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LSD, psilocybin, mescaline +2 moreLSD, psilocybin, mescaline, DOx compounds, other 5-HT2A agonists show less
Methallylescaline
3,5-dimethoxy-4-(2-methylallyloxy)phenethylamine
Methallylescaline (MAL) is a synthetic psychedelic of the phenethylamine class. It is a mescaline structural analog, roughly six times more potent than its parent compound.[1] It activates serotonin receptors in the brain, producing the visual and introspective shifts characteristic of classical psychedelics.[1]
Methallylescaline is a synthetic psychedelic of the phenethylamine class. It is a mescaline structural analog of the scaline family, roughly six times more potent than its parent compound.[1] MAL is a full 5-HT₂A receptor agonist, producing its effects by disrupting serotonin-mediated sensory gating in the prefrontal cortex.[1]
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LSD, psilocybin, mescaline +2 moreLSD, psilocybin, mescaline, DOx compounds, other 5-HT2A agonists show less
Shulgin synthesized MAL at his California laboratory in 1981–1982 and documented it as entry #99 in PiHKAL (1991).[2] The compound remained obscure for over three decades, with almost no scientific study. Online discussion surged in late 2023, and by 2024 drug surveillance systems had issued formal alerts about its steep dose-response curve.[3]
Subjective effects include color enhancement, geometric visual patterns, introspective depth, tactile enhancement, and body load.[2][3] The experience carries mescaline's warm visual saturation and introspective warmth at a fraction of the dose. Nausea, overstimulation, and a heavy come-up body load are characteristic undesired effects.
MAL produces no physical dependence, and the toxic dose in humans is unknown.[4] The defining risk is a steep dose-response curve — small increases in dose produce disproportionate jumps in intensity.[3] Understanding rests on a single pharmacological study,[1] one case report,[5] and community data — the evidence base is thin.
History[edit]
Discovery
Shulgin synthesized MAL at his private laboratory in Lafayette, California, in 1981–1982 and confirmed its psychoactive properties through self-administration.[2] He published it as entry #99 in PiHKAL: A Chemical Love Story (1991).[2] For nearly three decades, that entry was the entirety of published knowledge on MAL.
Scientific characterization
The first formal pharmacological study appeared in 2021, mapping MAL's receptor binding profile alongside a series of mescaline analogs.[1] A separate 2018 study identified how the body metabolizes MAL, providing data useful for forensic detection.[6]
Modern emergence
MAL remained obscure through most of the 2010s. Online discussion surged in late 2023, and a formal surveillance alert was issued in May 2024 highlighting the compound's steep dose-response curve and absent clinical safety data.[7][3]
Shulgin himself noted that the name "methallylescaline" is misleading — the compound is not a union of methallyl with escaline, but rather mescaline with a methallyloxy group at the 4-position.[2] A 2013 Erowid report documenting a severe adverse event at 130 mg is the earliest publicly available case data, and suggests poison control had no prior familiarity with MAL at the time.[5]
Chemistry[edit]
Structural class
Methallylescaline belongs to the scaline family — mescaline analogs in which the 4-methoxy group is replaced by a longer alkoxy substituent. MAL's branched methallyloxy group at the 4-position places it alongside allylescaline, escaline, and proscaline in a series where chain length and branching shape potency.[1] Extending the 4-alkoxy chain generally increases potency up to an optimum, beyond which affinity falls.[8]
Molecular properties
The molecular formula is C₁₄H₂₁NO₃ (molecular weight 251.32 g/mol). The terminal alkene of the methallyloxy group is the primary site of hepatic oxidative metabolism.[6] The hydrochloride salt crystallizes as a white solid with a melting point of 153–154°C.[2]
Pharmacology[edit]
Mechanism of action
MAL activates serotonin receptors in the brain, where it acts as a potent full agonist.[1] It does not act through dopamine or norepinephrine pathways, ruling out stimulant-type mechanisms.[1] This mechanism is confirmed by blocking studies: a selective serotonin receptor antagonist reduces the subjective effects of mescaline-class compounds in controlled settings.[9]
Pharmacokinetics
No human pharmacokinetic data have been published. Onset occurs 20–60 minutes after oral ingestion; peak effects last 3–5 hours, and total duration ranges from 8–16 hours depending on dose.[2][1][3]
Metabolism
The body metabolizes MAL primarily through oxidation of the methallyloxy group, producing four hydroxylated metabolites.[6] Some individuals carry a genetic variant that slows one of the main metabolizing enzymes (CYP2D6); certain medications — including fluoxetine, paroxetine, and ketoconazole — can also inhibit these enzymes and prolong MAL's effects.[6]
Neuroscience[edit]
Where it acts
MAL activates serotonin receptors on neurons in the prefrontal cortex.[1] This disrupts the brain's normal filtering of sensory input — the thalamus usually acts as a gatekeeper, limiting what reaches conscious awareness.[4] When that filter loosens, sensory experience intensifies, visual patterns emerge, and perceptual shifts become possible.
Why it matters
Serotonergic psychedelics reduce activity in the default mode network — the brain system linked to self-referential thinking and narrative identity — while increasing communication between regions that don't normally interact. This pattern is consistent with MAL's reported introspective depth and self-connective quality.[2] The REBUS model adds that psychedelics loosen the brain's top-down expectations, letting raw sensory experience override established mental models.[1]
Several questions remain unresolved. Does MAL's steep dose-response curve reflect metabolic saturation or a receptor-level phenomenon[3]? Does adrenergic activity contribute to the cardiovascular effects seen at high doses[5]? And what accounts for MAL's prolonged duration (up to 16 hours) given mescaline's much shorter plasma half-life[9]?
Subjective Effects[edit]
The MAL experience is built on a tension between sensory richness and physical discomfort. A heavy body load and nausea typically dominate the come-up before receding as vivid color enhancement, introspective depth, and complex visual geometry consolidate. The experience is acutely sensitive to set and setting — identical doses in different contexts produce markedly different trajectories.
The overall character sits between mescaline and allylescaline — sharing mescaline's warm color saturation and introspective warmth at roughly one-sixth the dose. Intensity scales steeply with dose, and small increments can shift the experience from contemplative to overwhelming — more so than most users familiar with psilocybin or LSD expect.
Synthesized and self-administered by Alexander Shulgin between 1981 and 1982, MAL was published as entry #99 in PiHKAL: A Chemical Love Story.[2] No formal pharmacological data appeared until 2021, when the first receptor binding and functional activation study was published.[1] Online discussion surged from late 2023, and MAL now circulates as a research chemical of increasing interest.[3]
Subjective effects include color enhancement, geometric visual patterns, introspective depth, tactile enhancement, and body load.[2][3] The experience carries mescaline's warm visual saturation at a fraction of the dose, underscored by a somatic heaviness and steep dose-sensitivity that define its character. Nausea, overstimulation, and a pronounced come-up body load are characteristic unsought effects.
MAL produces no physical dependence, and the toxic dose in humans is unknown.[4] Its steep dose-response curve is the defining risk — small dose increments produce disproportionate jumps in intensity, making accidental over-exposure more likely than with most psychedelics.[3] No clinical trials have been conducted; the current understanding rests on a single pharmacological study,[1] one case report,[5] and community experience data.
History[edit]
Discovery
Alexander Shulgin synthesized methallylescaline at his private laboratory in Lafayette, California, between 1981 and 1982, confirming its psychoactive properties through self-administration.[2] The compound was published as entry #99 in PiHKAL: A Chemical Love Story (1991), which remains the sole primary account of the original bioassay.[2] For nearly three decades, this entry constituted the entirety of published knowledge on MAL.
Scientific characterization
The first formal pharmacological study appeared in 2021, when Kolaczynska and colleagues characterized MAL's receptor binding profile alongside a series of mescaline analogs, establishing the quantitative data that had been absent since Shulgin's qualitative reports.[1] Separately, Kim and colleagues published the only study of MAL's metabolic fate in 2018, identifying hydroxylated metabolites via in vitro hepatocyte incubation to support forensic detection.[6]
Modern emergence
MAL circulated sporadically on research chemical markets throughout the 2010s but remained obscure. National Drug Early Warning System surveillance identified a marked increase in online discussion from late 2023, with a formal alert issued in May 2024 highlighting the compound's steep dose-response curve and absence of clinical safety data.[7][3]
Shulgin himself noted that the name "methallylescaline" is "completely unsound" — the compound is not a union of methallyl with escaline but rather mescaline with a methallyloxy group replacing the 4-methoxy substituent.[2] Despite this terminological objection, the name has persisted in both scientific and community usage. A 2013 Erowid experience report documenting a severe adverse event at 130 mg represents the earliest publicly available case data, suggesting poison control had no prior familiarity with the compound at that time.[5]
Chemistry[edit]
Structural class
Methallylescaline belongs to the scaline family of substituted phenethylamines — mescaline analogs in which the 4-methoxy group is replaced by a longer alkoxy substituent. Where mescaline carries a simple methoxy group at the 4-position, MAL bears a 2-methylprop-2-en-1-yloxy (methallyloxy) substituent, with the 3- and 5-methoxy groups retained.
This places MAL alongside allylescaline (unsubstituted allyl), escaline (ethyl), and proscaline (propyl) within a systematic structure-activity series exploring how 4-alkoxy chain length and branching affect potency and duration.[1] The branched methallyloxy group distinguishes MAL from allylescaline: the additional methyl on the terminal alkene introduces steric bulk that modestly reduces 5-HT₂A binding relative to the straight-chain allyl analog.[1]
Within the broader landscape of mescaline derivatives, extending the 4-alkoxy chain generally increases potency up to an optimum, beyond which affinity declines.[8]
Molecular properties
| Molecular formula | C₁₄H₂₁NO₃ |
| Molecular weight | 251.32 g/mol |
The core scaffold is a 3,5-dimethoxyphenethylamine backbone — the pharmacophore shared by all mescaline-class compounds — with the 4-position oxygen bearing the methallyl ether. The terminal alkene of the methallyloxy group is the primary site of hepatic oxidative metabolism.[6]
Stereochemistry
MAL does not possess a chirality center. The phenethylamine backbone is unsubstituted at the α-carbon, and the methallyloxy side chain contains no stereogenic element. Stereochemical considerations do not apply to this compound.
Physical properties
The hydrochloride salt crystallizes as a white solid with a melting point of 153–154°C.[2] No published data exist for free base melting point, aqueous solubility, partition coefficient, or pKa. The terminal alkene suggests potential susceptibility to oxidative degradation, but this has not been experimentally characterized.
Pharmacology[edit]
Mechanism of action
Methallylescaline produces its psychedelic effects primarily through activation of the serotonin 5-HT₂A receptor, where it acts as a potent full agonist.[1] It binds with near-equal strength at the 5-HT₂C receptor and shows roughly nine-fold selectivity for 5-HT₂A over 5-HT₁A.[1]
This mechanism is confirmed by blocking studies: the selective 5-HT₂A antagonist ketanserin attenuates the subjective effects of mescaline-class compounds in controlled human settings.[9] MAL is essentially inactive at 5-HT₂B — a finding with practical relevance, since chronic 5-HT₂B activation is the mechanism behind drug-induced heart valve damage seen with some other serotonergic compounds.[1]
MAL does not act through monoamine transporter activity — it has negligible binding at dopamine, norepinephrine, and serotonin transporters, ruling out stimulant-type or empathogen mechanisms.[1] At higher doses, some affinity at adrenergic α₂A receptors could theoretically contribute to cardiovascular effects, though this remains unconfirmed in humans.[1]
Pharmacokinetics
No human pharmacokinetic studies have been published for methallylescaline. Absorption, bioavailability, volume of distribution, and clearance are unmeasured.
Onset of subjective effects occurs 20–60 minutes after oral ingestion, with peak effects sustained for 3–5 hours. Total duration ranges from 8–16 hours depending on dose — Shulgin reported 12–16 hours at higher doses,[2] while later sources cite 8–12 hours at lower ranges.[1]
The discrepancy likely reflects dose-dependency: higher doses produce proportionally longer experiences, consistent with the steep dose-response curve documented in surveillance data.[3]
Metabolism
The sole published metabolic study used in vitro human hepatocyte incubation to identify four hydroxylated metabolites, with oxidation occurring predominantly on the methallyloxy group.[6] The metabolizing enzymes include CYP2D6, CYP2J2, CYP1A2, and CYP3A4.[6]
The CYP2D6 involvement has practical significance: individuals who are poor CYP2D6 metabolizers (roughly 5–10% of European populations) may clear MAL more slowly and experience prolonged effects. Medications that inhibit CYP2D6 (fluoxetine, paroxetine, bupropion) or CYP3A4 (ketoconazole, grapefruit juice) could theoretically increase MAL exposure.[6]
Neuroscience[edit]
Where it acts
As a full agonist at cortical 5-HT₂A receptors,[1] MAL is expected to engage the same neural mechanisms established for other serotonergic psychedelics. Activation of these receptors on layer V pyramidal neurons in the prefrontal cortex disrupts the thalamic filter that normally constrains sensory input,[4] producing the perceptual flooding and visual intensification characteristic of the psychedelic state.
Serotonergic psychedelics also reduce connectivity within the default mode network — the system associated with self-referential thought and narrative identity — while increasing communication between brain regions that do not normally interact. MAL's reported introspective depth and self-connective effects[2] are consistent with this pattern.
Why it matters
The REBUS framework (Relaxed Beliefs Under Psychedelics) proposes that 5-HT₂A agonists loosen the brain's top-down expectations, allowing raw sensory experience to override established mental models. MAL's potent 5-HT₂A agonism suggests strong engagement of this mechanism at adequate doses.[1]
Separately, 5-HT₂A agonists promote structural neuroplasticity — increased dendritic branching and new synaptic connections — through downstream signaling pathways. Whether MAL produces equivalent neuroplastic effects has not been tested.
Several questions remain unresolved. Does MAL's steep dose-response curve reflect saturation of metabolic capacity, or a pharmacodynamic phenomenon at the receptor level[3]? Does the α₂A adrenergic component contribute to the pronounced cardiovascular activation seen at high doses[5]? And what accounts for MAL's prolonged duration (up to 16 hours) given that mescaline has a plasma half-life of only ~3.5 hours[9]?
Subjective Effects[edit]
The methallylescaline experience is built on a tension between sensory richness and physical discomfort. A diffuse body load during the come-up — nausea, muscle tension, overstimulation — typically recedes as vivid color enhancement, introspective depth, and complex visual phenomena consolidate. The experience is highly sensitive to set and setting: identical doses in different psychological contexts produce markedly different trajectories. Intensity scales steeply with dose, and small increments can shift the experience from contemplative to overwhelming.
The overall character sits between mescaline and allylescaline — sharing mescaline's warm color saturation and introspective warmth at roughly one-sixth the dose, but with a body load and dose-sensitivity that exceed what most users familiar with psilocybin or LSD expect.
Effect Grid
Vivid color saturation dominates the visual field — environmental patterning, open-eye visual drifting, and symmetrical texture repetition become pronounced. Closed-eye imagery begins to develop complexity. Introspective depth increases substantially, with enhanced emotional processing and conceptual thinking.
The body load during come-up is a defining feature at this tier: nausea, muscle tension, and a sense of overstimulation that typically recedes as peak effects consolidate. Tactile enhancement and spontaneous body sensations are common. Pupil dilation is noticeable. Increased urination persists.
This represents the core psychedelic experience for MAL. Expect 10–14 hours of commitment. Sleep is difficult for at least 8 hours after ingestion. The steep dose-response curve means even 5 mg above this range can shift the experience significantly toward strong-tier intensity.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Depth perception distortion · Perspective distortion · Brightness alteration · Tracers · Auditory enhancement · Visual breathing · Touch enhancement · Symmetrical texture repetition · After-images · Environmental patterning · Light sensitivity · Sound sensitivity · Visual morphing · Visual acuity enhancement · Visual diffraction · Auditory distortion · Auditory misinterpretation · Holotropic state · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Visual haze / noise · Visual melting · Synesthesia · Vestibular distortion · Visual processing acceleration · Internal hallucinations · External hallucinations · Object activation · Object transformations · Visual recursion · Environmental orbism / cubism · Perspective hallucinations · Auditory hallucinations
Auditory enhancement · Visual breathing · Touch enhancement · Symmetrical texture repetition · After-images · Environmental patterning · Light sensitivity · Sound sensitivity · Visual morphing · Visual acuity enhancement · Visual diffraction · Auditory distortion · Auditory misinterpretation · Holotropic state · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Visual haze / noise · Visual melting · Synesthesia · Vestibular distortion · Visual processing acceleration · Internal hallucinations · External hallucinations · Object activation · Object transformations · Visual recursion · Environmental orbism / cubism · Perspective hallucinations · Auditory hallucinations
Appetite suppression · Body high · Wakefulness · Tactile euphoria · Nausea · Muscle tension · Dry mouth · Heart rate perception changes · Insomnia · Restlessness · Bodily lightness · Sexual arousal enhancement · Body schema distortion · Dehydration sensation · Dizziness · Excessive sweating · Laughter fits · Tingling / electric sensations · Vibrations / buzzing · Increased urination · Bodily pressures · Headache · Motor control impairment · Abnormal heartbeat · Trembling · Vomiting · Yawning
Tactile euphoria · Nausea · Muscle tension · Dry mouth · Heart rate perception changes · Insomnia · Restlessness · Bodily lightness · Sexual arousal enhancement · Body schema distortion · Dehydration sensation · Dizziness · Excessive sweating · Laughter fits · Tingling / electric sensations · Vibrations / buzzing · Increased urination · Bodily pressures · Headache · Abnormal heartbeat · Trembling · Vomiting · Yawning
Immersion enhancement · Conceptual thinking · Pattern recognition enhancement · Increased nature relatedness · Introspection enhancement · Openness enhancement · Thought connectivity · Thought acceleration · Cognitive flexibility · Multiple thought streams · Creativity enhancement · Memory suppression · Thought loops · Analysis enhancement · Cognitive impairment · Focus suppression · Humor enhancement · Synchronicity · Information processing enhancement · Motivation enhancement · Confusion · Language suppression · Memory fragmentation · Thought disorganization · Delusions of sobriety · Delusions
Increased nature relatedness · Introspection enhancement · Openness enhancement · Thought connectivity · Thought acceleration · Cognitive flexibility · Multiple thought streams · Creativity enhancement · Memory suppression · Thought loops · Analysis enhancement · Cognitive impairment · Focus suppression · Humor enhancement · Synchronicity · Information processing enhancement · Motivation enhancement · Confusion · Language suppression · Memory fragmentation · Thought disorganization · Delusions
Simultaneous emotions · Anxiety · Catharsis
Sociability enhancement · Trust enhancement · Communication enhancement · Flow state · Depersonalization · Boundary dissolution · Identity alteration · Ego dissolution
Depersonalization · Boundary dissolution · Identity alteration · Ego dissolution
Non-dual awareness · Entity contact
Recursive awareness
Timeline
First awareness of effects — mild body sensations, subtle perceptual brightening, and a faint physical hum. Easily mistaken for anticipation at lower doses.
Body load intensifies — nausea, muscle tension, and overstimulation are common. Visual and cognitive effects build steadily. Often the most physically uncomfortable phase.
Full visual, cognitive, and emotional effects. Vivid color enhancement, introspective depth, tactile enhancement, and possible ego softening. Time alteration is pronounced.
Gradual reduction in visual intensity. Residual stimulation, restlessness, and insomnia are common. Cognitive clarity begins returning but perceptual traces may linger.
Residual mood effects, enhanced dreaming, and physical fatigue. Cognitive clarity returns but sleep may remain difficult for several hours.
⚠ Do not drive or operate heavy machinery for at least 16 hours after ingestion at strong doses, or until all perceptual and cognitive effects have fully resolved.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- No data
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
No controlled toxicity studies have been conducted. The toxic dose in humans is unknown.
Acute toxicity
The only human safety data at high doses come from a single case report: 130 mg oral — roughly twice the upper end of Shulgin's reported effective range.[5] The individual experienced rapid heart rate (>120 bpm), elevated blood pressure (160/80 mmHg), facial flushing, delirium, and urinary retention.
All laboratory values — kidney function, liver enzymes, cardiac markers — remained normal.[5] The patient recovered fully after intravenous fluids, lorazepam, and supportive monitoring.
Heart and circulation
The cardiovascular stimulation seen at 130 mg is consistent with mescaline's known effects.[9] MAL is essentially inactive at a receptor subtype that, when chronically activated, causes drug-induced heart valve damage — suggesting lower chronic cardiac risk than some other serotonergic compounds.[1] No long-term cardiac data exist.
Nausea and body load
Nausea and vomiting are prominent adverse effects, particularly at higher doses.[9][3] Community reports describe the body load as encompassing unease, shortness of breath, and overstimulation.[3]
Psychological risks
MAL carries the class-level psychological risks of serotonergic psychedelics. Its steep dose-response curve makes accidental intensity escalation a distinctive concern.[3]
- Acute anxiety, panic, and dysphoria — particularly at higher doses or in unfavorable settings.
- Psychotic episodes — serotonergic psychedelics can trigger acute psychosis in individuals with a personal or family history of psychosis or schizophrenia-spectrum disorders.[4]
- Persistent visual disturbances — visual anomalies that outlast the experience; no MAL-specific cases have been published, but the risk is presumed present given the compound's potency.[10]
- Trauma re-emergence — introspective deepening can surface distressing material, particularly in individuals with trauma histories.[2]
Tolerance and dependence
MAL is not habit-forming and produces no physical dependence.[4] Its pharmacological profile — no DAT activity, no monoamine releasing activity[1] — is inconsistent with the mechanisms that drive compulsive drug-seeking.
Tolerance builds rapidly after a single dose and takes approximately 7 days to resolve.[11] Cross-tolerance extends to LSD, psilocybin, mescaline, and DOx-series compounds.[11] No withdrawal has been documented.
Drug Interactions
No published interaction studies exist for MAL. All guidance comes from class-level evidence and pharmacological inference.
Monoamine oxidase inhibitors (MAOIs). MAOIs block the breakdown of serotonin. Combined with MAL, this risks a dangerous buildup of serotonin activity — a potentially life-threatening reaction.[12] This combination is contraindicated. safety citation needed
SSRIs and SNRIs. These medications may reduce psychedelic effects through chronic receptor changes, though serotonergic potentiation cannot be excluded in all cases.[12]
Lithium. Psychedelic–lithium combinations have been associated with seizures across the serotonergic psychedelic class. Contraindicated. safety citation needed
Stimulants. Stimulants raise heart rate and blood pressure. Combined with MAL's documented cardiovascular stimulation at 130 mg,[5] the combination risks serious cardiac complications.
Cannabis. Potentiates psychedelic intensity, with increased risk of anxiety and psychosis.
CYP2D6 and CYP3A4 inhibitors. MAL is metabolized by these liver enzymes.[6] Inhibitors — including fluoxetine, paroxetine (CYP2D6) and ketoconazole, grapefruit juice (CYP3A4) — can increase MAL exposure and prolong effects.
Contraindications
7 knownNo substance-specific contraindication studies exist. The following are based on class-level evidence and available case data.
Heart conditions or high blood pressure. Cardiovascular stimulation documented at 130 mg (heart rate >120 bpm, blood pressure 160/80 mmHg)[5] and mescaline's sympathomimetic profile[9] indicate risk for individuals with pre-existing cardiac conditions.
Personal or family history of psychosis. Serotonergic psychedelics can trigger psychotic episodes in vulnerable individuals.[4]
Concurrent MAOI use. Risk of dangerous serotonin overload.[12]
Concurrent lithium use. Class-level seizure risk. safety citation needed
Pregnancy. No reproductive safety data exist.
Liver impairment. MAL is metabolized by multiple liver enzymes;[6] impaired clearance could increase exposure.
Harm Reduction[edit]
Forms & Identification
MAL's steep dose-response curve makes accurate identification and purity assessment more consequential than with most oral psychedelics.[3] Reagent testing confirms the substance class but cannot verify potency or purity. Quantitative analysis through a drug checking service provides the most meaningful safety information for this compound.
Guidelines
- Use a milligram-precision scale for every dose. Visual estimation is dangerous with MAL's steep dose-response curve.
- Start at the lower end of the dose range and wait at least 90 minutes before considering the come-up complete — onset can be slow.
- Do not redose. The long duration and steep curve mean full intensity may not be apparent until hours in.
- Eat a light meal 2–3 hours before ingestion to reduce nausea.
- Keep ginger tea or anti-nausea aids available — nausea during onset is common with mescaline-class compounds.
- Clear the full day and following morning of obligations. Experiences at moderate doses can last 12+ hours.
- Have a sober sitter present, especially at unfamiliar doses.
Set & Setting
Set and setting are primary drivers of the MAL experience. The long duration — potentially up to 16 hours — demands a stable, comfortable environment with no obligations for the full day and following morning.
First-time use benefits from a sober, experienced sitter who can provide reassurance during the come-up body load and any anxious passages. Choose a familiar, physically safe space.
Aftercare & integration. The extended duration of MAL means physical and psychological recovery may take longer than with shorter-acting psychedelics. Prioritize sleep, hydration, and light nutrition in the 24 hours following the experience. Some users report lingering body fatigue or emotional sensitivity for one to two days.
Journaling or discussing the experience within the first few days can help process intense introspective or emotional material. If distressing thoughts, persistent visual disturbances, or difficulty returning to baseline continue beyond a week, seek support from a mental health professional experienced with psychedelic experiences.
Recovery & Support
MAL does not produce physical dependence or withdrawal. However, repeated use of any psychedelic as a coping mechanism warrants self-examination. If psychedelic use is becoming driven by avoidance rather than intention, peer support communities and professional counseling can provide perspective and structure.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Uncomfortable body load, nausea, and anxiety during the come-up are common and generally resolve. Seek immediate help if any of the following occur: chest pain, sustained heart rate above 120 bpm that does not settle with rest, severe confusion or delirium, inability to recognize surroundings or people, self-harm risk, or loss of consciousness.
Immediate steps:
- 1. Move the person to a quiet, safe space.
- 2. Call emergency services if symptoms listed above are present.
- 3. Do not restrain the person unless there is immediate danger to themselves or others.
- 4. Keep them cool and hydrated while waiting for help.
- 5. If the person is unconscious, place them in the recovery position.
What to tell the dispatcher: Name the substance (methallylescaline / MAL), the dose if known, the time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
No reversal agent exists for serotonergic psychedelics. Hospital treatment is supportive — benzodiazepines for agitation, monitoring for cardiovascular symptoms.
Legal Status[edit]
Methallylescaline occupies an ambiguous legal position in most jurisdictions — not widely scheduled by name, but often captured under blanket psychoactive substance laws. In the United States, the Federal Analogue Act creates potential criminal liability when MAL is intended for human consumption, based on its structural and pharmacological similarity to mescaline (Schedule I).
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not specifically scheduled | Federal Analogue Act (21 U.S.C. § 813) may apply when intended for human consumption; structural and pharmacological analog of mescaline (Schedule I) |
| United Kingdom | Controlled — Psychoactive Substances Act 2016 | Blanket prohibition effective May 26, 2016; covers all psychoactive substances not specifically exempted |
| Germany | Controlled — NpSG | Neue-psychoaktive-Stoffe-Gesetz, effective November 26, 2016 |
| Sweden | Specifically scheduled | Classified as a controlled substance, January 2016 |
| Canada | Not controlled (as of 2012) | Health Canada status determination A-2013-00235 concluded MAL not controlled under CDSA; this determination may be outdatedcitation needed |
| Australia | Not specifically scheduled | Likely captured under state or federal NPS provisions; no specific scheduling confirmation availablecitation needed |
Legal status changes frequently and varies significantly by jurisdiction. This information is not legal advice. Verify current status in the relevant jurisdiction before relying on it.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- No data
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 7 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
No controlled toxicity studies have been conducted for methallylescaline in any species, and no lethal dose has been established. The toxic dose in humans is unknown.
Acute toxicity
The only available human safety data at high doses come from a single case report at 130 mg oral — roughly twice the upper end of Shulgin's reported effective range.[5] The individual experienced rapid heart rate (>120 bpm), elevated blood pressure (160/80 mmHg), facial flushing, delirium, and urinary retention.
All laboratory values — kidney function, liver enzymes, and cardiac markers — remained normal.[5] The patient recovered fully after treatment with intravenous fluids, lorazepam, and supportive monitoring.
Heart and circulation
The cardiovascular stimulation observed at 130 mg is consistent with effects documented for mescaline in controlled settings.[9] MAL's adrenergic α₂A activity could theoretically contribute at high doses.[1]
MAL is essentially inactive at the serotonin₂B receptor.[1] Chronic 5-HT₂B activation causes drug-induced heart valve damage — MAL's inactivity at this target suggests lower chronic cardiac risk than 5-HT₂B-active compounds. No long-term cardiac data exist.
Nausea and body load
Nausea and vomiting are prominent adverse effects, particularly at higher doses, consistent with the mescaline class.[9][3] Community reports describe the body load as encompassing unease, shortness of breath, and overstimulation.[3]
Psychological risks
No controlled studies of MAL's psychological adverse effects exist. Class-level risks for serotonergic psychedelics apply:
- Acute anxiety, panic, and dysphoria — particularly at higher doses or in unfavorable settings. MAL's steep dose-response curve[3] makes accidental dose escalation a distinctive risk factor.
- Psychotic episodes — serotonergic psychedelics can trigger acute psychotic symptoms in individuals with a personal or family history of psychosis or schizophrenia-spectrum disorders.[4]
- Hallucinogen persisting perception disorder (HPPD) — persistent visual disturbances after psychedelic use have been documented with potent novel psychoactive substances.[10] No MAL-specific cases have been published, but the risk is presumed present.
- Trauma re-emergence — introspective deepening can surface distressing material, particularly in individuals with trauma histories.[2]
Tolerance and dependence
MAL is not habit-forming and carries no physical dependence liability.[4] Its pharmacological profile — no DAT activity, no monoamine releasing activity, no D₂ receptor engagement[1] — is inconsistent with the neural mechanisms that produce compulsive drug-seeking.
Tolerance develops rapidly after a single dose, consistent with 5-HT₂A downregulation. Full receptor recovery takes approximately 7 days.[11] Cross-tolerance extends to other serotonergic psychedelics including LSD, psilocybin, mescaline, and DOx-series compounds.[11]
No withdrawal has been documented.
Drug Interactions
No published interaction studies exist for methallylescaline. All guidance is derived from class-level evidence and mechanistic inference.
Monoamine oxidase inhibitors (MAOIs). MAOIs combined with serotonergic psychedelics carry risk of serotonin syndrome.[12] MAOI co-administration would be expected to potentiate and prolong MAL's effects. This combination is contraindicated. safety citation needed
SSRIs and SNRIs. These medications may reduce psychedelic effects through chronic receptor changes, but serotonergic potentiation cannot be excluded in all cases.[12]
Lithium. Psychedelic–lithium combinations have been associated with seizures across the serotonergic psychedelic class. This combination is considered contraindicated. safety citation needed
Stimulants. Additive cardiovascular strain is the primary concern. Given the documented rapid heart rate and elevated blood pressure at 130 mg MAL,[5] concurrent stimulant use represents a risk for cardiovascular complications.
Cannabis. Potentiation of psychedelic intensity with increased risk of anxiety and psychosis is a well-documented class interaction.
CYP2D6 and CYP3A4 inhibitors. MAL is metabolized by CYP2D6, CYP2J2, CYP1A2, and CYP3A4.[6] Inhibitors of these enzymes — including fluoxetine, paroxetine, bupropion (CYP2D6) and ketoconazole, ritonavir, grapefruit juice (CYP3A4) — may increase MAL exposure and prolong effects.
Contraindications
7 knownNo substance-specific contraindication studies exist. The following are derived from class-level evidence and available case data:
Heart conditions or high blood pressure. Cardiovascular stimulation documented at 130 mg (heart rate >120 bpm, blood pressure 160/80 mmHg)[5] and mescaline's sympathomimetic effects[9] indicate risk for individuals with pre-existing cardiac conditions.
Personal or family history of psychosis. Serotonergic psychedelics can precipitate psychotic episodes in vulnerable individuals.[4]
Concurrent MAOI use. Risk of serotonin toxicity.[12]
Concurrent lithium use. Class-level seizure risk. safety citation needed
Pregnancy. No reproductive safety data exist. Class-level precautionary contraindication applies.
Liver impairment. MAL is metabolized by multiple liver enzymes;[6] impaired liver function could reduce clearance and increase exposure.
Harm Reduction[edit]
Forms & Identification
MAL's steep dose-response curve makes accurate identification and purity assessment more consequential than with most oral psychedelics. Because small differences in actual versus expected potency translate to large differences in effect intensity,[3] reagent testing confirms the substance class but cannot guarantee purity or potency. Quantitative analysis — such as sending a sample to a drug checking service — provides the most meaningful safety information for this compound.
Guidelines
- Use a milligram-precision scale for every dose. Visual estimation is dangerous with MAL's steep dose-response curve.
- Start at the lower end of the dose range and wait at least 90 minutes before considering the come-up complete — MAL's onset can be slow.
- Do not redose. The long duration and steep curve mean the full intensity may not be apparent until hours in.
- Eat a light meal 2–3 hours before ingestion to reduce nausea.
- Keep ginger tea or anti-nausea aids available — nausea during onset is common with mescaline-class compounds.
- Clear the full day and following morning of obligations. Experiences at moderate doses can last 12+ hours.
- Have a sober sitter present, especially at unfamiliar doses.
Set & Setting
Set and setting are primary modulators of the MAL experience across all dose ranges. The long duration (potentially up to 16 hours) demands a stable, comfortable environment with no time-sensitive obligations for the full day and following morning. First-time users benefit from a sober, experienced sitter who can provide reassurance during the come-up body load and any anxious passages.
Choose a familiar, physically safe space — the extended timeline means anything unsettling in the environment will be amplified across many hours.
Aftercare & integration. The extended duration of MAL means physical and psychological recovery may take longer than with shorter-acting psychedelics. Prioritize sleep, hydration, and light nutrition in the 24 hours following the experience. Some users report lingering body fatigue or emotional sensitivity for one to two days.
Journaling or discussing the experience with a trusted person within the first few days can help process intense introspective or emotional material. If distressing thoughts, persistent visual disturbances, or difficulty returning to baseline functioning continue beyond a week, seek support from a mental health professional experienced with psychedelic experiences.
Recovery & Support
MAL does not produce physical dependence or withdrawal. However, repeated use of any psychedelic as a coping mechanism warrants self-examination. If psychedelic use is becoming a pattern driven by avoidance rather than intention, peer support communities and professional counseling can provide perspective and structure.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Uncomfortable body load, nausea, and anxiety during the come-up are common and generally resolve. Seek immediate help if any of the following occur: chest pain, sustained heart rate above 120 bpm that does not settle with rest, severe confusion or delirium, inability to recognize surroundings or people, self-harm risk, or loss of consciousness.
Immediate steps:
- 1. Move the person to a quiet, safe space.
- 2. Call emergency services if symptoms listed above are present.
- 3. Do not restrain the person unless there is immediate danger to themselves or others.
- 4. Keep them cool and hydrated while waiting for help.
- 5. If the person is unconscious, place them in the recovery position.
What to tell the dispatcher: Name the substance (methallylescaline / MAL), the dose if known, the time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
No reversal agent exists for serotonergic psychedelics. Hospital treatment is supportive — benzodiazepines for agitation, monitoring for cardiovascular symptoms.
Legal Status[edit]
Methallylescaline occupies an ambiguous legal position in most jurisdictions. It is not widely scheduled by name, but several countries capture it under blanket psychoactive substance controls or novel psychoactive substance (NPS) frameworks. In the United States, the Federal Analogue Act creates potential criminal liability when MAL is intended for human consumption, based on its structural and pharmacological similarity to mescaline (Schedule I).
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not specifically scheduled | Federal Analogue Act (21 U.S.C. § 813) may apply when intended for human consumption; structural and pharmacological analog of mescaline (Schedule I) |
| United Kingdom | Controlled — Psychoactive Substances Act 2016 | Blanket prohibition effective May 26, 2016; covers all psychoactive substances not specifically exempted |
| Germany | Controlled — NpSG | Neue-psychoaktive-Stoffe-Gesetz, effective November 26, 2016 |
| Sweden | Specifically scheduled | Classified as a controlled substance, January 2016 |
| Canada | Not controlled (as of 2012) | Health Canada status determination A-2013-00235 concluded MAL not controlled under CDSA; this determination may be outdatedcitation needed |
| Australia | Not specifically scheduled | Likely captured under state or federal NPS provisions; no specific scheduling confirmation availablecitation needed |
The regulatory trajectory has been one of gradual inclusion through blanket NPS legislation rather than substance-specific scheduling. Three European jurisdictions (Sweden, UK, Germany) independently controlled MAL within a single calendar year (2016), reflecting the broader regulatory response to novel psychoactive substances during that period.
Frequently asked questions
What is Methallylescaline?
Methallylescaline (MAL) is a synthetic psychedelic phenethylamine of the scaline series, structurally derived from mescaline. First synthesized by Alexander Shulgin in 1981, it acts as a 5-HT2A/2C agonist with an oral duration of 8–16 hours and no clinical trial data.
How long does Methallylescaline last?
Total duration by route of administration — Oral: 8 – 16 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 Methallylescaline?
Psychedex publishes a dosage table for Methallylescaline on this page covering these routes of administration: oral. Dose values are presented only in that table, always alongside their route of administration.
What are dangerous combinations with Methallylescaline?
The highest-severity documented interactions for Methallylescaline: MAOIs (Lethal), Buspirone (Dangerous), Dopamine agonists (Dangerous), GHB, Baclofen (Dangerous), GHB, GBL (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is Methallylescaline addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for Methallylescaline: tolerance builds rapid; full reset takes 7 days; cross-tolerance develops with LSD, psilocybin, mescaline, DOx compounds, other 5-HT2A agonists. See the article's dependence and safety sections for recorded dependence data.
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