4-AcO-DMT
4-acetoxy-N,N-dimethyltryptamine
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4-AcO-DMT (O-acetylpsilocin) — also known as psilacetin — is a synthetic psychedelic of the tryptamine class. It is the acetate ester prodrug of psilocin, the active metabolite shared with psilocybin mushrooms. 4-AcO-DMT is a 5-HT₂A receptor agonist, producing its effects both directly[1] and through enzymatic conversion to psilocin.[2]
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Synthesized by Hofmann and Troxler at Sandoz in 1963, the compound was patented as part of a systematic exploration of psilocin derivatives but never pharmacologically examined.[3] Shulgin described it as interchangeable with psilocin in 1997,[4] and Nichols proposed it as a practical research substitute for psilocybin in 1999.[5] It now circulates primarily through unregulated research chemical markets and is the most commonly encountered novel tryptamine in European drug monitoring.
Subjective effects include geometric visual patterns, perceptual intensification, emotional enhancement, thought connectivity, and ego dissolution. The experience is warm, introspective, and body-centered — widely described as indistinguishable from psilocybin mushrooms at equivalent doses, with a gentler emotional saturation compared to the analytical edge of LSD. Nausea, anxiety escalation, thought loops, and transient confusion are common unsought effects.
4-AcO-DMT produces no physical dependence, and rapid tolerance after a single dose makes compulsive redosing self-limiting.[6] The primary risk is psychological — high doses can trigger panic, paranoid ideation, and identity disruption, scaling with dose and psychiatric vulnerability. No controlled human studies have been conducted; the current understanding rests on animal pharmacology, in vitro metabolism data, and computational toxicity modeling.[7]
History[edit]
Discovery
Albert Hofmann and Franz Troxler first synthesized 4-AcO-DMT in 1963 at Sandoz Pharmaceuticals in Basel, Switzerland.[3] The compound appeared in a Swiss patent covering ether and ester derivatives of 4-hydroxytryptamines — a systematic chemical exploration rather than a pharmacological investigation. Hofmann and Troxler did not examine its psychoactive properties, and the compound received no further scientific attention for over thirty years.
Academic Recognition
Alexander Shulgin brought 4-AcO-DMT to broader awareness in TiHKAL (1997), describing the acetate ester and the phosphate ester (psilocybin) as "completely interchangeable" in their pharmacological properties.[4] Two years later, David Nichols and Stephen Frescas published the first peer-reviewed paper proposing 4-AcO-DMT as a practical, economical alternative to psilocybin for psychopharmacology research.[5] Psilocybin's complex synthesis and Schedule I status had created barriers; psilacetin offered equivalent pharmacology with simpler preparation.
Market Emergence and Modern Research
4-AcO-DMT began appearing on research chemical markets in the early 2000s. By 2007, Erowid described it as a novel compound used primarily by "psychedelic connoisseurs".[8] Europol documented its presence as a designer drug in Europe in 2009, and it subsequently became the most commonly encountered novel tryptamine in European drug monitoring.[9]
From the 2010s onward, a series of pharmacological studies expanded the evidence base — metabolite profiling,[2] in vivo prodrug validation,[10] receptor binding characterization,[11] and computational toxicology.[7] No clinical trials have been initiated as of April 2026.
The name psilacetin — a portmanteau of psilocin and acetyl — reflects the compound's identity as psilocin's acetate ester. The abbreviation 4-AcO-DMT follows systematic tryptamine naming conventions: the 4-position acetyloxy substitution and the N,N-dimethyltryptamine backbone. Among users, the compound is sometimes called "synthetic shrooms" for its subjective similarity to psilocybin mushrooms, though this label obscures the pharmacological differences between a pure compound and a complex fungal preparation.
Chemistry[edit]
Structural Class
4-AcO-DMT (O-acetylpsilocin, psilacetin) is a substituted tryptamine built on an indole ring system with a dimethylaminoethyl side chain at the 3-position — the defining scaffold of psychedelic tryptamines. An acetyloxy group (–OC(O)CH₃) at the 4-position makes it the acetate ester of psilocin. This ester is hydrolyzable: enzymes cleave it to yield psilocin, the same pharmacologically active compound produced by psilocybin.[2][10]
Within the 4-substituted tryptamine series, the 4-position substituent determines both direct receptor affinity and prodrug behavior. The N,N-dimethyl configuration on the side chain is essential for psychedelic activity — secondary and quaternary amine variants fail to produce psychedelic-type responses in animal models.[1]
Molecular Properties
| Molecular formula | C₁₄H₁₈N₂O₂ |
| Molecular weight | 246.30 g/mol |
The acetyloxy group at C-4 is the sole structural difference from psilocin and increases lipophilicity relative to the parent 4-hydroxy compound. The indole nitrogen is unsubstituted, and the side chain terminates in an N,N-dimethylamine.
Stereochemistry
4-AcO-DMT contains no stereocenters and exists as a single achiral species. No enantioselective pharmacological considerations apply.
Physical Properties
The compound is most commonly encountered as the fumarate salt, whose crystal structure was characterized by X-ray diffraction in 2019.[12] The acetate ester is thermally stable but hydrolyzes readily under basic conditions — a property with significant implications for forensic analysis.[13]
Pharmacology[edit]
Mechanism of Action
4-AcO-DMT produces its psychedelic effects primarily through activation of serotonin 5-HT₂A receptors.[14][15] The compound operates through a dual mechanism: it functions as a prodrug of psilocin, with the acetate ester undergoing hydrolysis to yield psilocin as the dominant metabolic product,[2][10] while also activating 5-HT₂A receptors directly in its intact form.[1]
This dual action distinguishes 4-AcO-DMT from psilocybin, which has minimal direct receptor activity and relies entirely on conversion to psilocin. In animal models, intact 4-AcO-DMT produces psychedelic-type behavioral responses at potencies comparable to psilocin itself.[1]
At higher doses, secondary activation of 5-HT₁A receptors contributes sedation and reduced locomotor activity — producing a biphasic profile in which 5-HT₁A-mediated calming partially counteracts the 5-HT₂A-driven psychedelic stimulation.[11]
Pharmacokinetics
No human pharmacokinetic data specific to 4-AcO-DMT have been published. The following draws on in vitro metabolism studies, animal experiments, and pharmacokinetic characterization of the active metabolite psilocin.
In human liver preparations, hydrolysis to psilocin is the primary metabolic transformation, confirmed as the most abundant product.[2] In mice, 4-AcO-DMT yields approximately 70% of the circulating psilocin levels compared to an equivalent dose of psilocybin — the first direct in vivo confirmation that the compound functions as a prodrug.[10]
Once liberated, psilocin is cleared primarily by MAO-A, which handles roughly 80% of hepatic breakdown.[16] Published psilocin parameters from psilocybin studies indicate a half-life of 1.5–4 hours and time to peak levels of 1.8–4 hours after oral dosing.[17][18]
Metabolite profiling identified 15 breakdown products of 4-AcO-DMT, including hydroxylation and glucuronide products that could serve as forensic biomarkers distinguishing its use from psilocybin consumption.[2]
Neuroscience[edit]
Where It Acts
As a serotonin 2A receptor agonist that delivers psilocin as its active metabolite, 4-AcO-DMT is expected to engage the same cortical and limbic circuits characterized in psilocybin neuroimaging research. No direct brain imaging data for 4-AcO-DMT have been published.
In rats, the compound attenuates innate fear responses through 5-HT₂A receptors on specific inhibitory neurons in the prefrontal cortex,[19] identifying a cortical microcircuit through which psychedelics may modulate threat processing. In reward circuitry, conditioned place preference studies show that 4-AcO-DMT produces sustained positive motivational states without the compensatory rebound effect that characterizes addictive substances.[6]
Why It Matters
The dominant theoretical framework — relaxed beliefs under psychedelics (REBUS) — proposes that psychedelics loosen the brain's top-down predictions, allowing sensory input greater influence on conscious experience. Under this model, 4-AcO-DMT's reported effects — perceptual intensification, loosened categorical thinking, emotional lability, and ego dissolution — reflect a transient flattening of the brain's predictive hierarchy.citation needed
Psilocin also promotes structural neural changes — growth of new dendritic branches and synaptic connections — through growth factor signaling pathways. Whether 4-AcO-DMT engages these plasticity mechanisms at relevant doses has not been tested directly, though the shared active metabolite makes equivalent effects likely.citation needed
Key unresolved questions include whether the approximately 30% lower psilocin exposure from 4-AcO-DMT compared to psilocybin[10] translates to clinically meaningful differences in therapeutic efficacy or neuroplasticity outcomes. The compound's direct 5-HT₂A activity — prior to conversion to psilocin — could theoretically produce a temporally distinct neural activation profile, but this has not been tested.
Subjective Effects[edit]
The 4-AcO-DMT experience is warm, introspective, and body-centered. At lower doses, perceptual enrichment and gentle mood elevation predominate; as dose increases, geometric visual patterning intensifies, thought patterns become fluid and interconnected, and emotional responses deepen significantly. At high doses, ego dissolution and mystical-type states can emerge. Set and setting exert outsized influence — the same dose in a calm, supportive environment may produce contemplative euphoria, while anxiety or interpersonal tension can redirect the experience toward paranoia and thought loops.
Subjectively, 4-AcO-DMT is widely described as indistinguishable from psilocybin mushrooms at equivalent doses — consistent with Shulgin's assessment and the shared active metabolite.[4] Compared to LSD, the experience is shorter, less stimulating, and more emotionally saturated, with a heavier somatic quality characteristic of the tryptamine family.
Effect Grid
At common doses (15–25 mg oral), the full psychedelic experience unfolds. Visual effects become pronounced — geometric patterning overlaying surfaces, colour shifting and enhancement, drifting and morphing of objects and textures, and closed-eye visuals with kaleidoscopic imagery. Time distortion is significant; minutes may feel stretched or compressed. Thought connectivity increases, producing novel associations and conceptual linkages. Emotional amplification is marked — responses to music, nature, and interpersonal interaction can feel deeply meaningful.
Physically, nausea during the come-up is common and may lead to vomiting in some individuals. Body load is noticeable as diffuse heaviness or waves of physical sensation. Pupil dilation is prominent. Temperature dysregulation — alternating sensations of warmth and cold — is typical.
Functional impairment is substantial. Sleep is not possible for the duration of effects (4–7 h). Activities requiring coordination, concentration, or social composure are significantly impaired.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual drifting · Color alteration · Visual breathing · Environmental patterning · Auditory enhancement · Tracers · Symmetrical texture repetition · Perspective distortion · Visual morphing · Brightness alteration · Touch enhancement · Visual haze / noise · After-images · Depth perception distortion · Visual diffraction · Visual melting · Light sensitivity · Sound sensitivity · Spatial disorientation · Proprioceptive distortion · Peripheral vision distortion · Auditory distortion · Synesthesia · Vestibular distortion · Visual magnification · Auditory misinterpretation · Dreaming enhancement · Peripheral misidentification · Visual acuity enhancement · Visual acuity suppression · Taste enhancement · Olfactory enhancement · Internal hallucinations · Object transformations · External hallucinations · Visual recursion · Auditory hallucinations · Environmental orbism / cubism · Object activation · Visual scenery slicing · Perspective hallucinations · Olfactory hallucination
Auditory enhancement · Tracers · Symmetrical texture repetition · Perspective distortion · Visual morphing · Brightness alteration · Touch enhancement · Visual haze / noise · After-images · Depth perception distortion · Visual diffraction · Visual melting · Light sensitivity · Sound sensitivity · Spatial disorientation · Proprioceptive distortion · Peripheral vision distortion · Auditory distortion · Synesthesia · Vestibular distortion · Visual magnification · Auditory misinterpretation · Dreaming enhancement · Peripheral misidentification · Visual acuity enhancement · Visual acuity suppression · Taste enhancement · Olfactory enhancement · Internal hallucinations · Object transformations · External hallucinations · Visual recursion · Auditory hallucinations · Environmental orbism / cubism · Object activation · Visual scenery slicing · Perspective hallucinations · Olfactory hallucination
Body scan awareness · Stimulation · Body schema distortion · Muscle relaxation · Nausea · Tingling / electric sensations · Vibrations / buzzing · Physical fatigue · Insomnia · Appetite suppression · Laughter fits · Sedation · Bodily heaviness · Muscle tension · Watery eyes · Increased urination · Dizziness · Headache · Wakefulness · Bodily pressures · Heart rate perception changes · Restlessness · Tactile euphoria · Yawning · Excessive sweating · Trembling · Dry mouth · Bodily lightness · Pain suppression · Breathing alteration · Kundalini-like energy · Nasal congestion · Salivation · Bruxism · Brain zaps · Vomiting · Involuntary body movements · Nystagmus (eye wobbles) · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Muscle relaxation · Nausea · Tingling / electric sensations · Vibrations / buzzing · Physical fatigue · Insomnia · Appetite suppression · Laughter fits · Sedation · Bodily heaviness · Muscle tension · Watery eyes · Increased urination · Dizziness · Headache · Wakefulness · Bodily pressures · Heart rate perception changes · Restlessness · Tactile euphoria · Yawning · Excessive sweating · Trembling · Dry mouth · Bodily lightness · Pain suppression · Breathing alteration · Kundalini-like energy · Nasal congestion · Salivation · Bruxism · Brain zaps · Vomiting · Involuntary body movements · Nystagmus (eye wobbles) · Bodily dissociation · Tactile hallucination
Conceptual thinking · Cognitive euphoria · Thought connectivity · Pattern recognition enhancement · Cognitive flexibility · Openness enhancement · Aesthetic enhancement · Multiple thought streams · Language suppression · Memory suppression · Thought loops · Confusion · Increased nature relatedness · Synchronicity · Focus suppression · Cognitive impairment · Creativity enhancement · Humor enhancement · Thought deceleration · Thought acceleration · Thought disorganization · Memory fragmentation · Memory replays · Information processing suppression · Cognitive fatigue · Thought organization · Analysis enhancement · Information processing enhancement · Delusions
Pattern recognition enhancement · Cognitive flexibility · Openness enhancement · Aesthetic enhancement · Multiple thought streams · Language suppression · Memory suppression · Thought loops · Confusion · Increased nature relatedness · Synchronicity · Focus suppression · Cognitive impairment · Creativity enhancement · Humor enhancement · Thought deceleration · Thought acceleration · Thought disorganization · Memory fragmentation · Memory replays · Information processing suppression · Cognitive fatigue · Thought organization · Analysis enhancement · Information processing enhancement
Euphoria · Emotional lability · Simultaneous emotions · Dysphoria
Trust enhancement · Disinhibition · Sociability enhancement · Flow state · Communication enhancement · Ego inflation · Compulsive behavior reduction · Boundary dissolution · Identity alteration · Ego dissolution
Communication enhancement · Ego inflation · Compulsive behavior reduction · Boundary dissolution · Identity alteration · Ego dissolution
Time cessation
Non-dual awareness · Entity contact · Death-rebirth sequence
Recursive awareness
Timeline
First alerts emerge as a subtle shift in body awareness — slight tingling, mild stomach unease, or a gentle brightening of visual perception. Effects are easily dismissed as anticipation.
Effects build steadily. Nausea peaks during this phase and typically resolves by its end. Colours begin to saturate, yawning intensifies, and the first visual distortions appear.
Full psychedelic intensity. Visual patterning, colour enhancement, time distortion, and thought connectivity are at maximum. Emotional amplification is pronounced.
Effects recede gradually. Visuals lose intensity, thought patterns begin to normalize, and a sense of re-integration emerges. Emotional processing continues — insights from the peak may crystallize during this phase.
A residual state of emotional openness, mild mood elevation, or reflective introspection lasting hours to days. Some individuals report subtle visual after-images or enhanced pattern sensitivity. Appetite and sleep typically normalize within 4–6 hours of the resolution phase.
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 experimental lethal dose data exist for 4-AcO-DMT in any species, and the toxic dose in humans is unknown. Computational modeling predicts moderate-to-high acute oral toxicity, low cardiac risk relative to other tryptamines, and no mutagenic or endocrine-disrupting activity.[7]
No published case reports of fatal overdose solely attributable to 4-AcO-DMT were identified. Given the compound's low prevalence and uncontrolled market status, the absence of fatality reports does not confirm safety.
Cardiovascular Effects
Elevated heart rate and transient blood pressure increases are expected acute effects consistent with the serotonergic psychedelic class. No 4-AcO-DMT-specific cardiovascular data have been published. Computational predictions indicate lower cardiac channel inhibition risk than DMT and 5-MeO-DMT.[7]
Psychological Risks
Acute psychological distress, anxiety escalation, and paranoia are documented adverse effects of serotonergic psychedelics. At high doses, thought loops, confusion, delusions, identity disruption, and ego dissolution can occur. No controlled studies have characterized these risks specifically for 4-AcO-DMT; class-level data from psilocybin clinical trials provide the best available risk estimates.
Hallucinogen persisting perception disorder (HPPD) — persistent visual disturbances following psychedelic use — can occur after single or repeated exposure to serotonergic psychedelics.[20] The most commonly reported triggers are LSD and psilocybin; by shared active metabolite and class analogy, 4-AcO-DMT carries the same risk.
Individuals with personal or family histories of psychotic disorders, schizophrenia, or bipolar disorder face elevated risk of psychotic episode precipitation.safety citation needed
Tolerance and Dependence
Tolerance develops almost immediately after a single dose through 5-HT₂A downregulation.[21][22] Full sensitivity recovery requires approximately 7 days. Cross-tolerance extends to all 5-HT2A agonist psychedelics — LSD, psilocybin, DMT, mescaline.[14]
No physical dependence or withdrawal has been described for any serotonergic psychedelic. Psychological dependence liability is low. In conditioned place preference tests, 4-AcO-DMT produces a motivational pattern inconsistent with addiction — the compound is rewarding both acutely and at 24 hours, lacking the rebound effect negativity that drives compulsive use.[6]
Drug Interactions
Tramadol
Tramadol inhibits serotonin reuptake. Combined with 4-AcO-DMT's direct serotonin receptor activation, this creates a confirmed risk of serotonin syndrome.[23] Multiple fatalities have been documented from tramadol combined with other serotonergic drugs.[24] This combination is dangerous.
MAOIs
MAOIs block the primary enzyme responsible for psilocin breakdown (approximately 80% of liver clearance).[16] Co-administration would significantly prolong and intensify effects while elevating the risk of serotonin-related adverse events.[24]
SSRIs and SNRIs
Chronic SSRI use may blunt psychedelic effects through receptor desensitization. Concurrent use also raises serotonin syndrome risk, though no 4-AcO-DMT-specific interaction data exist.
Cannabis
No published interaction data exist for 4-AcO-DMT and cannabis. Evidence for receptor-level interaction between cannabinoid and serotonin systems suggests theoretical potential for unpredictable effects.citation needed
Detection
4-AcO-DMT is not detectable by standard drug screening panels.[25]
Contraindications
Psychiatric vulnerability: Personal or family history of psychotic disorders, schizophrenia spectrum disorders, or bipolar I disorder. Psychedelics can precipitate or worsen psychotic episodes.[24]
Concurrent tramadol use: Serotonin toxicity risk from combined mechanisms. Absolute contraindication.[23]
Concurrent MAOI use: Dangerous intensification of serotonergic effects through blockade of psilocin's primary breakdown pathway.[24][16]
Heart conditions: Elevated heart rate and blood pressure are expected acute effects. Pre-existing cardiovascular disease or conditions predisposing to irregular heart rhythm are relative contraindications.
Seizure disorders: Possible seizure threshold reduction has been reported at the class level for serotonergic psychedelics.safety citation needed
Harm Reduction[edit]
Forms & Identification
4-AcO-DMT is most commonly sold as the fumarate salt — a white to off-white powder or crystalline solid. Because the compound converts to psilocin (the same metabolite produced by psilocybin), standard reagent testing confirms the presence of a 4-substituted tryptamine but cannot distinguish between psilocin prodrugs. Active doses are measured in milligrams; volumetric dosing from a prepared solution is strongly recommended for powder forms, as even small measurement errors can shift the experience from mild to overwhelming. Drug checking services offering mass spectrometry provide the most reliable substance identification.
Guidelines
- Test your substance using reagent kits and, ideally, a drug checking service before use
- Start low. If unfamiliar with the batch or your sensitivity, begin at the lower end of the common dose range and wait at least 90 minutes before considering any additional dose
- Measure carefully. Use a milligram-precision scale (0.001 g). Never estimate powder doses by eye
- Prepare your environment. Remove hazards, ensure access to water and comfortable seating, and have a calm playlist ready
- Eat lightly 2–3 hours beforehand. A full stomach may delay onset; an empty stomach may increase nausea
- Clear your schedule. Allow the full duration plus several hours of afterglow. Do not drive or operate machinery
- Have a sitter. A sober, trusted companion can provide reassurance, manage logistics, and intervene if distress escalates
- Surrender to the experience. Resistance to emerging effects — especially at higher doses — frequently amplifies anxiety. Controlled breathing and a change of environment can help redirect difficult moments
Set & Setting
Psychedelic experiences are profoundly shaped by mindset and environment. Choose a calm, familiar space free from obligations or interruptions. A trusted, sober companion ("trip sitter") is strongly recommended, especially for first experiences or higher doses.
Avoid using during periods of emotional distress, unresolved interpersonal conflict, or significant anxiety — these states tend to amplify under psychedelics. Physical comfort matters: access to water, soft lighting, blankets, and a pre-prepared playlist can meaningfully ease the experience.
Aftercare & integration. The days following a psychedelic experience are a window for processing what emerged. Journaling, artwork, or voice recording within the first 24 hours can help capture insights before they fade. Discuss the experience with a trusted friend or integration therapist — particularly if difficult emotions, unresolved memories, or existential themes surfaced.
Mild mood shifts, reflectiveness, and altered dream activity are common in the days following use and typically resolve within a week. If anxiety, depersonalization, or intrusive thoughts persist beyond two weeks, seek professional support from a therapist experienced with psychedelic integration.
Recovery & Support
Serotonergic psychedelics carry low abuse liability, and compulsive use patterns are rare. However, problematic use can develop — particularly when psychedelics are used to escape rather than explore, or when integration is neglected. If use is becoming a way to avoid addressing life circumstances, reducing frequency or pausing entirely is advisable.
Support resources include psychedelic integration circles, harm reduction organizations such as the Zendo Project and DanceSafe, and therapists trained in psychedelic integration. For broader substance use concerns, SAMHSA's National Helpline (1-800-662-4357) provides free, confidential referrals.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Most difficult psychedelic experiences are distressing but not medically dangerous. Seek immediate help if the person is a danger to themselves or others, is completely unresponsive, experiences seizures, shows signs of severe overheating, or has taken a combination with serotonergic drugs and develops muscle rigidity, tachycardia, and high fever (signs of serotonin syndrome).
Immediate steps:
- 1. Stay with the person. Speak calmly and simply.
- 2. Move them to a quiet, safe space if possible.
- 3. If unresponsive, place them in the recovery position.
- 4. Call emergency services if symptoms escalate or you are unsure.
- 5. Do not restrain the person unless there is immediate danger of self-harm.
What to tell the dispatcher: Name the substance (4-AcO-DMT, a synthetic psilocin structural analog), estimated dose, time of ingestion, current symptoms, and any other substances taken. Good Samaritan laws in many jurisdictions protect those who call for help during a drug emergency.
Legal Status[edit]
4-AcO-DMT occupies a fragmented legal position internationally. As a synthetic tryptamine not found in nature, it falls outside natural product scheduling frameworks. Its structural relationship to psilocin — differing only by a single acetyloxy group — places it within reach of structural analog and ester provisions in some jurisdictions, but explicit scheduling varies substantially by country.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States (federal) | Not explicitly scheduled | Not listed in the Controlled Substances Act. Potentially prosecutable under the Federal Analog Act (21 U.S.C. § 813) as a structural analog of psilocin (Schedule I) when intended for human consumption. No known FAA prosecution specific to 4-AcO-DMT as of 2026[8][26] |
| United States (Alabama) | Schedule I | Explicitly named and scheduled under Alabama state law — one of the few US states to list 4-AcO-DMT by name[26] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled as an ester of psilocin under MDA 1971 Schedule 2, Paragraph 3, which extends control to "any ester or ether" of listed substances. Also covered by the Psychoactive Substances Act 2016[9] |
| Germany | Anlage I (BtMG) | Controlled under the strictest category of the Betäubungsmittelgesetz, covering esters, ethers, and salts of scheduled indole alkaloids[27] |
| Canada | Not controlled | Not listed in any CDSA schedule (I–VIII). Possession and acquisition are legal. Canada's CDSA lacks a generic analogue provision equivalent to the US Federal Analog Act[27] |
| Australia | Schedule 9 (TGA Poisons Standard) | Highest restriction category — prohibited substance. Manufacture, possession, supply, and use prohibited[27] |
| Sweden | Controlled substance | Among the first Scandinavian countries to schedule novel research chemicals[27] |
Analog and Prodrug Considerations
The US Federal Analog Act applies only to substances "substantially similar" in chemical structure or pharmacological effect to a Schedule I or II substance, and only when intended for human consumption. As the acetate ester of psilocin (Schedule I), 4-AcO-DMT meets the structural similarity criterion. Enforcement has been inconsistent, and no published case law specifically addresses 4-AcO-DMT under the FAA.[26]
In the United Kingdom, the ester clause in MDA 1971 Schedule 2 provides unambiguous coverage without requiring analogue reasoning. The Advisory Council on the Misuse of Drugs has advised that tryptamine esters are captured by the generic tryptamine definition.[9]
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references
- [1] ^abcdGlatfelter GC, Pottie E, Partilla JS, Sherwood AM, et al. (2022) Structure-Activity Relationships for Psilocybin, Baeocystin, Aeruginascin, and Related Analogues to Produce Pharmacological Effects in Mice — ACS Pharmacology and Translational Science doi:10.1021/acsptsci.2c00177
- [2]
- [3]
- [4]
- [5] ^abNichols DE, Frescas S (1999) Improvements to the Synthesis of Psilocybin and a Facile Method for Preparing the O-Acetyl Prodrug of Psilocin — Synthesis doi:10.1055/s-1999-3490
- [6] ^abcVargas-Perez H, Minauro-Sanmiguel F, Ting-A-Kee R, Grieder TE, Méndez-Díaz M, Próspero-García O, van der Kooy D (2024) Rewarding Effects of the Hallucinogen 4-AcO-DMT Administration and Withdrawal in Rats: A Challenge to the Opponent-Process Theory — Neuroscience Letters doi:10.1016/j.neulet.2023.137597