generation run 2026-05-10
76 min completedmodel pipeline-v5plan not recordedrun/8709d570…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
4 further caveats recorded as free text — readable on the working page
Reproduce
- inputs
- 29 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
17 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed · absence | 5-methoxy-N,N-diisopropyltryptamine benzofuran analog pharmacology | 0 | — | Query too specific for 5-MeO-DiBF |
| 2 | ClinicalTrials.gov · absence | 5-MeO-DiBF benzofuran tryptamine psychedelic | 0 | — | Expected; compound is research chemical with no human trials |
| 3 | OpenAlex | 5-MeO-DiPT foxy methoxy tryptamine pharmacology serotonin receptor | 10 | 7 | All directly relevant to 5-methoxytryptamine pharmacology class |
| 4 | PubMed | 5-MeO-DiPT pharmacology receptor binding serotonin | 1 | 1 | 5-MeO-DiPT GTPgammaS binding data useful as structural analog reference |
| 5 | PubMed | 5-MeO-DiPT foxy methoxy tryptamine toxicity animal study pharmacology | 4 | 4 | All 4 directly relevant to closest structural analog 5-MeO-DiPT |
| 6 | PubMed | benzofuran tryptamine analog serotonin 5-HT2A receptor binding novel psychoactive | 1 | 1 | Directly relevant benzofuran pharmacology paper |
| 7 | PubChem | 5-MeO-DiBF | 1 | 1 | Primary chemical identity confirmation |
| 8 | OpenAlex | 5-MeO-DiBF benzofuran psychedelic novel psychoactive | 4 | 2 | — |
| 9 | PubMed | 5-MeO-DiBF benzofuran psychedelic | 10 | 1 | — |
| 10 | ClinicalTrials.gov · absence | 5-MeO-DiBF benzofuran tryptamine psychedelic | 0 | — | Expected for research chemical |
| 11 | WebSearch | 5-MeO-DiBF legal status scheduling UK US EU Australia | 10 | 3 | Legal status data not available via API tools |
| 12 | WebSearch | 5-MeO-DiPT DEA Schedule I 2004 | 10 | 2 | US legal analog context for 5-MeO-DiBF |
| 13 | PubChem REST API | CID 125276632 chemical properties | 1 | 3 | Complete chemical identity verification |
| 14 | Erowid | 5-MeO-DiBF Disappointed experience report ID 107325 | 1 | 3 | Only detailed individual user report with dose information |
| 15 | HandWiki | 5-MeO-DiBF | 1 | 3 | Only secondary source with specific historical data |
| 16 | EUDA (formerly EMCDDA) | 5-MeO-DiBF first identified forensic Slovenia 2015 | 1 | 2 | Historical origin data |
| 17 | Erowid | 5-MeO-DiBF experience reports | 4 | 1 | Only primary user experience data available for dose and effect characterization |
57 claims by section — every cited sentence, checked against its source
safety15 · 11 ok
The Mohr et al. (2022) comprehensive review of NPS adverse events from 2017–2020, covering 1,319 cases and over 60 confirmed novel psychoactive substances, did not include 5-MeO-DiBF.supported
Review of 1,319 NPS adverse events 2017-2020; 60+ NPS with confirmed adverse events documented; no 5-MeO-DiBF cases identified. bkac023
Claim in safety — inconclusiveinconclusiveworking →
Compton et al. (2006) found that repeated adolescent 5-MeO-DiPT exposure (5 mg/kg) produced persistent impairment in response-learning tasks, consistent with long-term serotonergic disruptionsupported
Repeated adolescent 5-MeO-DiPT (5 mg/kg) impaired response-learning tasks, suggesting serotonergic disruption similar to MDMA. pmid:16933659
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Gatch et al. (2011) assessed DiPT-class tryptamines in DOM-trained rodent models and found low potency in abuse paradigms (ED₅₀ = 1.94 mg/kg for DiPT substitution in DOM discrimination)supported
Abuse liability of three substituted tryptamines in rodent models; DiPT substituted in DOM-trained rats at ED50=1.94 mg/kg. jpet.111.179705
Serotonin syndrome involves excessive 5-HT₁A and 5-HT₂A activation and can be life-threatening.supported
SS is life-threatening condition from excessive serotonergic activity; involves 5-HT1A and 5-HT2A. pjnns.106987
Serotonin syndrome involves excessive 5-HT₁A and 5-HT₂A activation and can be life-threatening.supported
Review of serotonin toxicity pathophysiology, Hunter criteria, severity assessment and management. Severe cases require aggressive supportive care including benzodiazepines, intubation, and active cooling. bcp.16152
Tramadol functions as a weak serotonin reuptake inhibitor and has been implicated in fatal serotonin toxicity reactions when combined with other serotonergic drugssupported
Tramadol is a weak SRI involved in serotonin toxicity with MAOIs. Combination of serotonergic drugs by different mechanisms can raise intra-synaptic serotonin to life-threatening levels. pmid:16051647
This is a class-level contraindication applicable to 5-MeO-DiBF.supported
Combination of serotonergic drugs by different mechanisms can raise intra-synaptic serotonin to life-threatening levels. pmid:16051647
CYP2D6 inhibitors: If 5-MeO-DiBF is metabolized by CYP2D6 as predicted, co-administration of potent CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion) could increase plasma concentrations unpredictably.supported
CYP2D6 plays polymorphic role in metabolism of indolealkylamine drugs of abuse. DDIs can occur leading to serotonin toxicity. s12248-008-9028-5
Cyproheptadine (a 5-HT₂A antagonist) has been used as an antidote in clinical settings, though evidence for its efficacy remains limited.supported
Systematic review of cyproheptadine for serotonin toxicity; 12 articles (11 case reports, 1 series); evidence very low quality; efficacy not established. 1742-6723.14554
Concurrent tramadol use: Elevated serotonin toxicity risk via dual serotonergic mechanisms. Absolute contraindication.supported
Tramadol is a weak SRI involved in serotonin toxicity with MAOIs. Combination of serotonergic drugs by different mechanisms can raise intra-synaptic serotonin to life-threatening levels. pmid:16051647
Concurrent CYP2D6 inhibitor use: Potential for pharmacokinetic potentiation if 5-MeO-DiBF is a CYP2D6 substrate. Relative contraindication.supported
CYP2D6 plays polymorphic role in metabolism of indolealkylamine drugs of abuse. DDIs can occur leading to serotonin toxicity. s12248-008-9028-5
pharmacology12 · 7 ok
In vitro, 5-MeO-DiPT displays much higher affinity for 5-HT₁A receptors than for 5-HT₂A or 5-HT₂C receptors, the latter showing only micromolar-range bindingsupported
Micromolar 5-HT2A/2C affinity but higher 5-HT1A affinity in vitro. pmid:16460788
Despite this apparent 5-HT₁A selectivity in binding assays, the hallucinogenic effects of 5-MeO-DiPT are mediated primarily through 5-HT₂A: the selective 5-HT₂A antagonist M100907 potently antagonizes both the head-twitch response in mice and LSD-discrimination generalization in rats, while the 5-HT₁A antagonist WAY-100635 produces no significant effectsupported
5-MeO-DiPT induces head-twitch response in mice (M100907-reversible). 75% LSD-discrimination generalization in rats. 5-HT2A primary site of hallucinogenic action despite in vitro 5-HT1A selectivity. pmid:16460788
Sogawa et al. (2007) demonstrated inhibition of [³H]serotonin uptake in COS-7 cells and rat striatal synaptosomes without reverse transport — distinguishing 5-MeO-DiPT from MDMA-type releaserssupported
5-MeO-DiPT competitively inhibits SERT at concentrations similar to cocaine; does not cause reverse transport. pmid:17382495
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
The broader receptorome context is relevant: Ray (2010) profiled 25 psychedelic drugs at 51 receptor sites via NIMH-PDSP and found that psychedelic drugs interact with up to 42 of 49 tested sites, indicating that receptor selectivity is less absolute than commonly assumed. 5-MeO-DiBF is expected to be a multi-target agent, with 5-HT₁A and 5-HT₂A as its primary sites.supported
Receptor affinity pharmacology of 25 psychedelic drugs at 51 receptors, transporters, and ion channels (NIMH-PDSP). Phenylalkylamines interact with 42 of 49 sites. journal.pone.0009019
Warren et al. (2024) published cryo-EM structures of 5-HT₁A in complex with 5-MeO-DMT and analogs, characterizing how N-substituent bulk and 5-methoxy positioning determine selectivity between 5-HT₁A and 5-HT₂A — and thus whether a compound produces primarily psychedelic (5-HT₂A-dominant) or anxiolytic (5-HT₁A-dominant) effectssupported
Cryo-EM structures of 5-HT1A with 5-MeO-DMT and analogues; SAR of 5-methoxytryptamines at 5-HT1A and 5-HT2A; 5-HT1A-selective analogue devoid of hallucinogenic effects while retaining anxiolytic/antidepressant activity. s41586-024-07403-2
The N,N-diisopropyl substitution pattern, shared with 5-MeO-DiPT, is expected to confer oral bioavailability by reducing susceptibility to monoamine oxidase (MAO-A) deamination — the primary first-pass metabolic pathway for DMT-class tryptaminessupported
DMT acts via 5-HT1A/2A/2C agonism; MAO-A substrate; beta-carboline MAOIs increase bioavailability and duration. s00018-024-05353-6
Claim in pharmacology — not_supportednot supportedworking →
CYP2D6 is the major enzyme involved in indolealkylamine metabolism, with genetic polymorphism in CYP2D6 representing an additional toxicity risk factor for this classsupported
CYP2D6 plays polymorphic role in metabolism of indolealkylamine drugs of abuse. DDIs can occur leading to serotonin toxicity. s12248-008-9028-5
Claim in pharmacology — inconclusiveinconclusiveworking →
comparative-pharmacology5 · 4 ok
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Neurotoxicity: 5-MeO-DiPT produces persistent DNA strand breaks in rat brain tissue up to 60 days post-treatment at 5–20 mg/kg and impairs response learning after repeated adolescent exposure. Whether the benzofuran modification alters this toxicological profile is unknown.supported
DNA strand breaks persist 60 days post-treatment indicating neurotoxicity. s12640-016-9654-0
Neurotoxicity: 5-MeO-DiPT produces persistent DNA strand breaks in rat brain tissue up to 60 days post-treatment at 5–20 mg/kg and impairs response learning after repeated adolescent exposure. Whether the benzofuran modification alters this toxicological profile is unknown.partially supported
Repeated adolescent 5-MeO-DiPT (5 mg/kg) impaired response-learning tasks, suggesting serotonergic disruption similar to MDMA. pmid:16933659
The APB compounds — 5-APB, 6-APB, 5-MAPB — function primarily as monoamine transporter substrates and releasers (entactogen/empathogen profile), with in vitro pharmacology characterized by Rickli et al. (2015). 5-MeO-DiBF is a direct serotonin receptor agonist with predicted SERT inhibition (not release)supported
Benzofurans pharmacologically characterized in vitro; act as indirect monoamine agonists interacting with transporters similarly to MDMA. bph.13128
Glatfelter et al. (2023) provided comprehensive receptor binding profiles for tryptamine psychedelics, establishing the multi-target binding framework within which 5-MeO-DiBF is predicted to operatesupported
Receptor binding profiles of tryptamine-based psychedelics. Multiple 5-HT receptors targeted including 5-HT1A. 5-HT2A mediates HTR; 5-HT1A mediates hypothermia and hypolocomotion. acsptsci.2c00222
neuroscience5 · 3 ok
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
Compton et al. (2006) found that repeated adolescent exposure to 5-MeO-DiPT (5 mg/kg) produced persistent impairment in response-learning tasks, consistent with long-term serotonergic disruption analogous to MDMA-type neurotoxicitysupported
Repeated adolescent 5-MeO-DiPT (5 mg/kg) impaired response-learning tasks, suggesting serotonergic disruption similar to MDMA. pmid:16933659
The SERT inhibition demonstrated for 5-MeO-DiPT adds a reuptake-inhibition component to the pharmacological profile that pure 5-HT₂A agonists (e.g., psilocin) lacksupported
5-MeO-DiPT competitively inhibits SERT at concentrations similar to cocaine; does not cause reverse transport. pmid:17382495
Nakagawa (2008) reviewed the neuropsychotoxicity mechanisms of 5-MeO-DiPT, further documenting serotonergic neurotoxicity.supported
In vitro studies on molecular targets and neural adaptation of 5-MeO-DiPT using Xenopus oocytes and organotypic slice cultures. pmid:18198474
pharmacokinetic-detail5 · 3 ok
By analogy with indolealkylamines, CYP2D6 is predicted to be a major metabolic enzyme, with CYP2D6 polymorphism representing an additional toxicity risk factor in poor or ultrarapid metabolizerssupported
CYP2D6 plays polymorphic role in metabolism of indolealkylamine drugs of abuse. DDIs can occur leading to serotonin toxicity. s12248-008-9028-5
The N,N-diisopropyl substitution reduces susceptibility to MAO-A deamination — the principal first-pass barrier for unsubstituted tryptamines such as DMTsupported
DMT acts via 5-HT1A/2A/2C agonism; MAO-A substrate; beta-carboline MAOIs increase bioavailability and duration. s00018-024-05353-6
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
For structurally related benzofuran and benzothiophene psychedelics (APBT class), CYP1A2, CYP2D6, CYP3A4, and CYP3A5 have been identified as the principal metabolic isozymes, with aromatic hydroxylation as the dominant Phase I reactionsupported
APBT psychedelics: CYP1A2, CYP2D6, CYP3A4, CYP3A5 involved in hydroxylation; metabolic patterns similar to related 5- and 6-APB analogues. j.tox.2026.154402
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
summary5 · 2 ok
Claim in summary — inconclusiveinconclusiveworking →
Its pharmacological class — 5-HT₁A and 5-HT₂A agonism — is inferred entirely from structural analogy with 5-MeO-DiPT, whose hallucinogenic effects are mediated primarily through 5-HT₂A despite higher in vitro affinity at 5-HT₁Asupported
Micromolar 5-HT2A/2C affinity but higher 5-HT1A affinity in vitro. 5-HT2A primary site of hallucinogenic action despite in vitro 5-HT1A selectivity. pmid:16460788
The structural analog 5-MeO-DiPT produces persistent DNA strand breaks in rat brain tissue at doses of 5–20 mg/kg, raising unresolved questions about the neurotoxic potential of the benzofuran derivativesupported
DNA strand breaks persist 60 days post-treatment indicating neurotoxicity. s12640-016-9654-0
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
receptor-pharmacology4 · 4 ok
M100907 (a selective 5-HT₂A antagonist) potently blocked both the head-twitch response and LSD-like discriminative stimulus effects, while WAY-100635 (a selective 5-HT₁A antagonist) had no significant effectsupported
5-MeO-DiPT induces head-twitch response in mice (M100907-reversible). 75% LSD-discrimination generalization in rats. 5-HT2A primary site of hallucinogenic action despite in vitro 5-HT1A selectivity. pmid:16460788
Warren et al. (2024) provide the structural framework for understanding how the 5-methoxy group and N-substituent bulk determine 5-HT₁A versus 5-HT₂A selectivity in the tryptamine scaffold, but the benzofuran modification was not tested in that study.supported
Cryo-EM structures of 5-HT1A with 5-MeO-DMT and analogues; SAR of 5-methoxytryptamines at 5-HT1A and 5-HT2A. s41586-024-07403-2
Nichols et al. (2014) characterized SAR of 5-methoxytryptamines at the 5-HT₂ receptor family, providing potency context for the structural class, though benzofuran analogs were not includedsupported
N-Benzyl-5-methoxytryptamine analogues at 5-HT2A/2B/2C; EC50 7.6-63 nM for potent compounds; head-twitch response correlated with 5-HT2A potency. cn500292d
Kozell et al. (2023) published broad receptor binding data for substituted tryptamines including 5-methoxy analogs, further defining the pharmacological space 5-MeO-DiBF is predicted to occupy.supported
21 substituted tryptamines at 5-HT1A, 5-HT2A, 5-HT2C and SERT; 4-substituted compounds show high selectivity for 5-HT2AR. jpet.122.001454
history3 · 2 ok
Claim in history — inconclusiveinconclusiveworking →
Its structural parent is 5-MeO-DiPT (5-methoxy-N,N-diisopropyltryptamine), a synthetic tryptamine colloquially known as "Foxy" or "Foxy Methoxy" that appeared on the United States recreational market in 1999. 5-MeO-DiPT was permanently placed into Schedule I of the US Controlled Substances Act on September 29, 2004supported
DEA permanently places AMT and 5-MeO-DiPT into Schedule I of the CSA based on DHHS recommendation. pmid:15455477
Chapman (2017) published ¹H NMR spectral data for 5-MeO-DiBF and related benzofuran tryptamine analogs purchased from grey-market internet vendors, confirming that the spectra were consistent with the labelled compoundssupported
1H NMR spectra of 43 alleged psychedelic tryptamines and benzofuran analogues from grey-market vendors; spectra consistent with labelled compounds. isomerdesign-5
chemistry1 · 1 ok
5-MeO-DiBF is structurally distinct from the aminopropylbenzofuran (APB) class — compounds such as 5-APB, 6-APB, and 5-MAPB — which attach the aminoalkyl chain at the 1-position of the benzofuran ring and function as monoamine transporter releasers (entactogens) rather than direct serotonin receptor agonistssupported
Benzofurans pharmacologically characterized in vitro; act as indirect monoamine agonists interacting with transporters similarly to MDMA. bph.13128
clinical-evidence1 · 1 ok
The Mohr et al. (2022) comprehensive review of NPS adverse events from 2017–2020, covering 1,319 cases and over 60 confirmed novel psychoactive substances, did not include 5-MeO-DiBF — indicating an absence of published clinical case reports during the review period.supported
Review of 1,319 NPS adverse events 2017-2020; 60+ NPS with confirmed adverse events documented; no 5-MeO-DiBF cases identified. bkac023
legal-status1 · 1 ok
In the United States, while not explicitly listed under the Controlled Substances Act, the Federal Analogue Act may apply given its structural and pharmacological similarity to the Schedule I substance 5-MeO-DiPTsupported
DEA permanently places AMT and 5-MeO-DiPT into Schedule I of the CSA based on DHHS recommendation. pmid:15455477