DMT, psilocybin, LSD +2 moreDMT, psilocybin, LSD, mescaline, serotonergic psychedelics show less
MET
N-methyl-N-ethyltryptamine
MET (N-methyl-N-ethyltryptamine) is a synthetic psychedelic of the tryptamine class. It sits structurally between DMT and DET, the symmetric N,N-dialkyltryptamines it most closely resembles. It activates serotonin receptors in the brain, disrupting normal sensory filtering and producing the perceptual and cognitive shifts characteristic of classical psychedelics.[1]
MET (N-ethyl-N-methyltryptamine) is a synthetic psychedelic of the tryptamine class. It sits between DMT and DET in the N,N-dialkyltryptamine series, distinguished by its asymmetric substitution. MET is a presumed 5-HT₂A receptor agonist, producing its effects by disrupting serotonergic filtering of sensory and cognitive input.[1]
DMT, psilocybin, LSD +2 moreDMT, psilocybin, LSD, mescaline, serotonergic psychedelics show less
MET first appeared in Michael Valentine Smith's Psychedelic Chemistry in 1981,[2] and was briefly referenced by Alexander Shulgin in TiHKAL[3] — but it did not receive a dedicated profile. It surfaced on research chemical markets in the 2010s and attracted minimal community engagement.[4] It has no approved medical use and circulates exclusively through research chemical channels.
Subjective effects include geometric visual patterns, color enhancement, euphoria, time alteration, and a buzzing physical energy throughout the experience. The overall character is stimulating and grounded — more energized than DMT and without DMT's immersive perceptual overwhelm, with a persistent physical buzz defining the dose range. Body load, anxiety, and cardiovascular stimulation are characteristic undesired effects.
MET does not produce physical dependence, and no lethal dose has been established in any species.[5] The primary risks are psychological — panic, paranoia, and psychotic reactions — amplified by the compound's stimulating character; combining it with monoamine oxidase inhibitors or lithium creates risk of life-threatening serotonin overload or seizures.[6] No controlled studies of any kind exist — everything known comes from structural analogy to better-characterized tryptamines.
History[edit]
Discovery
MET first appeared in Michael Valentine Smith's Psychedelic Chemistry in 1981,[2] a clandestine chemistry reference documenting synthesis procedures for numerous tryptamine derivatives. Alexander Shulgin later mentioned it in TiHKAL (1997),[3] noting its oral activity — but MET did not earn a dedicated profile among the book's 55 characterized tryptamines.
Research chemical era
MET appeared on research chemical markets during the 2010s.[7][4] It attracted almost no community engagement compared to relatives such as DET, DPT, or 4-AcO-MET — the Erowid vault holds only four user experience reports.
Absence of formal investigation
No research group has published any study of MET's pharmacology, toxicology, or subjective effects. As of 2026, the entire evidence base consists of its brief TiHKAL mention, a handful of community reports, and structural analogy to related tryptamines.
The name MET follows the standard abbreviation convention for N,N-dialkyltryptamines: the first letters of each alkyl substituent combined with the tryptamine suffix (Methyl + Ethyl + Tryptamine). The compound has no known street names, slang terminology, or cultural identity outside specialist research chemical communities.
Chemistry[edit]
Structural class
MET belongs to the substituted tryptamine family — an indole ring attached via an ethylamine chain to a terminal nitrogen. Its defining feature is asymmetric N-dialkylation: one methyl and one ethyl group on the terminal nitrogen, placing it between DMT (two methyls) and DET (two ethyls) in the N,N-dialkyltryptamine series.
Across this series, adding bulk to the N-alkyl groups progressively reduces serotonin receptor binding strength,[8] predicting intermediate potency for MET — a prediction not yet confirmed by direct measurement. The N-ethyl group also partially resists breakdown by MAO-A, which is why MET can be taken orally without requiring a monoamine oxidase inhibitor.[3]
Molecular properties
MET's molecular formula is C₁₃H₁₈N₂, with a molecular weight of 202.30 g/mol.[9] It contains no stereogenic centers — no mirror-image forms exist. No CAS registry number has been assigned; full chemical identifiers are available via PubChem.[9]
Pharmacology[edit]
Mechanism of action
MET activates serotonin receptors — principally the same receptor engaged by psilocybin, LSD, and DMT.[1] This disrupts the brain's normal filtering of sensory and self-referential information, producing the perceptual flooding characteristic of classical psychedelics.[10] A secondary action on a different serotonin receptor tends to soften intensity and help regulate body temperature.[11]
Across the tryptamine series, adding bulk to the N-alkyl groups progressively reduces serotonin receptor binding strength.[8] MET's mixed methyl/ethyl substitution predicts intermediate potency between DMT and DET. No direct binding data confirm this.inferred
Pharmacokinetics
Unlike DMT — which is rapidly broken down by MAO-A before oral absorption[12][5] — MET is orally active at approximately 80–100 mg.[3] The N-ethyl group reduces the enzyme's efficiency enough to permit oral uptake without a monoamine oxidase inhibitor. No plasma levels, bioavailability estimates, or half-life values have been published.inferred
Neuroscience[edit]
Where it acts
As a presumed serotonin agonist, MET is expected to engage the same brain systems studied in psilocybin, LSD, and DMT research.[1] This includes disruption of the default mode network — the brain system underlying self-referential thought — and interference with the thalamus's role in filtering incoming sensory signals. No neuroimaging or brain-recording studies have been conducted with MET directly.
Why it matters
Serotonergic psychedelics promote new brain cell connections through signaling cascades triggered by serotonin receptor activation. Whether MET specifically drives these changes is unknown. MET's reported stimulating character could produce a distinct neural signature from DMT, but this remains entirely speculative.
- Does MET promote neuroplasticity through the same signaling pathways demonstrated for other serotonergic psychedelics?
- Does the asymmetric N-alkyl substitution produce distinct receptor activation patterns compared to DMT or DET?
- Does the stimulating character reported by users correlate with measurable differences in noradrenergic or dopaminergic activity?
Subjective Effects[edit]
MET produces an experience defined by an unusual pairing: psychedelic perceptual shifts alongside a persistent, energizing body quality. Visuals and cognitive changes are present throughout, but the overall feel is animated and grounded rather than immersive or dissociating.
Within the tryptamine family, MET sits between DMT and DET. It is more grounded and stimulating than DMT's rapid perceptual flood, and lacks the emotional depth attributed to DET. Those familiar with psilocybin would find it lighter in psychological weight but more physically energized.
MET first appeared in Michael Valentine Smith's Psychedelic Chemistry (1981)[2] and was subsequently referenced by Alexander Shulgin in TiHKAL (1997), where it received a passing mention rather than a dedicated entry.[3] The compound surfaced on research chemical markets during the 2010s but attracted far less attention than related tryptamines such as DET or 4-AcO-MET.[4] It remains one of the least documented psychedelic tryptamines in active circulation.
Subjective effects include geometric visual patterns, color enhancement, euphoria, and time alteration. The experience carries a notably stimulating somatic character — more energized and grounded than DMT's overwhelming perceptual immersion, with a buzzing physical quality that permeates the dose range. Body load, anxiety, and cardiovascular stimulation are characteristic unsought effects.
MET does not produce physical dependence, and no lethal dose has been established in any species.[5] The primary acute risk is psychological — anxiety, panic, and psychotic reactions — amplified by the compound's stimulating character and by dangerous interactions with monoamine oxidase inhibitors and lithium at the class level.[6] No controlled studies of any kind exist for MET; virtually all safety and pharmacological claims rest on structural analogy to better-characterized tryptamines.
History[edit]
Discovery
MET first appeared in print in Michael Valentine Smith's Psychedelic Chemistry (1981),[2] a clandestine chemistry reference that documented synthesis procedures for numerous tryptamine derivatives. Alexander Shulgin later referenced the compound in TiHKAL (1997),[3] noting its oral activity within the MiPT entry — MET did not receive a dedicated profile among the book's 55 fully characterized tryptamines, reflecting its marginal status even within psychedelic chemistry circles.
Research chemical era
MET appeared on research chemical markets during the 2010s as part of the broader expansion of novel tryptamine availability.[7][4] The compound attracted minimal community engagement compared to relatives such as DET, DPT, or 4-AcO-MET — the Erowid MET vault catalogues only four user experience reports.
Absence of formal investigation
No academic research group has published a study specifically investigating MET's pharmacology, toxicology, or subjective effects. The compound has not been the subject of any registered clinical trial. As of 2026, MET's evidence base consists entirely of its brief mention in TiHKAL, a handful of community reports, and structural analogy to the N,N-dialkyltryptamine series.
The name MET follows the standard abbreviation convention for N,N-dialkyltryptamines: the first letters of each alkyl substituent combined with the tryptamine suffix (Methyl + Ethyl + Tryptamine). The compound has no known street names, slang terminology, or cultural identity independent of its chemical designation — a reflection of its near-total obscurity outside specialist research chemical communities.
Chemistry[edit]
Structural class
MET belongs to the substituted tryptamine family — an indole ring system linked via an ethylamine side chain to a terminal nitrogen. Its distinguishing feature is asymmetric N-dialkylation: one methyl and one ethyl group on the terminal amine, placing it between DMT (symmetric dimethyl) and DET (symmetric diethyl) in the N,N-dialkyltryptamine series.
The asymmetry is pharmacologically meaningful. Across indolealkylamines, increasing the bulk of N-alkyl groups progressively reduces serotonin receptor binding affinity.[8] MET's mixed substitution predicts intermediate affinity between DMT and DET, though this has not been confirmed by direct measurement. The N-ethyl group also provides partial resistance to enzymatic breakdown by MAO-A, enabling oral activity without monoamine oxidase inhibitor co-administration.[3]
Molecular properties
| Molecular formula | C₁₃H₁₈N₂ |
| Molecular weight | 202.30 g/mol |
Full chemical identifiers (PubChem CID 824845, InChIKey, SMILES) are available via PubChem.[9] No CAS Registry Number has been assigned.
Stereochemistry
MET contains no stereogenic centers. The molecule is achiral — no enantiomeric or diastereomeric forms exist.
Physical properties
No published data exist for MET's melting point, solubility, or stability. A computed XLogP of 2.9 indicates moderate lipophilicity.[9] As a free base, MET is expected to be an oily liquid at room temperature, consistent with other N,N-dialkyltryptamines. No salt forms have been formally characterized in published literature.
Pharmacology[edit]
Mechanism of action
MET is classified as a serotonin 5-HT₂A receptor agonist with secondary partial agonist activity at 5-HT₁A — the standard dual-target profile shared by classical psychedelic tryptamines.[1] No substance-specific binding data have been published for MET at any receptor.
Psychedelic effects arise primarily from 5-HT₂A activation, which disrupts the brain's normal filtering of sensory and self-referential information.[10] The 5-HT₁A component modulates the overall experience, generally softening intensity and contributing calming and body-temperature regulation effects.[11]
Structure-activity data across the tryptamine series show that increasing N-alkyl bulk reduces serotonin receptor binding strength.[8] MET's mixed methyl/ethyl substitution predicts intermediate potency between DMT and DET — somewhat weaker than DMT due to the added bulk of the ethyl group. This prediction has not been confirmed by direct measurement.inferred
Pharmacokinetics
No human pharmacokinetic data exist for MET. No plasma levels, bioavailability estimates, or half-life values have been published for any route.
The closest well-characterized structural analog, DMT, is rapidly broken down by MAO-A (MAO-A), rendering it orally inactive unless combined with an monoamine oxidase inhibitor.[12][5] MET's oral activity — documented at approximately 80–100 mg[3] — is attributed to the N-ethyl group partially shielding the molecule from MAO-A degradation. The ethyl group's bulk reduces the enzyme's efficiency enough to permit oral absorption without MAO inhibitor co-administration.
This intermediate metabolic protection — greater than DMT's but less than DET's two ethyl groups — is biochemically plausible but has not been confirmed by formal pharmacokinetic study.inferred
Neuroscience[edit]
Where it acts
As a presumed serotonin 2A receptor agonist, MET is expected to engage the same neural systems characterized in studies of psilocybin, LSD, and DMT.[1] These include disruption of the default mode network — the brain system underlying self-referential thought — and interference with thalamic sensory filtering, producing the perceptual flooding characteristic of the psychedelic state. No neuroimaging or electrophysiology studies have been conducted with MET directly.
Why it matters
Serotonergic psychedelics promote structural brain changes — new dendritic growth and synapse formation — through signaling cascades triggered by 5-HT₂A activation. Whether MET specifically drives these neuroplastic changes is unknown.
The REBUS model proposes that 5-HT₂A agonists loosen the brain's reliance on prior expectations, allowing new sensory information to reshape perception and belief.citation needed MET's reported stimulating character could theoretically produce a distinct neural signature from DMT, but this remains entirely speculative.
- Does MET promote neuroplasticity through the same signaling pathways demonstrated for other serotonergic psychedelics?
- Does the asymmetric N-alkyl substitution produce distinct receptor activation patterns compared to DMT or DET?
- Does the stimulating character reported by users correlate with measurable differences in noradrenergic or dopaminergic activity?
Subjective Effects[edit]
MET produces a broadly psychedelic experience shaped substantially by route of administration. Smoked doses deliver rapid, intense immersion comparable in onset speed to DMT but with a more stimulating physical quality; oral and insufflated routes produce a gradual arc that permits greater psychological navigation. A persistent body load — buzzing, energized, sometimes tense — distinguishes MET from the relative somatic neutrality of psilocin-type tryptamines and may increase anxiety susceptibility in unprepared individuals. Set and setting remain primary modulators of experiential valence across all routes.
Within the N,N-dialkyltryptamine series, MET sits between DMT and DET: more grounded and stimulating than DMT's characteristically overwhelming perceptual immersion, but without the distinctive body feel and emotional tone attributed to DET. The asymmetric substitution produces a qualitative character that has not been systematically differentiated from either symmetric structural analog.
Effect Grid
Full psychedelic effects are present. Visual geometry, significant color enhancement, visual drifting, and environmental patterning dominate the perceptual field. Tracers and after-images appear with eye movement. Internal hallucinations may emerge during eyes-closed states. Music enhancement is prominent.
Cognitive euphoria, conceptual thinking, and thought connectivity define the mental landscape. Time alteration is substantial — minutes may feel stretched or compressed. Introspection enhancement and novelty enhancement color the thought stream. Emotional enhancement and empathy enhancement may arise in social contexts.
Stimulation is the dominant physical effect, accompanied by pronounced wakefulness, pupil dilation, and spontaneous body sensations. Muscle tension and temperature dysregulation are common. Sleep is typically disrupted for 6+ hours after oral dosing. NOTE: The oral common dose (120–150 mg) exceeds Shulgin's published reference of 80–100 mg — this range reflects community consensus and may require editorial review.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Perspective distortion · Music enhancement · Brightness alteration · Tracers · Auditory enhancement · Visual breathing · Visual morphing · Holotropic state · Visual haze / noise · Depth perception distortion · Symmetrical texture repetition · Touch enhancement · Auditory distortion · Light sensitivity · Sound sensitivity · Spatial disorientation · After-images · Visual diffraction · Auditory misinterpretation · Dreaming enhancement · Peripheral vision distortion · Proprioceptive distortion · Vestibular distortion · Visual melting · Visual acuity enhancement · Synesthesia · Peripheral misidentification · Visual magnification · Visual processing acceleration · Internal hallucinations · Object transformations · Auditory hallucinations · External hallucinations · Visual recursion · Visual scenery slicing · Environmental orbism / cubism · Object activation · Perspective hallucinations · Visual flipping
Auditory enhancement · Visual breathing · Visual morphing · Holotropic state · Visual haze / noise · Depth perception distortion · Symmetrical texture repetition · Touch enhancement · Auditory distortion · Light sensitivity · Sound sensitivity · Spatial disorientation · After-images · Visual diffraction · Auditory misinterpretation · Dreaming enhancement · Peripheral vision distortion · Proprioceptive distortion · Vestibular distortion · Visual melting · Visual acuity enhancement · Synesthesia · Peripheral misidentification · Visual magnification · Visual processing acceleration · Internal hallucinations · Object transformations · Auditory hallucinations · External hallucinations · Visual recursion · Visual scenery slicing · Environmental orbism / cubism · Object activation · Perspective hallucinations · Visual flipping
Wakefulness · Stimulation · Dizziness · Heart rate perception changes · Nausea · Tingling / electric sensations · Vibrations / buzzing · Muscle tension · Laughter fits · Appetite suppression · Bodily lightness · Body schema distortion · Dry mouth · Physical fatigue · Tactile euphoria · Yawning · Abnormal heartbeat · Muscle relaxation · Bodily pressures · Breathing alteration · Excessive sweating · Restlessness · Trembling · Vasoconstriction · Bruxism · Sexual arousal enhancement · Headache · Involuntary body movements · Vomiting · Bodily dissociation · Tactile hallucination
Heart rate perception changes · Nausea · Tingling / electric sensations · Vibrations / buzzing · Muscle tension · Laughter fits · Appetite suppression · Bodily lightness · Body schema distortion · Dry mouth · Physical fatigue · Tactile euphoria · Yawning · Muscle relaxation · Bodily pressures · Breathing alteration · Excessive sweating · Restlessness · Trembling · Vasoconstriction · Bruxism · Sexual arousal enhancement · Headache · Involuntary body movements · Vomiting · Bodily dissociation · Tactile hallucination
Thought connectivity · Aesthetic enhancement · Introspection enhancement · Pattern recognition enhancement · Focus suppression · Immersion enhancement · Confusion · Cognitive flexibility · Cognitive impairment · Multiple thought streams · Openness enhancement · Creativity enhancement · Memory suppression · Thought loops · Language suppression · Thought deceleration · Increased nature relatedness · Information processing suppression · Thought acceleration · Thought disorganization · Humor enhancement · Analysis suppression · Cognitive fatigue · Memory fragmentation · Synchronicity · Analysis enhancement · Information processing enhancement · Cognitive dysphoria · Memory replays · Focus enhancement
Focus suppression · Immersion enhancement · Confusion · Cognitive flexibility · Cognitive impairment · Multiple thought streams · Openness enhancement · Creativity enhancement · Memory suppression · Thought loops · Language suppression · Thought deceleration · Increased nature relatedness · Information processing suppression · Thought acceleration · Thought disorganization · Humor enhancement · Analysis suppression · Cognitive fatigue · Memory fragmentation · Synchronicity · Analysis enhancement · Information processing enhancement · Cognitive dysphoria · Memory replays · Focus enhancement
Empathy enhancement · Anxiety · Catharsis · Dysphoria
Disinhibition · Social connection · Trust enhancement · Flow state · Sociability enhancement · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Sociability enhancement · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Time cessation
Transpersonal visions · Cessation · Death-rebirth sequence · Non-dual awareness · Voidness
Voidness
Recursive awareness
Timeline
Subtle awareness shift with possible mild gastrointestinal discomfort and initial stimulation. First perceptual brightening may appear at the edge of awareness.
Progressive visual and cognitive effects build — color enhancement, emerging geometry, and rising stimulation. Body high intensifies with spontaneous body sensations and mounting wakefulness.
Full psychedelic immersion with maximal visual geometry, color alteration, and time distortion. Cognitive euphoria, thought connectivity, and emotional enhancement dominate the mental landscape. Stimulation is prominent.
Gradual reduction of visual and cognitive effects. Stimulation persists longer than perceptual phenomena. Muscle tension and temperature dysregulation may linger.
Residual stimulation, reflective mood, and possible physical fatigue. Sleep may remain disrupted for several hours.
⚠ Do not drive or operate heavy machinery for at least 8 hours after oral ingestion.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- DMT · psilo · LSD
Toxicity
No controlled toxicity data exist for MET. No lethal dose has been established in any species, and no human fatalities have been attributed to the compound.
Cardiovascular effects
Increased heart rate and blood pressure are class-typical for serotonergic tryptamines but have not been formally measured for MET.[10] MET's stimulating character may increase acute cardiovascular strain compared to more sedating tryptamines.
Pulmonary considerations
Lung irritation is relevant for the smoked route. No specific data exist on combustion byproducts or lung toxicity from smoked MET.
Reagent testing
MET is expected to produce a purple-to-black reaction with Ehrlich's reagent, confirming the presence of an indole compound. A positive result means "a tryptamine is present" — not "this is MET." Definitive identification requires laboratory analysis.[13][12]
Psychological risks
Panic, paranoia, and psychotic breakdown are class-level risks, most likely in people with a personal or family history of psychotic or bipolar disorders.[5][12] These risks scale with dose and are strongly shaped by set and setting.
MET's stimulating character may increase anxiety and cardiovascular distress compared to more sedating tryptamines such as psilocin. Persistent perceptual changes after the experience occur across the serotonergic psychedelic class at low but non-negligible rates.citation needed
Tolerance and dependence
Serotonergic psychedelics produce rapid tolerance — serotonin receptors downregulate after each exposure, blunting effects within one to three uses.[5][12] Full receptor recovery takes approximately 7–14 days. Cross-tolerance with DMT, psilocybin, LSD, mescaline, and other serotonergic psychedelics is expected.
MET does not produce physical dependence and carries negligible compulsive use potential.[5] The rapid tolerance mechanism itself serves as a barrier to compulsive use. No MET-specific tolerance or dependence data exist.inferred
Drug Interactions
The most dangerous combinations are monoamine oxidase inhibitors (MAOIs) and lithium — both classified as dangerous.[6][14]safety citation needed MAOIs raise MET levels while simultaneously elevating serotonin, creating risk of a life-threatening overheating and seizure response. Lithium may lower the seizure threshold and produce neurotoxicity.
Tramadol raises serotonin through a separate mechanism and is a documented cause of serotonin syndrome when combined with serotonergic agents.[15][6] SSRIs and SNRIs blunt psychedelic effects through downregulation and carry theoretical serotonin toxicity risk in acute combination.[6] Cannabis potentiates perceptual distortion, anxiety, and paranoia, significantly increasing the probability of panic. All classifications are based on class-level evidence — no MET-specific interaction data have been published.
Contraindications
8 knownAbsolute contraindications:
- Concurrent use of monoamine oxidase inhibitors (irreversible or reversible) — risk of serotonin toxicity safety citation needed
- Concurrent use of lithium — risk of seizures and neurotoxicity safety citation needed
- Personal or family history of schizophrenia or psychotic disorders — risk of psychotic breakdown
Relative contraindications:
- Bipolar disorder — risk of manic episode
- Heart disease or uncontrolled high blood pressure — acute stimulant effects may worsen existing conditions
- Concurrent use of tramadol — additive serotonin toxicity risk
- Pregnancy and breastfeeding — no safety data exist
- Concurrent use of SSRIs or SNRIs — reduced efficacy and theoretical serotonin toxicity risk
All contraindications are class-level determinations. No MET-specific contraindication data have been published.inferred
Harm Reduction[edit]
Forms & Identification
MET circulates exclusively through research chemical channels with no pharmaceutical-grade reference standard. Purity, identity, and dosage accuracy are unreliable by default.
Ehrlich's reagent confirms an indole compound is present but cannot distinguish MET from other tryptamines — a positive result means "a tryptamine is present," not "this is MET." Definitive identification requires laboratory analysis or professional drug checking services.
Guidelines
- Test every batch with Ehrlich's reagent as a minimum; consider professional drug checking services where available
- Start with the lowest reported active dose and wait for full onset before considering redosing — MET's oral onset can be gradual
- Weigh doses carefully using a milligram-precision scale; volumetric measurement is unreliable for powders
- Choose a calm, familiar environment with a trusted, sober companion present
- Avoid combining with other psychoactive substances during first experiences
- Clear the schedule — do not plan demanding activities during or immediately after the experience
- Eat lightly several hours beforehand to reduce nausea risk
- Stay hydrated but avoid overhydration
Set & Setting
MET's stimulating body character makes environment and psychological preparation especially important. The energizing quality can amplify pre-existing anxiety in unfamiliar or chaotic settings.
A calm, familiar environment with access to a quiet retreat space reduces the probability of difficult experiences. An experienced, sober companion is strongly recommended, particularly for first experiences or higher doses.
Aftercare & integration. The days following a psychedelic experience are an important window for processing what occurred. Allow time for rest, adequate sleep, and gentle reentry into routine activities. Journaling or drawing can help capture impressions that fade quickly.
If the experience was difficult or raised distressing emotional material, consider speaking with a therapist experienced in psychedelic integration. Ongoing anxiety, persistent perceptual changes, or difficulty returning to baseline after several days warrant professional consultation.
Recovery & Support
Serotonergic psychedelics carry negligible physical dependence risk, and MET's rapid tolerance mechanism makes sustained compulsive use unlikely. However, psychological patterns of overuse can develop with any psychoactive substance. If psychedelic use is interfering with daily functioning, relationships, or mental health, support is available through harm reduction organizations and mental health professionals familiar with substance use.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
Most difficult psychedelic experiences are uncomfortable but not medically dangerous. Seek immediate help if any of the following occur: chest pain, seizure, loss of consciousness, self-harm behavior, or complete disconnection from reality with inability to respond to verbal communication.
Immediate steps:
- 1. Stay with the person. Do not leave them alone.
- 2. Move them to a quiet, low-stimulation environment if possible.
- 3. Speak calmly and reassuringly. Remind them what they have taken and that the effects are temporary.
- 4. If they are unconscious or having a seizure, place them in the recovery position and call emergency services immediately.
- 5. Do not restrain them unless there is immediate danger of self-harm.
- 6. Do not induce vomiting.
What to tell the dispatcher:
Provide the substance name, estimated amount taken, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
MET is not individually named in most national drug schedules but is captured by structural analog provisions in several countries.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not explicitly scheduled | Not listed under the Controlled Substances Act. Subject to the Federal Analogue Act (21 U.S.C. § 813) if intended for human consumption, as DMT is Schedule I and MET shares substantial structural similarity.[16] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Captured by the generic tryptamine definition covering derivatives with mono- or di-N-alkyl substitution. Possession: up to 7 years imprisonment. Supply: up to life imprisonment.[17] |
| Germany | Controlled (NpSG) | Covered under the Neue-psychoaktive-Stoffe-Gesetz since July 18, 2019. Production, import for commercial purposes, and supply are criminalized. Personal possession is illegal but not separately penalized.citation needed |
| Canada | Not scheduled | Not listed under the Controlled Drugs and Substances Act as of 2026.citation needed |
| New Zealand | Class C controlled substance | Controlled as an analogue of scheduled tryptamines.citation needed |
| Australia | Likely controlled (unconfirmed) | Specific scheduling status under the TGA Poisons Standard could not be confirmed. DMT and tryptamine analogs typically fall under Schedule 9 (prohibited substances).citation needed |
In the United States, the Federal Analogue Act requires case-by-case demonstration that a substance is substantially similar to a scheduled compound — it is not automatic scheduling. Whether MET would satisfy these criteria depends on evidence presented in a specific prosecution.
Legal status changes frequently and varies by jurisdiction. This table reflects available information as of 2026 and is not legal advice. Verify current law in the relevant jurisdiction before acting on this information.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- DMT · psilo · LSD
Toxicity
No controlled toxicity data exist for MET. No lethal dose has been determined in any species, and no human fatalities have been attributed to the compound.
Cardiovascular effects
Increased heart rate and blood pressure elevation are class-typical for serotonergic tryptamines but have not been formally measured for MET. The serotonergic psychedelic class generally shows low cardiac valve risk with intermittent use.[10] MET's stimulating character may increase acute cardiovascular strain relative to more sedating tryptamines.
Pulmonary considerations
Lung irritation is relevant primarily for the smoked route. No specific data exist on combustion byproducts or lung toxicity from smoked MET.
Reagent testing
MET-specific reagent test results are not published. As a tryptamine, it is expected to produce a purple-to-black reaction with Ehrlich's reagent, confirming the presence of an indole compound. Definitive identification requires laboratory analysis (GC-MS or LC-MS/MS).[13][12]
Psychological risks
Class-level psychological risks include acute anxiety, panic, paranoia, and psychotic breakdown in individuals with personal or family history of psychotic or bipolar spectrum disorders.[5][12] These risks scale with dose and are strongly shaped by set and setting.
No published data exist on HPPD (HPPD) specific to MET. HPPD occurs across the serotonergic psychedelic class at low but non-negligible rates.citation needed
MET's stimulating character may increase the likelihood of anxiety and cardiovascular distress during acute experiences compared to more sedating tryptamines such as psilocin.
Tolerance and dependence
Serotonergic psychedelics produce rapid tolerance through 5-HT₂A downregulation after each exposure. This tolerance develops within one to three uses, functionally preventing rewarding effects from repeated dosing in short intervals. Full receptor recovery takes approximately 7–14 days.[5][12]
Cross-tolerance with DMT, psilocybin, LSD, mescaline, and other 5-HT₂A agonists is expected.
Serotonergic psychedelics do not produce physical dependence and show negligible compulsive redosing potential.[5] The rapid tolerance mechanism itself serves as a barrier to compulsive use. No MET-specific tolerance or dependence data exist.inferred
Drug Interactions
Monoamine oxidase inhibitors (MAOIs) represent the most dangerous combination. Both irreversible MAOIs (phenelzine, tranylcypromine) and reversible inhibitors (moclobemide, harmaline in ayahuasca preparations) would substantially increase MET levels while simultaneously elevating serotonin, creating risk of serotonin syndrome. This combination is classified as dangerous.[6]safety citation needed
Lithium combined with serotonergic psychedelics is classified as dangerous. The interaction may reduce seizure threshold and produce neurotoxicity through disruption of the same signaling pathways engaged by 5-HT₂A activation.[14]safety citation needed
Tramadol carries dual risk as both a serotonin reuptake inhibitor and an opioid. It is a documented cause of serotonin toxicity when combined with serotonergic agents.[15][6]
SSRIs and SNRIs blunt psychedelic effects through chronic receptor downregulation while carrying theoretical serotonin toxicity risk in acute combination.[6]
Cannabis potentiates perceptual distortion, anxiety, and paranoia during the psychedelic state. This is a behavioral interaction that may significantly increase the probability of panic and adverse psychological reactions.
All interaction classifications are based on class-level evidence. No MET-specific interaction data have been published.
Contraindications
8 knownAbsolute contraindications:
- Concurrent use of monoamine oxidase inhibitors (irreversible or reversible) — risk of serotonin toxicity safety citation needed
- Concurrent use of lithium — risk of seizures and neurotoxicity safety citation needed
- Personal or family history of schizophrenia or psychotic disorders — risk of psychotic breakdown
Relative contraindications:
- Bipolar disorder — risk of manic episode
- Heart disease or uncontrolled high blood pressure — acute stimulant effects may worsen existing conditions
- Concurrent use of tramadol — additive serotonin toxicity risk
- Pregnancy and breastfeeding — no safety data exist
- Concurrent use of SSRIs or SNRIs — reduced efficacy and theoretical serotonin toxicity risk
All contraindications are class-level determinations. No MET-specific contraindication data have been published.inferred
Harm Reduction[edit]
Forms & Identification
MET circulates exclusively through research chemical channels, with no pharmaceutical-grade reference standard. The absence of standardized production means purity, identity, and dosage accuracy are unreliable by default. Ehrlich's reagent confirms the presence of an indole compound but cannot distinguish MET from other tryptamines — a positive result means "a tryptamine is present," not "this is MET." For definitive identification, laboratory analysis or professional drug checking services are the only reliable methods.
Guidelines
- Test every batch with Ehrlich's reagent as a minimum; consider professional drug checking services where available
- Start with the lowest reported active dose and wait for full onset before considering redosing — MET's oral onset can be gradual
- Weigh doses carefully using a milligram-precision scale; volumetric measurement is unreliable for powders
- Choose a calm, familiar environment with a trusted, sober companion present
- Avoid combining with other psychoactive substances during first experiences
- Clear your schedule — do not plan demanding activities during or immediately after the experience
- Eat lightly several hours beforehand to reduce nausea risk
- Stay hydrated but avoid overhydration
Set & Setting
MET's stimulating body character makes environment and psychological preparation especially important. The compound's energizing quality can amplify pre-existing anxiety in unfamiliar or chaotic settings. A calm, familiar environment with access to a quiet retreat space reduces the probability of difficult experiences. An experienced, sober companion is strongly recommended, particularly for first experiences or higher doses.
Aftercare & integration. The days following a psychedelic experience are an important window for processing what occurred. Allow time for rest, adequate sleep, and gentle reentry into routine activities. Journaling or drawing can help capture impressions that fade quickly.
If the experience was difficult or raised distressing emotional material, consider speaking with a therapist experienced in psychedelic integration. Ongoing anxiety, persistent perceptual changes, or difficulty returning to baseline after several days warrant professional consultation.
Recovery & Support
Serotonergic psychedelics carry negligible physical dependence risk, and MET's rapid tolerance mechanism makes sustained compulsive use unlikely. However, psychological patterns of overuse can develop with any psychoactive substance. If psychedelic use is interfering with daily functioning, relationships, or mental health, support is available through harm reduction organizations and mental health professionals familiar with substance use.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
Most difficult psychedelic experiences are uncomfortable but not medically dangerous. Seek immediate help if any of the following occur: chest pain, seizure, loss of consciousness, self-harm behavior, or complete disconnection from reality with inability to respond to verbal communication.
Immediate steps:
- 1. Stay with the person. Do not leave them alone.
- 2. Move them to a quiet, low-stimulation environment if possible.
- 3. Speak calmly and reassuringly. Remind them what they have taken and that the effects are temporary.
- 4. If they are unconscious or having a seizure, place them in the recovery position and call emergency services immediately.
- 5. Do not restrain them unless there is immediate danger of self-harm.
- 6. Do not induce vomiting.
What to tell the dispatcher:
Provide the substance name, estimated amount taken, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug-related emergency.
Legal Status[edit]
MET's legal status varies across jurisdictions. The compound is not individually named in most national controlled substance schedules but is captured by structural analog provisions in several countries. No international scheduling action has been taken against MET under United Nations drug control conventions.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not explicitly scheduled | Not listed under the Controlled Substances Act. Subject to the Federal Analogue Act (21 U.S.C. § 813) if intended for human consumption, as DMT is Schedule I and MET shares substantial structural similarity.[16] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Captured by the generic tryptamine definition covering derivatives with mono- or di-N-alkyl substitution. Possession: up to 7 years imprisonment. Supply: up to life imprisonment.[17] |
| Germany | Controlled (NpSG) | Covered under the Neue-psychoaktive-Stoffe-Gesetz since July 18, 2019. Production, import for commercial purposes, and supply are criminalized. Personal possession is illegal but not separately penalized.citation needed |
| Canada | Not scheduled | Not listed under the Controlled Drugs and Substances Act as of 2026.citation needed |
| New Zealand | Class C controlled substance | Controlled as an analogue of scheduled tryptamines.citation needed |
| Australia | Likely controlled (unconfirmed) | Specific scheduling status under the TGA Poisons Standard could not be confirmed. DMT and tryptamine analogs typically fall under Schedule 9 (prohibited substances).citation needed |
In the United States, the Federal Analogue Act warrants specific attention. MET differs from DMT (Schedule I) only in the substitution of one N-methyl group with an N-ethyl group. Application of the Analogue Act requires case-by-case demonstration that a substance is "substantially similar" in structure and pharmacological effect to a scheduled compound — it is not automatic scheduling. Whether MET would satisfy these criteria depends on the evidence presented in a specific prosecution.
Frequently asked questions
What is MET?
MET is a substituted tryptamine psychedelic with asymmetric N-methyl and N-ethyl groups, orally active without MAO inhibition. First referenced in Shulgin's TiHKAL (1997), it remains uncharacterized in formal pharmacological literature.
How long does MET last?
Total duration by route of administration — Smoked: 30 – 75 min; Insufflated: 2 – 4 hours; Oral: 4 – 6 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 MET?
Psychedex publishes a dosage table for MET on this page covering these routes of administration: oral, smoked, insufflated. Dose values are presented only in that table, always alongside their route of administration.
What are dangerous combinations with MET?
The highest-severity documented interactions for MET: MAOIs (Lethal), Dopamine agonists (Dangerous), GHB, Baclofen (Dangerous), GHB, GBL (Dangerous), Ibogaine (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is MET addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for MET: tolerance builds rapid; full reset takes 14 days; cross-tolerance develops with DMT, psilocybin, LSD, mescaline, serotonergic psychedelics. See the article's dependence and safety sections for recorded dependence data.
experience reports
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1] ^abcGlennon RA, Teitler M, Sanders-Bush E (1992) Hallucinogens and serotonergic mechanisms — NIDA Research Monograph PMID:1435968
- [2]
- [3]
- [4]
- [5]
- [6] ^abcdMalcolm B, Thomas K (2022) Serotonin toxicity of serotonergic psychedelics — Psychopharmacology doi:10.1007/s00213-021-05876-x
references
- [1] ^abcGlennon RA, Teitler M, Sanders-Bush E (1992) Hallucinogens and serotonergic mechanisms — NIDA Research Monograph PMID:1435968
- [2]
- [3]
- [4]
- [5]
- [6] ^abcdMalcolm B, Thomas K (2022) Serotonin toxicity of serotonergic psychedelics — Psychopharmacology doi:10.1007/s00213-021-05876-x