generation run 2026-05-11
56 min completedmodel pipeline-v5plan not recordedrun/8b3ac758…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
5 further caveats recorded as free text — readable on the working page
Reproduce
- inputs
- 26 source keys (listed under Sources)
- plan
- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
- streams
- none — agent transcripts are persisted from 2026-09 onward
22 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed | PMID 37082754 | 1 | 1 | Co-authored by Chadeayne (who published MPT crystal structure); may include MPT data. |
| 2 | Crossref | DOI 10.1107/s2414314619009623 | 1 | 1 | Primary crystallographic paper directly about MPT - essential. |
| 3 | PubMed · absence | MPT methylpropyltryptamine pharmacology | 0 | — | — |
| 4 | OpenAlex | N-methyl-N-propyltryptamine psychedelic tryptamine | 10 | 5 | Chadeayne 2019 is the only primary paper specifically about MPT. Others are relevant for class pharmacology and toxicology. |
| 5 | PubMed | N,N-dipropyltryptamine DPT psychedelic tryptamine pharmacology | 4 | 4 | DPT is the closest well-studied structural analogue to MPT; these papers inform class pharmacology. |
| 6 | PubChem · absence | N-methyl-N-propyltryptamine / [2-(1H-indol-3-yl)ethyl](methyl)propylamine | 0 | — | Will attempt CID-based lookup after finding CID via web search. |
| 7 | PubMed | PMID 36669875 | 1 | 1 | Directly tests multiple substituted tryptamines including potentially MPT; key pharmacology data source. |
| 8 | PubMed | serotonin syndrome tryptamine MAOI serotonin toxicity | 1 | 1 | Relevant for safety/interactions section. |
| 9 | PMC/Kozell 2023 | MPT in 21-compound tryptamine pharmacology study | 1 | 2 | 4-OH-MPT is the closest pharmacologically characterized structural analogue of MPT. |
| 10 | Erowid TIHKAL | TIHKAL MIPT entry #47, MPT reference | 1 | 1 | Primary historical source for MPT human experience data. Major finding: limited oral activity at tested doses. |
| 11 | PubChem | methylpropyltryptamine (CID 74405270) | 1 | 1 | Chemical identity confirmed via PubChem API. |
| 12 | PubMed | CYP2D6 tryptamine metabolism MAO monoamine oxidase | 4 | 3 | Directly relevant to MPT metabolism pathway via class pharmacology. |
| 13 | WebSearch | MPT methylpropyltryptamine legal status DEA analogue act UK scheduling | 10 | 2 | Legal status data not available in academic databases. |
| 14 | ClinicalTrials.gov · absence | methylpropyltryptamine MPT | 0 | — | Confirms no registered trials. |
| 15 | PubMed | DPT dipropyltryptamine psychotherapy clinical trial | 1 | 1 | DPT psychotherapy reference provides context for MPT analogue clinical history. |
| 16 | Psychedelic Science Review | MPT pharmacology effects dosage | 1 | — | Partially selected but errors flagged. Only qualitative narrative points used. |
| 17 | PsychonautWiki | MPT pharmacology effects dosage | 1 | — | Not selected as primary source due to incomplete and possibly erroneous data. |
| 18 | HandWiki | MPT pharmacology TIHKAL dose legal status | 1 | 3 | Confirmed key legal and dose data points. |
| 19 | OpenAlex | tryptamine 5-HT2A receptor binding SAR structure-activity | 8 | 2 | Context on SAR for tryptamine receptor binding; helps explain MPT predicted activity. |
| 20 | PubMed | psychedelic tryptamine psychiatric adverse effects anxiety psychosis | 2 | 2 | General safety framework for 5-HT2A psychedelics applicable to MPT class. |
| 21 | WebSearch | methylpropyltryptamine CAS number chemical registry | 10 | — | CAS number not confirmed; flagged for editorial review. |
| 22 | cross_reference | MPT vs DPT vs MIPT structural comparison | — | — | Important for context and SAR discussion. |
53 claims by section — every cited sentence, checked against its source
safety18 · 10 ok
SSRIs and SNRIs (moderate–unknown): SSRIs may blunt 5-HT₂A-mediated psychedelic effects through receptor downregulation while simultaneously increasing serotonin toxicity risk through pharmacodynamic summationsupported
Evaluates DDI risks and serotonin toxicity potential between serotonergic psychedelics and SSRIs/MAOIs. s00213-021-05876-x
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Absolute contraindications: * Concurrent MAOI use: Eliminates primary metabolic pathway; risk of fatal serotonin syndrome * Personal history of psychotic disorders (schizophrenia, schizoaffective disorder): 5-HT₂A agonism may precipitate or exacerbate psychosispartially supported
MAO-A inhibition by harmaline sharply increases 5-MeO-DMT exposure. dmd.112.050724
Claim in safety — inconclusiveinconclusiveworking →
Nonlinear pharmacokinetics at higher tryptamine doses — resulting from MAO-A saturation — mean that the transition from inactive to fully active doses may be abrupt and unpredictablesupported
5-MeO-DMT AUC increases nonproportionally with dose; Michaelis-Menten elimination; intoxication risk increases disproportionately at higher doses. dmd.111.039107
Claim in safety — inconclusiveinconclusiveworking →
Psychosis precipitation: Classic psychedelics can exacerbate or precipitate psychotic episodes in individuals with personal or family history of psychosis, bipolar disorder, or schizophreniasupported
potential harms include...exacerbation of mental illness in psychosis-predisposed individuals. j.neuropharm.2018.05.012
HPPD: Hallucinogen persisting perception disorder has been associated with 5-HT₂A agonist use. Risk factors, prevalence, and mechanism remain incompletely characterized for the classsupported
HPPD associated with 5-HT2A agonist drugs. Symptoms result from misbalance of inhibitory-excitatory visual processing. j.euroneuro.2014.05.008
HPPD: Hallucinogen persisting perception disorder has been associated with 5-HT₂A agonist use. Risk factors, prevalence, and mechanism remain incompletely characterized for the classsupported
Flashback phenomena can occur after 5-HT2A psychedelic use. s00213-022-06066-z
Smith et al. (2014) found that tolerance to head-twitch response did not develop with daily DPT or DiPT administration in mice — unlike phenethylamine hallucinogens (DOI, 2C-T-7) which produced rapid tolerancesupported
DPT and DIPT: tolerance to HTR did not develop with daily administration, unlike DOI and 2C-T-7. jpet.114.219337
Claim in safety — inconclusiveinconclusiveworking →
The 5-HT₂A psychedelic class demonstrates minimal reinforcing effects and low dependence liability in animal self-administration paradigmssupported
Psilocybin has limited reinforcing effects in preclinical models...Non-self-administering in non-human primates. j.neuropharm.2018.05.012
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Absolute contraindications: * Concurrent MAOI use: Eliminates primary metabolic pathway; risk of fatal serotonin syndrome * Personal history of psychotic disorders (schizophrenia, schizoaffective disorder): 5-HT₂A agonism may precipitate or exacerbate psychosispartially supported
potential harms include...exacerbation of mental illness in psychosis-predisposed individuals. j.neuropharm.2018.05.012
Relative contraindications: * Bipolar disorder: Risk of manic episode precipitation * Family history of psychosis: Elevated vulnerability to psychotic decompensation * Concurrent lithium: Possible seizure risk (community-reported, mechanism unclear) * Concurrent SSRI/SNRI therapy: Unpredictable effect modification and serotonin toxicity potential * Cardiovascular disease: Tryptamine-induced sympathomimetic effects may pose risk in compromised cardiac functionpartially supported
Evaluates DDI risks and serotonin toxicity potential between serotonergic psychedelics and SSRIs/MAOIs. s00213-021-05876-x
Claim in safety — inconclusiveinconclusiveworking →
pharmacology10 · 7 ok
As an unsubstituted N,N-dialkyltryptamine, MPT is presumed to act primarily as a serotonin 5-HT₂A receptor agonist — the established mechanism of psychedelic action for the tryptamine classsupported
M100907 (5-HT2A antagonist) more profound than WAY-100635 (5-HT1A antagonist). 5-HT2A is primary site; 5-HT1A modulates effects. pmid:17905422
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Additional targets may include the serotonin transporter (SERT), where N,N-dialkyltryptamines act as substrates rather than reuptake inhibitors — DPT shows a Ki of 0.594 μM for SERT inhibition in human plateletssupported
DPT Ki for SERT inhibition = 0.594 μM. High binding-to-uptake ratios support substrate (not blocker) behavior. s00702-009-0308-8
Whether MPT shares sigma-1 receptor affinity, as demonstrated for DMT, is unknown.supported
DMT bound to sigma-1 receptors...DMT is an endogenous sigma-1 receptor agonist. science.1166127
By class analogy, the primary inactivation pathway for non-ring-substituted tryptamines is MAO-A-mediated oxidative deaminationsupported
inactivated by MAO-A deamination. MAOI co-administration prolongs and amplifies effects. pmid:20942780
Claim in pharmacology — inconclusiveinconclusiveworking →
CYP2D6 serves a secondary metabolic role; polymorphism at this locus may produce inter-individual variability in exposure and effects.supported
CYP2D6 plays important polymorphic role in IAA metabolism. s12248-008-9028-5
CYP2D6 serves a secondary metabolic role; polymorphism at this locus may produce inter-individual variability in exposure and effects.supported
CYP2D6 mediates O-demethylation; unified PK model developed. dmd.112.050724
At higher doses, tryptamine exposure can increase non-proportionally due to saturation of MAO-A capacity, producing nonlinear pharmacokineticssupported
5-MeO-DMT AUC increases nonproportionally with dose; Michaelis-Menten elimination; brain concentrations also nonlinear. dmd.111.039107
pharmacokinetic-detail7 · 4 ok
Primary pathway: MAO-A-mediated oxidative deamination of the ethylamine side chain, producing indole-3-acetic acid derivativessupported
inactivated by MAO-A deamination. pmid:20942780
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Secondary pathway: CYP2D6-mediated N-dealkylation (removal of propyl or methyl group) and possible ring hydroxylationpartially supported
CYP2D6 mediates O-demethylation. dmd.112.050724
Shen et al. (2011) demonstrated nonlinear pharmacokinetics for 5-MeO-DMT in mice — at higher doses, plasma exposure increased disproportionately due to MAO-A saturationsupported
5-MeO-DMT AUC increases nonproportionally with dose; Michaelis-Menten elimination. dmd.111.039107
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
CYP2D6 inhibitors (paroxetine, fluoxetine, quinidine) may produce a secondary exposure increase.supported
CYP2D6 plays important polymorphic role in IAA metabolism. s12248-008-9028-5
summary6 · 3 ok
N-Methyl-N-propyltryptamine (MPT) is an unsubstituted tryptamine psychedelic with a mixed methyl–propyl N,N-dialkyl substitution pattern (molecular formula C₁₄H₂₀N₂, MW 216.32 g/mol)supported
The title compound {systematic name: [2-(1H-indol-3-yl)ethyl](methyl)propylamine}, C14H20N2 s2414314619009623
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
The 5-HT₂A psychedelic class carries minimal dependence liability, and tryptamine-class compounds may show reduced tolerance development compared to phenethylamine psychedelicspartially supported
Psilocybin has limited reinforcing effects in preclinical models...Non-self-administering in non-human primates. j.neuropharm.2018.05.012
The 5-HT₂A psychedelic class carries minimal dependence liability, and tryptamine-class compounds may show reduced tolerance development compared to phenethylamine psychedelicssupported
DPT and DIPT: tolerance to HTR did not develop with daily administration, unlike DOI and 2C-T-7. Tryptamine-derived hallucinogens may have reduced tolerance potential vs phenethylamine-derived 5-HT2A agonists. jpet.114.219337
receptor-pharmacology5 · 3 ok
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
McKenna et al. (1990) demonstrated that N,N-dialkyl group size is a secondary determinant of 5-HT receptor affinity, with groups larger than N,N-diisopropyl producing marked reductions in bindingsupported
N,N-dialkyl groups larger than diisopropyl markedly reduce affinity at both 5-HT2A and 5-HT1A. pmid:2139186
Puigseslloses et al. (2024) showed that amino group molecular size significantly influences SERT affinity for 5-methoxy-tryptamines, with smaller substituents conferring higher transporter affinitysupported
Molecular size of amino group influences SERT affinity. s41380-024-02506-8
N,N-dialkyltryptamines including DPT and MiPT function as SERT and VMAT2 substrates with high binding-to-uptake ratios, indicating they are transported into cells rather than simply blocking reuptakesupported
DMT, MIPT, DPT, and DIPT tested as SERT and VMAT2 substrates. High binding-to-uptake ratios support substrate (not blocker) behavior. s00702-009-0308-8
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
history3 · 2 ok
Claim in history — inconclusiveinconclusiveworking →
The Chadeayne group has published crystallographic structures of numerous structurally related tryptamines, including EPT (N-ethyl-N-propyltryptamine) and MiPT, as part of a systematic characterization effort focused on DMT analogues.supported
Solid-state structures of hydrofumarate salts of EPT (N-ethyl-N-propyltryptamine) and MALT. 2D hydrogen-bond networks in crystal structure. s2056989020008683
The Chadeayne group has published crystallographic structures of numerous structurally related tryptamines, including EPT (N-ethyl-N-propyltryptamine) and MiPT, as part of a systematic characterization effort focused on DMT analogues.supported
Crystal structures of MiPT and 4-HO-MiPT fumarate salts reported. Both possess protonated tryptammonium cation and hydrogen fumarate anion. s2056989019011253
comparative-pharmacology2 · 2 ok
Co-administration with MAO inhibitors would be expected to render MPT orally active — though this combination carries severe serotonin toxicity risksupported
MAO-A inhibition by harmaline sharply increases 5-MeO-DMT exposure; CYP2D6 mediates O-demethylation. dmd.112.050724
5-HT₂A Ki values from Kozell et al. (2023)supported
Pharmacologic activity of 21 substituted tryptamines at 5-HT1A, 5-HT2A, 5-HT2C receptors and SERT. jpet.122.001454
chemistry1 · 1 ok
Chadeayne et al. (2019) determined the crystal structure of MPT, reporting that the molecule crystallizes with a single molecule in the asymmetric unitsupported
The title compound {systematic name: [2-(1H-indol-3-yl)ethyl](methyl)propylamine}, C14H20N2, has a single molecule in the asymmetric unit. s2414314619009623
clinical-evidence1 · 1 ok
Reiche et al. (2018) identified one published clinical trial (N = 30) using DPT in the treatment of anxiety and depression in patients with life-threatening illnesssupported
Systematic review of 11 trials (N=445) of psychedelics for existential distress. One DPT trial (N=30) included. j.pnpbp.2017.09.012