generation run 2026-04-26
53 min completedmodel pipeline-v5plan not recordedrun/7f085aee…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
none raised on this run
Reproduce
- inputs
- 36 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
28 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | OpenAlex | 5-MeO-DiPT tryptamine psychedelic pharmacology | 10 | 4 | Selected highly-cited papers with direct relevance to 5-MeO-DiPT pharmacology and tryptamine class context |
| 2 | PubMed | foxy methoxy tryptamine Schedule I DEA scheduling | 2 | 2 | Primary regulatory documents for US legal status |
| 3 | PubMed · absence | 5-MeO-DIPT SERT 5-HT2A 5-HT1A receptor | 0 | — | — |
| 4 | PubMed · absence | 5-methoxy-N,N-diisopropyltryptamine receptor binding serotonin affinity | 0 | — | — |
| 5 | OpenAlex | 5-MeO-DiPT foxy methoxy receptor binding pharmacology | 10 | 4 | Key pharmacology papers with receptor binding data and metabolism data |
| 6 | PubChem | 5-MeO-DiPT | 1 | 1 | Confirms chemical identity; SMILES not returned but all other identity fields verified |
| 7 | PubMed | 5-MeO-DiPT foxy methoxy pharmacology | 15 | 15 | All selected as directly relevant to 5-MeO-DiPT pharmacology, toxicology, legal status, or case reports |
| 8 | PubMed | 5-methoxy diisopropyltryptamine head twitch response serotonin hallucinogen | 3 | 1 | Fantegrossi 2006 is key in vivo pharmacology paper with receptor binding assays |
| 9 | WebSearch/WebFetch | 5-MeO-DiPT UK Psychoactive Substances Act 2016 | 10 | 2 | — |
| 10 | PubMed | Shulgin Carter 1980 DiPT 5-MeO-DiPT original paper | 1 | 1 | — |
| 11 | WebSearch | 5-MeO-DiPT Ki binding affinity nM radioligand | 10 | — | — |
| 12 | PubMed | structural pharmacology 5-methoxytryptamines Nature 2024 | 1 | 1 | — |
| 13 | PubMed | 5-MeO-DIPT GC-MS LC-MS urinalysis detection forensic | 1 | 1 | — |
| 14 | PubMed | tryptamine hallucinogen discriminative stimulus abuse liability | 4 | 3 | — |
| 15 | PubMed/OpenAlex | receptor binding profiles novel tryptamines | 5 | 4 | — |
| 16 | WebSearch | 5-MeO-DiPT Canada Controlled Drugs Substances Act | 10 | — | — |
| 17 | PubMed | foxy methoxy tryptamine Schedule I DEA scheduling | 2 | 2 | — |
| 18 | WebSearch | 5-MeO-DiPT Japan Narcotics Control Law Schedule 2004 2005 | 10 | 1 | — |
| 19 | PubMed | 5-MeO-DiPT metabolism pharmacokinetics | 1 | 1 | — |
| 20 | PubMed | 5-MeO-DIPT Japanese drug abuse psychosis case | 1 | 1 | — |
| 21 | WebFetch | — | 1 | 1 | — |
| 22 | WebSearch | 5-MeO-DiPT PCP lethal interaction | 10 | — | — |
| 23 | Crossref/verify_doi | DOI 10.1111/j.1360-0443.2006.01573.x | 1 | 1 | — |
| 24 | WebFetch | — | 1 | 1 | — |
| 25 | WebSearch | 5-MeO-DiPT UK Psychoactive Substances Act Australia | 10 | 2 | — |
| 26 | WebFetch | — | 1 | 1 | — |
| 27 | ClinicalTrials.gov · absence | 5-MeO-DiPT foxy methoxy tryptamine | 0 | — | — |
| 28 | WebSearch | 5-MeO-DiPT CAS number SMILES melting point physical properties | 10 | 1 | — |
168 claims by section — every cited sentence, checked against its source
safety46 · 12 ok
Claim in safety — inconclusiveinconclusiveworking →
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Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
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Li et al. confirmed acute toxic effects in mice but did not report lethal dose parameterssupported
AMT showed acute toxic effects in mice. fbp.0000000000000841
Reported acute adverse effects from case reports, government data, and toxicology reviews include:supported
Review of tryptamine toxicology; morbidity considerable and underestimated. ijms21239279
Reported acute adverse effects from case reports, government data, and toxicology reviews include:supported
Comprehensive review on tryptamine hallucinogens including AMT; physiological and toxicological effects. s00204-015-1513-x
Reported acute adverse effects from case reports, government data, and toxicology reviews include:supported
Serotonergic effects predominate in toxicity; management primarily supportive. 15563650.2011.615318
Noworyta-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.supported
DNA strand breaks persist 60 days post-treatment indicating neurotoxicity. s12640-016-9654-0
Repeated-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 tissuesupported
Adolescent repeated 5-MeO-DIPT exposure: caspase-3 activation; oxidative DNA damage. Long-term neurotoxicity in developing brain. s11419-018-0433-x
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
No 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.supported
DOM used as training drug. DIPT fully substituted at ED50=1.94 mg/kg. jpet.111.179705
MAOIs 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 overactivationsupported
DDIs can occur at pharmacokinetic and pharmacodynamic levels leading to serotonin toxicity. s12248-008-9028-5
Added 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.partially supported
DDIs can occur at pharmacokinetic and pharmacodynamic levels leading to serotonin toxicity. s12248-008-9028-5
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
CYP2D6 inhibitors — including fluoxetine, paroxetine, and bupropion — impair 5-MeO-DiPT O-demethylation, producing phenocopied poor metabolizer kinetics with elevated parent compound exposure.supported
CYP2D6 polymorphism represents additional risk factor. DDIs can occur at pharmacokinetic and pharmacodynamic levels. s12248-008-9028-5
Claim in safety — not_supportednot supportedworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
cytochrome P450 2D6 poor metabolizer status — whether genetic or medication-induced — increases exposure and toxicity risk.supported
CYP2D6 polymorphism represents additional risk factor. DDIs can occur at pharmacokinetic and pharmacodynamic levels leading to serotonin toxicity. s12248-008-9028-5
Claim in safety — inconclusiveinconclusiveworking →
Pregnancy and breastfeeding are absolute contraindications given absent reproductive safety data and documented genotoxicity in animal models.supported
DNA strand breaks persist 60 days post-treatment indicating neurotoxicity. s12640-016-9654-0
pharmacology34 · 8 ok
Claim in pharmacology — inconclusiveinconclusiveworking →
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Claim in pharmacology — inconclusiveinconclusiveworking →
A 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.supported
Micromolar 5-HT2A/2C affinity but higher 5-HT1A affinity. 5-HT2A primary despite in vitro 5-HT1A selectivity. pmid:16460788
Fantegrossi 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 actionsupported
5-MeO-DIPT induced head-twitch in mice (M100907-reversible). pmid:16460788
In 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 hallucinogenspartially supported
Partial LSD-discrimination generalization in rats. pmid:16460788
Claim in pharmacology — not_supportednot supportedworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
SERT 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.supported
5-MeO-DiPT acts as potent SERT inhibitor. s12640-016-9654-0
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Li et al. documented significant effects on dopamine and its metabolites DOPAC and HVA across prefrontal cortex, nucleus accumbens, dorsolateral striatum, and hippocampussupported
Systematic study of DA, 5-HT and metabolite changes in PFC, NAc, DLS, hippocampus. j.neures.2025.04.006
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Poor metabolizers cannot efficiently O-demethylate 5-MeO-DiPT, potentially resulting in higher systemic exposure and prolonged duration of effectsupported
CYP2D6 plays important polymorphic role in metabolism of IAA drugs of abuse including tryptamine derivatives. CYP2D6 polymorphism represents additional risk factor. s12248-008-9028-5
Concurrent use of CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion) may produce the same phenocopy effect.supported
CYP2D6 polymorphism represents additional risk factor. DDIs can occur at pharmacokinetic and pharmacodynamic levels leading to serotonin toxicity. s12248-008-9028-5
Claim in pharmacology — inconclusiveinconclusiveworking →
Vorce and Sklerov confirmed urinary detection at 229 ng/mL by LC-MS with a limit of detection of 5 ng/mL.partially supported
LOD 5-10 ng/mL in blood, 25-1500 ng/mL range in urine by LC-MS. pmid:15516287
summary24 · 9 ok
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
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Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
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The 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 2004partially supported
DEA reported seizures in 12 states by February 2003. pmid:18072099
The 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 2004supported
DEA permanently places AMT into Schedule I of the CSA based on DHHS recommendation and DEA review. pmid:15455477
Claim in summary — inconclusiveinconclusiveworking →
5-MeO-DiPT acts through concurrent serotonin-transporter (SERT) inhibition, 5-ht1a receptor agonism, and 5-ht2a receptor agonismpartially supported
Micromolar 5-HT2A/2C affinity but higher 5-HT1A affinity. 5-HT2A primary despite in vitro 5-HT1A selectivity. pmid:16460788
In 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.partially supported
Micromolar 5-HT2A/2C affinity but higher 5-HT1A affinity. 5-HT2A primary despite in vitro 5-HT1A selectivity. pmid:16460788
In 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.partially supported
Pretreatment with M100907 (0.01 mg/kg) blocked AMT-induced HTR, confirming 5-HT2A involvement. fbp.0000000000000841
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
Rodent 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 basissupported
DNA strand breaks persist 60 days post-treatment indicating neurotoxicity. s12640-016-9654-0
Rodent 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 basissupported
Adolescent repeated 5-MeO-DIPT exposure: altered DA, 5-HT, glutamate in adult rats; caspase-3 activation; oxidative DNA damage. s11419-018-0433-x
The 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 documentedpartially supported
DDIs can occur at pharmacokinetic and pharmacodynamic levels leading to serotonin toxicity. s12248-008-9028-5
Alexander Shulgin and Michael Carter first synthesized and reported 5-MeO-DiPT in 1980supported
First published scientific report on DiPT human pharmacology. Reports oral activity and CNS effects. pmid:6949674
comparative-pharmacology12 · 4 ok
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
The 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.supported
All tested tryptamines showed selectivity for 5-HT1AR over 5-HT2AR; N-group size influences SERT affinity. s41380-024-02506-8
The 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.supported
SAR of 5-methoxytryptamines at 5-HT1A and 5-HT2A. 5-HT1A-selective analogue devoid of hallucinogenic effects. s41586-024-07403-2
The bulkier diisopropyl groups reduce 5-HT₂A functional activity relative to the dimethyl variant while increasing SERT interaction.supported
N-group size influences SERT affinity; HTR mediated primarily by 5-HT2A with 5-HT1A attenuating effect. s41380-024-02506-8
In 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.partially supported
DOM used as training drug. DIPT fully substituted at ED50=1.94 mg/kg. jpet.111.179705
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
history12 · 3 ok
Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
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Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
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Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
It 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 statessupported
DEA reported seizures in 12 states by February 2003. pmid:18072099
Claim in history — inconclusiveinconclusiveworking →
The 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 safetysupported
DEA temporarily places AMT into Schedule I of the CSA as an imminent hazard to public safety. Effective April 4, 2003. pmid:12678045
Permanent Schedule I placement followed in 2004 based on a Department of Health and Human Services scheduling recommendationsupported
DEA permanently places AMT into Schedule I of the CSA based on DHHS recommendation and DEA review. pmid:15455477
receptor-pharmacology12 · 5 ok
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
5-HT₂C receptor agonism is confirmed at micromolar concentrationssupported
Micromolar 5-HT2A/2C affinity. pmid:16460788
5-HT₂C receptor agonism is confirmed at micromolar concentrationssupported
5-MeO-DiPT acts as potent SERT inhibitor with high affinity at 5-HT1A, 5-HT2A, 5-HT2C. s12640-016-9654-0
Kozell 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 extractionsupported
21 substituted tryptamines at 5-HT1A, 5-HT2A, 5-HT2C and SERT. jpet.122.001454
The qualitative binding profile from Fantegrossi et al. is: micromolar affinity at 5-HT₂A and 5-HT₂C, submicromolar (higher) affinity at 5-HT₁Asupported
Micromolar 5-HT2A/2C affinity but higher 5-HT1A affinity. pmid:16460788
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Warren 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 classsupported
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
pharmacokinetic-detail10 · 3 ok
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Caspar et al. corroborated CYP1A2, CYP2C19, cyp2d6, and cyp3a4 involvement in the metabolism of 5-MeO-2-Me-DIPT, a close structural-analog.supported
CYP1A2, CYP2C19, CYP2D6, CYP3A4 involved in hydroxylation and N-dealkylation. dta.2197
Yu reviewed this as a general principle for indolealkylamines: CYP2D6 status alters both pharmacokinetics and drug-drug interaction potential for the class.supported
CYP2D6 plays important polymorphic role in metabolism of IAA drugs of abuse. DDIs can occur at pharmacokinetic and pharmacodynamic levels. s12248-008-9028-5
Vorce 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)partially supported
LOD 5-10 ng/mL in blood, 25-1500 ng/mL range in urine by LC-MS. pmid:15516287
neuroscience8 · 3 ok
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
Nakagawa 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.supported
In vitro studies on molecular targets and neural adaptation of 5-MeO-DiPT using Xenopus oocytes and organotypic slice cultures. pmid:18198474
Li 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.supported
Systematic study of DA, 5-HT and metabolite changes in PFC, NAc, DLS, hippocampus; DAergic and serotonergic systems both involved. j.neures.2025.04.006
Noworyta-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 cortexpartially supported
5-MeO-DiPT acts as potent SERT inhibitor. s12640-016-9654-0
Claim in neuroscience — inconclusiveinconclusiveworking →
clinical-evidence6 · 1 ok
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Smolinske et al. provided the first published medical toxicology report of 5-MeO-DiPT abuse, documenting clinical presentations and US poison center data.supported
Case report and poison center data on 5-MeO-DiPT. pmid:18072099
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Claim in clinical-evidence — inconclusiveinconclusiveworking →
chemistry4 · 1 ok
Claim in chemistry — inconclusiveinconclusiveworking →
Claim in chemistry — inconclusiveinconclusiveworking →
The 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.supported
All tested tryptamines showed selectivity for 5-HT1AR over 5-HT2AR; N-group size influences SERT affinity. s41380-024-02506-8
Claim in chemistry — inconclusiveinconclusiveworking →