit milligram quantities. No clinical trials, controlled pharmacokinetic studies, or systematic human toxicity data exist; the entire evidence base rests on self-experiments, forensic case reports, and preclinical animal models.
History[edit]
Discovery
5-MeO-MiPT was first synthesized by David Repke, David Grotjahn, and Alexander Shulgin, with results published in 1985 in the Journal of Medicinal Chemistry.[2] The paper evaluated eight N-methyl-N-isopropyltryptamines for hallucinogenic activity, and the 5-methoxy derivative demonstrated a substantial increase in potency and oral activity compared to its dimethyl homologues.[2] Shulgin expanded his account in TiHKAL (entry #40, 1997), providing synthesis instructions, multiple self-experiment narratives, and dosage guidance.[3]
Recreational emergence
5-MeO-MiPT entered recreational use through online research chemical vendors in the early 2000s. Forensic identification followed — first in Italy in 2014,[7] then in Germany and Switzerland by 2016,[8] and in Japanese NPS monitoring databases by 2007.[9] No institutional research program has ever been established for this compound; its entire pharmacological profile derives from Shulgin-era self-experiments, forensic case reports, and preclinical animal studies.
Regulatory history
The US DEA classified 5-MeO-MiPT as an structural analog of Schedule I substance 5-MeO-DiPT in a 2005 bulletin, making it potentially prosecutable under the Federal Analogue Act when intended for human consumption. A formal proposal to place 5-MeO-MiPT in Schedule I was published in January 2022, then withdrawn in July 2022 with the DEA requesting a new scientific evaluation from the Department of Health and Human Services.[4] Federal scheduling remains pending as of April 2026.
The name "Moxy" emerged in online user communities during the compound's initial circulation through research chemical markets. 5-MeO-MiPT is frequently discussed alongside its structural relatives 5-MeO-DiPT ("Foxy") and 4-HO-MiPT, forming a trio of asymmetrically N-alkylated tryptamines with overlapping but distinct experiential profiles. The compound occupies a niche reputation for its unusually body-focused psychedelia and aphrodisiac properties — characteristics that set it apart from most classical tryptamines in user discussions.
Chemistry[edit]
Structural class
5-MeO-MiPT belongs to the substituted tryptamine family, sharing the indole-ethylamine backbone common to DMT, psilocin, and 5-MeO-DMT. The nitrogen carries one methyl and one isopropyl group — an asymmetric pattern that distinguishes the MiPT series from the symmetrical dimethyl (DMT) and diisopropyl (DiPT) families. A methoxy group at the 5-position of the indole ring is critical for activity: the positional isomers 6-MeO-MiPT and 7-MeO-MiPT lack significant psychoactivity.[3]
Molecular properties
| Molecular formula | C₁₅H₂₂N₂O |
| Molecular weight | 246.35 g/mol |
Stereochemistry
5-MeO-MiPT possesses no chirality center. The isopropyl group on the terminal nitrogen does not create a stereogenic center in the ethylamine chain, so no stereoisomer considerations apply.[10]
Physical properties
The freebase melts at approximately 72–74 °C; the hydrochloride salt at 162–163 °C. The freebase dissolves in DMSO, ethanol, and DMF but is insoluble in water, while the hydrochloride salt dissolves readily in water.[10]
Pharmacology[edit]
Mechanism of action
5-MeO-MiPT acts primarily as a full agonist at the serotonin 5-HT₂A receptor, strongly activating G-protein signaling pathways in the brain.[1] This is the same receptor target through which classical psychedelics like psilocybin and LSD produce their effects. Among a series of 5-methoxytryptamines tested for G-protein activation in rat brain tissue, 5-MeO-MiPT ranked behind 5-MeO-DMT and 5-MeO-DALT but ahead of 5-MeO-DiPT.[9]
The compound does not significantly interact with the SERT,[1] distinguishing it from entactogenic compounds like MDMA that work by flooding the synapse with serotonin. Independent studies confirm only weak monoamine reuptake activity and minimal monoamine release.[11][12] Claims in some vendor literature that 5-MeO-MiPT is a "serotonin reuptake inhibitor" are not supported by pharmacological data.
Whether 5-MeO-MiPT also activates the 5-HT₁A receptor remains contested. One study found the compound inactive at this target,[1] while structural research on 5-methoxytryptamines as a class suggests they do engage 5-HT₁A.[13] The question is unresolved for this specific compound. citation needed
Like all serotonergic psychedelics, 5-MeO-MiPT likely interacts with multiple receptor targets beyond 5-HT₂A, including several other serotonin receptor subtypes.[14] The relative contribution of each target to the overall experience has not been established.
Pharmacokinetics
No controlled human pharmacokinetic studies have been published for 5-MeO-MiPT. No data exist for peak plasma time, half-life, or oral bioavailability.
Metabolism has been characterized using human liver microsomes and forensic biological samples.[8] The primary metabolic pathways involve removal of the N-methyl group and modification of the methoxy group. Four metabolites were detected in blood and seven in urine from a single forensic case.[8] No direct identification of which liver enzymes process the compound has been published, though related 5-methoxytryptamines are metabolized by several common cytochrome P450 enzymes. inferred
Route-dependent potency
An unusual feature of 5-MeO-MiPT is that it is several times more potent when taken orally than when smoked — the inverse of 5-MeO-DMT.[3] This pattern could reflect superior oral absorption or conversion to an active metabolite during first-pass liver processing, but neither mechanism has been formally investigated.
Neuroscience[edit]
Where it acts
No neuroimaging or brain activity studies have been conducted with 5-MeO-MiPT in humans or animals. As a full serotonin 2A receptor agonist,[1] it is expected to activate receptors on deep-layer neurons in the prefrontal cortex — the same mechanism through which other serotonergic psychedelics increase glutamate release, disrupt default mode network coherence, and alter the brain's filtering of sensory and cognitive input.
The experiential profile — somatic and cognitive rather than intensely visual — suggests the compound's effects may preferentially engage body-sensing and conceptual processing networks rather than visual cortex.
Why it matters
Two theoretical frameworks help explain 5-MeO-MiPT's effects. The REBUS model proposes that 5-HT₂A agonists loosen the brain's prior expectations, increasing neural flexibility — though the somatic emphasis of 5-MeO-MiPT's effects suggests this loosening manifests more in body awareness and thought than in visual perception.
The psychoplastogen hypothesis suggests serotonergic psychedelics promote structural brain changes via growth-factor signaling. Whether 5-MeO-MiPT does so is unknown, but its unusual signaling profile at 5-HT₂A[1] makes it a potentially informative test case for understanding which signaling pathways drive neuroplasticity.
Subjective Effects[edit]
5-MeO-MiPT produces an experience centered on the body rather than the visual field. Physical stimulation, tactile enhancement, and aphrodisiac warmth dominate the common dose range, with cognitive fluidity and empathogenic openness running alongside. Visual effects remain subtle below higher doses — altered depth perception and mild pattern enhancement rather than the rich geometric hallucinations typical of classical tryptamines. Set and setting strongly modulate the balance between euphoric sociability and introspective withdrawal.
The compound sits between 5-MeO-DMT and 4-HO-MiPT in experiential character: it lacks the ego-dissolving intensity of the former and the visual richness of the latter, occupying a niche defined by physical activation and conceptual fluidity.
Effect Grid
At common doses (4–6 mg oral), the full experiential profile described in TiHKAL manifests. Physical stimulation is prominent — tingling, body warmth, and tactile enhancement dominate the somatic landscape. Conceptual thinking is enhanced, with increased thought connectivity and philosophical ideation. Altered depth perception emerges, along with minor wave-like visual distortions in the peripheral field. Frank visual hallucinations are generally absent at this range.
Aphrodisiac and empathogenic qualities are frequently reported. Music enhancement is notable. Body load increases and may include vasoconstriction and mild tachycardia. Nausea is possible during the come-up phase.
Duration is 4–6 hours. Sleep is typically difficult for 1–2 hours after effects subside.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual breathing · Visual drifting · Tracers · After-images · Auditory enhancement · Brightness alteration · Light sensitivity · Sound sensitivity · Symmetrical texture repetition · Auditory distortion · Depth perception distortion · Environmental patterning · Perspective distortion · Proprioceptive distortion · Spatial disorientation · Synesthesia · Vestibular distortion · Visual diffraction · Visual haze / noise · Visual morphing · Visual acuity enhancement · Tinnitus · Visual melting · Taste enhancement · Visual processing acceleration · Object transformations · Internal hallucinations · Visual scenery slicing · Auditory hallucinations · External hallucinations
Auditory enhancement · Brightness alteration · Light sensitivity · Sound sensitivity · Symmetrical texture repetition · Auditory distortion · Depth perception distortion · Environmental patterning · Perspective distortion · Proprioceptive distortion · Spatial disorientation · Synesthesia · Vestibular distortion · Visual diffraction · Visual haze / noise · Visual morphing · Visual acuity enhancement · Tinnitus · Visual melting · Taste enhancement · Visual processing acceleration · Object transformations · Internal hallucinations · Visual scenery slicing · Auditory hallucinations · External hallucinations
Wakefulness · Body high · Muscle tension · Tingling / electric sensations · Nausea · Bodily pressures · Sexual arousal enhancement · Restlessness · Tactile euphoria · Vibrations / buzzing · Appetite suppression · Dry mouth · Heart rate perception changes · Insomnia · Abnormal heartbeat · Headache · Dehydration sensation · Breathing alteration · Bruxism · Dizziness · Excessive sweating · Kundalini-like energy · Laughter fits · Physical fatigue · Diarrhea · Body schema distortion · Involuntary body movements · Motor control impairment · Nystagmus (eye wobbles) · Respiratory stimulation · Trembling · Watery eyes · Vomiting · Bodily dissociation · Tactile hallucination
Tingling / electric sensations · Nausea · Bodily pressures · Sexual arousal enhancement · Restlessness · Tactile euphoria · Vibrations / buzzing · Appetite suppression · Dry mouth · Heart rate perception changes · Insomnia · Headache · Dehydration sensation · Breathing alteration · Bruxism · Dizziness · Excessive sweating · Kundalini-like energy · Laughter fits · Physical fatigue · Diarrhea · Body schema distortion · Involuntary body movements · Motor control impairment · Nystagmus (eye wobbles) · Respiratory stimulation · Trembling · Watery eyes · Vomiting · Bodily dissociation · Tactile hallucination
Openness enhancement · Pattern recognition enhancement · Conceptual thinking · Thought acceleration · Thought connectivity · Cognitive euphoria · Cognitive flexibility · Immersion enhancement · Creativity enhancement · Humor enhancement · Memory suppression · Cognitive impairment · Confusion · Focus suppression · Increased nature relatedness · Information processing suppression · Multiple thought streams · Thought disorganization · Thought loops · Analysis enhancement · Cognitive dysphoria · Memory fragmentation · Memory replays · Synchronicity · Information processing enhancement · Motivation enhancement
Thought connectivity · Cognitive euphoria · Cognitive flexibility · Immersion enhancement · Creativity enhancement · Humor enhancement · Memory suppression · Cognitive impairment · Confusion · Focus suppression · Increased nature relatedness · Information processing suppression · Multiple thought streams · Thought disorganization · Thought loops · Analysis enhancement · Cognitive dysphoria · Memory fragmentation · Memory replays · Synchronicity · Information processing enhancement · Motivation enhancement
Emotional lability · Catharsis · Simultaneous emotions · Dysphoria
Trust enhancement · Communication enhancement · Depersonalization · Derealization · Flow state · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration
Flow state · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration
Transpersonal visions · Entity contact
Timeline
First alerts emerge within 10–30 minutes — mild tingling, subtle mood shift, and slight physical activation. Shulgin reported onset as rapid (10–15 minutes); community reports average 20–40 minutes.
Physical stimulation intensifies progressively. Body tingling, rising tactile sensitivity, and the first hints of cognitive alteration. Nausea may occur during this phase.
Full expression of effects: pronounced somatic stimulation, conceptual enhancement, altered depth perception, and aphrodisiac qualities. Visual effects remain subtle at common doses — peripheral waviness rather than formed geometry. Peak lasts 1.
Effects sustain at reduced intensity. Physical stimulation remains present but cognitive effects begin to normalize. Mood elevation and tactile enhancement persist.
Gradual return to baseline over 1–1. 5 hours. Residual stimulation and mild mood elevation persist.
Mild residual stimulation and mood elevation may persist for 2–4 hours after primary effects resolve. Sleep may remain difficult.
⚠ Do not drive or operate machinery until after a full night of sleep, as residual stimulation and subtle cognitive effects may persist beyond subjective baseline.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Low
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
No controlled toxicity data exist for 5-MeO-MiPT in humans, and no fatalities have been attributed to the compound alone.
Acute toxicity
The best-documented human case involved a 23-year-old who developed rapid heart rate (107 bpm), elevated blood pressure (150/90 mmHg), catatonia, and sedation.[6] All symptoms resolved within 24 hours with supportive care.
Mouse studies showed a complex cardiovascular pattern — rapid heart rate followed by slowing and rebound effect acceleration, with blood pressure rising and falling in waves.[7][6] No human lethal dose has been established.
Chronic toxicity
Zebrafish exposed for 30 days showed anxiety-like behavior, liver-brain signaling disruption, and tissue damage.[14][15] This suggests chronic use carries toxicity risk, though zebrafish findings don't translate directly to human patterns.
Psychological risks
As a serotonergic psychedelic, 5-MeO-MiPT carries class-typical risks of acute anxiety, panic, and paranoia — especially at higher doses. Case reports describe agitated, disinhibited behavior: one person was found naked and aggressive;[8] another developed a substance-related mental disorder[16] — though both cases involved multiple substances.
The pronounced stimulant and body-load component may drive anxiety reactions distinct from those of more visually dominant psychedelics. No cases of HPPD have been specifically attributed to 5-MeO-MiPT.
Tolerance and dependence
Tolerance develops rapidly after a single dose, consistent with serotonin downregulation seen across the psychedelic class.[5] Near-complete reset occurs within approximately 7 days. Cross-tolerance is expected with LSD, psilocybin, mescaline, DMT, and other substituted tryptamines.[5]
No dependence studies exist. The rapid tolerance acts as an inherent brake on compulsive redosing, consistent with low abuse liability across serotonergic psychedelics.
Drug Interactions
Serotonergic compounds
Combining 5-MeO-MiPT with MAOIs, SSRIs, SNRIs, or other serotonergic drugs risks serotonin syndrome — a potentially life-threatening overheating and seizure response.[17] Even without flooding the synapse with serotonin, 5-MeO-MiPT's direct receptor activation is enough to trigger the syndrome in combination.[1]
Tramadol is specifically dangerous: it both blocks serotonin reuptake and lowers the seizure threshold.[17] Lithium is a class-level concern for all serotonergic psychedelics — documented seizures and severe reactions have occurred in combination. safety citation needed
Stimulants
5-MeO-MiPT raises heart rate and blood pressure. Adding stimulants compounds that cardiovascular stress. Forensic cases document severe agitation with concurrent cocaine use[8] and adverse outcomes with co-ingested methylone.[16]
MAOIs
The MAOI interaction has not been specifically studied. 5-MeO-MiPT's greater oral than smoked potency suggests it may not be heavily degraded by monoamine oxidase — which could moderate the amplification typically seen with MAOI-tryptamine combinations. The combination should still be considered high-risk. safety citation needed
Contraindications
9 knownCardiovascular conditions
Pre-existing high blood pressure, irregular heart rhythm, or structural heart disease represent elevated risk given the documented cardiovascular effects.[6][7]
Psychiatric conditions
5-MeO-MiPT is contraindicated in individuals with a personal or family history of psychotic disorders or bipolar disorder. The catatonia documented in the poisoning case[6] underscores the potential for severe acute psychiatric disturbance.
Concurrent serotonergic medication
MAOIs, SSRIs, SNRIs, tramadol, and lithium are contraindicated due to serotonin syndrome risk.[17]
Liver impairment
The compound is processed by liver enzymes,[8] and zebrafish data show liver disruption with chronic exposure.[14] Impaired liver function may increase exposure, though this remains a theoretical concern without clinical confirmation.
Harm Reduction[edit]
Forms & Identification
5-MeO-MiPT is active at very low doses — 4–6 mg orally — making visual estimation impossible. A milligram-precision scale (0.001 g resolution) is essential; standard gram-resolution scales cannot measure doses this small reliably.
The compound's low active dose means mislabeled or contaminated material poses heightened risk. Reagent testing confirms the presence of a tryptamine but cannot distinguish 5-MeO-MiPT from structurally similar compounds. Where available, a drug checking service providing quantitative analysis is the most useful identification tool.
Guidelines
- Use a milligram-precision scale (0.001 g) for every dose — never estimate by eye
- Start at the low end of the common dose range and wait the full onset period before considering any redose
- Reagent test all material; use a drug checking service where available
- Eat lightly beforehand — nausea during onset is common with tryptamines
- Stay hydrated with normal water intake; do not overhydrate
- Have a calm, comfortable environment prepared before dosing
- Avoid combining with other substances, particularly stimulants and serotonergic drugs
- Do not drive or operate machinery during or for several hours after the experience
Set & Setting
The pronounced physical stimulation makes physical comfort especially important. A familiar, temperature-controlled space with room to move helps manage the somatic intensity. The experience can shift between sociable warmth and introspective withdrawal depending on environment and mindset.
A trusted sitter is advisable for first experiences or doses above the common range. The compound's stimulant quality can mask fatigue — planning for adequate rest afterward is worthwhile.
Aftercare & integration. The body-focused intensity can leave residual physical tension and fatigue even after psychological effects subside. Light stretching, a warm shower, and a nutritious meal support physical recovery. Sleep may come easily once stimulant effects fade, but some people report restlessness.
Psychologically, the experience may surface unexpected emotional material. Writing down impressions within a day or two helps consolidate insights. If difficult emotions persist beyond several days or the experience produced significant distress, speaking with a therapist familiar with psychedelic experiences is advisable.
Recovery & Support
5-MeO-MiPT's rapid tolerance development makes compulsive daily use self-limiting, and no physical withdrawal syndrome has been documented. Psychological patterns of repeated use — particularly tied to aphrodisiac or empathogenic effects — may warrant attention if use feels compulsive or serves primarily to avoid difficult emotions.
Support resources include the Fireside Project (62-FIRESIDE / 623-473-7433), a free psychedelic peer support line, and MAPS integration therapy directories for finding experienced practitioners. General substance use support is available through SAMHSA's National Helpline (1-800-662-4357).
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Uncomfortable body load, mild anxiety, and nausea during onset are common and typically self-limiting. Seek immediate help if any of the following occur: chest pain or pressure, heart rate that feels dangerously fast or irregular, complete unresponsiveness, catatonia (frozen, unable to move or speak), seizure, or self-harm behavior.
Immediate steps:
- 1. Call emergency services if the person is unresponsive, seizing, experiencing chest pain, or appears catatonic
- 2. Keep the person in a safe, calm environment away from hazards
- 3. If unconscious but breathing, place in the recovery position (on their side)
- 4. Monitor breathing and heart rate continuously
- 5. Do not restrain unless there is immediate danger of self-harm
- 6. Do not induce vomiting
What to tell the dispatcher: Name the substance (5-MeO-MiPT or "Moxy"), the estimated amount taken, when it was taken, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
No reversal agent exists for serotonergic psychedelics. Treatment is supportive — managing symptoms until the drug clears.
Legal Status[edit]
5-MeO-MiPT occupies a legally ambiguous position in many jurisdictions — unscheduled at the US federal level as of April 2026, but controlled in several states and internationally under novel psychoactive substance frameworks.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States (federal) | Not scheduled; Federal Analogue Act may apply | DEA classified as analogue of 5-MeO-DiPT (Schedule I) in March 2005. Proposed Schedule I placement January 2022; withdrawn July 2022 pending updated HHS evaluation.[4] |
| Florida (US) | Schedule I | State-level scheduling.[18] |
| Louisiana (US) | Schedule I | Controlled since June 2013.[18] |
| Minnesota (US) | Banned | State-level prohibition.[18] |
| United Kingdom | Not specifically listed (MDA 1971); covered by Psychoactive Substances Act 2016 | Offence to produce, supply, or offer to supply any psychoactive substance. May also fall under MDA 1971 generic tryptamine definition.[18] |
| Germany | Controlled under NpSG (2016) | Generic NPS control under Neue-Psychoaktive-Stoffe-Gesetz. citation needed |
| Austria | Controlled under NpSG | National NPS framework. citation needed |
| China | Category I psychotropic substance | Controlled substance.[18] |
| Finland | Banned | Controlled since December 2014 under NPS regulations.[18] |
| Japan | Designated Substance | Controlled under pharmaceutical law; identified in NPS monitoring by 2007.[9][18] |
| Canada | Not confirmed | May be covered under analogue provisions or NPS frameworks. citation needed |
| Australia | Not confirmed | May be covered under analogue provisions. citation needed |
Analogue considerations
In the United States, 5-MeO-MiPT is structurally related to the Schedule I substance 5-MeO-DiPT, differing only in the N-alkyl chain. Under the Federal Analogue Act (21 U.S.C. § 813), substances substantially similar to Schedule I or II compounds may be treated as Schedule I when intended for human consumption. The withdrawn 2022 scheduling proposal[4] signals ongoing regulatory interest.
Legal status changes frequently and varies by jurisdiction. This information reflects publicly available sources as of April 2026 and is not legal advice.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Low
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
No controlled toxicity data exist for 5-MeO-MiPT in humans. No fatalities attributed solely to this compound have been reported, though the published case base is limited to three reports — all involving multiple substances or unquantified doses.
Acute toxicity
The single well-documented human case involved a 23-year-old male who developed rapid heart rate (107 bpm), elevated blood pressure (150/90 mmHg), catatonia, sedation, and muteness.[6] All symptoms resolved within 24 hours with supportive care. The ingested dose was not quantified.
Mouse studies at relevant doses showed a complex cardiovascular pattern: initial rapid heart rate followed by slowing and rebound effect acceleration, with blood pressure rising and falling in waves.[7][6] No human lethal dose has been established.
Chronic toxicity
Zebrafish exposed to 5-MeO-MiPT for 30 days showed anxiety-like behavior, disruption of liver-brain signaling, and tissue damage.[15][16] These findings suggest chronic use carries toxicity risk, though extrapolation from zebrafish to human use patterns requires caution.
Psychological risks
As a serotonergic psychedelic, 5-MeO-MiPT carries class-typical risks of acute anxiety, panic, and paranoia — particularly at higher doses. Case reports describe agitated, disinhibited behavior: one forensic case involved a person found naked and aggressive,[8] and another documented a substance-related mental disorder,[17] though multiple substances were involved in both.
The pronounced stimulant and body-load component at higher doses — intense physical stimulation, vasoconstriction, and overwhelming somatic pressure — may drive anxiety reactions distinct from the typical difficult experience of more visually dominant psychedelics. No cases of HPPD (HPPD) have been specifically attributed to 5-MeO-MiPT.
Tolerance and dependence
Tolerance develops rapidly after a single dose, consistent with 5-HT₂A downregulation observed across the psychedelic class.[5] Near-complete reset occurs within approximately 7 days. Cross-tolerance is expected with all classical psychedelics: LSD, psilocybin, mescaline, DMT, and other substituted tryptamines.[5]
No dependence studies exist. The rapid tolerance serves as an inherent brake on compulsive redosing — a pattern consistent with low abuse liability across the serotonergic psychedelic class.
Drug Interactions
Serotonergic compounds
Combining 5-MeO-MiPT with MAOIs, SSRIs, SNRIs, or other serotonergic drugs carries a risk of serotonin syndrome — a potentially life-threatening condition.[18] Although 5-MeO-MiPT itself does not significantly block serotonin reuptake,[1] its direct receptor activation provides sufficient serotonergic activity to contribute to the syndrome in combination.
Tramadol is specifically flagged as dangerous: it both inhibits serotonin reuptake and lowers the seizure threshold, compounding risk from both mechanisms.[18]
Lithium is a class-level concern for all serotonergic psychedelics due to documented seizures and severe reactions in combination. safety citation needed
Stimulants
The cardiovascular effects of 5-MeO-MiPT — elevated heart rate and blood pressure — compound with stimulant-induced cardiovascular stress. Published forensic cases document severe agitation with concurrent cocaine use[8] and adverse outcomes with co-ingested methylone.[17]
MAOIs
The MAOI interaction has not been specifically studied. 5-MeO-MiPT's unusual potency pattern — more potent orally than smoked — suggests it may not be heavily degraded by monoamine oxidase, which could moderate the potentiation typically seen with MAOI-tryptamine combinations. This remains speculative, and the combination should be considered high-risk. safety citation needed
Contraindications
9 knownCardiovascular conditions
Pre-existing high blood pressure, irregular heart rhythm, and structural heart disease represent elevated risk factors given the documented cardiovascular effects.[6][7]
Psychiatric conditions
5-MeO-MiPT is contraindicated in individuals with a personal or family history of psychotic disorders or bipolar disorder. The catatonia observed in the documented poisoning case[6] underscores the potential for severe acute psychiatric disturbance.
Concurrent serotonergic medication
MAOIs, SSRIs, SNRIs, tramadol, and lithium are contraindicated due to serotonin syndrome risk.[18]
Liver impairment
The compound is metabolized by liver enzymes,[8] and zebrafish data show liver pathway disruption with chronic exposure.[15] Impaired liver function may alter metabolism and increase exposure, though this is a theoretical concern without clinical confirmation.
Harm Reduction[edit]
Forms & Identification
5-MeO-MiPT is active at very low doses (4–6 mg oral), making accurate measurement critical and visual estimation impossible. The difference between a threshold and a strong experience can be as little as 2–3 mg. A milligram-precision scale (0.001 g) is essential — standard kitchen or gram-resolution scales cannot measure doses this small reliably.
The compound's low active dose also means that mislabeled or contaminated material poses heightened risk. Reagent testing confirms the presence of a tryptamine but cannot distinguish 5-MeO-MiPT from structurally similar compounds. Where available, quantitative analysis through a drug checking service provides the most useful information for substances active at single-digit milligram doses.
Guidelines
- Use a milligram-precision scale (0.001 g) for every dose — never estimate by eye
- Start at the low end of the common dose range and wait the full onset period before considering any redose
- Reagent test all material; use a drug checking service where available
- Eat lightly beforehand — nausea during onset is common with tryptamines
- Stay hydrated with normal water intake; do not overhydrate
- Have a calm, comfortable environment prepared before dosing
- Avoid combining with other substances, particularly stimulants and serotonergic drugs
- Do not drive or operate machinery during or for several hours after the experience
Set & Setting
5-MeO-MiPT's pronounced physical stimulation and body-focused effects make physical comfort especially important. A familiar, temperature-controlled space with room to move helps manage the somatic intensity. The experience can shift between sociable warmth and introspective withdrawal depending on environment and mindset — choosing a setting that accommodates both reduces the chance of a difficult experience.
A trusted sitter is advisable, particularly for first experiences or doses above the common range. The compound's stimulant quality can mask fatigue, so planning for adequate rest afterward is worthwhile.
Aftercare & integration. The body-focused intensity of 5-MeO-MiPT can leave residual physical tension and fatigue even after psychological effects subside. Light stretching, a warm shower, and a nutritious meal support physical recovery. Sleep may come easily once stimulant effects fade, but some people report restlessness — a calm environment and normal sleep hygiene help.
Psychologically, the experience may surface unexpected emotional material or altered perspectives. Writing down impressions within a day or two helps consolidate insights before they fade. If difficult emotions persist beyond several days, or if the experience produced significant distress, speaking with a therapist familiar with psychedelic experiences is advisable.
Recovery & Support
5-MeO-MiPT's rapid tolerance development makes compulsive daily use self-limiting, and no physical withdrawal syndrome has been documented. Psychological patterns of repeated use — particularly related to the compound's aphrodisiac or empathogenic effects — may warrant attention if use begins to feel compulsive or serves primarily to avoid processing difficult emotions.
Support resources include the Fireside Project (62-FIRESIDE / 623-473-7433), a free psychedelic peer support line, and MAPS integration therapy directories for finding experienced practitioners. General substance use support is available through SAMHSA's National Helpline (1-800-662-4357).
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Uncomfortable body load, mild anxiety, and nausea during onset are common and typically self-limiting. Seek immediate help if any of the following occur: chest pain or pressure, heart rate that feels dangerously fast or irregular, complete unresponsiveness, catatonia (frozen, unable to move or speak), seizure, or self-harm behavior.
Immediate steps:
- 1. Call emergency services if the person is unresponsive, seizing, experiencing chest pain, or appears catatonic
- 2. Keep the person in a safe, calm environment away from hazards
- 3. If unconscious but breathing, place in the recovery position (on their side)
- 4. Monitor breathing and heart rate continuously
- 5. Do not restrain unless there is immediate danger of self-harm
- 6. Do not induce vomiting
What to tell the dispatcher: Name the substance (5-MeO-MiPT or "Moxy"), the estimated amount taken, when it was taken, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
No reversal agent exists for serotonergic psychedelics. Treatment is supportive — managing symptoms until the drug clears.
Legal Status[edit]
5-MeO-MiPT occupies a legally ambiguous position in many jurisdictions. It is not explicitly scheduled under US federal law as of April 2026, but a formal scheduling proposal has been initiated and withdrawn, and it is controlled in several US states and internationally under various novel psychoactive substance frameworks.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States (federal) | Not scheduled; Federal Analogue Act may apply | DEA classified as analogue of 5-MeO-DiPT (Schedule I) in March 2005. Proposed Schedule I placement January 2022; withdrawn July 2022 pending updated HHS evaluation.[4] |
| Florida (US) | Schedule I | State-level scheduling.[19] |
| Louisiana (US) | Schedule I | Controlled since June 2013.[19] |
| Minnesota (US) | Banned | State-level prohibition.[19] |
| United Kingdom | Not specifically listed (MDA 1971); covered by Psychoactive Substances Act 2016 | Offence to produce, supply, or offer to supply any psychoactive substance. May also fall under MDA 1971 generic tryptamine definition.[19] |
| Germany | Controlled under NpSG (2016) | Generic NPS control under Neue-Psychoaktive-Stoffe-Gesetz. citation needed |
| Austria | Controlled under NpSG | National NPS framework. citation needed |
| China | Category I psychotropic substance | Controlled substance.[19] |
| Finland | Banned | Controlled since December 2014 under NPS regulations.[19] |
| Japan | Designated Substance | Controlled under pharmaceutical law; identified in NPS monitoring by 2007.[9][19] |
| Canada | Not confirmed | May be covered under analogue provisions or NPS frameworks. citation needed |
| Australia | Not confirmed | May be covered under analogue provisions. citation needed |
Analogue considerations
In the United States, 5-MeO-MiPT is structurally related to the Schedule I substance 5-MeO-DiPT, differing only in the N-alkyl chain. The DEA's 2005 classification explicitly established this structural analog relationship. Under the Federal Analogue Act (21 U.S.C. § 813), substances "substantially similar" to Schedule I or II compounds may be treated as Schedule I when intended for human consumption. The withdrawn 2022 scheduling proposal[4] signals ongoing regulatory interest.
Frequently asked questions
How long does 5-MeO-MiPT last?
Total duration by route of administration — Oral: 4 – 6 hours; Smoked: 1.5 – 3 hours. 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 5-MeO-MiPT?
Psychedex publishes a dosage table for 5-MeO-MiPT 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 5-MeO-MiPT?
The highest-severity documented interactions for 5-MeO-MiPT: MAOIs (Lethal), 5-HTP, Tryptophan (Dangerous), Alpha-2 adrenergic receptor antagonist (Dangerous), Amphetamines (Dangerous), Anticholinergics (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is 5-MeO-MiPT addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 5-MeO-MiPT: tolerance builds rapid; full reset takes 7 days; cross-tolerance develops with LSD, psilocybin, mescaline, DMT, 5-MeO-DMT, other serotonergic psychedelics. 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
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references
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- [5] ^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
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