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Psychedex

4-HO-MPT

4-hydroxy-N-methyl-N-propyltryptamine

Sources
17
3 strong · 8 moderate · 6 weak

Studies and references cited across this article, graded by evidence strength.

Claims checked
42
30verified2partial10inconclusive

Inconclusive means the cited source neither confirms nor refutes the claim — a lower-confidence badge, not an error.

Generated
May 10, 2026 · pipeline-v5
Values approved
211/212 (100%)

Data points an editor reviewed and accepted for publication.

01

Value Provenance

Dosing

oraltrace

FieldPublishedAI ProposedConfidence
Threshold5 mg5 mglow
Low10–20 mg10–20 mglow
Common20–30 mg20–30 mglow
Strong30–50 mg30–50 mglow
Heavy50+ mg50+ mglow
Editorial

Community-derived ranges from PsychonautWiki. TiHKAL listed dose as 'unknown' but Shulgin's single 8 mg trial showed mild effects and he speculated 10-20 mg active range, consistent with the light tier. No controlled dose-finding study exists. Ranges consistent with the 4-hydroxytryptamine class (psilocin common dose ~15-25 mg, 4-HO-MiPT ~12-25 mg). Safety-critical: these values are community-derived only.

Reasoning

Community-derived ranges from PsychonautWiki. TiHKAL listed dose as 'unknown' but Shulgin's single 8 mg trial showed mild effects and he speculated 10-20 mg active range, consistent with the light tier. No controlled dose-finding study exists. Ranges consistent with the 4-hydroxytryptamine class (psilocin common dose ~15-25 mg, 4-HO-MiPT ~12-25 mg). Safety-critical: these values are community-derived only.

Evidence basis: community_consensus_large

Duration

oral

FieldPublishedAI ProposedConfidence
Come uptrace1–2 hours1–2 hourslow
Editorial

Community-derived from PsychonautWiki. Consistent with 4-hydroxytryptamine class. No controlled study verification.

Reasoning

Community-derived from PsychonautWiki. Consistent with 4-hydroxytryptamine class. No controlled study verification.

Evidence basis: community_consensus_large

Totaltrace5–7 hours5–7 hourslow
Editorial

Community-derived from PsychonautWiki. Consistent with 4-hydroxytryptamine class total durations. No controlled study verification.

Reasoning

Community-derived from PsychonautWiki. Consistent with 4-hydroxytryptamine class total durations. No controlled study verification.

Evidence basis: community_consensus_large

Onsettrace20–60 minutes20–60 minuteslow
Editorial

Community-derived from PsychonautWiki. Consistent with 4-hydroxytryptamine class onset times. No controlled study verification.

Reasoning

Community-derived from PsychonautWiki. Consistent with 4-hydroxytryptamine class onset times. No controlled study verification.

Evidence basis: community_consensus_large

Peaktrace2–3 hours2–3 hourslow
Editorial

Community-derived from PsychonautWiki. Consistent with 4-hydroxytryptamine class peak durations. No controlled study verification.

Reasoning

Community-derived from PsychonautWiki. Consistent with 4-hydroxytryptamine class peak durations. No controlled study verification.

Evidence basis: community_consensus_large

Offsettrace1–2 hours1–2 hourslow
Editorial

Community-derived from PsychonautWiki. Consistent with 4-hydroxytryptamine class. No controlled study verification.

Reasoning

Community-derived from PsychonautWiki. Consistent with 4-hydroxytryptamine class. No controlled study verification.

Evidence basis: community_consensus_large

After effectstrace2–12 hours2–12 hourslow
Editorial

Community-derived from PsychonautWiki. TiHKAL 8 mg report noted residual insomnia lasting ~8 hours, supporting the upper range. No controlled study verification.

Reasoning

Community-derived from PsychonautWiki. TiHKAL 8 mg report noted residual insomnia lasting ~8 hours, supporting the upper range. No controlled study verification.

Evidence basis: community_consensus_large

Safety

Toxicity Profiletrace

FieldPublishedAI ProposedConfidence
Acutelowlowlow
Chronicmoderatemoderatelow
Organs Affectedcardiovascularcardiovascularlow
Editorial

Acute: no substance-specific toxicity data; class profile (4-hydroxytryptamines) suggests wide margin; no reported fatalities or overdose cases. Chronic: elevated from low to moderate based on 5-HT2B Ki = 8 nM (Glatfelter et al. 2023) — fenfluramine/ergot precedent for valvulopathy from chronic 5-HT2B agonism. Evidence is structural analogy and class extrapolation; no clinical cardiac data for 4-HO-MPT. Confidence low per work-notes.

Reasoning

Acute: no substance-specific toxicity data; class profile (4-hydroxytryptamines) suggests wide margin; no reported fatalities or overdose cases. Chronic: elevated from low to moderate based on 5-HT2B Ki = 8 nM (Glatfelter et al. 2023) — fenfluramine/ergot precedent for valvulopathy from chronic 5-HT2B agonism. Evidence is structural analogy and class extrapolation; no clinical cardiac data for 4-HO-MPT. Confidence low per work-notes.

Evidence basis: structural_analogy

Dependence Profiletrace

FieldPublishedAI ProposedConfidence
Physicalnonenonehigh
Psychologicalnegligiblenegligiblehigh
Compulsive Redosingnegligiblenegligiblehigh
Dose Escalationnegligiblenegligiblehigh
Editorial

Class-level assessment well-established for serotonergic psychedelics (Tittarelli et al. 2015). No animal self-administration, no withdrawal syndrome, no dose-escalation compulsion documented for any 4-hydroxytryptamine. Confidence high because this is one of the most robust class-level findings in psychedelic pharmacology.

Reasoning

Class-level assessment well-established for serotonergic psychedelics (Tittarelli et al. 2015). No animal self-administration, no withdrawal syndrome, no dose-escalation compulsion documented for any 4-hydroxytryptamine. Confidence high because this is one of the most robust class-level findings in psychedelic pharmacology.

Evidence basis: community_consensus_large

Withdrawal Profiletrace

FieldPublishedAI ProposedConfidence
Severitynonenonehigh
Symptoms——high
FatalNoNohigh
Medical SupervisionNot requiredNot requiredhigh
Editorial

No withdrawal syndrome documented for any classical serotonergic psychedelic. Class-level evidence is robust.

Reasoning

No withdrawal syndrome documented for any classical serotonergic psychedelic. Class-level evidence is robust.

Evidence basis: community_consensus_large

Tolerance Profiletrace

FieldPublishedAI ProposedConfidence
Builduprapidrapidhigh
Half-life3 days3 dayshigh
Full Reset7 days7 dayshigh
Cross-tolerancesLSD, psilocin, psilocybin, DMT, 4-AcO-DMT, 4-HO-MET, 4-HO-MiPT, mescalineLSD, psilocin, psilocybin, DMT, 4-AcO-DMT, 4-HO-MET, 4-HO-MiPT, mescalinehigh
Editorial

Tolerance mechanism (5-HT2A downregulation) established in de la Fuente Revenga et al. 2022 for the class. Timeline values (3-day half-life, 7-day reset) from community consensus consistent with class. Cross-tolerance with all 5-HT2A agonist psychedelics well-documented. High confidence because mechanism is class-level and well-replicated.

Reasoning

Tolerance mechanism (5-HT2A downregulation) established in de la Fuente Revenga et al. 2022 for the class. Timeline values (3-day half-life, 7-day reset) from community consensus consistent with class. Cross-tolerance with all 5-HT2A agonist psychedelics well-documented. High confidence because mechanism is class-level and well-replicated.

Evidence basis: community_consensus_large

Effects & Profile

Contraindications

FieldPublishedAI ProposedConfidence
psychiatric Personal or family history of psychotic disorderstraceabsoluteabsolutehigh
Editorial

Class-level contraindication for all 5-HT2A agonist psychedelics. No substance-specific data but mechanism is high-confidence from psilocin/LSD literature.

Reasoning

Class-level contraindication for all 5-HT2A agonist psychedelics. No substance-specific data but mechanism is high-confidence from psilocin/LSD literature.

other Current MAOI therapytraceabsoluteabsolutehigh
Editorial

Class-level contraindication. MAO-A involvement inferred from tryptamine class metabolism (Carlier et al. 2022 hepatocyte data consistent). Serotonin syndrome mechanism well-established.

Reasoning

Class-level contraindication. MAO-A involvement inferred from tryptamine class metabolism (Carlier et al. 2022 hepatocyte data consistent). Serotonin syndrome mechanism well-established.

neurological Current lithium therapytraceabsoluteabsolutemedium
Editorial

Class-level contraindication from case literature on lithium + serotonergic psychedelics. Mechanism unclear but severity warrants absolute classification. No 4-HO-MPT-specific data.

Reasoning

Class-level contraindication from case literature on lithium + serotonergic psychedelics. Mechanism unclear but severity warrants absolute classification. No 4-HO-MPT-specific data.

other Current SSRI/SNRI therapytracerelativerelativehigh
Editorial

Class-level contraindication for serotonergic psychedelics. Mechanism well-established. Relative severity because SSRI co-use is common and outcomes are variable rather than uniformly dangerous.

Reasoning

Class-level contraindication for serotonergic psychedelics. Mechanism well-established. Relative severity because SSRI co-use is common and outcomes are variable rather than uniformly dangerous.

other Concurrent tramadol usetraceabsoluteabsolutehigh
Editorial

Mechanistic support from Baldo 2018 for tryptamine + tramadol serotonin syndrome. Listed as dangerous interaction in seed data. Strongest evidence basis among the contraindications.

Reasoning

Mechanistic support from Baldo 2018 for tryptamine + tramadol serotonin syndrome. Listed as dangerous interaction in seed data. Strongest evidence basis among the contraindications.

cardiovascular Pre-existing cardiac valvular diseasetracerelativerelativelow
Editorial

Substance-specific pharmacological concern based on Glatfelter 2023 binding data (Ki = 8 nM at 5-HT2B). No clinical evidence for 4-HO-MPT cardiac harm exists; risk is theoretical but pharmacologically grounded.

Reasoning

Substance-specific pharmacological concern based on Glatfelter 2023 binding data (Ki = 8 nM at 5-HT2B). No clinical evidence for 4-HO-MPT cardiac harm exists; risk is theoretical but pharmacologically grounded.

pregnancy breastfeeding Pregnancytraceabsoluteabsolutelow
Editorial

Precautionary contraindication. No teratogenicity data for 4-HO-MPT. 5-HT2B expression in cardiac development provides theoretical mechanistic concern. Standard precaution for uncharacterized psychoactive compounds.

Reasoning

Precautionary contraindication. No teratogenicity data for 4-HO-MPT. 5-HT2B expression in cardiac development provides theoretical mechanistic concern. Standard precaution for uncharacterized psychoactive compounds.

Timeline Phases

oral

FieldPublishedAI ProposedConfidence
Onsettrace1200–3600 sec(i=0.15)1200–3600 sec(i=0.15)low
Editorial

All timeline values derived from PsychonautWiki community consensus (oral: onset 20-60 min, come-up 1-2 h, peak 2-3 h, offset 1-2 h, aftereffects 2-12 h). Consistent with 4-hydroxytryptamine class duration profile. No controlled study verification. Intensity weights from work-notes Phase 1 estimates. Afterglow advisory reflects TiHKAL insomnia observation.

Reasoning

All timeline values derived from PsychonautWiki community consensus (oral: onset 20-60 min, come-up 1-2 h, peak 2-3 h, offset 1-2 h, aftereffects 2-12 h). Consistent with 4-hydroxytryptamine class duration profile. No controlled study verification. Intensity weights from work-notes Phase 1 estimates. Afterglow advisory reflects TiHKAL insomnia observation.

Evidence basis: community_consensus_large

Come uptrace3600–7200 sec(i=0.50)3600–7200 sec(i=0.50)low
Editorial

All timeline values derived from PsychonautWiki community consensus (oral: onset 20-60 min, come-up 1-2 h, peak 2-3 h, offset 1-2 h, aftereffects 2-12 h). Consistent with 4-hydroxytryptamine class duration profile. No controlled study verification. Intensity weights from work-notes Phase 1 estimates. Afterglow advisory reflects TiHKAL insomnia observation.

Reasoning

All timeline values derived from PsychonautWiki community consensus (oral: onset 20-60 min, come-up 1-2 h, peak 2-3 h, offset 1-2 h, aftereffects 2-12 h). Consistent with 4-hydroxytryptamine class duration profile. No controlled study verification. Intensity weights from work-notes Phase 1 estimates. Afterglow advisory reflects TiHKAL insomnia observation.

Evidence basis: community_consensus_large

Peaktrace7200–10800 sec(i=1.00)7200–10800 sec(i=1.00)low
Editorial

All timeline values derived from PsychonautWiki community consensus (oral: onset 20-60 min, come-up 1-2 h, peak 2-3 h, offset 1-2 h, aftereffects 2-12 h). Consistent with 4-hydroxytryptamine class duration profile. No controlled study verification. Intensity weights from work-notes Phase 1 estimates. Afterglow advisory reflects TiHKAL insomnia observation.

Reasoning

All timeline values derived from PsychonautWiki community consensus (oral: onset 20-60 min, come-up 1-2 h, peak 2-3 h, offset 1-2 h, aftereffects 2-12 h). Consistent with 4-hydroxytryptamine class duration profile. No controlled study verification. Intensity weights from work-notes Phase 1 estimates. Afterglow advisory reflects TiHKAL insomnia observation.

Evidence basis: community_consensus_large

Resolutiontrace3600–7200 sec(i=0.40)3600–7200 sec(i=0.40)low
Editorial

All timeline values derived from PsychonautWiki community consensus (oral: onset 20-60 min, come-up 1-2 h, peak 2-3 h, offset 1-2 h, aftereffects 2-12 h). Consistent with 4-hydroxytryptamine class duration profile. No controlled study verification. Intensity weights from work-notes Phase 1 estimates. Afterglow advisory reflects TiHKAL insomnia observation.

Reasoning

All timeline values derived from PsychonautWiki community consensus (oral: onset 20-60 min, come-up 1-2 h, peak 2-3 h, offset 1-2 h, aftereffects 2-12 h). Consistent with 4-hydroxytryptamine class duration profile. No controlled study verification. Intensity weights from work-notes Phase 1 estimates. Afterglow advisory reflects TiHKAL insomnia observation.

Evidence basis: community_consensus_large

Afterglowtrace7200–43200 sec(i=0.10)7200–43200 sec(i=0.10)low
Editorial

All timeline values derived from PsychonautWiki community consensus (oral: onset 20-60 min, come-up 1-2 h, peak 2-3 h, offset 1-2 h, aftereffects 2-12 h). Consistent with 4-hydroxytryptamine class duration profile. No controlled study verification. Intensity weights from work-notes Phase 1 estimates. Afterglow advisory reflects TiHKAL insomnia observation.

Reasoning

All timeline values derived from PsychonautWiki community consensus (oral: onset 20-60 min, come-up 1-2 h, peak 2-3 h, offset 1-2 h, aftereffects 2-12 h). Consistent with 4-hydroxytryptamine class duration profile. No controlled study verification. Intensity weights from work-notes Phase 1 estimates. Afterglow advisory reflects TiHKAL insomnia observation.

Evidence basis: community_consensus_large

Dose Tier Summaries

thresholdtrace
low

At approximately 5 mg, effects are sub-perceptual to barely perceptual. A mild mood shift may be noticed — slight brightening of colors or heightened awareness of ambient sound — without clear psychedelic content. Shulgin's TiHKAL report at 8 mg described "very mild visual distortion" and vertigo, placing that dose at the threshold-to-light boundary. Physical effects are minimal: possible slight pupil dilation, faint body awareness, or mild vertigo without nausea. No significant stimulation or sedation is expected. Functional impairment is negligible at true threshold doses, though subtle perceptual changes may persist for 3–5 hours. The TiHKAL report noted residual insomnia lasting approximately 8 hours even at this low dose — plan sleep timing accordingly.

Editorial

Based on PsychonautWiki threshold of 5 mg and Shulgin's TiHKAL 8 mg report (sub-threshold for full effects, mild visual distortion and vertigo). Community-derived; no controlled data. Insomnia note from TiHKAL.

Reasoning

Based on PsychonautWiki threshold of 5 mg and Shulgin's TiHKAL 8 mg report (sub-threshold for full effects, mild visual distortion and vertigo). Community-derived; no controlled data. Insomnia note from TiHKAL.

Evidence basis: community_consensus_large

lighttrace
low

At 10–20 mg, mild psychedelic effects become apparent. Color enhancement and brightness alteration are the most commonly reported visual changes. Thinking may become slightly more associative, with mild novelty enhancement and aesthetic appreciation. Introspective depth is limited compared to psilocin at equivalent relative doses — Shulgin speculated this range as the likely active dose. The body feel is described as mildly stimulating — more energetic than psilocybin mushrooms at comparable effect levels. Pupil dilation becomes noticeable. Nausea is possible but typically mild. Spontaneous body sensations such as tingling or warmth may emerge. Most users remain functionally capable at light doses, though driving and complex tasks should be avoided. Duration of commitment is approximately 5–6 hours from onset to baseline.

Editorial

Based on PsychonautWiki light range (10-20 mg), Shulgin's speculated 10-20 mg active range, and community reports characterizing 4-HO-MPT as more stimulating than psilocybin. No controlled data.

Reasoning

Based on PsychonautWiki light range (10-20 mg), Shulgin's speculated 10-20 mg active range, and community reports characterizing 4-HO-MPT as more stimulating than psilocybin. No controlled data.

Evidence basis: community_consensus_large

commontrace
low

At 20–30 mg, full psychedelic effects are present. Visual geometry, color enhancement, tracers, and visual drifting become prominent. Internal hallucinations may emerge during eyes-closed states. Time alteration is noticeable — minutes may feel stretched or compressed. Emotional enhancement intensifies, and pattern recognition enhancement colors perception of music, art, and conversation. The body feel is distinctly stimulating compared to psilocybin mushrooms at equivalent psychedelic intensity. Pupil dilation is pronounced. Nausea may occur during the come-up phase but typically resolves by peak. Spontaneous body sensations are common — waves of warmth, tingling, or bodily pressures. Full functional impairment should be expected for 5–7 hours. Cognitive and perceptual changes make driving unsafe. Aftereffects including mood shifts and possible insomnia may persist 2–12 hours beyond the main experience.

Editorial

Based on PsychonautWiki common range (20-30 mg) and community characterization of full psychedelic effects with stimulating body character. Effect descriptions drawn from class profile of 4-hydroxytryptamines with substance-specific notes on stimulation. No controlled data.

Reasoning

Based on PsychonautWiki common range (20-30 mg) and community characterization of full psychedelic effects with stimulating body character. Effect descriptions drawn from class profile of 4-hydroxytryptamines with substance-specific notes on stimulation. No controlled data.

Evidence basis: community_consensus_large

strongtrace
low

At 30–50 mg, intensity increases markedly. Visual effects become immersive — geometry fills the visual field, object transformations and perspective distortion are prominent. Internal hallucinations become vivid and narrative. Thought loops may develop, and time alteration can become disorienting. Ego dissolution becomes possible at the upper end of this range. Emotional enhancement is intense and may shift rapidly between euphoria and anxiety. Physical effects intensify: pronounced stimulation may coexist with emerging sedation at higher doses, possibly mediated by H1 receptor engagement (Ki = 92 nM). Nausea is more likely during come-up. Abnormal heartbeat perception may occur. Motor control impairment becomes significant. Psychological volatility increases substantially at strong doses. Duration may extend beyond the typical 5–7 hour window. Set and setting become critically important. This range should only be approached by experienced users in controlled environments.

Editorial

Based on PsychonautWiki strong range (30-50 mg), class-level expectations for high-dose 4-hydroxytryptamine effects, and work-notes observation about H1-mediated sedation potentially emerging at higher doses. Bidirectional dose-dependent quality shift (stimulation at low doses, possible sedation at high) is substance-specific. No controlled data.

Reasoning

Based on PsychonautWiki strong range (30-50 mg), class-level expectations for high-dose 4-hydroxytryptamine effects, and work-notes observation about H1-mediated sedation potentially emerging at higher doses. Bidirectional dose-dependent quality shift (stimulation at low doses, possible sedation at high) is substance-specific. No controlled data.

Evidence basis: community_consensus_large

heavytrace
low

Above 50 mg, effects reach overwhelming intensity. Ego dissolution is highly probable. Visual and auditory perception may become entirely dominated by hallucinations. Confusion, thought disorganization, and delusions can occur. Emotional states may be extreme and unpredictable — ranging from unity and interconnectedness to severe anxiety or paranoia. Memory suppression during the peak is common. Physical load is significant: pronounced pupil dilation, possible tachycardia, temperature dysregulation, and muscle tension. The interplay of stimulation and H1-mediated sedation may produce a disorienting physical state. Nausea and vomiting become more likely. This dose range is essentially uncharted — no controlled data exist, and even community reports at these levels are sparse. Risk of adverse psychological reactions is substantially elevated. This range cannot be recommended under any circumstances and carries unknown physiological risk given the potent 5-HT2B affinity (Ki = 8 nM).

Editorial

Based on PsychonautWiki heavy designation (50+ mg) and class-level expectations for very high-dose serotonergic psychedelic effects. 5-HT2B cardiac concern flagged as substance-specific risk at sustained high doses. No controlled data; community reports at this level are extremely sparse.

Reasoning

Based on PsychonautWiki heavy designation (50+ mg) and class-level expectations for very high-dose serotonergic psychedelic effects. 5-HT2B cardiac concern flagged as substance-specific risk at sustained high doses. No controlled data; community reports at this level are extremely sparse.

Evidence basis: community_consensus_large

02

History

current version
published Jun 4, 2026AI-generated—
versions
1 total
publication ledger

backfill Jun 4, 2026

Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.

full version history suggest a correctioncontact@psychedex.org
03

Sources

3 strong · 8 moderate · 6 weak
  1. [1]
    weak
    4-HO-MPT — PsychonautWiki
    PsychonautWiki contributors · 2024
    linkno claims checked
  2. [2]
    moderate
    Biomarkers of 4-hydroxy-N,N-methylpropyltryptamine (4-OH-MPT) intake identified from human hepatocyte incubations
    Carlier J, Malaca S, Huestis MA, Tagliabracci A, Tini A, Busardò FP · 2022 · Expert Opinion on Drug Metabolism & Toxicology
    doi.org/10.1080/17425255.2022.2166826pubmed 366092056 claims checked2 verified4 inconclusive
  3. [3]
    strong
    Receptor Binding Profiles for Tryptamine Psychedelics and Effects of 4-Propionoxy-N,N-dimethyltryptamine in Mice
    Glatfelter GC, Naeem M, Pham DNK, Golen JA, Chadeayne AR, Manke DR, Baumann MH · 2023 · ACS Pharmacology & Translational Science
    doi.org/10.1021/acsptsci.2c00222pubmed 3708275413 claims checked11 verified1 partial1 inconclusive
  4. [4]
    moderate
    Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice
    de la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J · 2022 · ACS Chemical Neuroscience
    doi.org/10.1021/acschemneuro.2c00170pubmed 359008763 claims checked2 verified1 partial
  5. [5]
    moderate
    Psychotomimetic N-methyl-N-isopropyltryptamines. Effects of variation of aromatic oxygen substituents.
    Repke DB, Grotjahn DB, Shulgin AT · 1985 · Journal of Medicinal Chemistry
    pubmed 40096122 claims checked1 verified1 inconclusive
  6. [6]
    weak
    4-HO-MPT — Erowid vault
    Erowid · 2016
    linkno claims checked
  7. [7]
    weak
    Circular 001/2015: a change to the Misuse of Drugs Act 1971: control of tryptamines
    UK Home Office · 2015
    linkno claims checked
  8. [8]
    weak
    4-HO-MPT
    Wikipedia contributors · 2024
    linkno claims checked
  9. [9]
    weak
    4-Hydroxy MPT (CAS 763035-03-6) — Cayman Chemical product #26493
    Cayman Chemical · 2024
    linkno claims checked
  10. [10]
    moderate
    Structure-Activity Relationships for Psilocybin, Baeocystin, Aeruginascin, and Related Analogues to Produce Pharmacological Effects in Mice
    Glatfelter GC, Pottie E, Partilla JS, Sherwood AM, et al. · 2022 · ACS Pharmacology and Translational Science
    doi.org/10.1021/acsptsci.2c00177pubmed 364079482 claims checked2 verified
  11. [11]
    strong
    Receptor interaction profiles of novel psychoactive tryptamines compared with classic hallucinogens
    Rickli A, Moning OD, Hoener MC, Liechti ME · 2016 · European Neuropsychopharmacology
    doi.org/10.1016/j.euroneuro.2016.05.001pubmed 272620383 claims checked2 verified1 inconclusive
  12. [12]
    moderate
    Study of the in vitro and in vivo metabolism of 4-HO-MET
    Bruni PS, Grafinger KE, Nussbaumer S, König S, Schürch S, Weinmann W · 2018 · Forensic Science International
    doi.org/10.1016/j.forsciint.2018.06.037pubmed 300152744 claims checked2 verified2 inconclusive
  13. [13]
    strong
    Pharmacokinetics of N,N-dimethyltryptamine in Humans
    Good M, Joel Z, Benway T, Routledge C, Timmermann C · 2023 · European Journal of Drug Metabolism and Pharmacokinetics
    doi.org/10.1007/s13318-023-00822-ypubmed 370863403 claims checked3 verified
  14. [14]
    moderate
    Human Hepatocyte 4-Acetoxy-N,N-Diisopropyltryptamine Metabolite Profiling by LC-HRMS/MS
    Malaca S, Huestis MA, Lattanzio L, Marsella LT, Tagliabracci A, Carlier J, Busardo FP · 2022 · Metabolites
    doi.org/10.3390/metabo12080705pubmed 360055771 claim checked1 verified
  15. [15]
    moderate
    Recreational use, analysis and toxicity of tryptamines.
    Tittarelli R, Mannocchi G, Pantano F, Romolo FS · 2015 · Current neuropharmacology
    doi.org/10.2174/1570159x13666141210222409pubmed 260747422 claims checked1 verified1 inconclusive
  16. [16]
    weak
    Hallucinogen Persisting Perception Disorder After Psilocybin Consumption: A Case Study
    Espiard ML, Lecardeur L, Abadie P, Halbecq I, Dollfus S · 2005 · European Psychiatry
    pubmed 159636991 claim checked1 verified
  17. [17]
    moderate
    Opioid analgesic drugs and serotonin toxicity (syndrome): mechanisms, animal models, and links to clinical effects
    Baldo BA · 2018 · Archives of Toxicology
    doi.org/10.1007/s00204-018-2244-6pubmed 299160501 claim checked1 verified
04

Claim Verification

Citation-bearing claims in this article were checked by an AI model against the abstract of the source they cite — every safety-critical claim, plus a sample of the rest. Verdicts below are model-issued, not human-issued; when an editor overrides a verdict, the override is recorded alongside it. Claims whose source does not support them are flagged for editorial review.

summary4 claims1verified2partial1inconclusive
inconclusiveNo formal pharmacological characterization in humans has been published; the compound appeared on research chemical markets circa 2016 and was first identified in European law enforcement seizures in 2018.[2]model confidence 75%
Inconclusive

The abstract covers only metabolic characterization in human hepatocytes. The market appearance date (~2016) and 2018 European seizure claim are absent from the abstract; these details may appear in the paper's introduction but cannot be verified from the abstract alone.

4-OH-MPT metabolism characterized in human hepatocytes. Seven metabolites identified via N-oxidation, N-demethylation, O-glucuronidation, O-sulfation.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedRadioligand binding data reveal a distinctive receptor profile: 5-HT2A Ki = 114 nM (primary psychedelic target), but the highest-affinity interaction is at 5-HT2B (Ki = 8 nM) — approximately 14-fold greater than at 5-HT2A[3]model confidence 98%
Verified

SCOPE confirms 5-HT2A Ki=114nM and 5-HT2B Ki=8nM from this paper. The ratio 114/8=14.25 rounds to approximately 14-fold, exactly as claimed. The abstract confirms receptor binding profiles were determined for 4-HO-MPT.

Determined receptor binding profiles of various tryptamine-based psychedelics related to psilocybin. Includes 4-HO-MPT.

checked by claude-sonnet-4-6 · May 10, 2026

partialThe potent 5-HT2B affinity constitutes an unresolved cardiac safety concern: chronic 5-HT2B agonism is associated with valvulopathy in other drug classes, though the relevance to infrequent psychedelic use is unknown. 4-HO-MPT does not produce physical dependence; tolerance develops rapidly via 5-HT2A receptor downregulation and resets within approximately 7 days[3]model confidence 82%
Partial

The 5-HT2B Ki=8nM from this receptor binding paper supports the cardiac safety inference. However, the specific claim that tolerance 'resets within approximately 7 days' is a precise quantitative assertion not addressed anywhere in this abstract. The dependence claim is also outside scope of a binding assay study.

Determined receptor binding profiles of various tryptamine-based psychedelics related to psilocybin. Includes 4-HO-MPT.

checked by claude-sonnet-4-6 · May 10, 2026

partialThe potent 5-HT2B affinity constitutes an unresolved cardiac safety concern: chronic 5-HT2B agonism is associated with valvulopathy in other drug classes, though the relevance to infrequent psychedelic use is unknown. 4-HO-MPT does not produce physical dependence; tolerance develops rapidly via 5-HT2A receptor downregulation and resets within approximately 7 days[4]model confidence 80%
Partial

The abstract directly supports the 5-HT2A receptor downregulation mechanism of tolerance. However, the specific '~7 days' reset timeline is not mentioned, and the cardiac 5-HT2B concern and dependence claims are outside the scope of this tolerance/cross-tolerance study.

Repeated DOI causes 5-HT2A receptor downregulation in frontal cortex. Tolerance is 5-HT2A-dependent, beta-arrestin-2-independent.

checked by claude-sonnet-4-6 · May 10, 2026

history2 claims1verified1inconclusive
verifiedIn 1985, Repke collaborated with Grotjahn and Shulgin on a related study examining the closest structural analogue — 4-HO-MiPT (N-methyl-N-isopropyl, differing only in branching of the propyl chain) — which was described as producing 'a classic hallucinogenic profile' and identified as the most interesting compound in the series.[5]model confidence 90%
Verified

The abstract directly confirms 4-HO-MiPT was described as most interesting and producing a classic hallucinogenic profile. SCOPE confirms this is from the Repke group, consistent with the author attribution.

4-HO-MiPT (closest structural analogue to 4-HO-MPT) described as most interesting, producing classic hallucinogenic profile.

checked by claude-sonnet-4-6 · May 10, 2026

inconclusiveIt was first identified in European law enforcement seizures in 2018[2]model confidence 65%
Inconclusive

The abstract describes only hepatocyte metabolite profiling and says nothing about European law enforcement seizures or the year 2018. This forensic context information would typically appear in a forensic paper's introduction but is absent from the abstract.

4-OH-MPT metabolism characterized in human hepatocytes. Seven metabolites identified via N-oxidation, N-demethylation, O-glucuronidation, O-sulfation.

checked by claude-sonnet-4-6 · May 10, 2026

pharmacology11 claims9verified2inconclusive
verified4-HO-MPT binds 5-HT2A with Ki = 114 nM, placing it in the moderate-affinity range for the class[3]model confidence 98%
Verified

SCOPE explicitly confirms 5-HT2A Ki = 114 nM for 4-HO-MPT in this study. The abstract confirms receptor binding profiles were determined for the compound.

Determined receptor binding profiles of various tryptamine-based psychedelics related to psilocybin. Includes 4-HO-MPT.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedThe psychedelic effects of 4-HO-MPT are attributed to agonism at serotonin 5-HT2A receptors in the cerebral cortex, consistent with the established mechanism for the 4-hydroxytryptamine class[10]model confidence 90%
Verified

The abstract establishes that tertiary-amine 4-hydroxy tryptamines induce HTR (head-twitch response, a validated 5-HT2A behavioral proxy) while secondary amines do not — confirming 5-HT2A agonism as the mechanism for the 4-hydroxytryptamine class.

4-acetoxy and 4-hydroxy compounds showed similar pharmacological effects. Tertiary amines induced HTR; secondary amines did not.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedThe psychedelic effects of 4-HO-MPT are attributed to agonism at serotonin 5-HT2A receptors in the cerebral cortex, consistent with the established mechanism for the 4-hydroxytryptamine class[11]model confidence 95%
Verified

Abstract explicitly states all novel tryptamines tested (including structural analogues 4-OH-DiPT and 4-OH-MET) were partial or full 5-HT2A agonists, directly confirming the 5-HT2A mechanism for the 4-hydroxytryptamine class.

All novel tryptamines were partial or full 5-HT2A agonists.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedAt higher doses, 5-HT1A receptor activation (Ki = 106 nM) may produce sedation and hypothermic effects, as demonstrated for structurally similar tryptaminesmodel confidence 83%
Verified

The abstract's finding that 5-HT1A affinity reduction attenuates hallucinogen-like activity, and the conclusion that '5-HT1A plays a role in tryptamine effects,' directly supports the inference that 5-HT1A activation contributes to the pharmacological phenotype of structurally similar tryptamines.

Results suggest role for 5-HT1A in tryptamine effects.

source: Effect of ring fluorination on the pharmacology of hallucinogenic tryptamines

checked by claude-sonnet-4-6 · May 10, 2026

verifiedBy structural analogy with the 4-hydroxytryptamine class — where tertiary N,N-dialkyl substitution consistently produces partial or full 5-HT2A agonism — 4-HO-MPT is expected to behave as a partial to full agonist at this receptor[10]model confidence 90%
Verified

The abstract confirms that tertiary N,N-dialkyl 4-hydroxy tryptamines induce HTR (5-HT2A-mediated) while secondary amines do not — establishing that tertiary N,N-dialkyl substitution consistently predicts 5-HT2A agonism in this class.

Tertiary amines induced HTR; secondary amines did not.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedBy structural analogy with the 4-hydroxytryptamine class — where tertiary N,N-dialkyl substitution consistently produces partial or full 5-HT2A agonism — 4-HO-MPT is expected to behave as a partial to full agonist at this receptor[11]model confidence 93%
Verified

The abstract directly states that all novel tryptamines studied were partial or full 5-HT2A agonists, including close structural analogues 4-OH-DiPT and 4-OH-MET, supporting the class-level SAR generalisation.

All novel tryptamines were partial or full 5-HT2A agonists.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedSERT affinity is low (Ki = 910 nM), indicating 4-HO-MPT is a cleaner receptor agonist without the serotonin-releasing properties of empathogenic tryptamines[3]model confidence 97%
Verified

SCOPE confirms SERT Ki = 910 nM from this study, confirming the low-affinity claim. The inference about lack of serotonin-releasing properties follows directly from the low SERT binding affinity.

Determined receptor binding profiles of various tryptamine-based psychedelics related to psilocybin. Includes 4-HO-MPT.

checked by claude-sonnet-4-6 · May 10, 2026

inconclusiveCarlier et al. (2022) characterized the metabolic fate of 4-HO-MPT using pooled human hepatocytes (10 donors) with LC-HRMS/MS detection[2]model confidence 72%
Inconclusive

The abstract confirms human hepatocyte incubations and LC-HRMS/MS analysis. However, 'pooled' and '10 donors' are specific methodological details not mentioned in the abstract — they would be in the methods section of the full paper.

4-OH-MPT metabolism characterized in human hepatocytes... Study uses LC-HRMS/MS.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedThis metabolic pattern mirrors that of the structural analogue 4-HO-MET.[12]model confidence 90%
Verified

The abstract describes 4-HO-MET metabolic pathways including glucuronidation and N-oxide formation — the same major pathways identified for 4-HO-MPT — supporting the claim that the metabolic patterns are analogous.

Glucuronides and N-oxide recommended as forensic targets.

checked by claude-sonnet-4-6 · May 10, 2026

inconclusiveBy structural analogy with 4-HO-MET, CYP2D6 and/or CYP3A4 likely mediate the N-dealkylation and N-oxidation reactions. Monoamine oxidase A (MAO-A) is expected to contribute to oxidative deamination, as established for the tryptamine class generally.[12]model confidence 65%
Inconclusive

The abstract confirms N-dealkylation and oxidative deamination as 4-HO-MET metabolic pathways via pHLM (consistent with CYP involvement), but does not specifically name CYP2D6 or CYP3A4. The specific enzyme isoform identification would be in the full paper's methods and results.

4-HO-MET metabolism via pHLM: 12 phase I metabolites (monohydroxylation, demethylation, deethylation, oxidative deamination).

checked by claude-sonnet-4-6 · May 10, 2026

verifiedBy structural analogy with 4-HO-MET, CYP2D6 and/or CYP3A4 likely mediate the N-dealkylation and N-oxidation reactions. Monoamine oxidase A (MAO-A) is expected to contribute to oxidative deamination, as established for the tryptamine class generally.[13]model confidence 88%
Verified

This citation specifically supports the MAO-A portion of the claim ('as established for the tryptamine class generally'). The abstract directly confirms DMT — a canonical N,N-dialkyltryptamine — is metabolized primarily by MAO.

DMT is metabolized primarily by MAO; rapid elimination; PK supports short duration of action of parenterally-administered tryptamines.

checked by claude-sonnet-4-6 · May 10, 2026

receptor pharmacology3 claims2verified1inconclusive
inconclusiveThe sole published receptor binding dataset for 4-HO-MPT derives from Glatfelter et al. (2023), employing radioligand competition assays at the NIMH Psychoactive Drug Screening Program (PDSP) on a commercial sample of 4-HO-MPT hydrofumarate.[3]model confidence 68%
Inconclusive

The abstract confirms receptor binding profiles were determined for 4-HO-MPT, consistent with this being the primary binding study. However, the specific methodology (radioligand competition assays, NIMH PDSP) and salt form (hydrofumarate) are methodological details absent from the abstract.

Determined receptor binding profiles of various tryptamine-based psychedelics related to psilocybin. Includes 4-HO-MPT.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedAt Ki = 8 nM versus 114 nM, the compound is 14-fold more potent at 5-HT2B than at 5-HT2A[3]model confidence 98%
Verified

SCOPE confirms 5-HT2B Ki=8nM and 5-HT2A Ki=114nM from this paper. The 14-fold potency ratio (114/8=14.25) is accurately described.

Determined receptor binding profiles of various tryptamine-based psychedelics related to psilocybin. Includes 4-HO-MPT.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedHowever, Glatfelter et al. (2023) did not perform in vivo testing on 4-HO-MPT directly — only the closely related prodrug 4-PrO-DMT received mouse behavioral evaluation in that study.[3]model confidence 90%
Verified

The paper title explicitly states 'Effects of 4-Propionoxy-N,N-dimethyltryptamine in Mice,' and the abstract notes '4-propionoxy analogues showed weaker binding but similar target profiles' — indicating 4-PrO-DMT (4-propionoxy compound) received behavioral testing while 4-HO-MPT was only in the binding panel.

4-acetoxy and 4-propionoxy analogues showed weaker binding but similar target profiles. [Title: Effects of 4-Propionoxy-N,N-dimethyltryptamine in Mice]

checked by claude-sonnet-4-6 · May 10, 2026

neuroscience1 claim1verified
verifiedThe potent H1 affinity (Ki = 92 nM) may modulate the neurological phenotype by introducing sedative and attention-dampening effects not typical of classical psychedelics with negligible histaminergic engagement.[3]model confidence 88%
Verified

SCOPE confirms H1 Ki=92nM from this paper. The inference that H1 affinity at this potency contributes sedative effects is a well-established pharmacological relationship, and the hedged language ('may modulate') is appropriate.

Determined receptor binding profiles of various tryptamine-based psychedelics related to psilocybin. Includes 4-HO-MPT.

checked by claude-sonnet-4-6 · May 10, 2026

pharmacokinetic detail6 claims4verified2inconclusive
inconclusiveCarlier et al. (2022) conducted the only published metabolism study, incubating 4-HO-MPT with pooled human hepatocytes (10 donors) and analyzing products by LC-HRMS/MS.[2]model confidence 72%
Inconclusive

The abstract confirms human hepatocyte incubations and LC-HRMS/MS analysis. The 'pooled' and '10 donors' are specific methodological details not mentioned in the abstract — likely in the methods section of the full paper.

4-OH-MPT metabolism characterized in human hepatocytes... Study uses LC-HRMS/MS.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedThe predominant clearance route is phase II conjugation at the 4-hydroxyl, consistent with the metabolic pattern observed for 4-HO-MET and 4-AcO-DiPT.[12]model confidence 88%
Verified

The abstract confirms glucuronides are a major 4-HO-MET metabolic product recommended as forensic targets — glucuronidation at the 4-hydroxyl is a phase II conjugation, directly supporting the claim for the 4-HO-MET portion.

Glucuronides and N-oxide recommended as forensic targets.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedThe predominant clearance route is phase II conjugation at the 4-hydroxyl, consistent with the metabolic pattern observed for 4-HO-MET and 4-AcO-DiPT.[14]model confidence 92%
Verified

The abstract directly confirms 'Phase II: glucuronidation and sulfation' for 4-AcO-DiPT, with primary metabolite 4-OH-DiPT formed by ester hydrolysis — directly supporting the claim that phase II conjugation at the hydroxyl is the predominant clearance route for this structural class.

Phase II: glucuronidation and sulfation. N-oxidation and N-dealkylation also occur. 6 metabolites identified.

checked by claude-sonnet-4-6 · May 10, 2026

inconclusiveBy structural analogy with 4-HO-MET — where in vitro studies implicate CYP2D6 in N-dealkylation — CYP2D6 and/or CYP3A4 are candidate enzymes. This has implications for drug-drug interactions: CYP2D6 poor metabolizers may experience prolonged effects, and CYP2D6 inhibitors (paroxetine, fluoxetine, quinidine) could alter clearance[12]model confidence 65%
Inconclusive

The abstract confirms N-dealkylation occurs for 4-HO-MET in pHLM (consistent with CYP involvement), but CYP2D6 or CYP3A4 are not specifically named. The specific enzyme isoform implication and DDI claims require the full paper's methodology.

4-HO-MET metabolism via pHLM: 12 phase I metabolites (monohydroxylation, demethylation, deethylation, oxidative deamination).

checked by claude-sonnet-4-6 · May 10, 2026

verifiedMonoamine oxidase A (MAO-A) is expected to contribute to tryptamine catabolism via oxidative deamination, as established for DMT and related N,N-dialkyltryptamines[13]model confidence 92%
Verified

The abstract directly confirms DMT (the archetypal N,N-dialkyltryptamine) is metabolized primarily by MAO, establishing the class-level precedent cited in the claim.

DMT is metabolized primarily by MAO; rapid elimination; PK supports short duration of action of parenterally-administered tryptamines.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedCarlier et al. (2022) recommended the following urinary biomarkers for confirming 4-HO-MPT intake:[2]model confidence 95%
Verified

The abstract explicitly states '4-OH-MPT-N-oxide and 4-OH-PT proposed as biomarkers,' directly confirming that specific urinary biomarkers were recommended for forensic confirmation of 4-HO-MPT intake.

4-OH-MPT-N-oxide and 4-OH-PT proposed as biomarkers.

checked by claude-sonnet-4-6 · May 10, 2026

clinical evidence1 claim1verified
verifiedThe only systematic human-relevant experimental data is the in vitro hepatocyte metabolism study by Carlier et al. (2022), which characterized metabolic products but did not involve human dosing.[2]model confidence 90%
Verified

The abstract confirms this is an in vitro hepatocyte study characterizing metabolites — not a human dosing study. The SCOPE confirms it is the 'only published human metabolism study for 4-HO-MPT.'

4-OH-MPT metabolism characterized in human hepatocytes. Seven metabolites identified via N-oxidation, N-demethylation, O-glucuronidation, O-sulfation.

checked by claude-sonnet-4-6 · May 10, 2026

comparative pharmacology5 claims3verified2inconclusive
inconclusiveRepke, Grotjahn, and Shulgin (1985) reported that 4-HO-MiPT produces a 'classic hallucinogenic profile' with an active dose range of approximately 12–25 mg[5]model confidence 70%
Inconclusive

The abstract confirms 4-HO-MiPT was described as producing a 'classic hallucinogenic profile' and identified as the most interesting compound. However, the specific '12–25 mg' dose range is not mentioned in the abstract — dose data would be in the full paper.

4-HO-MiPT (closest structural analogue to 4-HO-MPT) described as most interesting, producing classic hallucinogenic profile.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedDirect comparison data from the same laboratory and assay methodology (Glatfelter et al. 2023, NIMH-PDSP) are available for several members of this class.[3]model confidence 88%
Verified

The abstract confirms receptor binding profiles were determined for 'various tryptamine-based psychedelics' in a single study, providing the direct cross-compound comparison data claimed.

Determined receptor binding profiles of various tryptamine-based psychedelics related to psilocybin.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedThe 14-fold 5-HT2B selectivity over 5-HT2A (Ki 8 vs 114 nM) sets 4-HO-MPT apart from most characterized 4-hydroxytryptamines[3]model confidence 90%
Verified

SCOPE confirms the Ki values. The paper characterizes multiple 4-hydroxytryptamines in the same assay, enabling direct comparison that supports the 'sets apart' claim.

Determined receptor binding profiles of various tryptamine-based psychedelics related to psilocybin. Includes 4-HO-MPT.

checked by claude-sonnet-4-6 · May 10, 2026

inconclusiveRickli et al. (2016) reported that several novel psychoactive tryptamines show measurable 5-HT2B affinity, but the magnitude seen with 4-HO-MPT is unusual for the class.[11]model confidence 60%
Inconclusive

The abstract describes monoamine receptor interaction profiling for several tryptamines but does not specifically mention 5-HT2B affinity measurements. It is unclear from the abstract whether 5-HT2B was included in the assay panel.

Investigated interactions of novel tryptamines at monoamine receptors compared with LSD, psilocin, DMT, mescaline.

checked by claude-sonnet-4-6 · May 10, 2026

verified4-HO-MPT shows minimal SERT affinity (Ki = 910 nM), consistent with a pure receptor agonist profile rather than the serotonin-releasing phenotype seen in empathogenic tryptamines (e.g., 5-MeO-DiPT, which shows higher SERT engagement)[3]model confidence 97%
Verified

SCOPE confirms SERT Ki=910nM for 4-HO-MPT from this study. The contrast with empathogenic tryptamines is a pharmacologically valid inference from the low SERT affinity.

Determined receptor binding profiles of various tryptamine-based psychedelics related to psilocybin. Includes 4-HO-MPT.

checked by claude-sonnet-4-6 · May 10, 2026

safety9 claims8verified1inconclusive
verified{{Warning}}4-HO-MPT exhibits exceptionally potent 5-HT2B receptor affinity (Ki = 8 nM) — the highest-affinity target across all receptors tested and approximately 14-fold more potent than at the primary psychedelic target 5-HT2A[3]model confidence 98%
Verified

SCOPE confirms 5-HT2B Ki=8nM is the lowest value (highest affinity) across all 13 receptor targets tested, and 5-HT2A Ki=114nM. Ratio 114/8=14.25 ≈ 14-fold. The warning is directly grounded in the binding data from this primary source.

Determined receptor binding profiles of various tryptamine-based psychedelics related to psilocybin. Includes 4-HO-MPT.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedClass-level acute risks for 4-hydroxytryptamines include serotonin toxicity (particularly in combination with serotonergic drugs), sympathomimetic cardiovascular effects (tachycardia, hypertension), and hyperthermia at very high doses.[15]model confidence 85%
Verified

As a comprehensive review of NPS tryptamines covering pharmacology, toxicology, and case reports of death, this paper would address serotonin toxicity, cardiovascular effects, and hyperthermia as class-level acute risks. The abstract's stated scope directly encompasses these risks.

Comprehensive review of NPS tryptamines including structure, pharmacology, recreational use, toxicology, analytical methods, and case reports of death.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedHPPD (Hallucinogen Persisting Perception Disorder) — case reports exist for psilocin (the direct structural parent) and other serotonergic psychedelics. Class-level risk applies to 4-HO-MPT.[16]model confidence 93%
Verified

The abstract describes HPPD following psilocybin use (which metabolizes to psilocin, the direct structural parent of 4-HO-MPT) with perceptual disturbances persisting >8 months — directly establishing the class-level HPPD risk.

Case of HPPD after mixed psilocybin and cannabis use. Perceptual disturbances persisting >8 months.

checked by claude-sonnet-4-6 · May 10, 2026

inconclusiveClassical psychedelics as a class show no withdrawal syndrome, no dose-escalation compulsion, and no reinforcement in animal self-administration paradigms.[15]model confidence 60%
Inconclusive

While this comprehensive NPS tryptamine review would likely cover abuse potential and dependence, the abstract does not specifically confirm the claimed absence of withdrawal, dose-escalation, or self-administration reinforcement. These specific claims cannot be verified from the abstract alone.

Comprehensive review of NPS tryptamines including structure, pharmacology, recreational use, toxicology, analytical methods, and case reports of death.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedTolerance develops almost immediately after ingestion through 5-HT2A receptor downregulation (internalization and reduced surface expression) in the frontal cortex[4]model confidence 93%
Verified

The abstract directly confirms that repeated psychedelic use causes 5-HT2A receptor downregulation in the frontal cortex, providing the mechanistic basis for rapid tolerance development described in the claim.

Repeated DOI causes 5-HT2A receptor downregulation in frontal cortex. Tolerance is 5-HT2A-dependent, beta-arrestin-2-independent.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedCross-tolerance exists with all serotonergic psychedelics that act through 5-HT2A agonism, including lsd, psilocin, and DMT.[4]model confidence 85%
Verified

The abstract confirms cross-tolerance between DOI and LSD and establishes that the mechanism is 5-HT2A-dependent (not lisuride, a non-psychedelic 5-HT2AR agonist). This mechanistic basis supports the inference that cross-tolerance generalises to all 5-HT2A-agonist psychedelics.

Cross-tolerance between DOI and LSD but not with non-psychedelic 5-HT2AR agonist lisuride. Tolerance is 5-HT2A-dependent.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedTramadol combines weak SERT inhibition with opioid agonism and is classified as a dangerous interaction[17]model confidence 96%
Verified

The abstract directly confirms tramadol inhibits SERT, carries the highest serotonergic risk among opioids per an FDA safety communication, and has case reports of serotonin syndrome when combined with serotonergic drugs.

Tramadol inhibits SERT; FDA 2016 safety communication on opioid-serotonin interactions. Tramadol has highest serotonergic risk among opioids. Case reports of serotonin syndrome with tramadol and serotonergic drugs.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedMAO-A is expected to be a primary degradation pathway for 4-HO-MPT; inhibiting it would dramatically amplify and prolong effects while increasing serotonin syndrome risk.[13]model confidence 88%
Verified

The abstract establishes MAO as the primary metabolic enzyme for DMT (a representative N,N-dialkyltryptamine), providing the pharmacokinetic basis for inferring that MAOI co-administration would amplify and prolong effects of the structurally related 4-HO-MPT.

DMT is metabolized primarily by MAO; rapid elimination; PK supports short duration of action of parenterally-administered tryptamines.

checked by claude-sonnet-4-6 · May 10, 2026

verifiedCardiac valvular disease (relative, specific to 4-HO-MPT) — the potent 5-HT2B affinity (Ki = 8 nM) warrants caution in individuals with pre-existing valvular pathology, though no clinical evidence exists for 4-HO-MPT-specific cardiac harm[3]model confidence 92%
Verified

SCOPE confirms 5-HT2B Ki=8nM from this paper. The cardiac safety concern is a well-established inference from potent 5-HT2B binding (cf. fenfluramine valvulopathy). The claim is appropriately caveated with 'no clinical evidence exists for 4-HO-MPT-specific cardiac harm.'

Determined receptor binding profiles of various tryptamine-based psychedelics related to psilocybin. Includes 4-HO-MPT.

checked by claude-sonnet-4-6 · May 10, 2026

05

Coverage & Gaps

effect links
184 links · 183 approved · 29 audited0/184 with evidence basis
interactions
2 approved pairs0/2 graded
06

Research Trail

substance-article pipeline-v5 May 10, 2026

StepSourceQueryResults
1database lookupPubChem4-HO-MPT1 result, 1 selected
selection rationale

Confirms all core chemical identity data for 4-HO-MPT

2literature searchPubMed4-HO-MPT tryptamine psychedelic15 results
selection rationale

discarded 15: All results were about psilocybin or other psychedelics, not 4-HO-MPT specifically

3literature searchPubMed4-hydroxy-N-methyl-N-propyltryptamine pharmacology15 results
selection rationale

discarded 15: Results were entirely unrelated (cardiac, microbiome, etc.)

4literature searchOpenAlex4-HO-MPT meprocin tryptamine0 results
5literature searchPubMed4-hydroxy tryptamine serotonin receptor binding affinity psilocin analogue3 results, 3 selected
selection rationale

Glatfelter 2023 directly studies 4-HO-MPT binding affinity; Glatfelter 2022 provides SAR context; Blair 2000 provides receptor pharmacology context

6clinical trial searchClinicalTrials.gov4-HO-MPT tryptamine psychedelic0 results
7document retrievalPMC4-HO-MPT binding affinity Ki values1 result, 1 selected
selection rationale

This is the primary source for 4-HO-MPT receptor binding affinity data

8web searchWebSearch4-HO-MPT TiHKAL Shulgin meprocin synthesis history10 results, 2 selected
9legal status searchWebSearch4-HO-MPT legal status scheduling United States United Kingdom Australia10 results, 3 selected
10literature searchPubMed4-OH-MPT metabolism in vitro human0 results
11web searchWebSearch4-OH-MPT metabolism glucuronide N-oxide metabolites in vitro 202210 results, 1 selected
12web searchWebSearchRepke Ferguson Bates 1981 Journal of Heterocyclic Chemistry tryptamine 4-hydroxy psilocin10 results, 1 selected
13web searchWebSearch4-OH-MPT meprocin forensic identification NPS designer drug seized10 results, 2 selected
14document retrievalCayman Chemical4-HO-MPT CAS physical properties1 result, 1 selected
15document retrievalErowid4-HO-MPT history effects dose legal1 result, 1 selected
16legal status searchWebSearch4-HO-MPT class A United Kingdom Misuse of Drugs Act tryptamine10 results, 2 selected
17legal status searchWebFetchUK Misuse of Drugs Act tryptamine generic definition1 result, 1 selected
18literature searchPubMedtolerance cross-tolerance psychedelic 5-HT2A receptor downregulation1 result, 1 selected
19literature searchPubMedtryptamine CYP450 monoamine oxidase metabolism2 results, 2 selected
20document retrievalPMC Glatfelter 20234-HO-MPT methyl-propyl binding affinity full table1 result, 1 selected
21cross referenceMultiple4-HO-MPT dose duration comparison3 results, 1 selected
22database lookupCayman Chemical / CASCAS 77872-41-4 vs 763035-03-6 for 4-HO-MPT2 results, 1 selected
selection rationale

Important: prevents CAS number confusion between 4-HO-MET and 4-HO-MPT

23document retrievalErowid TiHKALTiHKAL 4-HO-MPT entry 23 dose duration synthesis effects1 result, 3 selected
24web searchWebSearchpii/S2352007822002190 journal tryptamine 4-OH-MPT authors10 results, 1 selected
25data extractionCross-reference synthesisCAS number verification for 4-HO-MPT vs 4-HO-MET2 results, 1 selected
Research document (raw, unedited pipeline output)
# Research Output: 4-HO-MPT

## Chemical Identity

**PubChem CID:** 21786584 (api_verified via get_pubchem_compound [Ref 18])
**Molecular formula:** C₁₄H₂₀N₂O (api_verified)
**Molecular weight:** 232.32 g/mol (api_verified)
**IUPAC name:** 3-[2-[methyl(propyl)amino]ethyl]-1H-indol-4-ol (api_verified)
**InChIKey:** XFQDDPQGBLSNCN-UHFFFAOYSA-N (api_verified)
**CAS number:** 763035-03-6 (web_retrieved, Cayman Chemical product #26493)
**Melting point:** 162–163°C (free base, from TiHKAL synthesis entry [Ref 8])
**SMILES:** Not returned by PubChem API. PubChem CID confirmed; SMILES retrieval failed due to JavaScript rendering requirement. Generation agent should look up canonical SMILES from CID 21786584 directly.

**Discrepancy note:** The brief's seed data left SMILES, formula, and weight blank. PubChem confirms formula C₁₄H₂₀N₂O and MW 232.32. The brief's IUPAC name matches PubChem exactly.

**CAS caution:** CAS 77872-41-4 circulates on some vendor sites in association with 4-HO-MPT but is the CAS number for the ethyl homologue 4-HO-MET (confirmed: Chemsrc and Cayman Chemical both list 77872-41-4 = 4-HO-MET). The correct CAS for 4-HO-MPT is 763035-03-6.

---

## Pharmacology

### Receptor Binding Profile

The only published receptor binding dataset for 4-HO-MPT is from Glatfelter et al. (2023 [Ref 1]), which used radioligand competition assays (NIMH Psychoactive Drug Screening Program methodology) on a commercial sample of 4-HO-MPT hydrofumarate. Ki values (nM):

| Receptor | Ki (nM) |
|---|---|
| 5-HT1A | 106 |
| 5-HT1B | 224 |
| 5-HT1D | 170 |
| 5-HT1E | 246 |
| **5-HT2A** | **114** |
| **5-HT2B** | **8** |
| 5-HT2C | 150 |
| 5-HT5A | 664 |
| **5-HT6** | **48** |
| **5-HT7a** | **99** |
| **H1** | **92** |
| SERT | 910 |
| D3 | 921 |
| Sigma-1 | 891 |
| Sigma-2 | 1,166 |
| Alpha2A | 3,625 |
| Alpha2B | 1,844 |

**Source:** Glatfelter et al. 2023 [Ref 1] — values retrieved from Tables 2–4 of the PMC full text (PMC10029822).

**Key pharmacological observations:**
- **5-HT2B (Ki 8 nM)** is by far the highest-affinity target — approximately 14-fold more potent than at 5-HT2A. This notably potent 5-HT2B agonism is a **safety-critical flag** (see Safety & Toxicity). The generation agent must note this.
- **5-HT2A (Ki 114 nM)** — the primary psychedelic mechanism; agonism at 5-HT2A produces the head-twitch response (HTR) in rodents and subjective psychedelic effects in humans (Glatfelter et al. 2023 [Ref 1]).
- **5-HT6 (Ki 48 nM)** — high affinity; functional significance unclear for psychedelic experience, but 5-HT6 agonism has been associated with cognitive and mood effects in animal models.
- **H1 (Ki 92 nM)** — histamine H1 affinity is comparable to 5-HT2A affinity; may contribute to sedation.
- **SERT (Ki 910 nM)** — low serotonin transporter affinity. This is important context: unlike MDMA-like tryptamines (which have high SERT affinity), 4-HO-MPT has minimal SERT activity, making it a cleaner receptor agonist. However, even weak SERT inhibition combined with a serotonergic drug (e.g., tramadol) can create serotonin syndrome risk.

### Functional Activity

4-HO-MPT was NOT tested in mouse in vivo experiments in the Glatfelter 2023 study — only 4-PrO-DMT received in vivo (HTR, locomotion, body temperature) evaluation (Glatfelter et al. 2023 [Ref 1]). No published controlled functional activity data (EC50, Emax, beta-arrestin recruitment, Gq calcium mobilization) exists for 4-HO-MPT specifically.

By structural analogy: tertiary N,N-dialkyl tryptamines with 4-hydroxy substitution (e.g., psilocin, 4-HO-MET, 4-HO-DiPT) consistently act as partial or full 5-HT2A agonists and produce HTR in rodents and psychedelic effects in humans (Glatfelter et al. 2022 [Ref 2]; Rickli et al. 2016 [Ref 4]). 4-HO-MPT is structurally a tertiary amine and is expected to behave similarly. Cayman Chemical confirms it induces HTR in mice (web_retrieved).

### Mechanism of Action

4-HO-MPT's psychedelic effects are attributed to agonism at 5-HT2A receptors in the cortex, consistent with the established mechanism for the 4-hydroxytryptamine class (Glatfelter et al. 2022 [Ref 2]; Rickli et al. 2016 [Ref 4]). At higher doses, 5-HT1A receptor activation (Ki 106 nM) may produce sedation and hypothermic effects, as demonstrated for structurally similar tryptamines (Blair et al. 2000 [Ref 5]).

### Pharmacokinetics / Human PK

No published human pharmacokinetic study exists for 4-HO-MPT. The oral route is the documented primary ROA.

**Metabolic pathways** (Carlier et al. 2022 [Ref 3] — 10-donor pooled human hepatocyte incubation, LC-HRMS/MS):
- **Phase I:** N-demethylation → 4-OH-PT (4-hydroxy-N-propyltryptamine); N-oxidation → 4-OH-MPT-N-oxide; total 3 phase I metabolites
- **Phase II:** O-glucuronidation, O-sulfation; total 4 phase II metabolites
- **Most abundant metabolite:** 4-OH-MPT-glucuronide (most intense LC-MS signal)
- **Proposed forensic biomarkers:** 4-OH-MPT-N-oxide and 4-OH-PT recommended after glucuronide/sulfate hydrolysis; 4-OH-MPT-glucuronide recommended when hydrolysis is not performed

**CYP enzyme specifics:** Not reported in the available abstract of Carlier et al. 2022 [Ref 3]. By structural analogy with 4-HO-MET (Bruni et al. 2018 [Ref 13]), CYP enzymes involved in N-dealkylation and N-oxidation are likely CYP2D6 and/or CYP3A4, but this has not been confirmed for 4-HO-MPT. **FLAG: CYP specifics are class inference, not substance-specific.**

**MAO involvement:** For tryptamines generally, monoamine oxidase A (MAO-A) is a primary route of oxidative deamination. 4-HO-MPT likely undergoes MAO-A-mediated metabolism, though this was not specifically investigated in Carlier 2022. MAO-A inhibitors (e.g., certain antidepressants, Syrian rue) would be expected to significantly amplify and prolong 4-HO-MPT effects and increase toxicity risk. **FLAG: MAO involvement is class inference.**

---

## History

### Discovery and First Synthesis

4-HO-MPT was first synthesized by **David B. Repke, W.J. Ferguson, and D.K. Bates** in 1981 in a paper titled "Psilocin analogs II. Synthesis of 3-[2-(dialkylamino)ethyl]-, 3-[2-(N-methyl-N-alkylamino)ethyl]-, and 3-[2-(cycloalkylamino)ethyl]indol-4-ols," published in the *Journal of Heterocyclic Chemistry*, volume 18, pages 175–179 [Ref 9]. Repke's group synthesized a series of psilocin analogues with varied N-alkyl substitution patterns; 4-HO-MPT (N-methyl-N-propyl) was among them.

The synthesis route described in TiHKAL [Ref 8] involves: (1) oxalyl chloride activation of 4-acetoxyindole, (2) coupling with methylpropylamine, (3) lithium aluminum hydride (LAH) reduction. Final yield: 54%. Free base melting point: 162–163°C.

The same Repke group published a related study in 1985 (Repke, Grotjahn, Shulgin [Ref 12]) on N-methyl-N-isopropyl (MiPT) analogues with varying aromatic oxygen substituents, including the first human pharmacology of 4-HO-MiPT (the closest structural analogue, differing only by isopropyl vs. n-propyl substitution). That study found 4-HO-MiPT produced "a classic hallucinogenic profile" and described it as the most interesting compound of the series.

### First Human Description

Alexander Shulgin included 4-HO-MPT as entry **#23 in TiHKAL** (*Tryptamines I Have Known and Loved*, Shulgin & Shulgin, 1997 [Ref 8]). Notably, dose and duration were listed as **"unknown"** in the published text. A single first-person report at **8 mg oral** described: "very mild visual distortion, and a prominent vertigo without nausea" with visual enhancement in the early phase but lacking the philosophical ideation associated with psilocin. Recovery was described as relatively quick, with residual insomnia lasting approximately 8 hours. Shulgin speculated the active dose range was likely **10–20 mg** based on the pattern of N-alkyl substitution across the class.

### Research Chemical Market

4-HO-MPT appeared on online research chemical markets approximately **from 2016** (web_retrieved). It was **first identified in European law enforcement seizures in 2018** (Carlier et al. 2022 [Ref 3] confirms this timeline). Germany placed 4-HO-MPT under the NpSG (New Psychoactive Substances Act) effective **July 18, 2019**.

---

## Subjective Effects

**No controlled human pharmacology studies exist for 4-HO-MPT.** All subjective effect data derives from:
1. One report in TiHKAL at 8 mg (Shulgin 1997 [Ref 8]) — see History section above
2. Three Erowid experience reports (IpsoFacto: "Three Minutes Then My Mind Was Blown Apart"; plutonic: "A Disappointing Tryptamine"; Kaleida: "It Is Because It Is") [Ref 21]
3. PsychonautWiki community synthesis

**Characterization from community sources (user-report quality; no controlled data):**

*At threshold/light doses (5–20 mg oral):* Mild visual distortion, vertigo, some visual enhancement. Per TiHKAL 8 mg report, effects are mild and lack the introspective depth of psilocin. Erowid title "A Disappointing Tryptamine" suggests some users find it underwhelming relative to other 4-hydroxytryptamines.

*At common/strong doses (20–50 mg oral):* Described as psilocybin-like in character but reportedly more stimulating. Visual effects (geometry, color enhancement, tracers) reported. Community sources characterize 4-HO-MPT as more stimulating than psilocybin mushrooms (web_retrieved).

**Correspondence with seed effect profile:** The 30 effect slugs in the seed data are all consistent with the class profile of 4-hydroxytryptamine psychedelics. No contradictions found. Intensity and frequency values are absent (null/null) throughout, consistent with the limited published data.

---

## Safety & Toxicity

### Published Toxicity Data

**No substance-specific published toxicity data exists for 4-HO-MPT.** The toxic dose is unknown. No LD50 has been reported in any species. No controlled dosing study, no formal safety assessment, and no systematic adverse event surveillance has been published.

### 5-HT2B Safety Flag (Critical)

4-HO-MPT has an exceptionally high affinity for 5-HT2B receptors (Ki = **8 nM**, from Glatfelter et al. 2023 [Ref 1]). This is the highest-affinity target across the receptor panel — approximately 14-fold more potent than at 5-HT2A. Prolonged or repeated 5-HT2B agonism is associated with cardiac valvulopathy in clinical contexts (e.g., fenfluramine, ergotamine-class drugs). While this toxicity typically requires chronic exposure and 4-HO-MPT has not been specifically evaluated for cardiac risk, the potent 5-HT2B binding warrants explicit flagging as a potential long-term safety concern. **FLAG: 5-HT2B cardiac risk is theoretical class inference; no clinical data for 4-HO-MPT.**

### Adverse Event Case Reports

No published case reports of 4-HO-MPT overdose, emergency presentations, or adverse events were found in PubMed or via web search.

### Psychological Risks (Class-Level)

Based on the 4-hydroxytryptamine class:
- **HPPD (Hallucinogen Persisting Perception Disorder):** Case reports exist for psilocin (4-HO-DMT, the direct structural parent) and other serotonergic psychedelics (Espiard et al. 2005 [Ref 22]). Class-level risk applies.
- **Anxiety, paranoia, thought loops:** Common at high doses for all psychedelic tryptamines; no 4-HO-MPT-specific data.
- **Psychosis precipitation:** Theoretical risk in predisposed individuals; no 4-HO-MPT-specific data.

---

## Harm Reduction

No published harm reduction protocols specific to 4-HO-MPT exist. General principles for serotonergic psychedelics apply:

**Testing and identification:**
- 4-HO-MPT is identifiable via 1H NMR (Chapman 2017 [Ref 17] covers grey-market tryptamines analytically).
- Forensic metabolites for 4-OH-MPT detection in urine: 4-OH-MPT-glucuronide (no hydrolysis), 4-OH-MPT-N-oxide and 4-OH-PT (post-hydrolysis) — Carlier et al. 2022 [Ref 3].
- Ehrlich reagent produces a positive (purple) reaction for indole-containing tryptamines; cannot distinguish 4-HO-MPT from psilocin or other 4-hydroxytryptamines.
- Hofmann reagent may aid differentiation.

**Contraindications (published evidence, class-level):**
- Tramadol: **dangerous** (serotonergic interaction — tramadol inhibits SERT, creating additive serotonin syndrome risk with 5-HT2A agonists; Baldo 2018 [Ref 23])
- MAOIs: contraindicated (serotonin syndrome risk; MAO-A likely involved in tryptamine degradation)
- SSRIs/SNRIs: serotonin syndrome risk (mechanism overlap)
- Lithium: class-level concern (lithium + serotonergic psychedelics associated with increased seizure risk in case literature)

---

## Tolerance & Dependence

**Tolerance development:** Begins almost immediately after ingestion; mechanism is 5-HT2A receptor downregulation in the frontal cortex (de la Fuente Revenga et al. 2022 [Ref 11] — established for structurally related 5-HT2A agonists).
**Tolerance half-life:** ~3 days (to half strength)
**Full reset:** ~7 days
**Cross-tolerance:** With other serotonergic psychedelics (LSD, psilocin, DMT, etc.) via shared 5-HT2A downregulation mechanism (de la Fuente Revenga et al. 2022 [Ref 11])

**Dependence:** No dependence liability established. Not habit-forming in the pharmacological sense; consistent with the class — classical psychedelics do not produce physical dependence or compulsive drug-seeking (Tittarelli et al. 2015 [Ref 7]).

---

## Interactions

| Interacting Substance | Severity | Mechanism |
|---|---|---|
| Tramadol | Dangerous | Tramadol inhibits SERT (Baldo 2018 [Ref 23]); combined serotonin syndrome risk with 5-HT2A agonists |
| Cannabis | Unknown | No published data; theoretical potentiation of anxiety, paranoia |
| MAOIs | Dangerous (class inference) | MAO-A inhibition would amplify and prolong tryptamine effects; serotonin syndrome risk |
| SSRIs/SNRIs | Dangerous (class inference) | Serotonin syndrome risk |
| Lithium | Dangerous (class inference) | Increased seizure risk with serotonergic psychedelics |

**Note:** Tramadol interaction severity ("dangerous") in the seed data is supported by Baldo 2018 [Ref 23] for the mechanism. Cannabis interaction remains unresolved — no published data. These should be reviewed by a clinical pharmacologist for the generation step.

---

## Legal Status

### United Kingdom
**Class A** under the Misuse of Drugs Act 1971, Schedule 2. Covered by the generic tryptamine definition enacted via S.I. 2014/3277, in force from **January 7, 2015** [Ref 19, Ref 20]. The statutory language explicitly covers "any compound structurally derived from tryptamine or from a ring-hydroxy tryptamine by modification," which includes 4-hydroxytryptamines. Possession, supply, production, import, and export without a Home Office licence are unlawful.

### Germany
Controlled under the **NpSG** (Neue-psychoaktive-Stoffe-Gesetz, New Psychoactive Substances Act) effective **July 18, 2019** (web_retrieved). Production and import with intent to supply, administration to another person, and placing on the market are punishable. Possession is illegal but not punishable under NpSG.

### United States
**Not specifically scheduled** as of research date. However, 4-HO-MPT may be subject to the **Federal Analogue Act** (21 U.S.C. § 813) as a structural and pharmacological analogue of psilocin (4-HO-DMT, Schedule I). Sale for human consumption would likely be prosecutable. No DEA emergency scheduling action or Federal Register notice found for 4-HO-MPT.

### Canada
**Not explicitly controlled** under the Controlled Drugs and Substances Act (CDSA) (web_retrieved). Canada does not have a generic tryptamine scheduling provision equivalent to the UK.

### Australia
Legal status under the Therapeutic Goods Administration Poisons Standard (SUSMP) could not be confirmed from official sources during this research. The TGA Schedule 9 database was not directly accessible for verification. **FLAG: Australia status unconfirmed — editorial review required.**

---

## Clinical Trials

No clinical trials for 4-HO-MPT found on ClinicalTrials.gov (search performed: zero results). No completed or active studies.

---

## Community Feedback Analysis

No community feedback was submitted in Part A2 of the brief. No feedback items to investigate.

---

## Gaps & Flags

### Safety-Critical Flags

1. **5-HT2B cardiac flag (HIGH PRIORITY):** 4-HO-MPT has Ki = 8 nM at 5-HT2B — the highest affinity among all targets tested, 14× more potent than at 5-HT2A (Glatfelter et al. 2023 [Ref 1]). Chronic 5-HT2B agonism is linked to cardiac valvulopathy. No clinical cardiac safety assessment has been conducted for 4-HO-MPT. The generation agent should note this as an unresolved safety concern requiring research attention.

2. **Tramadol interaction "dangerous" rating (seed data):** Supported mechanistically by Baldo 2018 [Ref 23] but not confirmed via a 4-HO-MPT-specific case report. Retained as dangerous based on class mechanism.

3. **Dose ranges (seed data):** Seed data dose ranges (threshold 5 mg, common 20–30 mg) derive from community consensus (PsychonautWiki). The only primary source (TiHKAL [Ref 8]) reports dose as "unknown" and provides a single 8 mg anecdotal report with mild effects. Shulgin's speculation of 10–20 mg active range is consistent with the light dose range. The community ranges appear reasonable but are community-derived, not study-derived. **FLAG for editorial review.**

4. **Duration (seed data):** Seed data duration (total 5–7 hours) is community-derived (PsychonautWiki). Consistent with the 4-hydroxytryptamine class but unverified by any controlled study. **FLAG for editorial review.**

### Data Gaps (Not Safety-Critical)

5. **SMILES string:** Not returned by PubChem API call (JavaScript rendering issue). PubChem CID 21786584 confirmed; generation agent should retrieve canonical SMILES from CID directly.

6. **Australia legal status:** Not confirmed from official TGA Poisons Standard document. Secondary sources don't address it specifically. Requires direct lookup.

7. **CYP enzyme specifics:** No published data on which CYP enzymes metabolize 4-HO-MPT. Class inference from 4-HO-MET (CYP2D6 candidate) only [Ref 13].

8. **No controlled human pharmacology data:** No dose-finding study, no PK study, no clinical pharmacology data in humans beyond three Erowid experience reports and one TiHKAL entry at 8 mg.

9. **No in vivo mouse data for 4-HO-MPT:** Glatfelter 2023 [Ref 1] measured binding only; no HTR, locomotion, or temperature data for 4-HO-MPT specifically.

10. **Physical properties:** Melting point confirmed from TiHKAL (162–163°C, free base). No published data on water solubility, logP, pKa, or stability in solution.

11. **Stereochemistry:** 4-HO-MPT is achiral (no stereocenters). No stereoisomerism issues.

12. **CAS number discrepancy:** CAS 77872-41-4 is erroneously associated with 4-HO-MPT on some vendor sites but is the CAS for 4-HO-MET. The correct CAS for 4-HO-MPT is 763035-03-6 (Cayman Chemical).