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MPT
N-methyl-N-propyltryptamine
MPT (N-methyl-N-propyltryptamine) is a synthetic psychedelic of the tryptamine class. It is a constitutional isomer of MiPT and DET — same molecular formula, different nitrogen geometry. It is presumed to activate serotonin receptors in the brain, though no binding data have been published.[1]
MPT (N-methyl-N-propyltryptamine) is an emerging synthetic psychedelic of the tryptamine class. It is a constitutional isomer of both MiPT and DET, distinguished by its straight-chain propyl group. MPT is a presumed 5-HT₂A receptor agonist, though no binding affinity data have been published.[1]
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Shulgin first described MPT in TiHKAL (1997) — as a structural footnote in the MiPT chapter, where oral doses up to 20 mg produced no effects.[2] The compound was set aside. As of 2026, the only peer-reviewed paper dedicated to MPT is a 2019 crystal structure determination[3] — no pharmacology, no trials, no experience reports have followed.
Subjective effects include none on record — no experience report documents any psychoactive response at any dose or by any route. If an active dose exists, MPT's structural position between DMT and DPT suggests effects somewhere between the two, but this is entirely speculative. No unsought effects have been documented either, because no active dose has been found.
No physical dependence data exist, and the toxic dose is entirely unknown.safety citation needed At doses high enough to overwhelm the enzyme that breaks MPT down in the gut, exposure could spike sharply and without warning.[4] MPT is among the most poorly characterized compounds in the psychedelic literature — virtually nothing known about it rests on direct observation.[5][6]
History[edit]
History
Discovery
MPT was first synthesized and self-administered by Alexander Shulgin, with results published in TiHKAL (1997).[2] The compound did not receive its own chapter — Shulgin discussed it within the MiPT entry as a structural relative that failed to produce effects at 20 mg oral. He attributed the failure to the straight-chain propyl group's vulnerability to enzymatic breakdown, in contrast to the branched isopropyl geometry that appeared to protect MiPT.
Scientific characterization
The only peer-reviewed work dedicated to MPT is a 2019 crystal structure determination by Chadeayne, Golen, and Manke,[3] part of a broader crystallographic survey of DMT analogues that also covered EPT[7] and MiPT.[8]
Modern status
As of 2026, MPT remains essentially uncharacterized. No pharmacological studies, clinical trials, or experience reports exist. PsychonautWiki carries no documented effects or dosage information for the compound.[9]
The name MPT follows standard tryptamine nomenclature: M for N-methyl, P for N-propyl, T for tryptamine. No street names, slang, or cultural identity have developed around the compound — a direct consequence of its near-total absence from human use. Even in research chemical communities, MPT appears only as a structural footnote in discussions of its better-known isomers.
Chemistry[edit]
Chemistry
Structural class
MPT belongs to the unsubstituted N,N-dialkyltryptamine family — the same class as DMT and DPT. Its molecular formula is C₁₄H₂₀N₂, making it a constitutional isomer of both MiPT and DET. All three share identical molecular weight but differ in the geometry of their nitrogen substituents — a difference with significant consequences for how the body processes each compound.
Physical properties
The crystal structure was determined in 2019 by Chadeayne et al., who found that MPT molecules assemble into chains through hydrogen bonds between adjacent indole groups.[3] No published data exist for melting point, solubility, or storage stability.citation needed
Pharmacology[edit]
Pharmacology
Mechanism of action
No receptor binding data for MPT have been published. Based on its structural class, it is presumed to activate serotonin receptors in the brain[10][11] — the shared mechanism of all classical psychedelics. A second serotonin receptor likely plays a moderating role, softening the primary effect, as observed in the closely related compound DPT.[10]
inferred
Pharmacokinetics
MPT appears inactive by mouth because an enzyme in the gut and liver — MAO-A — breaks it down before enough reaches the brain.[12][13] Shulgin found no effects at oral doses up to 20 mg and attributed this to MPT's straight-chain propyl group offering little protection against that enzyme.[2]
At higher doses, this enzyme can become saturated, causing exposure to rise sharply and unpredictably.[4] The gap between inactive and active doses may be much narrower than it appears.
Neuroscience[edit]
Neuroscience
Where it acts
No neuroimaging or electrophysiology data exist for MPT. Based on its presumed serotonin receptor activity, it would be expected to disrupt the brain's sensory filtering — allowing normally suppressed information to reach conscious awareness.citation needed Classical psychedelics also reduce the coherence of self-referential brain networks, which correlates with experiences of ego dissolution.citation needed
Why it matters
Related tryptamines promote rapid growth of neural connections in cortical tissue — a property that has attracted interest in therapeutic contexts.citation needed Whether MPT shares this capacity at any achievable dose has not been tested.
inferred
Subjective Effects[edit]
Subjective Effects
MPT's experiential character is entirely unknown. The only documented human trial produced no perceptible effects, and no community report describes psychoactive experience at any dose or route. Until an active dose is established, characterization of the experience remains impossible.
If MPT does produce effects at higher doses or via routes that bypass the gut, its mixed methyl–propyl substitution places it structurally between DMT and DPT. Whether this translates to an intermediate experience — somewhere between DMT's intensity and DPT's reported emotional depth — is entirely speculative.
First documented by Alexander Shulgin in TiHKAL (1997), MPT was mentioned only in passing within the MiPT chapter after oral doses up to 20 mg produced no effects.[2] The only dedicated peer-reviewed publication is a 2019 crystal structure determination.[3] It remains one of the least-explored tryptamines in existence, with no pharmacological studies, clinical trials, or systematic experience reports.
Subjective effects are entirely uncharacterized — no experience report from any source documents psychoactive effects at any dose or route. If active doses are achieved, its structural position between DMT and DPT suggests effects potentially intermediate between the two, though this remains wholly speculative. No unsought effects have been documented because no active dose has been established.
No physical dependence data exist, and the toxic dose is entirely unknown.safety citation needed The compound's apparent oral inactivity at tested doses likely reflects rapid metabolic destruction rather than inherent safety — at higher doses, abrupt onset from enzyme saturation could produce unpredictable effects.[4] MPT is among the most poorly characterized psychoactive compounds in the literature; virtually nothing about it rests on direct observation.[5][6]
History[edit]
History
Discovery
MPT was first synthesized and self-administered by Alexander Shulgin, with results published in TiHKAL (1997).[2] The compound did not receive its own chapter — Shulgin discussed it within the MiPT entry as a structural relative that failed to produce psychoactive effects at oral doses up to 20 mg. He attributed the difference to the straight-chain propyl group's vulnerability to metabolic breakdown, contrasting it with the branched isopropyl geometry that appeared to protect MiPT.
Scientific characterization
The only peer-reviewed publication dedicated to MPT is a 2019 crystal structure determination by Chadeayne, Golen, and Manke.[3] This work confirmed the molecular formula and characterized the solid-state geometry as part of a systematic crystallographic survey of DMT analogues that also covered EPT[7] and MiPT.[8] A 2005 publication by Brandt et al. may represent the earliest formal synthetic chemistry reference, though this could not be independently confirmed.[9]
Modern status
As of 2026, MPT remains essentially uncharacterized. No pharmacological studies, clinical trials, experience reports, or forensic case reports have been published. PsychonautWiki's MPT page contains no documented effects or dosage information.[10] The compound sits at the intersection of synthetic simplicity and pharmacological obscurity — easy to make, but apparently inactive at the only doses anyone has tried.
The name MPT follows standard tryptamine nomenclature: the M denotes N-methyl and the P denotes N-propyl, with T for tryptamine. No street names, slang, or cultural identity have developed around the compound — a direct consequence of its near-total absence from human use. Even among research chemical communities, MPT appears only as a structural footnote in discussions of its better-known isomers MiPT and DET.
Chemistry[edit]
Chemistry
Structural class
MPT belongs to the unsubstituted N,N-dialkyltryptamine family — an indole ring fused to an ethylamine side chain, with methyl and straight-chain propyl groups on the terminal nitrogen as the sole modifications. It occupies an intermediate position in the tryptamine N-alkyl series: one carbon larger than MET, and a constitutional isomer of both MiPT (branched isopropyl) and DET (two ethyl groups).
All three C₁₄H₂₀N₂ isomers share identical molecular weight but differ in the geometry of their nitrogen substituents — a distinction with significant consequences for metabolic stability and receptor fit.
| Molecular formula | C₁₄H₂₀N₂ |
| Molecular weight | 216.32 g/mol |
Stereochemistry
MPT contains no chirality centers. Although the nitrogen bears three different substituents, rapid nitrogen inversion at room temperature prevents optical isomerism. The compound exists as a single achiral species.
Physical properties
Chadeayne et al. (2019) determined the crystal structure, finding that MPT molecules assemble into infinite one-dimensional chains through hydrogen bonds between the indole NH and the amine nitrogen of adjacent molecules.[3] No published data exist for melting point, solubility, or storage stability. As a free base tryptamine, MPT is expected to be a liquid or low-melting solid with moderate lipophilicity and susceptibility to oxidative degradation in light and air.citation needed
Structure-activity relationships
The critical SAR comparison is between MPT and its branched isomer MiPT. MiPT is orally active at 10–25 mg; MPT showed no effects at 20 mg. Shulgin hypothesized that the branched isopropyl group creates steric bulk that slows enzymatic degradation, while the straight-chain propyl group leaves MPT vulnerable to rapid metabolic inactivation.[2] This suggests MPT's apparent inactivity reflects pharmacokinetic failure rather than lack of receptor affinity — the molecule may be destroyed before reaching the brain in sufficient quantity.
Pharmacology[edit]
Pharmacology
Mechanism of action
No receptor binding or functional potency data specific to MPT have been published. All mechanistic understanding is inferred from structurally related tryptamines.
As an unsubstituted N,N-dialkyltryptamine, MPT is presumed to act primarily through serotonin 5-HT₂A receptor agonism — the established mechanism of psychedelic action for the tryptamine class.[11][12] The 5-HT₁A receptor likely plays a modulatory role, tempering the intensity of 5-HT₂A-driven effects. This dual mechanism has been demonstrated in the closely related compound DPT, where selective blockade of 5-HT₂A abolished head-twitch response while 5-HT₁A blockade only shifted the dose-response curve.[11]
MPT may also interact with the SERT (SERT), acting as a substrate rather than a reuptake blocker — a pattern observed in DPT.[13] Whether MPT shares sigma-1 receptor affinity, as demonstrated for DMT,[14] is unknown.
inferred
Pharmacokinetics
No pharmacokinetic data for MPT exist in any species. All parameters — bioavailability, half-life, onset, duration — remain uncharacterized.
By class analogy, the primary inactivation pathway for unsubstituted tryptamines is MAO-A-mediated oxidative deamination.[15][16] The straight-chain propyl group offers minimal steric protection against this enzyme, likely explaining Shulgin's observation of no effects at 20 mg oral.[2] Genetic variation in CYP2D6 may produce inter-individual differences in exposure.[16][17]
At higher doses, MAO-A saturation can cause tryptamine exposure to rise disproportionately, producing nonlinear pharmacokinetics.[4] The practical implication: the jump from sub-threshold to fully active doses may be abrupt and difficult to predict.
Neuroscience[edit]
Neuroscience
Where it acts
No neuroimaging or electrophysiology data exist for MPT. Based on its presumed 5-HT₂A agonism, the compound would be expected to disrupt thalamic sensory filtering via action on prefrontal cortex neurons, allowing normally suppressed information to reach conscious awareness.citation needed Classic psychedelics also reduce the coherence of the default mode network — the brain system underlying self-referential thought — which correlates with experiences of ego dissolution.citation needed
Why it matters
The REBUS model proposes that 5-HT₂A agonists loosen the brain's reliance on learned expectations, allowing raw sensory input to reshape perception. Related tryptamines have also been classified as psychoplastogens — substances that promote rapid growth of neural connections in cortical tissue.citation needed Whether MPT shares these neuroplasticity-promoting properties at any achievable dose has not been tested.
inferred
Subjective Effects[edit]
Subjective Effects
MPT's experiential character is entirely unknown. The only documented human trial — Shulgin's oral administration up to 20 mg — produced no perceptible effects, and no community reports describe psychoactive experiences at any dose or route. Effect profiles associated with MPT in community databases appear templated from generic tryptamine data rather than derived from actual observations. Until an active dose is established, characterization of the experience remains impossible.
If MPT does produce psychedelic effects at higher doses or via parenteral routes, its mixed methyl–propyl substitution places it structurally between DMT and DPT. Whether this intermediate structural position translates to an intermediate experiential character — somewhere between DMT's intensity and DPT's reported emotional depth — is entirely speculative.
Effect Grid
No common-dose effects have been documented for MPT. The dose range producing a full psychedelic experience is entirely unknown.
If MPT produces psychedelic effects at sufficient concentrations — as predicted by its structural similarity to DPT and DMT — a common dose might be expected to produce geometry, color enhancement, time alteration, cognitive euphoria, and emotional enhancement consistent with the tryptamine class. Nausea and pupil dilation would be expected somatic accompaniments.
These predictions are structural analogy inferences from DPT and MiPT profiles and have never been observed in any human subject taking MPT.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Brightness alteration · Environmental patterning · Music enhancement · Visual breathing · Holotropic state · Auditory distortion · Auditory enhancement · Depth perception distortion · Light sensitivity · Perspective distortion · Sound sensitivity · Tracers · Visual haze / noise · Visual morphing · After-images · Auditory misinterpretation · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Symmetrical texture repetition · Touch enhancement · Visual diffraction · Visual melting · Visual acuity enhancement · Peripheral misidentification · Synesthesia · Vestibular distortion · Internal hallucinations · Object transformations · Auditory hallucinations · Environmental orbism / cubism · External hallucinations · Object activation · Visual recursion · Perspective hallucinations · Visual scenery slicing
Holotropic state · Auditory distortion · Auditory enhancement · Depth perception distortion · Light sensitivity · Perspective distortion · Sound sensitivity · Tracers · Visual haze / noise · Visual morphing · After-images · Auditory misinterpretation · Peripheral vision distortion · Proprioceptive distortion · Spatial disorientation · Symmetrical texture repetition · Touch enhancement · Visual diffraction · Visual melting · Visual acuity enhancement · Peripheral misidentification · Synesthesia · Vestibular distortion · Internal hallucinations · Object transformations · Auditory hallucinations · Environmental orbism / cubism · External hallucinations · Object activation · Visual recursion · Perspective hallucinations · Visual scenery slicing
Body scan awareness · Appetite suppression · Nausea · Tingling / electric sensations · Vibrations / buzzing · Wakefulness · Body schema distortion · Dizziness · Heart rate perception changes · Insomnia · Physical fatigue · Stimulation · Bodily heaviness · Bodily lightness · Bodily pressures · Breathing alteration · Dry mouth · Excessive sweating · Laughter fits · Muscle tension · Restlessness · Tactile euphoria · Bruxism · Headache · Involuntary body movements · Kundalini-like energy · Nystagmus (eye wobbles) · Trembling · Vasoconstriction · Vomiting · Yawning · Bodily dissociation · Tactile hallucination
Tingling / electric sensations · Vibrations / buzzing · Wakefulness · Body schema distortion · Dizziness · Heart rate perception changes · Insomnia · Physical fatigue · Stimulation · Bodily heaviness · Bodily lightness · Bodily pressures · Breathing alteration · Dry mouth · Excessive sweating · Laughter fits · Muscle tension · Restlessness · Tactile euphoria · Bruxism · Headache · Involuntary body movements · Kundalini-like energy · Nystagmus (eye wobbles) · Trembling · Vomiting · Yawning · Bodily dissociation · Tactile hallucination
Novelty enhancement · Openness enhancement · Thought connectivity · Cognitive flexibility · Cognitive impairment · Conceptual thinking · Focus suppression · Immersion enhancement · Pattern recognition enhancement · Confusion · Creativity enhancement · Humor enhancement · Increased nature relatedness · Information processing suppression · Memory fragmentation · Multiple thought streams · Synchronicity · Thought acceleration · Thought disorganization · Analysis enhancement · Analysis suppression · Cognitive fatigue · Language suppression · Memory replays · Memory suppression · Motivation suppression · Thought loops · Information processing enhancement · Language enhancement · Cognitive dysphoria · Thought deceleration
Cognitive impairment · Conceptual thinking · Focus suppression · Immersion enhancement · Pattern recognition enhancement · Confusion · Creativity enhancement · Humor enhancement · Increased nature relatedness · Information processing suppression · Memory fragmentation · Multiple thought streams · Synchronicity · Thought acceleration · Thought disorganization · Analysis enhancement · Analysis suppression · Cognitive fatigue · Language suppression · Memory replays · Memory suppression · Motivation suppression · Thought loops · Information processing enhancement · Language enhancement · Cognitive dysphoria · Thought deceleration
Empathy enhancement · Simultaneous emotions · Anxiety suppression · Catharsis · Dysphoria
Dysphoria
Trust enhancement · Communication suppression · Disinhibition · Communication enhancement · Flow state · Sociability enhancement · Ego inflation · Sociability suppression · Social disconnection · Boundary dissolution · Ego dissolution · Identity alteration · Cognitive disconnection · Telepathic feelings
Flow state · Sociability enhancement · Ego inflation · Sociability suppression · Social disconnection · Boundary dissolution · Ego dissolution · Identity alteration · Cognitive disconnection · Telepathic feelings
Transpersonal feelings · Transpersonal visions · Death-rebirth sequence · Transpersonal memory access · Near-death experience · Voidness
Near-death experience · Voidness
Recursive awareness
Timeline
First awareness of altered state, if activity is achieved at sufficient dose. Subtle shift in sensory processing. Inferred from DPT onset (20–60 min oral).
Maximum intensity of psychedelic effects, if achieved. Duration inferred from DPT peak (1–2 h) and MiPT total duration (3–4 h).
Gradual return toward baseline. Effects diminish progressively. Inferred from DPT and MiPT offset profiles.
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.
- LSD · psilo · mesc
Toxicity
No toxicity data exist for MPT in any species — no lethal dose, no organ toxicity assessments, and no case reports of adverse events.safety citation needed The absence of harm reports reflects the compound's extreme obscurity, not demonstrated safety.
Dose-response steepness
For unsubstituted tryptamines, the enzyme that destroys them in the gut can become overwhelmed at higher doses, causing blood levels to rise sharply and unpredictably.[4] For MPT, the territory above Shulgin's inactive 20 mg is entirely uncharted.safety citation needed
By class analogy, active doses may produce transient cardiovascular effects — increased heart rate, elevated blood pressure, and vasoconstriction.[14][15] A systematic review of classic psychedelic studies found no serious drug-attributable adverse events at standard doses,[16] but whether that applies to MPT at its unknown active dose cannot be determined.
Psychological risks
No psychological adverse events have been documented for MPT. By class inference from serotonin receptor agonists:
- Acute distress: anxiety, panic, paranoia, and brief psychotic symptoms occur in a minority of psychedelic experiences, scaling with dose and shaped by context[5]
- Psychosis risk: Classical psychedelics can worsen or trigger psychotic episodes in people with a personal or family history of psychosis, bipolar disorder, or schizophrenia[5]
- Persistent perceptual changes (HPPD): Lingering visual disturbances have been associated with serotonin receptor agonist use[17][18]
All risks listed are class-level inferences. No MPT-specific data exist.
Tolerance and dependence
No tolerance or dependence data exist for MPT. In mice, daily administration of DPT and DiPT did not produce tolerance — unlike phenethylamine hallucinogens, which produced rapid tolerance.[6] The serotonin receptor agonist class shows negligible abuse liability in animal studies,[5] and MPT is expected to share this profile.
Contraindications
6 knownNo MPT-specific contraindication data exist. The following are inferred from serotonin receptor agonist pharmacology:
Absolute contraindications:
- Concurrent MAOI use: Eliminates the primary metabolic pathway; risk of fatal serotonin syndrome — a dangerous overheating and seizure response[19]
- Personal history of psychotic disorders (schizophrenia, schizoaffective disorder): Serotonin receptor agonism may trigger or worsen psychosis[5]
Relative contraindications:
- Bipolar disorder: Risk of triggering a manic episode
- Family history of psychosis: Elevated vulnerability
- Concurrent lithium: Possible seizure risk (community-reported, mechanism unclear)
- Concurrent SSRI/SNRI therapy: Unpredictable effect changes and serotonin toxicity potential[20]
- Heart conditions: Tryptamine-induced cardiovascular stress may pose risk in compromised cardiac function[14]
inferred
Drug Interactions
No interaction data specific to MPT exist. All interactions below are inferred from tryptamine class pharmacology.
MAO inhibitors (life-threatening): The most dangerous interaction for any unsubstituted tryptamine. MAO-A inhibition eliminates the primary metabolic pathway, potentially increasing tryptamine exposure tenfold or more.[19][13] This includes pharmaceutical MAOIs (phenelzine, tranylcypromine, moclobemide), beta-carboline alkaloids (harmaline, harmine — present in ayahuasca and Syrian rue), and dietary monoamine oxidase substrates at extreme doses. Fatal serotonin syndrome — dangerous overheating and seizure — is the primary risk.
SSRIs and SNRIs (moderate–unknown): May blunt psychedelic effects while simultaneously increasing serotonin toxicity risk.[20] The net result is unpredictable.
Lithium (unknown severity): Associated with increased seizure risk when combined with serotonergic psychedelics across multiple community reports. No controlled data exist for any tryptamine-lithium combination.safety citation needed
Other serotonin receptor agonists: Additive or synergistic effects expected from action at the same receptor.
Tramadol: Serotonin syndrome risk through combined serotonergic activity.safety citation needed
inferred
Harm Reduction[edit]
Forms & Identification
MPT has no established market presence and no documented physical forms in circulation. Anyone encountering material claimed to be MPT should treat identification as the primary safety concern — without verified reference standards, confirming that a sample is actually MPT rather than a more potent tryptamine (DPT, DMT, or a 4-substituted structural analog) is essential before any consideration of dose.
Reagent testing can confirm the presence of an indole-containing tryptamine but cannot distinguish MPT from its isomers MiPT or DET, or from dozens of other tryptamines. Mass spectrometry or NMR is required for definitive identification. Given the compound's obscurity, mislabeling risk is substantial.
Guidelines
- Test the material. Use reagent kits to confirm an indole tryptamine is present. Pursue analytical testing through drug checking services if available — reagents alone cannot confirm MPT specifically.
- Start extremely low. With no established dose range, begin well below any anticipated threshold. Titrate upward across separate sessions, never within a single session.
- Have a sober sitter present. Essential for any uncharacterized compound. The sitter should have experience with psychedelic states and know how to contact emergency services.
- Avoid all MAOIs. This includes ayahuasca, Syrian rue, pharmaceutical MAOIs, and moclobemide. Monoamine oxidase inhibition could transform an inactive dose into a dangerously potent one.
- Do not combine with other serotonergic substances. SSRIs, SNRIs, tramadol, and other tryptamines all carry serotonin syndrome risk in combination.
- Keep the environment controlled. Remove access to vehicles, sharp objects, and heights. Ensure water is available.
- Document everything. Dose, time of administration, route, and all effects. Uncharacterized compounds benefit from careful record-keeping.
Set & Setting
Because MPT has no established active dose, any attempt at use is exploratory by definition. There is no established duration, intensity curve, or qualitative character to prepare for.
A calm, familiar, and physically safe environment with a sober sitter is non-negotiable. The sitter should be briefed on the possibility of unexpectedly intense effects due to dose-response unpredictability in uncharacterized tryptamines.
Aftercare & integration. Anyone who experiences psychoactive effects from MPT should treat the aftermath with care. Unexpected effects from uncharacterized compounds can leave residual emotional and perceptual changes that benefit from deliberate processing.
Journaling the experience in detail within 24 hours helps preserve observations useful for harm reduction purposes. If the experience produced significant anxiety, confusion, or disturbing content, speaking with a therapist familiar with psychedelic experiences is advisable. Allow at least two weeks before considering any subsequent use.
Recovery & Support
The serotonin receptor agonist class carries negligible physical dependence liability, and compulsive redosing patterns are rare. However, psychological habituation to altered states can develop with any psychoactive substance.
If use of MPT or related tryptamines becomes a pattern of avoidance or escalation, support resources include the SAMHSA National Helpline (1-800-662-4357), the Fireside Project psychedelic peer support line (62-FIRESIDE), and local harm reduction organizations. Psychedelic-informed therapists can be found through directories such as the Psychedelic Support Network.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Seizure activity or uncontrolled muscle rigidity
- Extremely rapid heart rate, chest pain, or difficulty breathing
- Loss of consciousness or inability to be roused
- Severe agitation, self-harm attempts, or complete disconnection from reality
- Body temperature hot to the touch (potential serotonin syndrome — a dangerous overheating response)
Immediate steps:
- 1. Call emergency services immediately if any of the above signs appear.
- 2. Place an unconscious person in the recovery position (on their side, airway clear).
- 3. Do not restrain a person in psychological crisis unless they are in immediate danger of harming themselves or others. Speak calmly and minimize stimulation.
- 4. Do not induce vomiting.
- 5. Monitor breathing and pulse until help arrives.
What to tell the dispatcher:
Name the substance (MPT / methylpropyltryptamine), the amount taken if known, the time of ingestion, the route, and current symptoms. Good Samaritan laws in many jurisdictions protect callers who report drug-related emergencies from prosecution.
Legal Status[edit]
Legal Status
MPT is not named in any international drug control convention, and its status varies by jurisdiction depending on whether national law includes generic tryptamine clauses or structural analog provisions.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled under the tryptamine catch-all clause, which schedules any compound with a 3-(2-aminoethyl)indole structure regardless of N-substitution[21] |
| United States | Not explicitly scheduled | Not listed in the Controlled Substances Act. MPT is a constitutional isomer of DET (Schedule I, C₁₄H₂₀N₂); the Federal Analogue Act may apply if intended for human consumption[21] |
| Canada | Not scheduled | No tryptamine catch-all provision; MPT not specifically listed[21] |
| Australia | Uncertain | DMT is Schedule 9 (prohibited); MPT not specifically named. Analogue provision status unclear |
| European Union | Not specifically scheduled | Not listed in EU scheduling instruments. Individual member states may control under national generic legislation |
Analogue act considerations
MPT shares its molecular formula with DET (N,N-diethyltryptamine), a Schedule I substance in the United States. The Federal Analogue Act treats as Schedule I any substance substantially similar in chemical structure and pharmacological effect to a scheduled compound when intended for human consumption. Given MPT's structural similarity to multiple scheduled tryptamines — DET, DMT, DPT — legal risk exists in jurisdictions with analogue provisions.citation needed
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.
- LSD · psilo · mesc
Toxicity
No toxicity data exist for MPT in any species — no lethal dose, no organ toxicity assessments, and no case reports of adverse events or overdose.safety citation needed The absence of harm reports reflects the compound's extreme obscurity, not demonstrated safety.
Dose-response steepness
For unsubstituted tryptamines, MAO-A saturation at higher doses can cause exposure to rise disproportionately, making the jump from inactive to fully active doses abrupt and unpredictable.[4] For MPT, the gap between Shulgin's inactive 20 mg and the putative threshold (>50 mg) is uncharted territory.safety citation needed
By class analogy, serotonergic tryptamines at active doses may produce transient cardiovascular effects including increased heart rate, blood pressure elevation, and vasoconstriction.[18][19] A systematic review of adverse events in classic psychedelic studies found no serious drug-attributable adverse events at standard doses,[20] but whether this applies to MPT at its unknown active dose cannot be determined.
Psychological risks
No psychological adverse events have been documented for MPT. By class inference from serotonin 2A receptor agonists:
- Acute distress: anxiety, panic, paranoia, and transient psychotic symptoms occur in a minority of psychedelic experiences, typically scaling with dose and shaped by context[5]
- Psychosis risk: Classic psychedelics can worsen or trigger psychotic episodes in people with personal or family history of psychosis, bipolar disorder, or schizophrenia[5]
- Persistent perceptual changes (HPPD): Lingering visual disturbances have been associated with 5-HT₂A agonist use[21][22]
All risks listed are class-level inferences. No MPT-specific data exist.
Tolerance and dependence
No tolerance or dependence data exist for MPT.
In mice, tolerance to head-twitch response did not develop with daily DPT or DiPT administration — unlike phenethylamine hallucinogens, which produced rapid tolerance.[6] This suggests tryptamine-class psychedelics may have reduced tolerance potential.
Cross-tolerance between 5-HT₂A agonists is expected but incompletely mapped. DOI-tolerant mice showed cross-tolerance to DPT, but the reverse was not established.[6]
The 5-HT₂A psychedelic class shows minimal reinforcement and negligible abuse liability in animal studies.[5] MPT is expected to share this low abuse potential.
Contraindications
6 knownNo MPT-specific contraindication data exist. The following are inferred from 5-HT₂A psychedelic class pharmacology:
Absolute contraindications:
- Concurrent MAOI use: Eliminates the primary metabolic pathway; risk of fatal serotonin syndrome[17]
- Personal history of psychotic disorders (schizophrenia, schizoaffective disorder): 5-HT₂A agonism may trigger or worsen psychosis[5]
Relative contraindications:
- Bipolar disorder: Risk of triggering a manic episode
- Family history of psychosis: Elevated vulnerability
- Concurrent lithium: Possible seizure risk (community-reported, mechanism unclear)
- Concurrent SSRI/SNRI therapy: Unpredictable effect changes and serotonin toxicity potential[23]
- Heart conditions: Tryptamine-induced cardiovascular stress may pose risk in compromised cardiac function[18]
inferred
Drug Interactions
No interaction data specific to MPT exist. All interactions below are inferred from tryptamine class pharmacology.
MAO inhibitors (life-threatening): The most dangerous interaction for any unsubstituted tryptamine. MAO-A inhibition eliminates the primary metabolic pathway, potentially increasing tryptamine exposure tenfold or more.[17][16] This includes pharmaceutical MAOIs (phenelzine, tranylcypromine, moclobemide), beta-carboline alkaloids (harmaline, harmine — present in ayahuasca and Syrian rue), and dietary monoamine oxidase substrates at extreme doses. Fatal serotonin syndrome is the primary risk.
SSRIs and SNRIs (moderate–unknown): May blunt psychedelic effects through receptor changes while simultaneously increasing serotonin toxicity risk.[23] The net result is unpredictable.
Lithium (unknown severity): Associated with increased seizure risk when combined with serotonergic psychedelics across multiple community reports. No controlled data exist for any tryptamine-lithium combination.safety citation needed
Other 5-HT₂A agonists: Additive or synergistic effects expected from action at the same receptor.
Tramadol: Serotonin syndrome risk through combined serotonergic activity.safety citation needed
inferred
Harm Reduction[edit]
Forms & Identification
MPT has no established market presence and no documented physical forms in circulation. Anyone encountering material claimed to be MPT should treat identification as the primary safety concern — without verified reference standards, confirming that a sample is actually MPT rather than a more potent tryptamine (DPT, DMT, or a 4-substituted structural analog) is essential before any consideration of dose.
Reagent testing can confirm the presence of an indole-containing tryptamine but cannot distinguish MPT from its isomers MiPT or DET, or from dozens of other tryptamines. Mass spectrometry or NMR would be required for definitive identification. Given the compound's obscurity, mislabeling risk is substantial.
Guidelines
- Test the material. Use reagent kits to confirm an indole tryptamine is present. Pursue analytical testing (e.g. through drug checking services) if available — reagents alone cannot confirm MPT specifically.
- Start extremely low. With no established dose range, begin well below any anticipated threshold. Titrate upward across separate sessions, never within a single session.
- Have a sober sitter present. Essential for any uncharacterized compound. The sitter should have experience with psychedelic states and know how to contact emergency services.
- Avoid all MAOIs. This includes ayahuasca, Syrian rue, pharmaceutical MAOIs, and moclobemide. Monoamine oxidase inhibition could transform an inactive dose into a dangerously potent one.
- Do not combine with other serotonergic substances. SSRIs, SNRIs, tramadol, and other tryptamines all carry serotonin syndrome risk in combination.
- Keep the environment controlled. Remove access to vehicles, sharp objects, and heights. Ensure water is available.
- Document everything. Dose, time of administration, route, and all effects. Uncharacterized compounds benefit from careful record-keeping — your observations may be among the first.
Set & Setting
Because MPT has no established active dose, any attempt at use is exploratory by definition. The complete absence of experience reports means there is no established duration, intensity curve, or qualitative character to prepare for.
If someone chooses to explore this compound, a calm, familiar, and physically safe environment with a sober sitter is non-negotiable. The sitter should be briefed on the possibility of unexpectedly intense effects due to dose-response unpredictability in uncharacterized tryptamines.
Aftercare & integration. Given that MPT's effects are uncharacterized, anyone who does experience psychoactive effects should treat the aftermath with particular care. Psychedelic experiences — especially unexpected ones from uncharacterized compounds — can leave residual emotional and perceptual effects that benefit from deliberate processing.
Journaling the experience in detail within 24 hours helps preserve observations that may be useful for harm reduction purposes. If the experience produced significant anxiety, confusion, or disturbing content, consider speaking with a therapist familiar with psychedelic experiences. Allow at least two weeks before considering any subsequent use.
Recovery & Support
The 5-HT₂A psychedelic class carries negligible physical dependence liability, and compulsive redosing patterns are rare. However, psychological habituation to altered states can develop with any psychoactive substance.
If use of MPT or related tryptamines becomes a pattern of avoidance or escalation, support resources include the SAMHSA National Helpline (1-800-662-4357), the Fireside Project psychedelic peer support line (62-FIRESIDE), and local harm reduction organizations. Psychedelic-informed therapists can be found through directories such as the Psychedelic Support Network.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Seizure activity or uncontrolled muscle rigidity
- Extremely rapid heart rate, chest pain, or difficulty breathing
- Loss of consciousness or inability to be roused
- Severe agitation, self-harm attempts, or complete disconnection from reality
- Body temperature hot to the touch (potential serotonin syndrome)
Immediate steps:
- 1. Call emergency services immediately if any of the above signs appear.
- 2. Place an unconscious person in the recovery position (on their side, airway clear).
- 3. Do not restrain a person in psychological crisis unless they are in immediate danger of harming themselves or others. Speak calmly and minimize stimulation.
- 4. Do not induce vomiting.
- 5. Monitor breathing and pulse until help arrives.
What to tell the dispatcher:
Name the substance (MPT / methylpropyltryptamine), the amount taken if known, the time of ingestion, the route, and current symptoms. Good Samaritan laws in many jurisdictions protect callers who report drug-related emergencies from prosecution.
Legal Status[edit]
Legal Status
MPT is not named in any international drug control convention. Its legal status varies by jurisdiction, shaped by whether national law includes generic tryptamine clauses or structural analog provisions.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled under the tryptamine catch-all clause, which schedules any compound with a 3-(2-aminoethyl)indole structure regardless of N-substitution[9] |
| United States | Not explicitly scheduled | Not listed in the Controlled Substances Act. MPT is a constitutional isomer of DET (Schedule I, C₁₄H₂₀N₂); the Federal Analogue Act may apply if intended for human consumption[9] |
| Canada | Not scheduled | No tryptamine catch-all provision; MPT not specifically listed[9] |
| Australia | Uncertain | DMT is Schedule 9 (prohibited); MPT not specifically named. Analogue provision status unclear |
| European Union | Not specifically scheduled | Not listed in EU scheduling instruments. Individual member states may control under national generic legislation |
Analogue act considerations
MPT shares its molecular formula with DET (N,N-diethyltryptamine), a Schedule I substance in the United States. The Federal Analogue Act treats as Schedule I any substance "substantially similar" in chemical structure and pharmacological effect to a scheduled compound when intended for human consumption. Given MPT's structural similarity to multiple scheduled tryptamines (DET, DMT, DPT), legal risk exists in jurisdictions with analogue provisions. Legal counsel would be required to assess prosecution risk in any specific case.
citation needed
Frequently asked questions
What is MPT?
MPT is a synthetic tryptamine psychedelic and constitutional isomer of MiPT and DET, with no confirmed psychoactive effects at tested doses. First documented in TiHKAL (1997), it remains one of the least characterized compounds in the N,N-dialkyltryptamine series.
Where can I find dosage information for MPT?
Psychedex publishes a dosage table for MPT 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 MPT?
The highest-severity documented interactions for MPT: MAOIs (Lethal), Alpha-2 adrenergic receptor antagonist (Dangerous), Dopamine agonists (Dangerous), DXM (Dangerous), GHB, Baclofen (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is MPT addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for MPT: tolerance builds rapid; full reset takes 7 days; cross-tolerance develops with LSD, psilocybin, mescaline, DMT, DPT, MiPT. See the article's dependence and safety sections for recorded dependence data.
experience reports
No experience reports yet. Be the first to contribute.
First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1] ^Kozell LB, Eshleman AJ, Swanson TL, Bloom SH, Wolfrum KM, et al. (2023) Pharmacologic Activity of Substituted Tryptamines at 5-HT2A, 5-HT2C, 5-HT1A Receptors and SERT — Journal of Pharmacology and Experimental Therapeutics doi:10.1124/jpet.122.001454
- [2]
- [3] ^abcChadeayne AR, Golen JA, Manke DR (2019) N-Methyl-N-propyltryptamine (MPT) — IUCrData doi:10.1107/s2414314619009623
- [4] ^abcShen HW, Jiang XL, Yu AM (2011) Nonlinear pharmacokinetics of 5-methoxy-N,N-dimethyltryptamine in mice — Drug Metabolism and Disposition doi:10.1124/dmd.111.039107
- [5]
- [6] ^abSmith DA, Bailey JM, Williams D, Fantegrossi WE (2014) Tolerance and cross-tolerance to head twitch behavior elicited by phenethylamine- and tryptamine-derived hallucinogens in mice. — The Journal of pharmacology and experimental therapeutics doi:10.1124/jpet.114.219337
references
- [1] ^Kozell LB, Eshleman AJ, Swanson TL, Bloom SH, Wolfrum KM, et al. (2023) Pharmacologic Activity of Substituted Tryptamines at 5-HT2A, 5-HT2C, 5-HT1A Receptors and SERT — Journal of Pharmacology and Experimental Therapeutics doi:10.1124/jpet.122.001454
- [2]
- [3] ^abcChadeayne AR, Golen JA, Manke DR (2019) N-Methyl-N-propyltryptamine (MPT) — IUCrData doi:10.1107/s2414314619009623
- [4] ^abcShen HW, Jiang XL, Yu AM (2011) Nonlinear pharmacokinetics of 5-methoxy-N,N-dimethyltryptamine in mice — Drug Metabolism and Disposition doi:10.1124/dmd.111.039107
- [5]
- [6] ^abcSmith DA, Bailey JM, Williams D, Fantegrossi WE (2014) Tolerance and cross-tolerance to head twitch behavior elicited by phenethylamine- and tryptamine-derived hallucinogens in mice. — The Journal of pharmacology and experimental therapeutics doi:10.1124/jpet.114.219337