αMT
α-methyltryptamine
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αMT (alpha-methyltryptamine) is a synthetic psychedelic-stimulant of the tryptamine class. It is structurally analogous to amphetamine within the tryptamine scaffold, distinguished by its unusually long duration and mixed pharmacological character. αMT is a 5-HT₂A receptor agonist and monoamine releaser, producing its effects through combined direct receptor activation and indirect serotonin, dopamine, and norepinephrine release.[1][2]
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Synthesised in the early 1960s by Upjohn and Sandoz as an antidepressant candidate, αMT was marketed in the Soviet Union as Indopan before withdrawal due to adverse effects.[3] The compound resurfaced as a recreational research chemical in the late 1990s, and the first documented US fatality in 2003 triggered permanent Schedule I placement.[4] It is now controlled in most Western jurisdictions with no active clinical development programme.
Subjective effects include geometric visual patterns, color enhancement, thought acceleration, euphoria, and wakefulness. The experience layers psychedelic perception over a persistent stimulant-empathogenic baseline — more physically activating and emotionally warm than classical tryptamines, with a pronounced body load throughout. Nausea during onset, jaw tension, and a stimulant-type comedown with low mood and fatigue are characteristic unsought effects.
αMT produces no documented physical dependence, and structural analog data suggest low reinforcement potential.[5] Its combined MAO-A inhibition[6] and serotonin release create inherent serotonin syndrome risk even in isolation[7] — combination with any serotonergic substance compounds this toward life-threatening serotonin syndrome, making the interaction profile broader and more dangerous than that of classical psychedelics. No controlled human studies have been conducted; the evidence base rests on animal pharmacology, forensic case reports, and user accounts.
History[edit]
Discovery
αMT was synthesised in the early 1960s independently by Upjohn Pharmaceuticals (compound code U-14,164E) and Sandoz (code IT-290), both pursuing monoamine oxidase inhibitors as antidepressant candidates.[3][8] The compound advanced to clinical use in the Soviet Union, where it was marketed as Indopan in 5 mg and 10 mg oral tablets for depression.[3] Indopan was eventually withdrawn from production due to serious adverse effects, the nature of which is poorly documented in English-language literature.citation needed
Recreational emergence and scheduling
αMT resurfaced in the late 1990s and early 2000s as a research chemical distributed via internet vendors, marketed as a legal psychedelic alternative.[9][10] The first documented US fatality occurred in February 2003 in Miami-Dade County, Florida,[11] triggering emergency DEA scheduling on April 4, 2003[4] and permanent Schedule I placement on September 29, 2004.[12] In the United Kingdom, αMT appeared on the drug market in 2011 and was classified as a Class A substance effective January 7, 2015.[8]
Current status
Deaths and serious poisonings have been reported across the United States, United Kingdom, Sweden, Norway, and Japan.[13] No clinical trials involving αMT have been registered under modern regulatory frameworks, and no clinical development programme exists.
The name alpha-methyltryptamine reflects the compound's defining structural feature: a methyl group at the alpha position of the tryptamine side chain — the same modification that distinguishes amphetamine from phenethylamine. The pharmaceutical brand name Indopan derives from the indole ring system. In recreational contexts, the DEA recorded the street name "Spirals," though αMT and AMT remain the dominant identifiers in online communities.[8]
Chemistry[edit]
Structural class
αMT belongs to the tryptamine family, sharing the core indole ring system with DMT, psilocybin, and serotonin. Its defining structural feature is an alpha-methyl group on the ethylamine side chain — the same modification that distinguishes amphetamine from phenethylamine. This alpha-methyl group protects the molecule from monoamine oxidase degradation, extending its biological half-life and enabling oral activity without a co-administered MAO inhibitor.[8]
Molecular properties
| Molecular formula | C₁₁H₁₄N₂ |
| Molecular weight | 174.24 g/mol |
The molecule consists of an indole bicyclic ring system with a propan-2-amine side chain at the 3-position. The systematic (IUPAC) name is 1-(1H-indol-3-yl)propan-2-amine.[3]
Stereochemistry
The alpha-methyl group introduces a chirality centre, and αMT exists as a racemic mixture in all documented preparations. No study has characterised the pharmacological differences between the R- and S-enantiomers of αMT specifically. Data from the close structural analog alpha-ethyltryptamine (αET) show stereoselective activity: only S(+)-αET produces partial 5-HT₂A agonism in calcium assays, though both enantiomers induce behavioural responses in vivo.[14] Whether αMT shows comparable enantioselectivity remains unstudied.
Physical properties
αMT has been encountered as powder, pellets or tablets, and capsules in forensic and harm reduction settings.[15] No formal characterisation of melting point, solubility, or stability has been published for the free base or salt forms.citation needed
Pharmacology[edit]
Mechanism of action
αMT operates through three concurrent mechanisms that produce its combined stimulant-psychedelic character.
MAO-A inhibition
αMT reversibly inhibits MAO-A (MAO-A), the enzyme primarily responsible for breaking down serotonin, dopamine, and norepinephrine in the brain.[3][6] This inhibition slows monoamine degradation, amplifying and prolonging the effects of both endogenous neurotransmitters and the serotonin that αMT itself releases. The alpha-methyl group also protects αMT from being broken down by monoamine oxidase, enabling oral activity at lower doses than unprotected tryptamines like DMT.[8]
Monoamine release
αMT promotes the release of serotonin, dopamine, and norepinephrine from nerve terminals.[1] This triple-release profile — confirmed across the prefrontal cortex, nucleus accumbens, striatum, and hippocampus in rats — distinguishes αMT from classical psychedelics (which primarily activate receptors directly) and positions it pharmacologically between classical psychedelics and entactogens like MDMA.
Data from the close structural analog alpha-ethyltryptamine (αET) demonstrate that behavioural effects depend on both direct receptor activation and SERT-mediated release; blocking the serotonin transporter abolished αET's hallucinogen-like response.[14] αMT is expected to share this dual dependence.
5-HT₂A receptor agonism
αMT activates the serotonin 5-HT₂A receptor, the primary target responsible for psychedelic effects across the tryptamine and phenethylamine classes.[9][16] In mice, αMT's hallucinogen-like behaviour is completely blocked by a selective 5-HT₂A antagonist, confirming that this receptor drives the psychedelic component.[2] No quantitative binding data have been published — the receptor interaction is established behaviourally but not characterised at the molecular level.
Pharmacokinetics
No controlled human pharmacokinetic study has been published for αMT. Bioavailability, peak plasma time, plasma half-life, and distribution remain uncharacterised. The prolonged 13–15 hour oral duration likely results from two reinforcing factors: the alpha-methyl group's protection of the molecule from enzymatic breakdown, and concurrent MAO-A inhibition that slows the clearance of both αMT itself and the monoamines it releases.
Malaca et al. identified nine metabolites in human hepatocyte incubations and additional metabolites in postmortem samples, including hydroxylated, sulfated, glucuronidated, and acetylated forms.[17] The specific liver enzymes responsible for αMT metabolism have not been identified.inferred
Neuroscience[edit]
Where it acts
αMT engages the same cortical serotonin receptors as classical psychedelics — 5-HT₂A receptors on layer V pyramidal neurons in the prefrontal cortex[2] — but simultaneously floods multiple brain regions with serotonin, dopamine, and norepinephrine.[1] The dopamine release in the nucleus accumbens implicates reward circuitry not typically engaged by classical psychedelics, while norepinephrine elevation likely drives the stimulant-like arousal and cardiovascular activation. This broad monoaminergic engagement explains why αMT feels like neither a pure psychedelic nor a pure stimulant.
Why it matters
Psychedelic 5-HT₂A agonists increase neural entropy — greater signal diversity and reduced predictability of brain activity — and promote structural changes in neurons including dendritic growth and new synaptic connections.inferred αMT's 5-HT₂A agonism suggests it shares this neuroplastic potential, supported by the finding that the close structural analog 5-MeO-AMT activates prefrontal 5-HT₂A receptors.[5]
The concurrent monoamine release introduces neuromodulatory variables absent from classical psychedelic models, and the extended duration raises questions about whether sustained receptor engagement produces different neuroplastic outcomes than shorter-acting agents.
Key unresolved questions include whether αMT produces neuroplastic changes comparable to classical psychedelics, how simultaneous MAO-A inhibition and monoamine release modify the neural signature of 5-HT₂A-mediated psychedelic states, and whether the R- and S-enantiomers differ in brain activity and subjective effects as demonstrated for αET.[14]
Subjective Effects[edit]
αMT produces a hybrid experience that interweaves psychedelic perception with stimulant energy and empathogenic warmth — pharmacologically distinct from either axis alone. At lower doses the stimulant character dominates: elevated mood, wakefulness, and physical activation with subtle perceptual shifts. As dose increases, visual patterning, colour saturation, and conceptual fluidity intensify while the empathogenic quality deepens. Set and setting exert strong influence across the entire range, and the extended time commitment means environmental stability and social context carry more weight than for shorter-acting compounds.
The closest experiential comparisons are MDA, which shares the psychedelic-stimulant-empathogenic blend through different mechanisms, and high-dose 2C-B, which produces a similar layering of visual psychedelia over physical activation. αMT is distinguished from both by its markedly longer duration and a pronounced stimulant comedown that resembles post-amphetamine recovery more than the gentle offset typical of classical tryptamines.
Effect Grid
At common doses (25–40 mg oral), the full combined stimulant-psychedelic experience manifests. Visual effects become prominent: geometric patterning on surfaces, colour saturation and shifting, drifting and morphing of objects, and vivid closed-eye visuals. Music enhancement is marked. Time distortion becomes significant — hours may feel compressed or expanded. Thought connectivity increases dramatically, producing novel associations and conceptual thinking.
Stimulant effects are strong: sustained wakefulness, elevated mood approaching euphoria, and pronounced empathy. Cardiovascular activation is evident — increased heart rate, elevated blood pressure, and temperature dysregulation. Nausea at onset is common. Appetite is suppressed throughout.
The total experience spans 13–15 hours. Functional impairment is significant for the duration. Sleep is impossible for 10–12 hours post-ingestion.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Geometry · Symmetrical texture repetition · After-images · Auditory enhancement · Environmental patterning · Light sensitivity · Perspective distortion · Sound sensitivity · Visual breathing · Auditory distortion · Auditory misinterpretation · Brightness alteration · Depth perception distortion · Peripheral misidentification · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Touch enhancement · Vestibular distortion · Visual haze / noise · Visual morphing · Synesthesia · Visual diffraction · Visual melting · Flashbacks · Object transformations · Internal hallucinations · External hallucinations · Visual recursion · Visual scenery slicing · Auditory hallucinations · Environmental orbism / cubism · Object activation · Persisting hallucinations
Environmental patterning · Light sensitivity · Perspective distortion · Sound sensitivity · Visual breathing · Auditory distortion · Auditory misinterpretation · Brightness alteration · Depth perception distortion · Peripheral misidentification · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Touch enhancement · Vestibular distortion · Visual haze / noise · Visual morphing · Synesthesia · Visual diffraction · Visual melting · Flashbacks · Object transformations · Internal hallucinations · External hallucinations · Visual recursion · Visual scenery slicing · Auditory hallucinations · Environmental orbism / cubism · Object activation · Persisting hallucinations
Nausea · Body high · Insomnia · Restlessness · Spontaneous body sensations · Excessive sweating · Appetite suppression · Dry mouth · Heart rate perception changes · Muscle tension · Physical fatigue · Tingling / electric sensations · Vibrations / buzzing · Increased urination · Dehydration sensation · Headache · Bruxism · Dizziness · Vasoconstriction · Bodily lightness · Tactile euphoria · Trembling · Vomiting · Abnormal heartbeat
Restlessness · Spontaneous body sensations · Excessive sweating · Appetite suppression · Dry mouth · Heart rate perception changes · Muscle tension · Physical fatigue · Tingling / electric sensations · Vibrations / buzzing · Increased urination · Dehydration sensation · Headache · Bruxism · Dizziness · Bodily lightness · Tactile euphoria · Trembling · Vomiting · Abnormal heartbeat
Cognitive euphoria · Immersion enhancement · Conceptual thinking · Aesthetic enhancement · Cognitive fatigue · Cognitive flexibility · Introspection enhancement · Novelty enhancement · Openness enhancement · Analysis enhancement · Memory suppression · Cognitive impairment · Creativity enhancement · Increased nature relatedness · Multiple thought streams · Thought loops · Humor enhancement · Motivation enhancement · Compulsive redosing urge · Confusion · Memory fragmentation · Memory replays · Synchronicity · Thought disorganization · Focus enhancement
Aesthetic enhancement · Cognitive fatigue · Cognitive flexibility · Introspection enhancement · Novelty enhancement · Openness enhancement · Analysis enhancement · Memory suppression · Cognitive impairment · Creativity enhancement · Increased nature relatedness · Multiple thought streams · Thought loops · Humor enhancement · Motivation enhancement · Confusion · Memory fragmentation · Memory replays · Synchronicity · Thought disorganization · Focus enhancement
Anxiety · Emotional lability · Simultaneous emotions · Anhedonia · Catharsis · Dysphoria · Irritability
Catharsis · Dysphoria · Irritability
Social connection · Trust enhancement · Communication enhancement · Flow state · Craving · Depersonalization · Identity alteration · Boundary dissolution · Ego dissolution
Craving · Depersonalization · Identity alteration · Boundary dissolution · Ego dissolution
Entity contact · Non-dual awareness
Timeline
First alerts emerge gradually — mild mood shift, subtle sensory brightening, faint body awareness. The unusually slow onset (60–180 minutes) is a primary redosing risk factor; effects may not be perceptible for over an hour.
Stimulant and psychedelic effects build in tandem. Nausea and possible vomiting are common during this phase. Heart rate rises noticeably, mood elevation increases, and faint visual distortions begin to appear.
Full psychedelic-stimulant experience: pronounced visual patterning, colour enhancement, thought connectivity, music enhancement, and euphoria. Cardiovascular stimulation (tachycardia, hypertension) is sustained. The peak is notably long compared to other tryptamines, reflecting αMT's MAO-A inhibition prolonging serotonergic activity.
Psychedelic intensity diminishes while stimulant activation persists. Visual effects recede to subtle colour shifts and mild pattern recognition. Mental stimulation and wakefulness continue.
Gradual return toward baseline over several hours. Residual stimulation prevents sleep. Mood may shift toward fatigue and irritability as the stimulant component wanes.
Residual effects include low mood, physical fatigue, flu-like symptoms, and lingering insomnia lasting 1–2 days. Some users report mild cognitive fog and emotional flatness.
⚠ Do not drive or operate machinery until after a full night of sleep following the experience — residual stimulant impairment and sleep deprivation significantly compromise reaction time and judgement.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 30 days
- Physical
- None
- Psychological
- Low
- Compulsive redosing
- Low
- Dose escalation
- Negligible
- Cross-tol.
- psilo · LSD · DMT
Toxicity
Acute toxicity
No formal lethal dose has been established for αMT in any species.[2] Two documented fatalities provide reference points: the first US death in 2003 showed a postmortem blood concentration of 2.0 mg/L,[11] while a later polydrug fatality showed 4.69 mg/L αMT alongside multiple other substances.[18] The wide concentration range and polydrug context prevent establishing a reliable lethal threshold.safety citation needed
αMT cross-reacts with amphetamine immunoassays in standard toxicology screening, meaning hospital drug tests may return a false positive for amphetamine.[11]
Serotonin toxicity
αMT's dual role as MAO-A inhibitor and serotonin releaser creates inherent serotonin syndrome risk even without other drugs present.[7] Symptoms follow the classic pattern: altered mental status, muscle rigidity and tremor, and autonomic instability (dangerously high body temperature, rapid heart rate, excessive sweating, high blood pressure).[8]
Heart and circulation
Clinical toxicity reports document rapid heart rate, high blood pressure, agitation, and confusion following αMT use.[19] Muscle breakdown has been documented in clinical cases, which can lead to kidney damage.[8] No chronic toxicology studies have been published.
Psychological risks
Acute anxiety, panic attacks, and paranoia are documented in clinical case series.[19] The 13–15 hour duration amplifies psychological distress — an adverse experience cannot be waited out quickly, and stimulant-driven insomnia compounds exhaustion. A comedown characterised by low mood and flu-like symptoms lasting 1–2 days is consistently reported.[8]
Persistent perceptual disturbances (HPPD) have not been formally studied for αMT but are plausible given its 5-HT₂A agonism.inferred Individuals with personal or family history of psychotic disorders or bipolar disorder face elevated risk, consistent with the profile of all 5-HT₂A agonists.inferred
Tolerance and dependence
αMT produces rapid tolerance to its psychedelic effects. A single dose of a psychedelic 5-HT₂A agonist induces tolerance within 24 hours via downregulation in the frontal cortex.[20] Community reports suggest a tolerance half-life of approximately 14 days with full reset at roughly one month; these values are plausible but unconfirmed by αMT-specific studies.citation needed
Cross-tolerance with other psychedelics — psilocybin, LSD, DMT, mescaline — is expected based on shared 5-HT₂A receptor mechanisms.[20]
The close structural analog 5-MeO-AMT showed no reward-seeking behaviour or self-administration in mice, suggesting low dependence potential.[5] No dependence or withdrawal studies specific to αMT have been published. The compound's dopamine-releasing activity may confer some psychological reinforcement beyond classical psychedelics, but compulsive use patterns have not been documented.
Drug interactions
αMT is both a reversible MAO-A inhibitor and a serotonin releaser. Combination with any serotonergic substance carries serious serotonin syndrome risk.
Serotonergic combinations (life-threatening)
MDMA: Both agents cause massive serotonin release through different mechanisms. The combination produces compounded serotonin accumulation with extreme serotonin syndrome risk.[6][7][21]
Tramadol: serotonin reuptake inhibitor plus mild MAOI activity from tramadol combined with αMT's MAO-A inhibition creates dangerous serotonin accumulation; tramadol also lowers the seizure threshold.[21]
Dextromethorphan (DXM): Serotonin reuptake inhibition and weak MAOI activity from DXM combined with αMT creates serotonin syndrome risk.[21]
SSRIs and SNRIs: Any serotonin reuptake inhibitor combined with αMT's MAO-A inhibition and serotonin release creates dangerous serotonin accumulation.[21]
Stimulant combinations
Cocaine: Dopamine and norepinephrine reuptake inhibition combined with αMT's monoamine release creates cardiovascular toxicity risk (dangerously high blood pressure, irregular heartbeat) and elevated body temperature.[21]
Other high-risk combinations
PCP, methoxetamine (MXE): Dissociatives combined with serotonergic agents may produce unpredictable behavioural toxicity.safety citation needed
Mescaline: Both compounds act on serotonin systems; combination increases 5-HT₂A stimulation.safety citation needed
Contraindications
αMT is contraindicated in individuals taking serotonergic medications (SSRIs, SNRIs, MAOIs, lithium, triptans, tramadol).[21] The washout period for SSRIs before αMT exposure should account for at least five elimination half-lives of the SSRI.
Personal or family history of psychotic disorders or bipolar disorder is a relative contraindication.inferred Heart conditions — high blood pressure, irregular heartbeat, structural heart disease — are relative contraindications given documented cardiovascular toxicity.[19]
Liver impairment may alter αMT metabolism, though the clinical significance is unknown.inferred Pregnancy and breastfeeding are absolute contraindications in the absence of reproductive toxicology data.safety citation needed
Harm Reduction[edit]
Forms & Identification
αMT circulates primarily as powder, capsules, and pressed pellets or tablets.[15] The powder form presents the highest dosing risk — small errors in weighing produce disproportionate changes in effect intensity, and a milligram-precision scale (0.001 g) is essential. Pressed tablets and pellets vary between batches, so dose claims cannot be assumed accurate without independent verification.
αMT cross-reacts with amphetamine immunoassays,[11] which means reagent testing is critical for confirming identity rather than relying on presumptive field tests. Because αMT shares visual characteristics with many other powdered tryptamines and phenethylamines, reagent testing alone may not distinguish it from all substitutes — laboratory analysis provides the highest confidence.
Guidelines
- Test the substance with multiple reagent kits before use. Consider laboratory analysis for unknown powder.
- Use a milligram-precision scale (0.001 g) for powder forms. Never estimate doses by eye.
- Start with a low dose and do not redose early. The slow onset (up to 2–3 hours oral) can tempt premature redosing, which dramatically increases risk.
- Clear a full 24-hour window. Active effects last 13–15 hours; residual stimulation and insomnia extend beyond that.
- Stay hydrated and eat lightly before and during the experience. The stimulant component increases water and electrolyte loss.
- Have a sober sitter present who understands the substance's long duration and stimulant character.
- Avoid all serotonergic substances including supplements like 5-HTP, St John's Wort, and tryptophan in the days surrounding use.
Set & Setting
The extended duration makes environmental planning unusually important. An interrupted or unstable setting that would be manageable during a 4-hour experience becomes a serious source of distress over half a day. Secure a private, comfortable space for the full duration and clear all obligations for the day and the following morning.
A trusted, sober sitter is strongly recommended, particularly for first experiences or higher doses. The stimulant component means sleep will not be possible for many hours after ingestion — plan timing so the experience does not extend into next-day obligations. Nausea during onset is near-universal; have a light or empty stomach and anti-nausea remedies available.
Aftercare & integration. The stimulant comedown after αMT typically involves low mood, physical fatigue, and flu-like symptoms lasting 1–2 days.[8] Prioritise sleep, hydration, and light nutrition in the 24–48 hours following the experience. Avoid stimulants (including excess caffeine) during recovery, as the nervous system is already depleted.
The psychedelic component may surface emotionally significant material that benefits from processing. Journaling within the first few days, conversation with a trusted person, or working with an integration-trained therapist can help make sense of the experience. If disturbing thoughts, persistent anxiety, or perceptual changes continue beyond a week, seek professional support.
Recovery & Support
αMT does not produce physical dependence in the conventional sense, and compulsive use patterns have not been documented. However, any pattern of repeated psychoactive substance use that interferes with daily functioning, relationships, or wellbeing warrants attention regardless of the substance's pharmacological dependence profile.
If use has become a coping mechanism or is escalating in frequency, harm reduction services, psychedelic integration circles, and substance use counsellors can provide non-judgmental support. SAMHSA's National Helpline (1-800-662-4357) offers free referrals in the United States. In the UK, FRANK (0300 123 6600) and Release (020 7324 2989) provide confidential advice.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognising an emergency:
Uncomfortable effects (nausea, anxiety, elevated heart rate) are common and do not themselves require medical intervention. Seek emergency help immediately if any of the following occur:
- Body temperature that is visibly or palpably dangerously high (hot, dry skin or profuse uncontrollable sweating)
- Severe muscle rigidity, tremor, or jerking movements (signs of serotonin syndrome)
- Seizure or loss of consciousness
- Chest pain or irregular heartbeat
- Extreme confusion, aggression, or complete disconnection from reality with self-harm risk
Immediate steps:
- 1. Call emergency services immediately if any of the above are present.
- 2. Move the person to a cool, quiet area. Remove excess clothing if body temperature is elevated.
- 3. If unconscious but breathing, place in the recovery position (on their side, airway clear).
- 4. Do not induce vomiting. Do not physically restrain unless there is immediate danger of self-harm.
- 5. Stay with the person until help arrives.
What to tell the dispatcher: State the substance (alpha-methyltryptamine / αMT), estimated amount if known, 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]
Overview
αMT is controlled in multiple jurisdictions, with scheduling driven primarily by recreational fatalities and emergence in the new psychoactive substances market during the early 2000s. No international scheduling under United Nations conventions has been enacted, though the WHO Expert Committee on Drug Dependence has conducted a review.[13]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Temporary placement April 4, 2003;[4] permanent September 29, 2004.[12] Triggered by first US fatality in February 2003.[11] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Effective January 7, 2015, following ACMD recommendation.[8] Possession: up to 7 years imprisonment and/or unlimited fine. Supply: up to life imprisonment and/or unlimited fine. |
| Australia | Schedule 8 (controlled drug) | [13] |
| Germany | Controlled (Betäubungsmittelgesetz, BtMG) | [13] |
| Japan | Controlled substance | [13] |
| Canada | Not explicitly scheduled (as of 2025) | Not controlled under CDSA schedules. Status should be verified against current Health Canada scheduling.citation needed |
Analog act considerations
In the United States, αMT's permanent Schedule I placement means the Federal Analogue Act does not apply to the parent compound. Novel αMT analogs (ring-substituted variants or other structural modifications) that are not specifically scheduled could fall under the Analogue Act if sold for human consumption, given αMT's Schedule I status as the reference compound.
references
- [1] ^abcLi K, Li N, Chen Y, Li X, Qiao Y, Wang D, Di B, Xu P (2025) A systematic study of changes in monoamine neurotransmitters in the rat brain following acute administration of alpha-methyltryptamine (AMT), 5-methoxy-alpha-methyltryptamine (5-MeO-AMT) and 5-methoxy-N,N-diisopropyltryptamine (5-MeO-DiPT). — Neuroscience research doi:10.1016/j.neures.2025.04.006
- [2] ^abcdLi K, Li N, Chen Y, Li X, Qiao Y, Wang D, Di B, Xu P (2025) Effects of three tryptamines: alpha-methyltryptamine, 5-methoxy-alpha-methyltryptamine, and 5-methoxy-N,N-diisopropyltryptamine on acute toxicity, locomotor activity, and hallucinogenic behavior in mice. — Behavioural pharmacology doi:10.1097/fbp.0000000000000841
- [3]
- [4] ^abcDEA Deputy Administrator (2003) Schedules of controlled substances: temporary placement of alpha-methyltryptamine and 5-methoxy-N,N-diisopropyltryptamine into Schedule I. Final rule. — Federal Register PMID:12678045
- [5] ^abcAbiero A, Botanas CJ, Sayson LV, Custodio RJ, de la Pena JB, Kim M, Lee HJ, Seo JW, Ryu IS, Chang CM, Yang JS, Lee YS, Jang CG, Kim HJ, Cheong JH (2019) 5-Methoxy-alpha-methyltryptamine (5-MeO-AMT), a tryptamine derivative, induces head-twitch responses in mice through the activation of serotonin receptor 2a in the prefrontal cortex. — Behavioural brain research doi:10.1016/j.bbr.2018.07.020
- [6] ^abcWagmann L, Brandt SD, Kavanagh PV, Maurer HH, Meyer MR (2017) In vitro monoamine oxidase inhibition potential of alpha-methyltryptamine analog new psychoactive substances for assessing possible toxic risks. — Toxicology letters doi:10.1016/j.toxlet.2017.03.007