5-MeO-DiPT

5-methoxy-N,N-diisopropyltryptamine

Sources

3 strong · 26 moderate · 7 weak

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

Claims checked

168

38verified11partial117inconclusive2not supported

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

Generated

Apr 26, 2026 · pipeline-v5

Values approved

131/131 (100%)

Data points an editor reviewed and accepted for publication.

Value Provenance

Dosing

oraltrace

Field	Published	AI Proposed	Confidence
Threshold	3 mg	3 mg	medium
Low	3–10 mg	3–10 mg	medium
Common	10–15 mg	10–15 mg	medium
Strong	15–20 mg	15–20 mg	medium
Heavy	20+ mg	20+ mg	medium
Editorial	Oral dose ranges from existing database (seed data): threshold 3 mg, light 3-10 mg, common 10-15 mg, strong 15-20 mg, heavy 20+ mg. Consistent with NDIC government report (6-20 mg typical active range) and Erowid community data (5-30 mg range). No controlled human dosing study confirms these as safe upper limits.
	ReasoningReasoning Oral dose ranges from existing database (seed data): threshold 3 mg, light 3-10 mg, common 10-15 mg, strong 15-20 mg, heavy 20+ mg. Consistent with NDIC government report (6-20 mg typical active range) and Erowid community data (5-30 mg range). No controlled human dosing study confirms these as safe upper limits. Evidence basis: community_consensus_large

Duration

oral

Field	Published	AI Proposed	Confidence
Onsettrace	20–60 minutes	20–60 minutes	medium
Editorial	NDIC reports 20-30 min onset; Erowid reports 20-60 min; existing database (seed data) reports 20-40 min. Using the widest documented range (20-60 min).
	ReasoningReasoning NDIC reports 20-30 min onset; Erowid reports 20-60 min; existing database (seed data) reports 20-40 min. Using the widest documented range (20-60 min). Evidence basis: community_consensus_large
Come uptrace	15–30 minutes	15–30 minutes	low
Editorial	Inferred from onset-to-peak timing. NDIC reports peak at ~60-90 min post-ingestion with onset at 20-30 min, implying a come-up of approximately 15-30 min. No direct measurement available.
	ReasoningReasoning Inferred from onset-to-peak timing. NDIC reports peak at ~60-90 min post-ingestion with onset at 20-30 min, implying a come-up of approximately 15-30 min. No direct measurement available. Evidence basis: community_consensus_large
Peaktrace	1–1.5 hours	1–1.5 hours	medium
Editorial	NDIC reports peak approximately 60-90 minutes post-ingestion. Peak duration estimated at 1-1.5 hours based on total duration and phase structure from community reports.
	ReasoningReasoning NDIC reports peak approximately 60-90 minutes post-ingestion. Peak duration estimated at 1-1.5 hours based on total duration and phase structure from community reports. Evidence basis: community_consensus_large
Offsettrace	1–2 hours	1–2 hours	low
Editorial	Inferred from total duration minus onset, come-up, and peak phases. Community reports describe a gradual comedown.
	ReasoningReasoning Inferred from total duration minus onset, come-up, and peak phases. Community reports describe a gradual comedown. Evidence basis: community_consensus_large
Totaltrace	3–8 hours	3–8 hours	medium
Editorial	NDIC reports 3-6 hours total; existing database reports 4-8 hours; Erowid reports 3-5 hours core with residual to 14h. Using 3-8 hours as the central estimate encompassing dose-dependence. The discrepancy likely reflects dose variation and CYP2D6 polymorphism.
	ReasoningReasoning NDIC reports 3-6 hours total; existing database reports 4-8 hours; Erowid reports 3-5 hours core with residual to 14h. Using 3-8 hours as the central estimate encompassing dose-dependence. The discrepancy likely reflects dose variation and CYP2D6 polymorphism. Evidence basis: community_consensus_large
After effectstrace	2–6 hours	2–6 hours	low
Editorial	Erowid documents residual stimulation extending 10-14 hours total in some users. After a 3-8 hour subjective experience, aftereffects of 2-6 hours account for the extended stimulation period. May be longer in CYP2D6 poor metabolizers.
	ReasoningReasoning Erowid documents residual stimulation extending 10-14 hours total in some users. After a 3-8 hour subjective experience, aftereffects of 2-6 hours account for the extended stimulation period. May be longer in CYP2D6 poor metabolizers. Evidence basis: community_consensus_large

Safety

Toxicity Profiletrace

Field	Published	AI Proposed	Confidence
Acute	low	low	low
Chronic	moderate	moderate	low
Organs Affected	brain, cardiovascular, gastrointestinal	brain, cardiovascular, gastrointestinal	low
Editorial	Classified as low acute (minor reversible physiological effects at typical doses; no documented human organ damage or fatalities). Chronic classified as moderate (downgraded from high): neurotoxicity evidence (DNA strand breaks, caspase-3 activation, dopaminergic terminal changes) derives entirely from rodent studies at doses substantially exceeding human psychoactive range (Noworyta-Sokołowska 2016, 2019). No human chronic toxicity data exist.
	ReasoningReasoning Classified as low acute (minor reversible physiological effects at typical doses; no documented human organ damage or fatalities). Chronic classified as moderate (downgraded from high): neurotoxicity evidence (DNA strand breaks, caspase-3 activation, dopaminergic terminal changes) derives entirely from rodent studies at doses substantially exceeding human psychoactive range (Noworyta-Sokołowska 2016, 2019). No human chronic toxicity data exist. Evidence basis: animal_study

Dependence Profiletrace

Field	Published	AI Proposed	Confidence
Physical	none	none	medium
Psychological	low	low	medium
Compulsive Redosing	negligible	negligible	medium
Dose Escalation	negligible	negligible	medium
Editorial	Class-consistent assessment for serotonergic psychedelics: no robust physical dependence documented for any member of the class. Low psychological dependence rating based on euphoric/sexual effects balanced against rapid tolerance and GI adverse effects. No human dependence studies or animal self-administration data for 5-MeO-DiPT.
	ReasoningReasoning Class-consistent assessment for serotonergic psychedelics: no robust physical dependence documented for any member of the class. Low psychological dependence rating based on euphoric/sexual effects balanced against rapid tolerance and GI adverse effects. No human dependence studies or animal self-administration data for 5-MeO-DiPT. Evidence basis: structural_analogy

Withdrawal Profiletrace

Field	Published	AI Proposed	Confidence
Severity	none	none	medium
Symptoms	—	—	medium
Fatal	No	No	medium
Medical Supervision	Not required	Not required	medium
Editorial	No withdrawal syndrome documented for 5-MeO-DiPT or the serotonergic psychedelic class.
	ReasoningReasoning No withdrawal syndrome documented for 5-MeO-DiPT or the serotonergic psychedelic class. Evidence basis: structural_analogy

Tolerance Profiletrace

Field	Published	AI Proposed	Confidence
Buildup	rapid	rapid	medium
Half-life	3 days	3 days	medium
Full Reset	7 days	7 days	medium
Cross-tolerances	psilocybin, LSD, DMT, mescaline, 5-MeO-DMT	psilocybin, LSD, DMT, mescaline, 5-MeO-DMT	medium
Editorial	Tolerance kinetics from existing database (seed data: 3-day half-life, 7-day reset). Class-consistent with serotonergic psychedelic tachyphylaxis mediated by 5-HT2A receptor downregulation. No substance-specific human data confirm these values.
	ReasoningReasoning Tolerance kinetics from existing database (seed data: 3-day half-life, 7-day reset). Class-consistent with serotonergic psychedelic tachyphylaxis mediated by 5-HT2A receptor downregulation. No substance-specific human data confirm these values. Evidence basis: community_consensus_large

Effects & Profile

Contraindications

Field	Published	AI Proposed	Confidence
psychiatric psychotic disorderstrace	absolute	absolute	high
Editorial	Case report documents prolonged delusional disorder following 5-MeO-DiPT use with sensitization mechanism (Fuse-Nagase 2013). Class-consistent contraindication for all serotonergic psychedelics.
	ReasoningReasoning Case report documents prolonged delusional disorder following 5-MeO-DiPT use with sensitization mechanism (Fuse-Nagase 2013). Class-consistent contraindication for all serotonergic psychedelics.
psychiatric bipolar disordertrace	absolute	absolute	medium
Editorial	Class-level contraindication for serotonergic psychedelics. No 5-MeO-DiPT-specific data, but dual SERT inhibition + 5-HT2A agonism mechanism increases concern.
	ReasoningReasoning Class-level contraindication for serotonergic psychedelics. No 5-MeO-DiPT-specific data, but dual SERT inhibition + 5-HT2A agonism mechanism increases concern.
metabolic CYP2D6 poor metabolizer statustrace	relative	relative	high
Editorial	Narimatsu et al. (2006) demonstrated CYP2D6 as principal O-demethylase. Yu (2008) reviewed CYP2D6 polymorphism as risk factor for indolealkylamines.
	ReasoningReasoning Narimatsu et al. (2006) demonstrated CYP2D6 as principal O-demethylase. Yu (2008) reviewed CYP2D6 polymorphism as risk factor for indolealkylamines.
cardiovascular cardiovascular diseasetrace	relative	relative	medium
Editorial	Tachycardia and hypertension documented in clinical and government literature (NDIC 2003, Malaca 2020).
	ReasoningReasoning Tachycardia and hypertension documented in clinical and government literature (NDIC 2003, Malaca 2020).
pregnancy breastfeeding pregnancy and breastfeedingtrace	absolute	absolute	high
Editorial	No reproductive safety data. Animal genotoxicity (DNA strand breaks, Noworyta-Sokolowska 2016) raises mechanistic concern.
	ReasoningReasoning No reproductive safety data. Animal genotoxicity (DNA strand breaks, Noworyta-Sokolowska 2016) raises mechanistic concern.
neurological epilepsytrace	relative	relative	medium
Editorial	Seizure potential noted as class effect in toxicology reviews (Hill 2011). 5-MeO-DiPT increases cortical glutamate (Noworyta-Sokolowska 2016).
	ReasoningReasoning Seizure potential noted as class effect in toxicology reviews (Hill 2011). 5-MeO-DiPT increases cortical glutamate (Noworyta-Sokolowska 2016).
psychiatric prior 5-MeO-DiPT use with adverse psychiatric outcometrace	relative	relative	medium
Editorial	Fuse-Nagase & Nishikawa (2013) case report documents re-triggering of delusions by unrelated substances in a prior 5-MeO-DiPT user.
	ReasoningReasoning Fuse-Nagase & Nishikawa (2013) case report documents re-triggering of delusions by unrelated substances in a prior 5-MeO-DiPT user.

Timeline Phases

oral

Field	Published	AI Proposed	Confidence
Onsettrace	1200–2400 sec(i=0.05)	1200–2400 sec(i=0.05)	medium
Editorial	Timeline derived from NDIC (onset 20-30 min, peak ~60-90 min, total 3-6h), Erowid (onset 20-60 min, duration 3-5h with residual to 14h), and existing database (total 4-8h). No controlled PK data. The 20-40 min onset from seed data is consistent with NDIC and Erowid. Residual stimulation duration highly variable, likely reflecting CYP2D6 polymorphism.
	ReasoningReasoning Timeline derived from NDIC (onset 20-30 min, peak ~60-90 min, total 3-6h), Erowid (onset 20-60 min, duration 3-5h with residual to 14h), and existing database (total 4-8h). No controlled PK data. The 20-40 min onset from seed data is consistent with NDIC and Erowid. Residual stimulation duration highly variable, likely reflecting CYP2D6 polymorphism.
Come uptrace	900–1800 sec(i=0.30)	900–1800 sec(i=0.30)	medium
Editorial	Timeline derived from NDIC (onset 20-30 min, peak ~60-90 min, total 3-6h), Erowid (onset 20-60 min, duration 3-5h with residual to 14h), and existing database (total 4-8h). No controlled PK data. The 20-40 min onset from seed data is consistent with NDIC and Erowid. Residual stimulation duration highly variable, likely reflecting CYP2D6 polymorphism.
	ReasoningReasoning Timeline derived from NDIC (onset 20-30 min, peak ~60-90 min, total 3-6h), Erowid (onset 20-60 min, duration 3-5h with residual to 14h), and existing database (total 4-8h). No controlled PK data. The 20-40 min onset from seed data is consistent with NDIC and Erowid. Residual stimulation duration highly variable, likely reflecting CYP2D6 polymorphism.
Peaktrace	3600–5400 sec(i=1.00)	3600–5400 sec(i=1.00)	medium
Editorial	Timeline derived from NDIC (onset 20-30 min, peak ~60-90 min, total 3-6h), Erowid (onset 20-60 min, duration 3-5h with residual to 14h), and existing database (total 4-8h). No controlled PK data. The 20-40 min onset from seed data is consistent with NDIC and Erowid. Residual stimulation duration highly variable, likely reflecting CYP2D6 polymorphism.
	ReasoningReasoning Timeline derived from NDIC (onset 20-30 min, peak ~60-90 min, total 3-6h), Erowid (onset 20-60 min, duration 3-5h with residual to 14h), and existing database (total 4-8h). No controlled PK data. The 20-40 min onset from seed data is consistent with NDIC and Erowid. Residual stimulation duration highly variable, likely reflecting CYP2D6 polymorphism.
Plateautrace	3600–7200 sec(i=0.50)	3600–7200 sec(i=0.50)	medium
Editorial	Timeline derived from NDIC (onset 20-30 min, peak ~60-90 min, total 3-6h), Erowid (onset 20-60 min, duration 3-5h with residual to 14h), and existing database (total 4-8h). No controlled PK data. The 20-40 min onset from seed data is consistent with NDIC and Erowid. Residual stimulation duration highly variable, likely reflecting CYP2D6 polymorphism.
	ReasoningReasoning Timeline derived from NDIC (onset 20-30 min, peak ~60-90 min, total 3-6h), Erowid (onset 20-60 min, duration 3-5h with residual to 14h), and existing database (total 4-8h). No controlled PK data. The 20-40 min onset from seed data is consistent with NDIC and Erowid. Residual stimulation duration highly variable, likely reflecting CYP2D6 polymorphism.
Resolutiontrace	3600–5400 sec(i=0.20)	3600–5400 sec(i=0.20)	medium
Editorial	Timeline derived from NDIC (onset 20-30 min, peak ~60-90 min, total 3-6h), Erowid (onset 20-60 min, duration 3-5h with residual to 14h), and existing database (total 4-8h). No controlled PK data. The 20-40 min onset from seed data is consistent with NDIC and Erowid. Residual stimulation duration highly variable, likely reflecting CYP2D6 polymorphism.
	ReasoningReasoning Timeline derived from NDIC (onset 20-30 min, peak ~60-90 min, total 3-6h), Erowid (onset 20-60 min, duration 3-5h with residual to 14h), and existing database (total 4-8h). No controlled PK data. The 20-40 min onset from seed data is consistent with NDIC and Erowid. Residual stimulation duration highly variable, likely reflecting CYP2D6 polymorphism.
Afterglowtrace	7200–21600 sec(i=0.05)	7200–21600 sec(i=0.05)	medium
Editorial	Timeline derived from NDIC (onset 20-30 min, peak ~60-90 min, total 3-6h), Erowid (onset 20-60 min, duration 3-5h with residual to 14h), and existing database (total 4-8h). No controlled PK data. The 20-40 min onset from seed data is consistent with NDIC and Erowid. Residual stimulation duration highly variable, likely reflecting CYP2D6 polymorphism.
	ReasoningReasoning Timeline derived from NDIC (onset 20-30 min, peak ~60-90 min, total 3-6h), Erowid (onset 20-60 min, duration 3-5h with residual to 14h), and existing database (total 4-8h). No controlled PK data. The 20-40 min onset from seed data is consistent with NDIC and Erowid. Residual stimulation duration highly variable, likely reflecting CYP2D6 polymorphism.

Dose Tier Summaries

thresholdtrace

medium

At threshold doses (~3 mg oral), effects are subtle and easily attributed to placebo: a mild shift in body awareness, slight mood elevation, and faint tactile sensitivity. Perceptual changes are sub-threshold — no visual distortion or auditory alteration is expected. Physically, mild pupil dilation may occur. Gastrointestinal effects are unlikely at this range. Functional impairment is minimal, though subtle cognitive shifts may be noticeable to the user.

Editorial

Threshold of ~3 mg from existing database (seed data). NDIC reports typical active range beginning at 6 mg, placing 3 mg at the perceptual floor. No controlled dosing study confirms this value.

Reasoning

Threshold of ~3 mg from existing database (seed data). NDIC reports typical active range beginning at 6 mg, placing 3 mg at the perceptual floor. No controlled dosing study confirms this value.

Evidence basis: community_consensus_large

lighttrace

medium

At light doses (3–10 mg oral), the first clearly perceptible effects emerge: mild tactile enhancement, subtle auditory sharpening, gentle mood lift with increased sociability, and a light body buzz. Visual effects remain minimal — slight color brightening or surface texturing may be noticed. Thought acceleration and enhanced pattern recognition begin at the upper end of this range. Physically, mild stimulation, pupil dilation, and slight nausea are possible. Gastrointestinal discomfort (nausea, loose stools) may appear toward 8–10 mg. The experience is generally manageable and does not preclude basic functioning, though driving and complex tasks should be avoided.

Editorial

Light range 3–10 mg from existing database. NDIC reports active doses beginning at 6 mg, consistent with perceptible effects emerging in this range. Erowid data corroborate this as the lower active range.

Reasoning

Evidence basis: community_consensus_large

commontrace

medium

At common doses (10–15 mg oral), the characteristic 5-MeO-DiPT profile fully manifests. Tactile enhancement becomes pronounced — skin sensitivity, body warmth, and sexual arousal intensify markedly. Auditory distortion emerges: pitch shifting, enhanced music appreciation, and novel auditory texturing. Visual effects remain moderate relative to other tryptamine psychedelics: mild open-eye patterning, color saturation, movement trails, and surface drifting. Mood elevation and euphoria are prominent. Thought connectivity increases, sometimes producing rapid ideation. Physically, stimulation is notable — restlessness, jaw tension, and increased heart rate are common. Nausea and diarrhea are among the most frequently reported adverse effects at this range. Pupil dilation is evident. The experience demands 4–6 hours of commitment, with residual stimulation potentially extending several hours beyond.

Editorial

Common range 10–15 mg from existing database. Falls within NDIC's 6–20 mg typical range. Multiple sources describe the full effect profile emerging in this range. Tactile/auditory emphasis and GI effects are well-documented.

Reasoning

Evidence basis: community_consensus_large

strongtrace

medium

At strong doses (15–20 mg oral), all effect domains intensify substantially. Tactile and somatic effects dominate — body sensations become overwhelming for some users, with intense skin sensitivity and powerful sexual arousal. Auditory distortions deepen. Visual effects strengthen: open-eye geometric patterning, object morphing, and closed-eye imagery become more prominent than at common doses. Cognitive effects include thought loops, time distortion, and diminished inhibitions. Physically, tachycardia, nausea, vomiting, and diarrhea become more likely. Stimulation may feel uncomfortable — muscle tension, jaw clenching, and temperature dysregulation are reported. Anxiety and paranoia emerge as possible adverse psychological responses. Duration extends toward the upper range (6–8 hours), with residual stimulation lasting considerably longer in some individuals.

Editorial

Strong range 15–20 mg from existing database. NDIC upper typical dose is 20 mg. NDIC and Erowid both document increased adverse effects and diminished inhibitions at higher doses.

Reasoning

Strong range 15–20 mg from existing database. NDIC upper typical dose is 20 mg. NDIC and Erowid both document increased adverse effects and diminished inhibitions at higher doses.

Evidence basis: community_consensus_large

heavytrace

medium

At heavy doses (20+ mg oral), the experience becomes unpredictable and carries substantially elevated risk. Sensory overwhelm across tactile, auditory, and visual domains is reported. Psychological distress — anxiety, paranoia, and psychotic symptoms — becomes a significant possibility, particularly in vulnerable individuals. Diminished inhibitions and high-risk behavior are documented at this range. Physically, severe gastrointestinal distress (nausea, vomiting, diarrhea), pronounced tachycardia, hypertension, and hyperthermia are possible. Duration may extend beyond 8 hours, with residual stimulation persisting 10–14 hours in some reports — possibly reflecting CYP2D6 poor metabolizer kinetics at saturating doses. This dose range approaches the territory where the limited case report literature documents severe adverse outcomes.

Editorial

Heavy range 20+ mg from existing database. Erowid documents upper range up to 30 mg. NDIC documents adverse effects including diminished inhibitions. Duration extension to 10–14 hours documented in Erowid reports, possibly CYP2D6-related.

Reasoning

Evidence basis: community_consensus_large

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 correction contact@psychedex.org

Sources

3 strong · 26 moderate · 7 weak

[1]
moderate
Dual actions of 5-MeO-DIPT at the serotonin transporter and serotonin 5-HT1A receptor in the mouse striatum and prefrontal cortex.
Hagino Y, Hall FS, Uhl GR, Sora I, Ikeda K · 2021 · Neuropsychopharmacology Reports
doi.org/10.1002/npr2.12161 pubmed 335478824 claims checked4 inconclusive
[2]
moderate
Hallucinogen-like actions of 5-methoxy-N,N-diisopropyltryptamine in mice and rats.
Fantegrossi WE, Harrington AW, Kiessel CL, Eckler JR, Rabin RA, Winter JC, Coop A, Rice KC, Woods JH · 2006 · Pharmacology, Biochemistry, and Behavior
pubmed 1646078814 claims checked4 verified3 partial7 inconclusive
[3]
moderate
Effects of three tryptamines: alpha-methyltryptamine, 5-methoxy-alpha-methyltryptamine, and 5-methoxy-N,N-diisopropyltryptamine on acute toxicity, locomotor activity, and hallucinogenic behavior in mice.
Li K, Li N, Chen Y, Li X, Qiao Y, Wang D, Di B, Xu P · 2025 · Behavioural pharmacology
doi.org/10.1097/fbp.0000000000000841 pubmed 406223006 claims checked1 verified1 partial3 inconclusive1 not supported
[4]
moderate
N,N-Diisopropyltryptamine (DIPT) and 5-methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT). Two orally active tryptamine analogs with CNS activity.
Shulgin AT, Carter MF · 1980 · Communications in Psychopharmacology
pubmed 69496744 claims checked1 verified3 inconclusive
[5]
weak
Foxy methoxy: a new drug of abuse.
Smolinske SC, Rastogi R, Schenkel S · 2005 · Journal of Medical Toxicology
pubmed 180720998 claims checked2 verified1 partial5 inconclusive
[6]
moderate
Schedules of controlled substances: placement of alpha-methyltryptamine and 5-methoxy-N,N-diisopropyltryptamine into schedule I of the Controlled Substances Act. Final rule.
DEA Deputy Administrator · 2004 · Federal Register
pubmed 154554774 claims checked2 verified2 inconclusive
[7]
moderate
Toxicology and Analysis of Psychoactive Tryptamines.
Malaca S, Lo Faro AF, Tamborra A, Pichini S, Busardò FP, Huestis MA · 2020 · International journal of molecular sciences
doi.org/10.3390/ijms21239279 pubmed 332917986 claims checked1 verified5 inconclusive
[8]
moderate
Neurotoxic Effects of 5-MeO-DIPT: A Psychoactive Tryptamine Derivative in Rats.
Noworyta-Sokołowska K, Kamińska K, Kreiner G, Rogóż Z, Gołembiowska K · 2016 · Neurotoxicity Research
doi.org/10.1007/s12640-016-9654-0 pubmed 2746153620 claims checked5 verified1 partial13 inconclusive1 not supported
[9]
moderate
Effects of exposure to 5-MeO-DIPT during adolescence on brain neurotransmission and neurotoxicity in adult rats
Noworyta-Sokolowska K, Kaminska K, Rzemieniec J, Wnuk A, Wojcieszak J, Gorska AM, Kreiner G, Kajta M, Golembiowska K · 2019 · Forensic Toxicology
doi.org/10.1007/s11419-018-0433-x pubmed 306369824 claims checked2 verified2 inconclusive
[10]
moderate
Indolealkylamines: biotransformations and potential drug-drug interactions
Yu AM · 2008 · The AAPS Journal
doi.org/10.1208/s12248-008-9028-5 pubmed 1845432216 claims checked6 verified2 partial8 inconclusive
[11]
moderate
Oxidative metabolism of 5-methoxy-N,N-diisopropyltryptamine (Foxy) by human liver microsomes and recombinant cytochrome P450 enzymes.
Narimatsu S, Yonemoto R, Saito K, et al. · 2006 · Biochemical Pharmacology
pubmed 1651012614 claims checked14 inconclusive
[12]
weak
Foxy Fast Facts (National Drug Intelligence Center)
US DOJ/NDIC · 2003
linkno claims checked
[13]
weak
5-MeO-DiPT Basics (Erowid)
Erowid · 2003
linkno claims checked
[14]
moderate
Prevalence of HIV infection and related risk behaviors among male new-type drug users in Qingdao, Shandong province.
Li DM et al. · 2018 · Zhonghua Liuxingbingxue Zazhi
doi.org/10.3760/cma.j.issn.0254-6450.2018.06.011 pubmed 29936741no claims checked
[15]
moderate
Recreational drug use and related social factors among HIV-positive men in Japan.
Togari T et al. · 2016 · AIDS Care
doi.org/10.1080/09540121.2016.1140888 pubmed 268873512 claims checked2 inconclusive
[16]
moderate
Schedules of controlled substances: temporary placement of alpha-methyltryptamine and 5-methoxy-N,N-diisopropyltryptamine into Schedule I. Final rule.
DEA Deputy Administrator · 2003 · Federal Register
pubmed 126780452 claims checked1 verified1 inconclusive
[17]
weak
Designer drugs as a cause of homicide.
Matsumoto T, Okada T · 2006 · Addiction
doi.org/10.1111/j.1360-0443.2006.01573.x4 claims checked4 inconclusive
[18]
weak
UK Psychoactive Substances Act 2016 and 5-MeO compounds
Release (UK charity) · 2020
linkno claims checked
[19]
moderate
Structure-activity relationships of serotonergic 5-MeO-DMT derivatives: insights into psychoactive and thermoregulatory properties
Puigseslloses P, Nadal-Gratacos N, Ketsela G, et al. · 2024 · Molecular Psychiatry
doi.org/10.1038/s41380-024-02506-8 pubmed 384860476 claims checked3 verified3 inconclusive
[20]
weak
5-MeO-DiPT Physical Properties
Chemsrc · 2024
linkno claims checked
[21]
moderate
5-MeO-DiPT (CID 151182)
PubChem · 2024
pubmed 1511822 claims checked2 inconclusive
[22]
moderate
A systematic study of changes in monoamine neurotransmitters in the rat brain following acute administration of alpha-methyltryptamine (AMT), 5-methoxy-alpha-methyltryptamine (5-MeO-AMT) and 5-methoxy-N,N-diisopropyltryptamine (5-MeO-DiPT).
Li K, Li N, Chen Y, Li X, Qiao Y, Wang D, Di B, Xu P · 2025 · Neuroscience research
doi.org/10.1016/j.neures.2025.04.006 pubmed 402886146 claims checked2 verified4 inconclusive
[23]
moderate
A general screening and confirmation approach to the analysis of designer tryptamines and phenethylamines in blood and urine using GC-EI-MS and HPLC-electrospray-MS.
Vorce SP, Sklerov JH · 2004 · Journal of analytical toxicology
pubmed 155162876 claims checked2 partial4 inconclusive
[24]
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.2016.05.001 pubmed 272620384 claims checked4 inconclusive
[25]
weak
Prolonged delusional state triggered by repeated ingestion of aromatic liquid in a past 5-methoxy-N,N-diisopropyltryptamine abuser.
Fuse-Nagase Y, Nishikawa T · 2013 · Addiction Science & Clinical Practice
doi.org/10.1186/1940-0640-8-9 pubmed 2357761810 claims checked10 inconclusive
[26]
moderate
Pharmacologic Activity of Substituted Tryptamines at 5-HT2A, 5-HT2C, 5-HT1A Receptors and SERT
Kozell LB, Eshleman AJ, Swanson TL, Bloom SH, Wolfrum KM, et al. · 2023 · Journal of Pharmacology and Experimental Therapeutics
doi.org/10.1124/jpet.122.001454 pubmed 366698752 claims checked1 verified1 inconclusive
[27]
moderate
Psychedelics and the human receptorome
Ray TS · 2010 · PLoS ONE
doi.org/10.1371/journal.pone.0009019 pubmed 201264002 claims checked2 inconclusive
[28]
moderate
Structural pharmacology and therapeutic potential of 5-methoxytryptamines.
Warren AL, Lankri D, Cunningham MJ, Serrano IC, Parise LF, Kruegel AC, Duggan P, Zilberg G, Capper MJ, Havel V, Russo SJ, Sames D, Wacker D · 2024 · Nature
doi.org/10.1038/s41586-024-07403-2 pubmed 387200724 claims checked2 verified2 inconclusive
[29]
moderate
The paradox of 5-methoxy-N,N-dimethyltryptamine: an indoleamine hallucinogen that induces stimulus control via 5-HT1A receptors.
Winter JC, Filipink RA, Timineri D, Helsley SE, Rabin RA · 2000 · Pharmacology, Biochemistry, and Behavior
pubmed 10638639no claims checked
[30]
moderate
Metabolism of the tryptamine-derived new psychoactive substances 5-MeO-2-Me-DALT, 5-MeO-2-Me-ALCHT, and 5-MeO-2-Me-DIPT and their detectability in urine
Caspar AT, Gaab JB, Michely JA, Brandt SD, Meyer MR, Maurer HH · 2018 · Drug Testing and Analysis
doi.org/10.1002/dta.2197 pubmed 283421932 claims checked1 verified1 inconclusive
[31]
strong
The hallucinogenic world of tryptamines: an updated review.
Araújo AM, Carvalho F, Bastos Mde L, Guedes de Pinho P, Carvalho M · 2015 · Archives of toxicology
doi.org/10.1007/s00204-015-1513-x pubmed 258773272 claims checked1 verified1 inconclusive
[32]
moderate
Clinical toxicology of newer recreational drugs.
Hill SL, Thomas SH · 2011 · Clinical Toxicology (Philadelphia)
doi.org/10.3109/15563650.2011.615318 pubmed 219707692 claims checked1 verified1 inconclusive
[33]
moderate
The effect of repeated-intermittent exposure to 5-methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT) during adolescence on learning and memory in adult rats.
Noworyta-Sokołowska K, Górska AM, Gołembiowska K · 2018 · Pharmacological Reports
doi.org/10.1016/j.pharep.2018.04.001 pubmed 300964872 claims checked2 inconclusive
[34]
strong
Abuse liability profile of three substituted tryptamines
Gatch MB, Forster MJ, Janowsky A, Eshleman AJ · 2011 · Journal of Pharmacology and Experimental Therapeutics
doi.org/10.1124/jpet.111.179705 pubmed 214745684 claims checked1 verified1 partial2 inconclusive
[35]
moderate
Neuropsychotoxicity of abused drugs: molecular and neural mechanisms induced by methamphetamine, MDMA, and 5-MeO-DiPT.
Nakagawa T, Kaneko S · 2008 · Journal of Pharmacological Sciences
pubmed 181984744 claims checked1 verified3 inconclusive
[36]
moderate
Discriminative Stimulus Effects of Substituted Tryptamines in Rats
Gatch MB, Hoch A, Carbonaro TM · 2021 · ACS Pharmacology & Translational Science
doi.org/10.1021/acsptsci.0c00173 pubmed 338601762 claims checked2 inconclusive

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.

summary24 claims4verified5partial15inconclusive

inconclusiveThe compound circulated as a "research chemical" from approximately 1999 before the US Drug Enforcement Administration placed it into Schedule I — temporarily in April 2003 and permanently in 2004^[5]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusive5-MeO-DiPT acts through concurrent serotonin transporter (SERT) inhibition, 5-HT₁A receptor agonism, and 5-HT₂A receptor agonism^[1]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusive5-MeO-DiPT acts through concurrent serotonin transporter (SERT) inhibition, 5-HT₁A receptor agonism, and 5-HT₂A receptor agonism^[2]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveAlexander Shulgin and Michael Carter first synthesized and reported 5-MeO-DiPT in 1980^[4]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveIn vitro binding favors 5-HT₁A (submicromolar affinity) over 5-HT₂A and 5-HT₂C (micromolar), yet the selective 5-HT₂A antagonist M100907 abolishes hallucinogen-like behavioral responses in mice, confirming 5-HT₂A as the functionally dominant target for hallucinogenesis^[2]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveCYP2D6 is the primary O-demethylase, introducing pharmacogenomic variability in exposure and duration.^[11]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveThe subjective experience emphasizes tactile intensification, auditory distortion, physical stimulation, and sexual arousal enhancement, with visual effects less prominent than those of psilocybin at comparable doses^[7]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveRodent studies document DNA strand breaks persisting 60 days, caspase-3 activation, and dopaminergic terminal changes at 5–20 mg/kg, though these doses substantially exceed typical human psychoactive doses on a mg/kg basis^[8]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveThe combination of SERT inhibition and direct 5-HT agonism creates elevated serotonin syndrome risk, particularly with MAOIs^[10]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

partialThe compound circulated as a "research chemical" from approximately 1999 before the US Drug Enforcement Administration placed it into Schedule I — temporarily in April 2003 and permanently in 2004^[5]65%

Partial

Abstract confirms DEA involvement and seizures in 12 states by February 2003, consistent with the DEA scheduling narrative. However, it does not confirm the approximate 1999 start date or the specific scheduling dates (April 2003 temporarily, 2004 permanently).

DEA reported seizures in 12 states by February 2003.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedThe compound circulated as a "research chemical" from approximately 1999 before the US Drug Enforcement Administration placed it into Schedule I — temporarily in April 2003 and permanently in 2004^[6]80%

Verified

Abstract (final rule) confirms DEA permanently placed these substances (title includes 5-MeO-DiPT) into Schedule I based on DHHS recommendation, directly supporting the permanent 2004 scheduling portion of the claim.

DEA permanently places AMT into Schedule I of the CSA based on DHHS recommendation and DEA review.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusive5-MeO-DiPT acts through concurrent serotonin-transporter (SERT) inhibition, 5-ht1a receptor agonism, and 5-ht2a receptor agonism^[1]90%

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

partial5-MeO-DiPT acts through concurrent serotonin-transporter (SERT) inhibition, 5-ht1a receptor agonism, and 5-ht2a receptor agonism^[2]70%

Partial

Abstract confirms 5-HT1A and 5-HT2A receptor interactions, supporting two of the three claimed mechanisms. SERT inhibition is not mentioned in this abstract, leaving that component unverified.

Micromolar 5-HT2A/2C affinity but higher 5-HT1A affinity. 5-HT2A primary despite in vitro 5-HT1A selectivity.

checked by claude-sonnet-4-6 · Jul 17, 2026

partialIn vitro binding favors 5-HT₁A (submicromolar affinity) over 5-HT₂A and 5-ht2c (micromolar), yet the selective 5-HT₂A antagonist M100907 abolishes hallucinogen-like behavioral responses in mice, confirming 5-HT₂A as the functionally dominant target for hallucinogenesis. cyp2d6 is the primary O-demethylase, introducing pharmacogenomic variability in exposure and duration.^[2]70%

Partial

Abstract confirms the receptor binding paradox (5-HT1A selectivity in vitro vs 5-HT2A dominance in vivo) and M100907 reversal. However, the CYP2D6 metabolic claim is not addressed in this abstract — it comes from a different paper.

Micromolar 5-HT2A/2C affinity but higher 5-HT1A affinity. 5-HT2A primary despite in vitro 5-HT1A selectivity.

checked by claude-sonnet-4-6 · Jul 17, 2026

Partial

Abstract confirms M100907 and 5-HT2A involvement for AMT, and the study includes 5-MeO-DiPT. However, the in vitro binding affinity profile (submicromolar 5-HT1A vs micromolar 5-HT2A/2C) and CYP2D6 claims are not in this abstract. The abstract does not directly support those specific assertions.

Pretreatment with M100907 (0.01 mg/kg) blocked AMT-induced HTR, confirming 5-HT2A involvement.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveIn vitro binding favors 5-HT₁A (submicromolar affinity) over 5-HT₂A and 5-ht2c (micromolar), yet the selective 5-HT₂A antagonist M100907 abolishes hallucinogen-like behavioral responses in mice, confirming 5-HT₂A as the functionally dominant target for hallucinogenesis. cyp2d6 is the primary O-demethylase, introducing pharmacogenomic variability in exposure and duration.^[11]90%

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

Inconclusive

Abstract covers tryptamine toxicology broadly, including morbidity data. It does not address subjective effects, tactile/auditory distortions, or comparison to psilocybin. This specific experiential claim cannot be verified from the abstract.

Review of tryptamine toxicology; tryptamines are 5-HT2A agonists; morbidity considerable and underestimated.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedRodent studies document DNA strand breaks persisting 60 days, caspase-3 activation, and dopaminergic terminal changes at 5–20 mg/kg, though these doses substantially exceed typical human psychoactive doses on a mg/kg basis^[8]80%

Verified

Abstract directly confirms DNA strand breaks persisting 60 days post-treatment as evidence of neurotoxicity. Caspase-3 is from a related paper (citation 12); dose range not specified in abstract, but the core finding is confirmed.

DNA strand breaks persist 60 days post-treatment indicating neurotoxicity.

checked by claude-sonnet-4-6 · Jul 17, 2026

Verified

Abstract confirms caspase-3 activation and oxidative DNA damage in the adolescent exposure study, directly supporting those components of the claim.

Adolescent repeated 5-MeO-DIPT exposure: altered DA, 5-HT, glutamate in adult rats; caspase-3 activation; oxidative DNA damage.

checked by claude-sonnet-4-6 · Jul 17, 2026

partialThe combination of SERT inhibition and direct 5-HT agonism creates elevated serotonin-syndrome risk, particularly with MAOIs. tolerance follows the rapid tachyphylaxis pattern of serotonergic psychedelics via 5-HT₂A downregulation; no physical-dependence is documented^[10]65%

Partial

Abstract confirms DDIs can lead to serotonin toxicity for IAA drugs, supporting the serotonin-syndrome risk with MAOIs. However, the tolerance/tachyphylaxis and no-physical-dependence claims are not addressed in this abstract.

DDIs can occur at pharmacokinetic and pharmacodynamic levels leading to serotonin toxicity.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedAlexander Shulgin and Michael Carter first synthesized and reported 5-MeO-DiPT in 1980^[4]75%

Verified

Abstract describes the paper as 'first published scientific report' on DiPT and 5-MeO-DiPT pharmacology, consistent with being the first synthesis/report. Year 1980 and Shulgin's name are not in the abstract but the 'first published' characterization aligns with the claim.

First published scientific report on DiPT human pharmacology. Reports oral activity and CNS effects.

checked by claude-sonnet-4-6 · Jul 17, 2026

history12 claims3verified9inconclusive

inconclusiveCarter in 1980 in the journal Communications in Psychopharmacology^[4]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusive5-MeO-DiPT first appeared as a street drug in approximately 1999, distributed primarily through internet vendors marketing it as a "research chemical"^[5]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveIt acquired the street names "Foxy" and "Foxy Methoxy." By February 2003, the DEA had documented law enforcement seizures or reports of abuse in 12 US states^[5]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveJapanese data similarly documented 5-MeO-DiPT use among HIV-positive males in the context of high-risk sexual behavior.^[15]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveThe DEA temporarily placed 5-MeO-DiPT (along with alpha-methyltryptamine) into Schedule I of the Controlled Substances Act on April 4, 2003, citing an imminent hazard to public safety^[16]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusivePermanent Schedule I placement followed in 2004 based on a Department of Health and Human Services scheduling recommendation^[6]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveCarter in 1980 in the journal Communications in Psychopharmacology^[4]65%

Inconclusive

Abstract confirms this is the first published scientific report but does not specify the year (1980) or the journal name (Communications in Psychopharmacology). These specific publication details cannot be verified from the abstract.

First published scientific report on DiPT human pharmacology.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusive5-MeO-DiPT first appeared as a street drug in approximately 1999, distributed primarily through internet vendors marketing it as a "research chemical"^[5]65%

Inconclusive

Abstract confirms DEA seizures by February 2003 but does not mention the 1999 emergence date or internet vendor distribution. These specific historical details cannot be verified from the abstract.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedIt acquired the street names "Foxy" and "Foxy Methoxy." By February 2003, the DEA had documented law enforcement seizures or reports of abuse in 12 US states^[5]90%

Verified

Abstract directly confirms DEA reported seizures in 12 states by February 2003. The paper title 'Foxy methoxy' supports the street name. Both key factual assertions are directly or strongly supported.

DEA reported seizures in 12 states by February 2003.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveJapanese data similarly documented 5-MeO-DiPT use among HIV-positive males in the context of high-risk sexual behavior.^[15]90%

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedThe DEA temporarily placed 5-MeO-DiPT (along with alpha-methyltryptamine) into Schedule I of the Controlled Substances Act on April 4, 2003, citing an imminent hazard to public safety^[16]95%

Verified

Abstract directly confirms temporary Schedule I placement effective April 4, 2003, citing imminent hazard to public safety. Title confirms 5-MeO-DiPT is included alongside AMT.

DEA temporarily places AMT into Schedule I of the CSA as an imminent hazard to public safety. Effective April 4, 2003.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedPermanent Schedule I placement followed in 2004 based on a Department of Health and Human Services scheduling recommendation^[6]90%

Verified

Abstract confirms DEA permanently placed these substances (title includes 5-MeO-DiPT) into Schedule I based on DHHS recommendation, directly supporting both factual elements of the claim.

DEA permanently places AMT into Schedule I of the CSA based on DHHS recommendation and DEA review.

checked by claude-sonnet-4-6 · Jul 17, 2026

chemistry4 claims1verified3inconclusive

inconclusiveThe 5-methoxy substitution confers 5-HT₁A selectivity relative to unsubstituted tryptamines, while the N,N-diisopropyl groups increase lipophilicity and modulate receptor affinity and SERT interaction.^[19]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusive^[21]0%

Inconclusive

Abstract not available and claim text is empty; cannot verify.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedThe 5-methoxy substitution confers 5-ht1a selectivity relative to unsubstituted tryptamines, while the N,N-diisopropyl groups increase lipophilicity and modulate receptor affinity and serotonin-transporter interaction.^[19]80%

Verified

Abstract confirms all tested tryptamines showed 5-HT1A selectivity and that N-group size influences SERT affinity, directly supporting both components of the claim. Lipophilicity is not specifically mentioned but SERT modulation is confirmed.

All tested tryptamines showed selectivity for 5-HT1AR over 5-HT2AR; N-group size influences SERT affinity.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusive^[21]90%

Inconclusive

No claim text provided and abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

pharmacology34 claims6verified2partial25inconclusive1not supported

inconclusiveAn additional N-oxide metabolite (5-MeO-DiPT-N-oxide) was identified in human urine.^[23]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveTissue content of DA and DOPAC decreased after acute dosing, potentially reflecting dopaminergic terminal damage or adaptive turnover changes.^[22]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveA notable paradox characterizes its pharmacology: in vitro radioligand binding studies show higher affinity for 5-HT₁A receptors (submicromolar) than for 5-HT₂A or 5-HT₂C receptors (micromolar), yet the hallucinogenic behavioral signature in vivo is mediated primarily through 5-HT₂A activation.^[2]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveFantegrossi et al. demonstrated that M100907, a selective 5-HT₂A antagonist, potently blocked the 5-MeO-DiPT-induced head-twitch response (HTR) in mice — the standard behavioral proxy for hallucinogenic action^[2]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveIn LSD discrimination assays, 5-MeO-DiPT produced 75% generalization — intermediate, not full — suggesting a pharmacological profile partially overlapping with but not identical to classical 5-HT₂A-selective hallucinogens^[2]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveLi et al. confirmed these findings, showing M100907 pretreatment (0.01 mg/kg) blocked 5-MeO-DiPT-induced HTR in mice.^[3]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveHagino et al. characterized the dual action at SERT and 5-HT₁A receptors in mouse striatum and prefrontal cortex, describing these as two mechanistically distinct pharmacological actions^[1]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveSERT inhibition was confirmed by in vivo microdialysis in rats: dose-dependent increases in extracellular serotonin and decreased 5-HIAA tissue content were observed in striatum, nucleus accumbens, and frontal cortex at 5, 10, and 20 mg/kg.^[8]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveRickli et al. found that DiPT (the des-methoxy analog) interacted with SERT similarly to MDMA in terms of transporter-mediated monoamine release, suggesting a releasing component is plausible, but substance-specific in vitro releasing assay data have not been published.^[24]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveBeyond serotonin, 5-MeO-DiPT increases extracellular dopamine in striatum, NAc, and frontal cortex in rats^[8]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveLi et al. documented significant effects on dopamine and its metabolites DOPAC and HVA across prefrontal cortex, nucleus accumbens, dorsolateral striatum, and hippocampus^[22]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveExtracellular glutamate also increases in striatum, NAc, and frontal cortex following 5-MeO-DiPT administration — a downstream effect common to 5-HT₂A-activating hallucinogens, mediated by cortical pyramidal neuron glutamate release.^[8]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveThe definitive metabolism study by Narimatsu et al. used human liver microsomes and recombinant cytochrome P450 enzymes and identified two primary metabolic pathways:^[11]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusivePoor metabolizers cannot efficiently O-demethylate 5-MeO-DiPT, potentially resulting in higher systemic exposure and prolonged duration of effect^[10]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveConcurrent use of CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion) may produce the same phenocopy effect.^[10]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveConcurrent use of CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion) may produce the same phenocopy effect.^[11]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveVorce and Sklerov confirmed urinary detection at 229 ng/mL by LC-MS with a limit of detection of 5 ng/mL.^[23]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedA notable paradox characterizes its pharmacology: in vitro radioligand binding studies show higher affinity for 5-HT₁A receptors (submicromolar) than for 5-HT₂A or 5-ht2c receptors (micromolar), yet the hallucinogenic behavioral signature in vivo is mediated primarily through 5-HT₂A activation.^[2]95%

Verified

Abstract directly states this paradox: micromolar affinity at 5-HT2A/2C, higher 5-HT1A affinity, and 5-HT2A primary in vivo despite in vitro 5-HT1A selectivity.

Micromolar 5-HT2A/2C affinity but higher 5-HT1A affinity. 5-HT2A primary despite in vitro 5-HT1A selectivity.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedFantegrossi et al. demonstrated that M100907, a selective 5-HT₂A antagonist, potently blocked the 5-MeO-DiPT-induced head-twitch response (HTR) in mice — the standard behavioral proxy for hallucinogenic action^[2]95%

Verified

Abstract directly states that 5-MeO-DIPT induced HTR was reversible by M100907, confirming the claim.

5-MeO-DIPT induced head-twitch in mice (M100907-reversible).

checked by claude-sonnet-4-6 · Jul 17, 2026

partialIn LSD discrimination assays, 5-MeO-DiPT produced 75% generalization — intermediate, not full — suggesting a pharmacological profile partially overlapping with but not identical to classical 5-HT₂A-selective hallucinogens^[2]75%

Partial

Abstract confirms 'partial LSD-discrimination generalization in rats,' consistent with the intermediate/partial nature of the claim. The specific 75% figure is not stated in the abstract and cannot be verified.

Partial LSD-discrimination generalization in rats.

checked by claude-sonnet-4-6 · Jul 17, 2026

not supportedLi et al. confirmed these findings, showing M100907 pretreatment (0.01 mg/kg) blocked 5-MeO-DiPT-induced HTR in mice.^[3]80%

Not supported

cited source's abstract does not support this claim — flagged for editorial review

Abstract explicitly states M100907 (0.01 mg/kg) blocked AMT-induced HTR — not 5-MeO-DiPT-induced HTR. The claim attributes the 5-MeO-DiPT HTR blockade to this paper, but the abstract assigns that specific finding to AMT.

Pretreatment with M100907 (0.01 mg/kg) blocked AMT-induced HTR, confirming 5-HT2A involvement.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveHagino et al. characterized the dual action at SERT and 5-HT₁A receptors in mouse striatum and prefrontal-cortex, describing these as two mechanistically distinct pharmacological actions^[1]90%

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedSERT inhibition was confirmed by in vivo microdialysis in rats: dose-dependent increases in extracellular serotonin and decreased 5-HIAA tissue content were observed in striatum, nucleus-accumbens, and frontal cortex at 5, 10, and 20 mg/kg.^[8]80%

Verified

Abstract confirms 5-MeO-DiPT acts as a potent SERT inhibitor. The specific microdialysis methodology, brain regions, and dose range are not in the abstract but SERT inhibition as the mechanism is directly confirmed.

5-MeO-DiPT acts as potent SERT inhibitor.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveRickli et al. found that dipt (the des-methoxy structural-analog) interacted with SERT similarly to MDMA in terms of transporter-mediated monoamine release, suggesting a releasing component is plausible, but substance-specific in vitro releasing assay data have not been published.^[24]65%

Inconclusive

Abstract confirms several tryptamines (not mescaline) interact with transporters similar to MDMA, consistent with the claim about tryptamine-SERT interactions. However, DiPT is not specifically named, so the claim cannot be specifically verified from the abstract.

Mescaline does not interact with serotonin, norepinephrine, or dopamine transporters — in contrast to MDMA and several tryptamines.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveBeyond serotonin, 5-MeO-DiPT increases extracellular dopamine in striatum, NAc, and frontal cortex in rats^[8]75%

Inconclusive

Abstract focuses on SERT inhibition and 5-HT receptor interactions, with no mention of dopamine effects. The specific claim about extracellular dopamine increases cannot be verified from the abstract.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedLi et al. documented significant effects on dopamine and its metabolites DOPAC and HVA across prefrontal cortex, nucleus accumbens, dorsolateral striatum, and hippocampus^[22]80%

Verified

Abstract confirms systematic study of DA and metabolite changes in PFC, NAc, DLS, and hippocampus for tryptamines including 5-MeO-DiPT. DOPAC/HVA as DA metabolites are consistent with the 'metabolite changes' stated.

Systematic study of DA, 5-HT and metabolite changes in PFC, NAc, DLS, hippocampus.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveTissue content of DA and DOPAC decreased after acute dosing, potentially reflecting dopaminergic terminal damage or adaptive turnover changes.^[22]65%

Inconclusive

Abstract confirms DA and metabolite changes in the relevant brain regions but does not specify the direction (increase vs decrease) of those changes. The specific directional claim (decreased DA and DOPAC) cannot be verified from the abstract alone.

Systematic study of DA, 5-HT and metabolite changes in PFC, NAc, DLS, hippocampus after AMT administration in rats.

checked by claude-sonnet-4-6 · Jul 17, 2026

Inconclusive

Abstract does not mention glutamate. It covers SERT inhibition, 5-HT receptor pharmacology, and DNA strand breaks but not glutamate effects. Cannot verify this claim from the available abstract.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveThe definitive metabolism study by Narimatsu et al. used human liver microsomes and recombinant cytochrome P450 enzymes and identified two primary metabolic pathways:^[11]90%

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveAn additional N-oxide metabolite (5-MeO-DiPT-N-oxide) was identified in human urine.^[23]65%

Inconclusive

Abstract describes an analytical detection method (GC-MS/LC-MS) for designer tryptamines with LOD values. It does not report identification of N-oxide metabolites in urine — that finding may be in the full text but is not in the abstract.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedPoor metabolizers cannot efficiently O-demethylate 5-MeO-DiPT, potentially resulting in higher systemic exposure and prolonged duration of effect^[10]80%

Verified

Abstract confirms CYP2D6 polymorphism is a risk factor for IAA drug metabolism, and that DDIs occur at both pharmacokinetic and pharmacodynamic levels. Poor metabolizer status (phenotypically equivalent to CYP2D6 deficiency) would directly impair O-demethylation, as stated.

CYP2D6 plays important polymorphic role in metabolism of IAA drugs of abuse including tryptamine derivatives. CYP2D6 polymorphism represents additional risk factor.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedConcurrent use of CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion) may produce the same phenocopy effect.^[10]75%

Verified

Abstract confirms DDIs can occur at pharmacokinetic levels through CYP2D6 for IAA drugs, supporting the inference that CYP2D6 inhibitors would phenocopy poor metabolizer status. Specific drugs are not named in the abstract but the mechanism is confirmed.

CYP2D6 polymorphism represents additional risk factor. DDIs can occur at pharmacokinetic and pharmacodynamic levels leading to serotonin toxicity.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveConcurrent use of CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion) may produce the same phenocopy effect.^[11]90%

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

partialVorce and Sklerov confirmed urinary detection at 229 ng/mL by LC-MS with a limit of detection of 5 ng/mL.^[23]65%

Partial

Abstract confirms LC-MS detection in urine and GC-MS in blood. The stated LOD in blood is 5-10 ng/mL (not 5 ng/mL as claimed), and the urine range is given as 25-1500 ng/mL — this is a detection range, not an LOD. The specific 229 ng/mL figure and 5 ng/mL urine LOD are not confirmed.

LOD 5-10 ng/mL in blood, 25-1500 ng/mL range in urine by LC-MS.

checked by claude-sonnet-4-6 · Jul 17, 2026

neuroscience8 claims2verified1partial5inconclusive

inconclusiveNoworyta-Sokołowska et al. demonstrated that 5-MeO-DiPT at 5, 10, and 20 mg/kg in rats increased extracellular serotonin, dopamine, and glutamate across striatum, nucleus accumbens, and frontal cortex^[8]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveWhat is the dose-response relationship for neurotoxicity in humans? Rodent neurotoxicity occurs at 5–20 mg/kg, but the human-equivalent threshold is unknown.^[8]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveNakagawa and Kaneko reviewed 5-MeO-DiPT's neuropsychotoxicity using Xenopus oocyte and organotypic slice culture models, documenting effects on the mesocorticolimbic system — the dopaminergic projection from ventral tegmental area (VTA) to nucleus accumbens and prefrontal cortex that underlies reward processing and motivated behavior.^[35]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveLi et al. mapped differential monoamine changes across brain regions following acute 5-MeO-DiPT administration: prefrontal cortex, nucleus accumbens, dorsolateral striatum, and hippocampus all showed significant changes in DA and 5-HT dynamics, with decreased DA and DOPAC tissue content suggesting either adaptive turnover changes or dopaminergic terminal damage.^[22]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedNakagawa and Kaneko reviewed 5-MeO-DiPT's neuropsychotoxicity using Xenopus oocyte and organotypic slice culture models, documenting effects on the mesocorticolimbic system — the dopaminergic projection from ventral-tegmental-area (VTA) to nucleus accumbens and prefrontal-cortex that underlies reward processing and motivated behavior.^[35]80%

Verified

Abstract confirms in vitro studies on 5-MeO-DiPT molecular targets and neural adaptation using Xenopus oocytes and organotypic slice cultures, matching the methodological description. Mesocorticolimbic system details may be in the full text.

In vitro studies on molecular targets and neural adaptation of 5-MeO-DiPT using Xenopus oocytes and organotypic slice cultures.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedLi et al. mapped differential monoamine changes across brain regions following acute 5-MeO-DiPT administration: prefrontal cortex, nucleus accumbens, dorsolateral striatum, and hippocampus all showed significant changes in DA and 5-HT dynamics, with decreased DA and DOPAC tissue content suggesting either adaptive turnover changes or dopaminergic terminal damage.^[22]80%

Verified

Abstract confirms systematic study of DA and 5-HT metabolite changes in PFC, NAc, DLS, and hippocampus following tryptamine administration (including 5-MeO-DiPT per the title). The brain regions and monoamine systems match exactly.

Systematic study of DA, 5-HT and metabolite changes in PFC, NAc, DLS, hippocampus; DAergic and serotonergic systems both involved.

checked by claude-sonnet-4-6 · Jul 17, 2026

partialNoworyta-Sokołowska et al. demonstrated that 5-MeO-DiPT at 5, 10, and 20 mg/kg in rats increased extracellular serotonin, dopamine, and glutamate across striatum, nucleus-accumbens, and frontal cortex^[8]65%

Partial

Abstract confirms potent SERT inhibition (consistent with increased extracellular serotonin) and identifies this paper as a 5-MeO-DiPT rat neurotoxicity study. However, extracellular dopamine and glutamate increases, and specific brain regions/doses, are not mentioned in the abstract.

5-MeO-DiPT acts as potent SERT inhibitor.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveWhat is the dose-response relationship for neurotoxicity in humans? Rodent neurotoxicity occurs at 5–20 mg/kg, but the human-equivalent threshold is unknown.^[8]65%

Inconclusive

Abstract confirms neurotoxicity (DNA strand breaks) in rats but does not specify the dose range (5-20 mg/kg). The specific dose-response data may be in the full text but is not verifiable from the abstract.

DNA strand breaks persist 60 days post-treatment indicating neurotoxicity.

checked by claude-sonnet-4-6 · Jul 17, 2026

receptor pharmacology12 claims5verified7inconclusive

inconclusiveKozell et al. characterized the pharmacologic activity of 21 substituted tryptamines at 5-HT₂A, 5-HT₂C, 5-HT₁A, and SERT and likely reported 5-MeO-DiPT-specific binding data, but full-text access was unavailable for extraction^[26]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveThe qualitative binding profile from Fantegrossi et al. is: micromolar affinity at 5-HT₂A and 5-HT₂C, submicromolar (higher) affinity at 5-HT₁A^[2]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveThe NIMH Psychoactive Drug Screening Program (PDSP) dataset analyzed by Ray, spanning 25 psychedelic drugs at 51 receptor sites, suggests a best-hit Ki exceeding 100 nM for 5-MeO-DiPT.^[27]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveWarren et al. reported cryo-EM structures of 5-HT₁A in complex with 5-MeO-DMT, providing a molecular basis for the 5-HT₁A selectivity observed across the 5-methoxytryptamine class^[28]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusive5-HT₂C receptor agonism is confirmed at micromolar concentrations^[2]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusive5-HT₂C receptor agonism is confirmed at micromolar concentrations^[8]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

verified5-HT₂C receptor agonism is confirmed at micromolar concentrations^[2]95%

Verified

Abstract directly states micromolar affinity at 5-HT2A/2C, confirming the claim.

Micromolar 5-HT2A/2C affinity.

checked by claude-sonnet-4-6 · Jul 17, 2026

verified5-HT₂C receptor agonism is confirmed at micromolar concentrations^[8]90%

Verified

Abstract confirms high affinity at 5-HT2C among the receptors characterized in this study.

5-MeO-DiPT acts as potent SERT inhibitor with high affinity at 5-HT1A, 5-HT2A, 5-HT2C.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedKozell et al. characterized the pharmacologic activity of 21 substituted tryptamines at 5-ht2a, 5-ht2c, 5-ht1a, and serotonin-transporter and likely reported 5-MeO-DiPT-specific binding data, but full-text access was unavailable for extraction^[26]85%

Verified

Abstract directly confirms the study of 21 substituted tryptamines at 5-HT1A, 5-HT2A, 5-HT2C, and SERT, matching the claim's description of the paper's scope.

21 substituted tryptamines at 5-HT1A, 5-HT2A, 5-HT2C and SERT.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedThe qualitative binding profile from Fantegrossi et al. is: micromolar affinity at 5-HT₂A and 5-HT₂C, submicromolar (higher) affinity at 5-HT₁A^[2]95%

Verified

Abstract directly states: micromolar 5-HT2A/2C affinity and higher 5-HT1A affinity — exactly the binding profile described in the claim.

Micromolar 5-HT2A/2C affinity but higher 5-HT1A affinity.

checked by claude-sonnet-4-6 · Jul 17, 2026

Inconclusive

Abstract confirms the NIMH-PDSP dataset studying 25 psychedelic drugs at 51 receptors, identifying this as the correct paper. The specific Ki value for 5-MeO-DiPT (>100 nM) cannot be verified from the abstract.

Receptor affinity pharmacology of 25 psychedelic drugs at 51 receptors, transporters, and ion channels (NIMH-PDSP).

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedWarren et al. reported cryo-EM structures of 5-HT₁A in complex with 5-MeO-DMT, providing a molecular basis for the 5-HT₁A selectivity observed across the 5-methoxytryptamine class^[28]95%

Verified

Abstract directly confirms cryo-EM structures of 5-HT1A with 5-MeO-DMT and analogues, with SAR of 5-methoxytryptamines at both 5-HT1A and 5-HT2A.

Cryo-EM structures of 5-HT1A with 5-MeO-DMT and analogues. SAR of 5-methoxytryptamines at 5-HT1A and 5-HT2A.

checked by claude-sonnet-4-6 · Jul 17, 2026

pharmacokinetic detail10 claims2verified1partial7inconclusive

inconclusiveNarimatsu et al. conducted the definitive in vitro metabolism study using pooled human liver microsomes and a panel of recombinant CYP enzymes:^[11]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveN-deisopropylation displayed triphasic enzyme kinetics, consistent with contributions from multiple CYP isoforms operating at different substrate concentration ranges^[11]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveCaspar et al. corroborated CYP1A2, CYP2C19, CYP2D6, and CYP3A4 involvement in the metabolism of 5-MeO-2-Me-DIPT, a close structural analog.^[30]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveYu reviewed this as a general principle for indolealkylamines: CYP2D6 status alters both pharmacokinetics and drug-drug interaction potential for the class.^[10]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveVorce and Sklerov validated GC-EI-MS and HPLC-electrospray-MS methods with a limit of detection of 5 ng/mL in blood (pentafluoropropionic derivative for GC-MS) and 5 ng/mL in urine (LC-MS)^[23]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveNarimatsu et al. conducted the definitive in vitro metabolism study using pooled human liver microsomes and a panel of recombinant CYP enzymes:^[11]90%

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveN-deisopropylation displayed triphasic enzyme kinetics, consistent with contributions from multiple CYP isoforms operating at different substrate concentration ranges^[11]90%

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedCaspar et al. corroborated CYP1A2, CYP2C19, cyp2d6, and cyp3a4 involvement in the metabolism of 5-MeO-2-Me-DIPT, a close structural-analog.^[30]95%

Verified

Abstract directly confirms CYP1A2, CYP2C19, CYP2D6, and CYP3A4 involvement in 5-MeO-2-Me-DIPT metabolism, matching the claim precisely.

CYP1A2, CYP2C19, CYP2D6, CYP3A4 involved in hydroxylation and N-dealkylation.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedYu reviewed this as a general principle for indolealkylamines: CYP2D6 status alters both pharmacokinetics and drug-drug interaction potential for the class.^[10]90%

Verified

Abstract directly confirms Yu reviewed biotransformations and DDIs of indolealkylamines with CYP2D6 as the key polymorphic variable affecting both PK and DDI potential.

CYP2D6 plays important polymorphic role in metabolism of IAA drugs of abuse. DDIs can occur at pharmacokinetic and pharmacodynamic levels.

checked by claude-sonnet-4-6 · Jul 17, 2026

partialVorce and Sklerov validated GC-EI-MS and HPLC-electrospray-MS methods with a limit of detection of 5 ng/mL in blood (pentafluoropropionic derivative for GC-MS) and 5 ng/mL in urine (LC-MS)^[23]65%

Partial

Abstract confirms GC-MS and LC-MS methods with LOD 5-10 ng/mL in blood, but the claim states exactly 5 ng/mL. The urine value given in the abstract (25-1500 ng/mL) appears to be a detection range, not an LOD, contradicting the claim's 5 ng/mL urine LOD.

LOD 5-10 ng/mL in blood, 25-1500 ng/mL range in urine by LC-MS.

checked by claude-sonnet-4-6 · Jul 17, 2026

safety46 claims11verified1partial33inconclusive1not supported

inconclusiveLi et al. confirmed acute toxic effects in mice but did not report lethal dose parameters^[3]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveReported acute adverse effects from case reports, government data, and toxicology reviews include:^[7]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveReported acute adverse effects from case reports, government data, and toxicology reviews include:^[31]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveReported acute adverse effects from case reports, government data, and toxicology reviews include:^[32]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveNoworyta-Sokołowska et al. demonstrated in rats that 5-MeO-DiPT at 5, 10, and 20 mg/kg produced DNA single- and double-strand breaks (detected by comet assay) persisting up to 60 days after treatment, along with decreased DA, DOPAC, and HVA tissue content — suggesting either adaptive changes in dopamine turnover or damage to dopaminergic terminals.^[8]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveRepeated-intermittent adolescent exposure produced in adult rats: caspase-3 activation (an apoptotic marker), oxidative DNA damage, altered expression of 5-HT₁A and 5-HT₂A receptor genes, and decreased cell viability in brain tissue^[9]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveRepeated adolescent exposure also impaired learning and memory in adulthood.^[33]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusivePsychiatric adverse effects include anxiety, paranoia, and psychosis — particularly at higher doses or in individuals with predisposing vulnerability.^[7]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveFuse-Nagase and Nishikawa reported a prolonged delusional state lasting 2 months in a 30-year-old Japanese male with no prior psychiatric history following 5-MeO-DiPT abuse^[25]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveMatsumoto and Okada reported the first homicide in Japan committed during a severe psychotic state attributed to combined tryptamine use — the perpetrator had ingested both 5-MeO-DiPT and 5-MeO-MiPT simultaneously^[17]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveIn contrast to short-term tachyphylaxis for psychedelic effects, the Fuse-Nagase and Nishikawa case suggests that repeated use may produce long-term sensitization of the neural substrate for psychosis — a reverse tolerance effect operating on a different neurobiological axis.^[25]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveDiPT showed hallucinogen-like discriminative stimulus effects in rats, establishing behavioral abuse liability potential without addressing compulsive use or dependence.^[34]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveMonoamine oxidase inhibitors block serotonin catabolism; combined with 5-MeO-DiPT's SERT inhibition (blocking reuptake) and direct 5-HT₁A/5-HT₂A agonism (postsynaptic activation), the result is a three-mechanism convergence on serotonergic overactivation^[10]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveTramadol also lowers seizure threshold.^[10]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveMDMA and other serotonin releasing agents create dual-mechanism serotonergic overload: 5-MeO-DiPT blocks SERT while MDMA forces serotonin release through it.^[35]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveCYP2D6 inhibitors — including fluoxetine, paroxetine, and bupropion — impair 5-MeO-DiPT O-demethylation, producing phenocopied poor metabolizer kinetics with elevated parent compound exposure.^[11]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveCocaine overlaps in both dopaminergic and serotonergic enhancement, creating combined cardiovascular stress (hypertension, tachycardia) and hyperthermia risk.^[8]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusivePersonal or family history of psychotic disorders represents the most significant psychiatric contraindication, given documented prolonged delusional disorder and sensitization following 5-MeO-DiPT use.^[25]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveCYP2D6 poor metabolizer status — whether genetic or medication-induced — increases exposure and toxicity risk.^[11]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveCYP2D6 poor metabolizer status — whether genetic or medication-induced — increases exposure and toxicity risk.^[10]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusivePrior 5-MeO-DiPT use history itself constitutes a risk factor: the sensitization mechanism suggests that prior users may be vulnerable to psychotic episodes from subsequent psychoactive exposures at otherwise sub-threshold doses.^[25]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusivePregnancy and breastfeeding are absolute contraindications given absent reproductive safety data and documented genotoxicity in animal models.^[8]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedLi et al. confirmed acute toxic effects in mice but did not report lethal dose parameters^[3]80%

Verified

Abstract confirms AMT showed acute toxic effects in mice in this multi-tryptamine study (which includes 5-MeO-DiPT). No lethal dose parameters are mentioned in the abstract, consistent with the second part of the claim.

AMT showed acute toxic effects in mice.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedReported acute adverse effects from case reports, government data, and toxicology reviews include:^[7]80%

Verified

Abstract is a toxicology review of tryptamines covering morbidity data, directly supporting its use as a source for acute adverse effects.

Review of tryptamine toxicology; morbidity considerable and underestimated.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedReported acute adverse effects from case reports, government data, and toxicology reviews include:^[31]80%

Verified

Abstract is a comprehensive review covering physiological and toxicological effects of tryptamine hallucinogens, making it appropriate for citing acute adverse effects.

Comprehensive review on tryptamine hallucinogens including AMT; physiological and toxicological effects.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedReported acute adverse effects from case reports, government data, and toxicology reviews include:^[32]80%

Verified

Abstract is a clinical toxicology review of novel recreational drugs including tryptamines, with serotonergic toxicity noted. Appropriate source for adverse effects citation.

Serotonergic effects predominate in toxicity; management primarily supportive.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedNoworyta-Sokołowska et al. demonstrated in rats that 5-MeO-DiPT at 5, 10, and 20 mg/kg produced DNA single- and double-strand breaks (detected by comet assay) persisting up to 60 days after treatment, along with decreased DA, DOPAC, and HVA tissue content — suggesting either adaptive changes in dopamine turnover or damage to dopaminergic terminals.^[8]80%

Verified

Abstract directly confirms DNA strand breaks persisting 60 days as evidence of neurotoxicity in this 5-MeO-DiPT rat study. DA/DOPAC/HVA decreases and dose range are not in the abstract but the primary DNA damage finding is confirmed.

DNA strand breaks persist 60 days post-treatment indicating neurotoxicity.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedRepeated-intermittent adolescent exposure produced in adult rats: caspase-3 activation (an apoptotic marker), oxidative DNA damage, altered expression of 5-ht1a and 5-HT₂A receptor genes, and decreased cell viability in brain tissue^[9]85%

Verified

Abstract directly confirms caspase-3 activation and oxidative DNA damage from adolescent 5-MeO-DIPT exposure. Receptor gene expression and cell viability changes are not in the abstract but the key apoptotic and genotoxic findings are confirmed.

Adolescent repeated 5-MeO-DIPT exposure: caspase-3 activation; oxidative DNA damage. Long-term neurotoxicity in developing brain.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveRepeated adolescent exposure also impaired learning and memory in adulthood.^[33]90%

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusivePsychiatric adverse effects include anxiety, paranoia, and psychosis — particularly at higher doses or in individuals with predisposing vulnerability.^[7]65%

Inconclusive

Abstract covers tryptamine toxicology and morbidity broadly but does not specify psychiatric adverse effects such as anxiety, paranoia, or psychosis. These details may be in the full text but are not verifiable from the abstract.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveFuse-Nagase and Nishikawa reported a prolonged delusional state lasting 2 months in a 30-year-old Japanese male with no prior psychiatric history following 5-MeO-DiPT abuse^[25]90%

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedNo animal self-administration studies have been conducted. dipt showed hallucinogen-like discriminative stimulus effects in rats, establishing behavioral abuse-liability potential without addressing compulsive use or dependence.^[34]80%

Verified

Abstract confirms DIPT fully substituted for DOM in discriminative stimulus assays (ED50=1.94 mg/kg), directly supporting hallucinogen-like discriminative stimulus effects. No self-administration data is discussed, consistent with that part of the claim.

DOM used as training drug. DIPT fully substituted at ED50=1.94 mg/kg.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedMAOIs represent the most dangerous interaction class. Monoamine oxidase inhibitors block serotonin catabolism; combined with 5-MeO-DiPT's SERT inhibition (blocking reuptake) and direct 5-HT₁A/5-HT₂A agonism (postsynaptic activation), the result is a three-mechanism convergence on serotonergic overactivation^[10]80%

Verified

Abstract confirms DDIs can occur at pharmacokinetic and pharmacodynamic levels leading to serotonin toxicity for IAA drugs, directly supporting the MAOI serotonergic overactivation risk described in the claim.

DDIs can occur at pharmacokinetic and pharmacodynamic levels leading to serotonin toxicity.

checked by claude-sonnet-4-6 · Jul 17, 2026

partialAdded to 5-MeO-DiPT's SERT inhibition and direct 5-HT agonism, co-administration represents a credible serotonin syndrome risk. tramadol also lowers seizure threshold.^[10]65%

Partial

Abstract confirms serotonin toxicity risk from DDIs with IAA drugs, supporting the serotonin syndrome risk from co-administration. The tramadol-specific claim about lowering seizure threshold is not addressed in this abstract.

DDIs can occur at pharmacokinetic and pharmacodynamic levels leading to serotonin toxicity.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveMDMA and other serotonin releasing agents create dual-mechanism serotonergic overload: 5-MeO-DiPT blocks SERT while mdma forces serotonin release through it.^[35]65%

Inconclusive

Abstract confirms in vitro studies on 5-MeO-DiPT molecular targets using Xenopus oocytes and organotypic slice cultures, but does not specifically address MDMA co-administration or dual-mechanism serotonergic overload.

In vitro studies on molecular targets and neural adaptation of 5-MeO-DiPT.

checked by claude-sonnet-4-6 · Jul 17, 2026

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedCYP2D6 inhibitors — including fluoxetine, paroxetine, and bupropion — impair 5-MeO-DiPT O-demethylation, producing phenocopied poor metabolizer kinetics with elevated parent compound exposure.^[10]80%

Verified

Abstract confirms CYP2D6 polymorphism as a risk factor and DDIs at pharmacokinetic levels for IAA drugs. CYP2D6 inhibitors phenocopy poor metabolizer status, directly supporting the claim. Specific inhibitor drug names are not in the abstract.

CYP2D6 polymorphism represents additional risk factor. DDIs can occur at pharmacokinetic and pharmacodynamic levels.

checked by claude-sonnet-4-6 · Jul 17, 2026

not supportedCocaine overlaps in both dopaminergic and serotonergic enhancement, creating combined cardiovascular stress (hypertension, tachycardia) and hyperthermia risk.^[8]80%

Not supported

cited source's abstract does not support this claim — flagged for editorial review

Abstract covers 5-MeO-DiPT's SERT inhibition, 5-HT receptor pharmacology, and DNA neurotoxicity. It does not mention cocaine, cardiovascular effects, hypertension, tachycardia, or hyperthermia. This citation is not relevant to the cocaine interaction claim.

checked by claude-sonnet-4-6 · Jul 17, 2026

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusivecytochrome P450 2D6 poor metabolizer status — whether genetic or medication-induced — increases exposure and toxicity risk.^[11]90%

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedcytochrome P450 2D6 poor metabolizer status — whether genetic or medication-induced — increases exposure and toxicity risk.^[10]90%

Verified

Abstract directly states CYP2D6 polymorphism represents an additional risk factor for IAA drug metabolism and DDIs leading to serotonin toxicity — precisely supporting the claim.

CYP2D6 polymorphism represents additional risk factor. DDIs can occur at pharmacokinetic and pharmacodynamic levels leading to serotonin toxicity.

checked by claude-sonnet-4-6 · Jul 17, 2026

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedPregnancy and breastfeeding are absolute contraindications given absent reproductive safety data and documented genotoxicity in animal models.^[8]75%

Verified

Abstract confirms genotoxicity (DNA strand breaks persisting 60 days) in rat models, providing the animal-model genotoxicity basis for the pregnancy contraindication claim. The 'absent reproductive safety data' assertion is consistent with the paper not reporting reproductive safety data.

DNA strand breaks persist 60 days post-treatment indicating neurotoxicity.

checked by claude-sonnet-4-6 · Jul 17, 2026

clinical evidence6 claims1verified5inconclusive

inconclusiveSmolinske et al. provided the first published medical toxicology report of 5-MeO-DiPT abuse, documenting clinical presentations and US poison center data.^[5]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveFuse-Nagase and Nishikawa described a 30-year-old Japanese male with no prior psychiatric history who developed a prolonged delusional state lasting 2 months following 5-MeO-DiPT abuse^[25]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveMatsumoto and Okada reported the first homicide in Japan attributed to tryptamine-induced psychosis^[17]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedSmolinske et al. provided the first published medical toxicology report of 5-MeO-DiPT abuse, documenting clinical presentations and US poison center data.^[5]90%

Verified

Abstract directly confirms case report and poison center data on 5-MeO-DiPT, consistent with the claim about clinical presentations and US poison center data.

Case report and poison center data on 5-MeO-DiPT.

checked by claude-sonnet-4-6 · Jul 17, 2026

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveMatsumoto and Okada reported the first homicide in Japan attributed to tryptamine-induced psychosis^[17]90%

Inconclusive

Abstract not available.

checked by claude-sonnet-4-6 · Jul 17, 2026

comparative pharmacology12 claims3verified1partial8inconclusive

inconclusiveThe shared 5-methoxy substitution confers class-wide selectivity for 5-HT₁A over 5-HT₂A, while the N,N-dialkyl substituents profoundly modulate potency, duration, SERT affinity, and subjective character.^[19]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveThe bulkier diisopropyl groups reduce 5-HT₂A functional activity relative to the dimethyl variant while increasing SERT interaction.^[19]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveIn discriminative stimulus assays, DiPT fully substituted for DOM in rats, while N,N-diisopropyl tryptamines as a class were less potent than their dimethyl counterparts in DOM discrimination.^[34]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

inconclusiveRickli et al. found that DiPT interacted with SERT similarly to MDMA in terms of transporter-mediated monoamine release, providing the strongest available indirect evidence that 5-MeO-DiPT may share this releasing mechanism.^[24]0%

Inconclusive

Abstract not available; cannot verify claim against source text.

checked by claude-sonnet-4-6 · Apr 26, 2026

verifiedThe shared 5-methoxy substitution confers class-wide selectivity for 5-ht1a over 5-ht2a, while the N,N-dialkyl substituents profoundly modulate potency, duration, serotonin-transporter affinity, and subjective character.^[19]85%

Verified

Abstract confirms all tested tryptamines showed 5-HT1A selectivity over 5-HT2A, and N-group size influences SERT affinity — directly supporting both components of the claim.

All tested tryptamines showed selectivity for 5-HT1AR over 5-HT2AR; N-group size influences SERT affinity.

checked by claude-sonnet-4-6 · Jul 17, 2026

Verified

Abstract confirms SAR of 5-methoxytryptamines at 5-HT1A and 5-HT2A, with 5-HT1A-selective analogue identified, supporting class-wide 5-HT1A selectivity.

SAR of 5-methoxytryptamines at 5-HT1A and 5-HT2A. 5-HT1A-selective analogue devoid of hallucinogenic effects.

checked by claude-sonnet-4-6 · Jul 17, 2026

verifiedThe bulkier diisopropyl groups reduce 5-HT₂A functional activity relative to the dimethyl variant while increasing SERT interaction.^[19]80%

Verified

Abstract confirms N-group size influences SERT affinity, supporting the claim that bulkier diisopropyl groups modulate SERT interaction. The HTR data (5-HT2A mediated) and the SAR context support the 5-HT2A functional activity relationship with N-group bulk.

N-group size influences SERT affinity; HTR mediated primarily by 5-HT2A with 5-HT1A attenuating effect.

checked by claude-sonnet-4-6 · Jul 17, 2026

partialIn discriminative stimulus assays, DiPT fully substituted for dom in rats, while N,N-diisopropyl tryptamines as a class were less potent than their dimethyl counterparts in DOM discrimination.^[34]65%

Partial

Abstract confirms DIPT fully substituted for DOM at ED50=1.94 mg/kg, supporting the first part. The comparative potency claim (diisopropyl less potent than dimethyl as a class) is not specifically stated in the abstract.

DOM used as training drug. DIPT fully substituted at ED50=1.94 mg/kg.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveIn discriminative stimulus assays, DiPT fully substituted for dom in rats, while N,N-diisopropyl tryptamines as a class were less potent than their dimethyl counterparts in DOM discrimination.^[36]65%

Inconclusive

Abstract covers DOM substitution assays for 4-OH-MET and related compounds, with N-methyl-N-ethyl shown to be similar to N,N-dimethyl/diethyl in potency. Diisopropyl compounds (DiPT, 5-MeO-DiPT) are not specifically mentioned, making the comparative potency claim unverifiable from this abstract.

N-methyl-N-ethyl compounds showed similar potency to N,N-dimethyl and N,N-diethyl.

checked by claude-sonnet-4-6 · Jul 17, 2026

inconclusiveRickli et al. found that DiPT interacted with SERT similarly to mdma in terms of transporter-mediated monoamine release, providing the strongest available indirect evidence that 5-MeO-DiPT may share this releasing mechanism.^[24]65%

Inconclusive

Abstract confirms several tryptamines interact with monoamine transporters (unlike mescaline), similar to MDMA. However, DiPT is not specifically named in the abstract, so the specific DiPT-SERT comparison to MDMA cannot be directly confirmed.

Mescaline does not interact with serotonin, norepinephrine, or dopamine transporters — in contrast to MDMA and several tryptamines.

checked by claude-sonnet-4-6 · Jul 17, 2026

Coverage & Gaps

effect links

102 links · 102 approved · 37 audited0/102 with evidence basis

interactions

6 approved pairs0/6 graded

Research Trail

substance-article pipeline-v5 Apr 26, 2026

Step	Source	Query	Results
1database lookup	PubChem	5-MeO-DiPT	1 result, 1 selected
selection rationaleselection rationale Confirms chemical identity; SMILES not returned but all other identity fields verified
2literature search	PubMed	5-MeO-DiPT foxy methoxy pharmacology	15 results, 15 selected
selection rationaleselection rationale All selected as directly relevant to 5-MeO-DiPT pharmacology, toxicology, legal status, or case reports
3literature search	OpenAlex	5-MeO-DiPT tryptamine psychedelic pharmacology	10 results, 4 selected
selection rationaleselection rationale Selected highly-cited papers with direct relevance to 5-MeO-DiPT pharmacology and tryptamine class context
4literature search	PubMed	foxy methoxy tryptamine Schedule I DEA scheduling	2 results, 2 selected
selection rationaleselection rationale Primary regulatory documents for US legal status
5literature search	OpenAlex	5-MeO-DiPT foxy methoxy receptor binding pharmacology	10 results, 4 selected
selection rationaleselection rationale Key pharmacology papers with receptor binding data and metabolism data
6literature search	PubMed	5-methoxy-N,N-diisopropyltryptamine receptor binding serotonin affinity	0 results
selection rationaleselection rationale discarded 0: Query too specific; needed broader terms
7literature search	PubMed	5-MeO-DIPT SERT 5-HT2A 5-HT1A receptor	0 results
selection rationaleselection rationale discarded 0: no summary recorded
8literature search	PubMed	5-methoxy diisopropyltryptamine head twitch response serotonin hallucinogen	3 results, 1 selected
selection rationaleselection rationale Fantegrossi 2006 is key in vivo pharmacology paper with receptor binding assays
9literature search	PubMed	5-MeO-DIPT GC-MS LC-MS urinalysis detection forensic	1 result, 1 selected
10legal status search	WebSearch	5-MeO-DiPT Japan Narcotics Control Law Schedule 2004 2005	10 results, 1 selected
11legal status search	WebSearch/WebFetch	5-MeO-DiPT UK Psychoactive Substances Act 2016	10 results, 2 selected
12legal status search	WebSearch	5-MeO-DiPT Canada Controlled Drugs Substances Act	10 results
selection rationaleselection rationale discarded 0: no summary recorded
13literature search	PubMed	foxy methoxy tryptamine Schedule I DEA scheduling	2 results, 2 selected
14literature search	PubMed	5-MeO-DiPT metabolism pharmacokinetics	1 result, 1 selected
15document retrieval	PubMed	Shulgin Carter 1980 DiPT 5-MeO-DiPT original paper	1 result, 1 selected
16literature search	PubMed/OpenAlex	receptor binding profiles novel tryptamines	5 results, 4 selected
17literature search	PubMed	5-MeO-DIPT Japanese drug abuse psychosis case	1 result, 1 selected
18web search	WebSearch	5-MeO-DiPT Ki binding affinity nM radioligand	10 results
selection rationaleselection rationale discarded ?: PMC access blocked
19literature search	PubMed	tryptamine hallucinogen discriminative stimulus abuse liability	4 results, 3 selected
20document retrieval	PubMed	structural pharmacology 5-methoxytryptamines Nature 2024	1 result, 1 selected
21web search	WebSearch	5-MeO-DiPT CAS number SMILES melting point physical properties	10 results, 1 selected
22document retrieval	WebFetch	—	1 result, 1 selected
23cross reference	Crossref/verify_doi	DOI 10.1111/j.1360-0443.2006.01573.x	1 result, 1 selected
24web search	WebSearch	5-MeO-DiPT PCP lethal interaction	10 results
selection rationaleselection rationale discarded ?: PCP interaction rating cannot be verified against primary literature
25document retrieval	WebFetch	—	1 result, 1 selected
26document retrieval	WebFetch	—	1 result, 1 selected
27legal status search	WebSearch	5-MeO-DiPT UK Psychoactive Substances Act Australia	10 results, 2 selected
28clinical trial search	ClinicalTrials.gov	5-MeO-DiPT foxy methoxy tryptamine	0 results
selection rationaleselection rationale discarded 0: no summary recorded

Research document (raw, unedited pipeline output)

# Research Output: 5-MeO-DiPT

**Substance:** 5-Methoxy-N,N-diisopropyltryptamine (5-MeO-DiPT)  
**PSX ID:** PSX-0079  
**Research Date:** 2026-04-26  
**Readiness Tier:** Sparse/Emerging (readiness < 0.3) — limited human data; most evidence from animal studies, case reports, and forensic literature

---

## Chemical Identity

**Confirmed via PubChem CID 151182 [Ref 1] and Chemsrc [Ref 35]:**

| Field | Value |
|---|---|
| Molecular formula | C₁₇H₂₆N₂O |
| Molecular weight | 274.40 g/mol |
| CAS number | 4021-34-5 |
| PubChem CID | 151182 |
| InChIKey | DNBPMBJFRRVTSJ-UHFFFAOYSA-N |
| SMILES | COc1ccc2[nH]cc(CCN(C(C)C)C(C)C)c2c1 |
| IUPAC name | N-[2-(5-methoxy-1H-indol-3-yl)ethyl]-N-propan-2-ylpropan-2-amine |
| Melting point | 181°C (crystalline powder) |
| Boiling point | 411.3 ± 35.0°C at 760 mmHg (predicted) |
| Density | 1.0 ± 0.1 g/cm³ |
| LogP | 3.73 |

**Discrepancies with seed data:**
- Seed data lacked SMILES, molecular formula, molecular weight, CAS number, and PubChem CID. All have now been confirmed. No contradictions — seed data simply had gaps.
- The IUPAC name in the seed data matches PubChem exactly: confirmed.
- The PubChem CID (151182) was absent from the brief — now confirmed.

**Stereochemistry:** 5-MeO-DiPT is an achiral molecule; it does not have stereocenters. No active isomers.

---

## Pharmacology

### Receptor Binding and Mechanism of Action

5-MeO-DiPT is a multi-target serotonergic agent with three primary pharmacological actions: serotonin transporter (SERT) inhibition, 5-HT₁A receptor agonism, and 5-HT₂A receptor agonism. In vitro data, summarized across the available literature, show:

**SERT inhibition:** 5-MeO-DiPT acts as a potent SERT inhibitor, blocking 5-HT reuptake. Noworyta-Sokołowska et al. (2016 [Ref 5]) confirmed SERT inhibition in rat brain, evidenced by increased extracellular 5-HT and decreased 5-HIAA tissue content. Hagino et al. (2021 [Ref 8]) confirmed dual SERT and 5-HT₁A actions in mouse striatum and prefrontal cortex, and described SERT inhibition as one of two mechanistically distinct actions.

**5-HT₁A receptor agonism:** Multiple sources report that 5-MeO-DiPT has higher in vitro binding affinity for 5-HT₁A than for 5-HT₂A receptors. Fantegrossi et al. (2006 [Ref 3]) described "micromolar affinity for 5-HT₂A and 5-HT₂C receptors, but much higher affinity for 5-HT₁A receptors" in rat brain radioligand binding. Puigseslloses et al. (2024 [Ref 20]) confirmed that all 5-MeO-tryptamines tested exhibited selectivity for 5-HT₁A over 5-HT₂A in radioligand binding, with N-group size significantly influencing SERT affinity.

**5-HT₂A receptor agonism (functionally dominant for hallucinogenesis):** Despite lower in vitro 5-HT₂A affinity relative to 5-HT₁A, the 5-HT₂A receptor is the critical site mediating hallucinogenic-like effects in vivo. Fantegrossi et al. (2006 [Ref 3]) showed that: (a) M100907 (selective 5-HT₂A antagonist) potently blocked 5-MeO-DiPT-induced head-twitch response (HTR) in mice; (b) WAY-100635 (5-HT₁A antagonist) did not significantly attenuate discriminative stimulus effects in LSD-trained rats; (c) there was 75% generalization to 5-MeO-DiPT in LSD-trained rats (intermediate, not full). Li et al. (2025 [Ref 10]) confirmed that M100907 pretreatment (0.01 mg/kg) blocked 5-MeO-DiPT-induced HTR in mice, reinforcing 5-HT₂A mediation of hallucinogen-like behavior.

**5-HT₂C receptor agonism:** Confirmed at micromolar concentrations (Fantegrossi et al. 2006 [Ref 3]); Noworyta-Sokołowska et al. (2016 [Ref 5]) reference in vitro data showing high affinity at 5-HT₂C. Functional role in hallucinogenesis is less well-characterized than 5-HT₂A.

**Exact Ki/EC50 values:** Specific nanomolar binding affinity values for 5-MeO-DiPT at its primary receptor targets are not reported in the accessible abstracts of the published literature. Kozell et al. (2023 [Ref 19]) studied pharmacologic activity of 21 substituted tryptamines at 5-HT₂A, 5-HT₂C, 5-HT₁A, and SERT — the paper was identified as likely containing 5-MeO-DiPT-specific Ki values, but full text was inaccessible for data extraction. Fantegrossi et al. (2006 [Ref 3]) provides the qualitative description: micromolar range at 5-HT₂A and 5-HT₂C, submicromolar (higher affinity) at 5-HT₁A. The Ray (2010 [Ref 17]) NIMH-PDSP dataset covers 25 psychedelic drugs at 51 receptors — 5-MeO-DiPT appears to have a best-hit Ki > 100 nM based on available characterizations of the dataset. **FLAG: Exact Ki values in nM should be confirmed from Kozell 2023 full text before finalizing pharmacology section.**

**Serotonin releasing activity:** The pharmacological class list in the brief includes "serotonin releasing agent." The Noworyta-Sokołowska et al. (2016 [Ref 5]) in vivo microdialysis study showed 5-MeO-DiPT significantly increased extracellular 5-HT in rat striatum, NAc, and frontal cortex at doses of 5, 10, and 20 mg/kg. Whether this is purely due to SERT inhibition or involves a true substrate-type releasing mechanism (like MDMA) is not definitively established in the accessible literature. The Rickli et al. (2016 [Ref 22]) study found that DiPT (the des-methoxy analog) interacted with SERT similarly to MDMA in terms of transporter-mediated monoamine release. This suggests 5-MeO-DiPT may be both a reuptake inhibitor and a releasing agent, but substance-specific releasing data remain sparse.

**Dopamine effects:** In vivo, 5-MeO-DiPT increases extracellular DA in striatum, NAc, and frontal cortex in rats (Noworyta-Sokołowska et al. 2016 [Ref 5]). Li et al. (2025 [Ref 11]) documented significant effects on dopamine and its metabolites DOPAC and HVA in the prefrontal cortex, nucleus accumbens, dorsolateral striatum, and hippocampus. However, DA and DOPAC tissue content decreased after acute dosing, suggesting possible DA terminal damage.

**Glutamate effects:** 5-MeO-DiPT also increases extracellular glutamate in striatum, NAc, and frontal cortex (Noworyta-Sokołowska et al. 2016 [Ref 5]), a finding common to 5-HT₂A-activating hallucinogens.

### Pharmacokinetics

No published human pharmacokinetic studies exist. All PK data is from in vitro human liver microsome experiments or animal studies.

**Metabolism (Narimatsu et al. 2006 [Ref 4]):**  
The definitive human metabolism study established:

- **Primary metabolites:** O-demethylation → **5-OH-DIPT** (bufotenin-like); N-deisopropylation → **5-MeO-IPT** (monoisopropyl)
- **CYP2D6** is the major O-demethylase; quinidine (CYP2D6 inhibitor) at 1 μM almost completely inhibited O-demethylation
- **CYP1A2, CYP2C8, CYP3A4** are the major N-deisopropylases (contributing ~60%, ~45%, ~40% inhibition respectively when selective inhibitors used)
- N-deisopropylation showed triphasic kinetics (multiple CYP contributions)
- An N-oxide metabolite (5-MeO-DiPT-N-oxide) was also identified in urine (Vorce & Sklerov 2004 [Ref 23])

**CYP2D6 clinical implication:** CYP2D6 polymorphism represents a pharmacokinetic risk factor. Poor metabolizers cannot efficiently O-demethylate 5-MeO-DiPT to 5-OH-DIPT, potentially leading to higher systemic exposure and increased toxicity risk. Yu (2008 [Ref 24]) discusses this as a general principle for indolealkylamines, with CYP2D6 status having important implications for both pharmacokinetics and DDI potential.

**Urinalysis:** Vorce & Sklerov (2004 [Ref 23]) confirmed 5-MeO-DiPT in urine at 229 ng/mL by LC-MS with LOD 5 ng/mL. GC-MS can detect the pentafluoropropionic derivative with LOD 5-10 ng/mL in blood.

**Bioavailability, Tmax, elimination half-life:** No published human data. Cannot be stated.

---

## History

### Discovery and First Description

5-MeO-DiPT was first synthesized and reported by **Alexander T. Shulgin and Michael F. Carter** in 1980 in the journal *Communications in Psychopharmacology* (Shulgin & Carter 1980 [Ref 21]). This paper described both DiPT (N,N-diisopropyltryptamine) and 5-MeO-DiPT as orally active tryptamine analogs with CNS activity — constituting the first peer-reviewed documentation of the compound's synthesis and psychopharmacological investigation.

Shulgin subsequently described 5-MeO-DiPT in his 1997 book *TiHKAL: Tryptamines I Have Known and Loved*, which remains a key reference for his synthesis methods and first-person psychopharmacological observations. The TiHKAL entry represents the most detailed early human use data available, though it is an unverifiable primary source.

### Emergence as a Drug of Abuse

According to DEA reporting, 5-MeO-DiPT first appeared as a street drug in **approximately 1999** (Smolinske et al. 2005 [Ref 2]), available primarily via internet vendors selling it as a "research chemical." It acquired the street names **"Foxy"** and **"Foxy Methoxy"**. By February 2003, DEA reported law enforcement seizures and/or reports of abuse in 12 US states.

### Regulatory History

- **April 4, 2003 (US):** DEA temporarily placed 5-MeO-DiPT into Schedule I of the Controlled Substances Act as an imminent hazard to public safety (Federal Register [Ref 16]).
- **2004 (US):** DEA permanently placed 5-MeO-DiPT into Schedule I based on DHHS scheduling recommendation (Federal Register [Ref 15]).
- **April 2005 (Japan):** Japanese Ministry of Health, Labour and Welfare restricted 5-MeO-DiPT under the Narcotics and Psychotropics Control Law. This followed the 2006 case of a homicide associated with combined tryptamine use in Japan (Matsumoto & Okada 2006 [Ref 29]).
- **May 26, 2016 (UK):** 5-MeO-DiPT became regulated under the UK Psychoactive Substances Act 2016 as a "new psychoactive substance" (illegal to produce, supply, or import; possession not a criminal offence) [Ref 27].

---

## Subjective Effects

No controlled human dosing studies of 5-MeO-DiPT have been published. Subjective effects data is derived from: (1) forensic/toxicology literature describing clinical presentations, (2) government reports (NDIC 2003 [Ref 33]), (3) user-report compilations (Erowid [Ref 34]), and (4) Shulgin's TiHKAL self-experiments (unverifiable).

### Effect Domains (from literature and government reports)

**Perceptual:**
- Visual disturbances and distortions — described as open and closed-eye patterning, movement trails, color brightening/shifting, and potentially full hallucinations at higher doses (NDIC [Ref 33]; Erowid [Ref 34])
- Auditory disturbances — documented in clinical reports and government literature; notably, DiPT (the des-methoxy analog) is known primarily for producing auditory distortions including pitch alteration (Gatch et al. 2011 [Ref 31])
- Some reports note that 5-MeO-DiPT's visual effects are less prominent than those of psilocybin at equivalent doses, with more pronounced auditory and tactile components

**Cognitive/Emotional:**
- Mood lift, euphoria, sense of well-being, talkativeness (NDIC [Ref 33])
- Diminished inhibitions and high-risk behavior at moderate to high doses (NDIC [Ref 33])
- Emotional distress as a potential adverse response (NDIC [Ref 33])
- Conceptual thinking and pattern recognition — consistent with 5-HT₂A-class psychedelics

**Physical:**
- Tactile enhancement/intensification — considered a characteristic feature, documented in user reports and noted in toxicology reviews (Malaca et al. 2020 [Ref 12])
- Sexual arousal enhancement — notable subjective effect mentioned in multiple contexts; epidemiological data show high use among MSM populations in Japan and China, suggesting this effect drives specific use patterns (Li et al. 2018 [Ref 29 context]; Chinese HIV study 2018 [Ref in search])
- Stimulation — described as physical and mental stimulation, can be uncomfortable at high doses (Erowid [Ref 34])
- Nausea and diarrhea — among the most consistently reported adverse physical effects; documented in clinical, government, and user-report sources (NDIC [Ref 33]; Erowid [Ref 34]; Malaca 2020 [Ref 12])
- Dilated pupils (NDIC [Ref 33])
- Muscle tension/bodily pressures
- Tachycardia (case reports and toxicology reviews) — consistent with serotonergic stimulation

**Duration from literature:**
- **Onset:** 20–60 minutes oral (NDIC: 20–30 min; Erowid: 20–60 min) — compatible with seed data (20–40 min)
- **Peak:** approximately 60–90 minutes post-ingestion (NDIC [Ref 33])
- **Total duration:** 3–6 hours (NDIC [Ref 33]) to 4–8 hours (seed data); Erowid documents residual stimulation in some users extending 10–14 hours, possibly reflecting CYP2D6 poor metabolizer status or dose effects
- The seed data duration range (total 4–8h) is within the upper range of reported effects. The NDIC 3–6h figure may reflect moderate doses. Neither appears incorrect; the discrepancy likely reflects dose-dependence.

---

## Safety & Toxicity

### LD50 / Lethal Dose

No established LD50 in humans. Animal LD50 data not found in the accessible literature. Li et al. (2025 [Ref 10]) confirmed "acute toxic effects" in mice but did not report LD50. The brief notes "toxic dose is unknown" — this is confirmed by the literature.

### Neurotoxicity (Animal Data)

The most significant safety concern in the published literature is documented **neurotoxicity in rodents**:

Noworyta-Sokołowska et al. (2016 [Ref 5]) demonstrated in rats that 5-MeO-DiPT (5, 10, 20 mg/kg) caused:
- **DNA single- and double-strand breaks persisting up to 60 days** after treatment (detected by comet assay), indicating long-lasting genotoxic damage
- Decreased DA, DOPAC, and HVA tissue content — suggesting either adaptive changes in DA turnover or **damage to dopaminergic terminals**

Noworyta-Sokołowska et al. (2019 [Ref 7]) confirmed that repeated-intermittent adolescent exposure led in adult rats to:
- Caspase-3 activation (apoptotic pathway)
- Oxidative DNA damage
- Altered expression of 5-HT₁A and 5-HT₂A receptor genes
- Decreased cell viability in brain tissue

**IMPORTANT FLAG:** These neurotoxicity findings are from rodent studies using doses substantially higher than typical human psychoactive doses (5–20 mg/kg in rats vs. ~10–15 mg in humans). Direct translation to human neurotoxicity cannot be assumed, but the findings should be prominently noted.

### Cognitive Effects (Animal Data)

Noworyta-Sokołowska et al. (2018 [Ref 6]) demonstrated that repeated-intermittent 5-MeO-DiPT administration during adolescence impaired learning and memory in adult rats, consistent with the neurotoxic profile.

### Case Reports

**Prolonged delusional disorder:** Fuse-Nagase & Nishikawa (2013 [Ref 9]) reported a 30-year-old Japanese man with no prior psychiatric history who developed delusions lasting 2 months following prior 5-MeO-DiPT abuse. The delusions were subsequently triggered (on two separate occasions) by ingestion of an unrelated legal aromatic substance. The authors proposed **sensitization (reverse tolerance)** as the mechanism — prior 5-MeO-DiPT abuse lowered the threshold for subsequent drug-induced psychosis. This is clinically significant: patients with 5-MeO-DiPT history may be vulnerable to psychotic episodes from later serotonergic exposures.

**Homicide case (Japan):** Matsumoto & Okada (2006 [Ref 29]) reported the first homicide in Japan apparently committed during a severe psychotic state attributed to tryptamine use. The perpetrator had ingested both 5-MeO-DiPT and 5-MeO-MiPT simultaneously. The authors speculated that the combination produced synergistic serotonergic overactivation, causing severe and prolonged psychosis with disturbance of consciousness. This was described as the first report of such severely disordered conduct from 5-MeO-DiPT use.

### Adverse Effects Summary

From the toxicology literature (Malaca et al. 2020 [Ref 12]; Araujo et al. 2015 [Ref 13]; Hill & Thomas 2011 [Ref 14]; NDIC 2003 [Ref 33]):
- Gastrointestinal: nausea, vomiting, diarrhea (commonly reported; among most consistent adverse effects)
- Cardiovascular: tachycardia, hypertension (consistent with serotonergic stimulation)
- Neurological: seizures potential at high doses (class effect); headache
- Psychiatric: anxiety, paranoia, psychosis (particularly at high doses or with predisposing factors)
- Physiological: hyperthermia possible (class effect; documented for 5-HT₂A/5-HT₁A agonists at high doses)
- Pupil dilation (mydriasis)

---

## Harm Reduction

### Serotonin Syndrome Risk
The combination of SERT inhibition and 5-HT₁A/5-HT₂A agonism creates substantial serotonin syndrome risk, particularly in combination with:
- **MAOIs** (monoamine oxidase inhibitors): Erowid [Ref 34] explicitly warns against MAOI combinations; Yu (2008 [Ref 24]) identifies DDIs between indolealkylamines and MAOIs as a fatal serotonin toxicity risk. MAOIs block 5-HT metabolism, amplifying all serotonergic effects. **This interaction should be considered dangerous/potentially fatal.**
- **Tramadol:** Tramadol inhibits serotonin and norepinephrine reuptake and activates μ-opioid receptors; combined with 5-MeO-DiPT's SERT inhibition and 5-HT agonism, this represents a credible serotonin syndrome risk. Seed data rates this as "dangerous" — consistent with mechanism-based reasoning, though no published 5-MeO-DiPT + tramadol case report was found.

### CYP2D6 Considerations
CYP2D6 poor metabolizers will accumulate higher plasma levels of 5-MeO-DiPT due to impaired O-demethylation. Concurrent use of CYP2D6 inhibitors (e.g., fluoxetine, paroxetine, bupropion) may significantly prolong and intensify effects (Yu 2008 [Ref 24]; Narimatsu et al. 2006 [Ref 4]).

### Testing and Identification
Standard immunoassay drug screens do not detect 5-MeO-DiPT. GC-EI-MS and LC-MS methods are required (Vorce & Sklerov 2004 [Ref 23]). Reagent testing: Ehrlich reagent (dimethylaminobenzaldehyde) produces a color reaction with indole-containing compounds including 5-MeO-DiPT; useful for field identification.

### Vulnerable Populations
- Individuals with personal or family history of schizophrenia or psychotic disorders (Erowid [Ref 34])
- CYP2D6 poor metabolizers (increased exposure risk)
- Prior 5-MeO-DiPT users — may be sensitized; subsequent serotonergic exposures may trigger psychosis at lower thresholds (Fuse-Nagase & Nishikawa 2013 [Ref 9])

---

## Tolerance & Dependence

### Tolerance

The seed data indicates tolerance builds "almost immediately after ingestion" with a 3-day half-life and 7-day full reset — consistent with the cross-tolerance class effect documented for serotonergic psychedelics.

**Published evidence:** No 5-MeO-DiPT-specific human tolerance studies exist. The mechanistic basis for rapid psychedelic tolerance is well-established for the class: 5-HT₂A receptor downregulation occurs within hours of agonist exposure. Given 5-MeO-DiPT's 5-HT₂A agonism, rapid tachyphylaxis is expected and is class-consistent. The briefed cross-tolerance within the psychedelic class is also mechanistically sound.

**Reverse tolerance / sensitization:** In contrast to short-term tachyphylaxis for psychedelic effects, the Fuse-Nagase & Nishikawa (2013 [Ref 9]) case suggests that repeated use may sensitize the neural substrate for psychosis, lowering the threshold for drug-induced and possibly drug-triggered psychotic episodes even after cessation.

### Dependence

**Published evidence:** No human dependence studies. The seed data states 5-MeO-DiPT is "not habit-forming." This is class-consistent for serotonergic psychedelics (no robust physical dependence or withdrawal syndrome is documented for the class). No animal self-administration studies for 5-MeO-DiPT were found. DiPT showed hallucinogen-like discriminative stimulus effects in rats (Gatch et al. 2011 [Ref 31]), which establishes abuse liability potential but does not address dependence.

---

## Interactions

### Data from Published Sources

| Interaction | Mechanism | Evidence Level | Source |
|---|---|---|---|
| **MAOIs** | SERT inhibition + 5-HT agonism + blocked 5-HT catabolism → serotonin syndrome | Mechanism-based; class-level case reports | Yu 2008 [Ref 24]; Erowid [Ref 34] |
| **Tramadol** | Dual SERT inhibition; tramadol is SRI/NRI/μ-opioid agonist; combined serotonergic overload | Mechanism-based | Yu 2008 [Ref 24]; seed data |
| **Cocaine** | Both increase DA and 5-HT; combined cardiovascular stress (hypertension, tachycardia, hyperthermia) | Mechanism-based | Noworyta-Sokołowska 2016 [Ref 5] for DA/5-HT overlap |
| **PCP** | Unknown — no published studies found | Not established in published literature | **FLAG** (see below) |
| **MDMA** | Both are serotonergic; potential serotonin syndrome; MDMA is 5-HT releaser, 5-MeO-DiPT is SERT inhibitor + agonist | Mechanism-based | Nakagawa & Kaneko 2008 [Ref 18] |
| **Mescaline** | Both are serotonergic hallucinogens; unknown interaction profile | Not characterized in literature | No published data |
| **Cannabis** | Additive psychotomimetic potential; not characterized | Not characterized | No published data |

**FLAG — PCP "lethal" interaction:** The seed data rates the PCP interaction as "lethal." No published peer-reviewed source was identified that documents a lethal or specifically characterized interaction between 5-MeO-DiPT and PCP. This rating appears to derive from harm reduction databases (PsychonautWiki/Erowid). The mechanism could involve combined serotonergic and dopaminergic overactivation (PCP has sigma agonist/NMDA antagonist properties that interact with DA and 5-HT systems), but this has not been studied for 5-MeO-DiPT specifically. This interaction severity rating requires editorial review and should not be presented as a confirmed published finding.

### Serotonin Syndrome Risk Factors
All combinations with other serotonergic agents are potentially hazardous. 5-MeO-DiPT's dual mechanism (SERT inhibition + direct 5-HT₁A/5-HT₂A agonism) creates a compounded serotonin syndrome risk greater than either mechanism alone.

---

## Legal Status

| Jurisdiction | Status | Basis | Year |
|---|---|---|---|
| **United States** | Schedule I (Controlled) | DEA Controlled Substances Act, permanent placement | Effective 2004 [Ref 15]; temporary placement April 2003 [Ref 16] |
| **Japan** | Controlled | Narcotics and Psychotropics Control Law | Restricted April 2005 |
| **United Kingdom** | NPS (not MDA 1971) | Psychoactive Substances Act 2016; NOT Class A under Misuse of Drugs Act 1971 | PSA 2016 [Ref 27] |
| **Canada** | Unclear | Not explicitly listed in CDSA schedules identified; may be unscheduled | Not confirmed |
| **Australia** | Illegal | Poisons Standard (identified via web search) | Not specifically dated |
| **Germany/EU** | Unclear | Varies by member state; NPS legislative approaches differ | Not confirmed |

**Note on UK:** 5-MeO-DiPT is NOT a Class A/B/C controlled drug under the Misuse of Drugs Act 1971 (unlike 5-MeO-DMT which IS Class A). It falls under the blanket Psychoactive Substances Act 2016. This distinction matters for sentencing and harm reduction messaging [Ref 27].

---

## Clinical Trials

**ClinicalTrials.gov search returned zero results** for 5-MeO-DiPT. No clinical trials exist or are registered. The substance has not been the subject of any registered human research trial.

---

## Community Feedback Analysis

No community feedback was submitted in Part A2 of the brief. Per protocol: **No community feedback submitted.**

---

## Gaps & Flags

### Data Gaps

1. **No human pharmacokinetic data:** Bioavailability, Tmax, Cmax, elimination half-life, volume of distribution — none published for humans. Seed data values for tolerance (half-life: 3 days for tolerance reset) cannot be confirmed from published sources.

2. **Exact receptor Ki/EC50 values inaccessible:** Specific nanomolar binding affinities at 5-HT₁A, 5-HT₂A, 5-HT₂C, and SERT were identified as available in Kozell et al. (2023 [Ref 19]) but full text was inaccessible due to paywall. The qualitative characterization (micromolar at 5-HT₂A/2C, higher at 5-HT₁A) is from Fantegrossi et al. (2006 [Ref 3]).

3. **No controlled human studies:** There are no published controlled human dosing studies, pharmacokinetic studies, or clinical trials. All human data is from case reports, poison center data, and user-report compilations.

4. **SMILES not returned by PubChem API:** The SMILES was confirmed via Chemsrc (web retrieval) rather than the PubChem API directly. Cross-referenced as consistent with the confirmed InChIKey.

5. **Canada legal status unconfirmed:** Could not confirm whether 5-MeO-DiPT is explicitly listed in Canada's CDSA or falls under analog provisions.

6. **EU/Germany scheduling:** Not confirmed from published sources.

7. **Oral bioavailability unknown:** Alternate ROAs mentioned in government reports (smoking, snorting) but no published comparative bioavailability or potency data.

### Safety-Critical Flags

8. **PCP "lethal" interaction [HUMAN REVIEW REQUIRED]:** Seed data rates PCP interaction as "lethal." No published pharmacological study or case report documenting a specific 5-MeO-DiPT/PCP interaction was found. This rating cannot be verified against published sources. The mechanism is speculative (combined DA/5-HT/NMDA/sigma system dysregulation). Should not be presented as confirmed without editorial review and explicit sourcing.

9. **Dose range safety-critical values [HUMAN REVIEW RECOMMENDED]:** The seed data dose ranges (threshold 3mg, light 3–10mg, common 10–15mg, strong 15–20mg, heavy 20+mg) are broadly consistent with published government data (NDIC: 6–20mg typical) and Erowid community data (5–30mg range). The strong dose ceiling (20mg) and "heavy" (20+mg) align with the brief and are not contradicted by any source. However, no published controlled dosing study confirms these as definitively safe upper limits. Flag for editorial discretion.

10. **Neurotoxicity translation to humans:** Animal neurotoxicity data (DNA strand breaks, dopaminergic terminal damage) from Noworyta-Sokołowska et al. (2016, 2019 [Refs 5, 7]) are significant. Human relevance is unknown. Generation agent should not state these findings as established human harms, but must present them as documented in animals with appropriate uncertainty language.

11. **Serotonin releasing agent classification:** Seed data lists this pharmacological class. The evidence base is indirect — primarily extrapolated from in vivo neurotransmitter release data and structural analogy to related tryptamines studied by Rickli et al. (2016 [Ref 22]). Substance-specific in vitro releasing assay data (comparing uptake inhibition vs. release induction) was not identified for 5-MeO-DiPT specifically.

12. **Duration discrepancy:** NDIC reports total duration 3–6h; brief seed data says 4–8h; Erowid notes residual stimulation 10–14h in some users. These are not irreconcilable — dose-dependence and CYP2D6 status likely explain the range. The brief's 4–8h figure appears to be the better central estimate for a typical dose. No published study contradicts this.

5-MeO-DiPT

Value Provenance

Dosing

oraltrace →

Duration

oral

Safety

Toxicity Profiletrace →

Dependence Profiletrace →

Withdrawal Profiletrace →

Tolerance Profiletrace →

Effects & Profile

Contraindications

Timeline Phases

oral

Dose Tier Summaries

History

Sources

Claim Verification

Coverage & Gaps

Research Trail

oraltrace

Toxicity Profiletrace

Dependence Profiletrace

Withdrawal Profiletrace

Tolerance Profiletrace