generation run 2026-04-26
64 min completedmodel pipeline-v5plan not recordedrun/265d510b…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
none raised on this run
Reproduce
- inputs
- 27 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
20 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | ClinicalTrials.gov | 4-OH-DiPT OR 4-hydroxy-diisopropyltryptamine OR RE104 | 5 | 5 | RE104 is a prodrug of 4-OH-DiPT, the active metabolite of 4-AcO-DiPT - highly relevant clinical data |
| 2 | OpenAlex | 4-AcO-DiPT tryptamine psychedelic pharmacology | 10 | 4 | Landmark papers on tryptamine pharmacology |
| 3 | PubMed | Shulgin tryptamine synthesis diisopropyltryptamine | 10 | 2 | Cozzi 2009 involves Shulgin as co-author and tests DiPT at SERT |
| 4 | PubMed | 4-OH-DiPT OR 4-hydroxy-N,N-diisopropyltryptamine pharmacology serotonin | 3 | 3 | 4-OH-DiPT is the active metabolite of 4-AcO-DiPT - directly relevant pharmacology |
| 5 | PubChem | 4-AcO-DiPT by name | 1 | 1 | Primary chemical identity verification |
| 6 | PubMed | tryptamine metabolism acetoxy 4-AcO hydrolysis psilocin prodrug | 1 | 1 | Informs likely metabolic pathway of 4-AcO-DiPT by analogy |
| 7 | PubMed | 4-AcO-DiPT OR 4-acetoxy-dipropyltryptamine OR dipropyltryptamine acetate pharmacology | 1 | 1 | Direct pharmacology study including 4-AcO-DiPT |
| 8 | PMC/PubMed | — | 1 | 1 | Critical finding on metabolic pathway |
| 9 | Erowid TIHKAL via isomerdesign.com | — | 1 | 1 | Shulgin documentation of 4-HO-DiPT history |
| 10 | PubChem | CID 24801868 full record | 1 | 1 | Chemical identity verification for seed data cross-check |
| 11 | ClinicalTrials.gov | RE104 | 5 | 5 | Active clinical program for 4-OH-DiPT prodrug validates pharmacological profile |
| 12 | Federal Register / DEA | — | 1 | 2 | Critical legal status finding - proposed scheduling withdrawn |
| 13 | Web search | 4-AcO-DiPT legal status Japan UK Germany Sweden Australia | 10 | 4 | Legal status across major jurisdictions |
| 14 | PubMed | 4-acetoxy diisopropyltryptamine metabolism hepatocyte | 1 | 1 | Critical paper - only dedicated 4-AcO-DiPT metabolism study |
| 15 | Erowid TIHKAL | — | 1 | 1 | Primary source for synthesis history and human effects of 4-OH-DiPT (active metabolite) |
| 16 | PubMed | psychedelic serotonin 5-HT2A receptor downregulation tolerance mechanism hallucinogen | 2 | 1 | Mechanism of psychedelic tolerance relevant to seed data claims |
| 17 | PubMed | 5-MeO-DiPT adverse events fatality rhabdomyolysis neurotoxicity clinical | 2 | 2 | Closest structural analog with neurotoxicity data; important safety distinction |
| 18 | Web search | 4-AcO-DiPT Germany NpSG Canada Australia legal status | 10 | 4 | Completing legal status across major jurisdictions |
| 19 | Multiple sources | 4-AcO-DiPT CAS number | 5 | 1 | CAS number not in seed data - verified from multiple commercial sources |
| 20 | PubMed | tolerance cross-tolerance head twitch response tryptamine phenethylamine hallucinogen | 3 | 1 | DIPT-specific tolerance data directly relevant to 4-AcO-DiPT |
70 claims by section — every cited sentence, checked against its source
safety18 · 15 ok
Claim in safety — inconclusiveinconclusiveworking →
4-OH-DiPT demonstrates strong agonist activity at 5-HT₂B receptorssupported
near full agonist at 5-HT2A/2B/2C s41386-023-01744-8
5-MeO-DiPT, a structurally related but pharmacologically distinct compound, produces neurotoxicity in rats at doses of 5–20 mg/kg: increased extracellular dopamine, serotonin, and glutamate; decreased dopamine tissue content suggesting terminal damage; and DNA strand breaks persisting for 60 dayspartially supported
Adolescent repeated 5-MeO-DIPT exposure: altered DA, 5-HT, glutamate in adult rats; caspase-3 activation; oxidative DNA damage. Long-term neurotoxicity in developing brain. s11419-018-0433-x
This neurotoxicity is attributed to 5-MeO-DiPT's potent SERT inhibition and serotonin-releasing properties — a mechanism analogous to MDMA. 4-AcO-DiPT/4-OH-DiPT has a different pharmacological profile: its SERT interaction is weaker, and its primary mechanism is 5-HT₂A agonismsupported
All novel tryptamines were partial or full 5-HT2A agonists. 4-OH-DiPT and DiPT interacted with SERT and partially NET. j.euroneuro.2016.05.001
Claim in safety — not_supportednot supportedworking →
Hallucinogen persisting perception disorder (HPPD) — persistent visual disturbances following serotonergic psychedelic use have been documented for the broader class. Muller et al. (2022) characterized flashback phenomena in controlled psilocybin and LSD studies, finding low incidence under supervised conditions. No substance-specific HPPD data exist for 4-AcO-DiPT.supported
HPPD characterization in phase I trials of LSD and psilocybin in healthy volunteers. s00213-022-06066-z
De la Fuente Revenga et al. (2022) demonstrated this mechanism for the DOI-induced head twitch response, showing it is β-arrestin-2 independent and specific to psychedelic (not non-psychedelic) 5-HT₂A agonistssupported
Tolerance to psychedelic HTR involves 5-HT2A receptor downregulation; not observed with non-psychedelic 5-HT2A agonists; β-arrestin-2 independent mechanism. acschemneuro.2c00170
Smith et al. (2014) found that DiPT — the N,N-diisopropyl backbone of 4-AcO-DiPT — does not develop tolerance to the head twitch response with daily dosing in mice, unlike the phenethylamine hallucinogens DOI and 2C-T-7supported
DIPT and DPT do NOT develop tolerance to HTR with daily dosing in mice (unlike DOI/2C-T-7). jpet.114.219337
Cross-tolerance with other serotonergic psychedelics (psilocybin, LSD, mescaline) is supported by shared 5-HT₂A receptor downregulationsupported
Tolerance to psychedelic HTR involves 5-HT2A receptor downregulation; not observed with non-psychedelic 5-HT2A agonists. acschemneuro.2c00170
Cross-tolerance with other serotonergic psychedelics (psilocybin, LSD, mescaline) is supported by shared 5-HT₂A receptor downregulationpartially supported
DIPT and DPT do NOT develop tolerance to HTR with daily dosing in mice (unlike DOI/2C-T-7). DOI-tolerant mice show cross-tolerance to DPT. jpet.114.219337
Claim in safety — inconclusiveinconclusiveworking →
Given DiPT's documented SERT substrate behavior and 4-OH-DiPT's SERT interaction, co-administration with MAOIs could substantially increase synaptic serotonin levels and precipitate serotonin syndrome — a potentially fatal condition characterized by hyperthermia, neuromuscular excitability, and autonomic instability.supported
DiPT KI for SERT = 2.32 ± 0.46 µM. All tryptamines show substrate (not blocker) behavior at both transporters. s00702-009-0308-8
Given DiPT's documented SERT substrate behavior and 4-OH-DiPT's SERT interaction, co-administration with MAOIs could substantially increase synaptic serotonin levels and precipitate serotonin syndrome — a potentially fatal condition characterized by hyperthermia, neuromuscular excitability, and autonomic instability.supported
4-OH-DiPT and DiPT interacted with SERT and partially NET. j.euroneuro.2016.05.001
The combination elevates serotonin syndrome risk through dual serotonergic mechanismssupported
Review of tramadol-serotonergic drug interactions and serotonin syndrome risk. 0897190013504957
While chronic SSRI use typically attenuates psychedelic effects through 5-HT₂A receptor downregulation, the SERT substrate properties of the DiPT class add pharmacological complexity: SSRIs block the transporter through which DiPT-class compounds enter neurons.supported
All tryptamines show substrate (not blocker) behavior at both transporters. s00702-009-0308-8
DiPT-class compounds inhibit CYP2D6 in vitro at IC₅₀ < 100 µMsupported
DiPTs inhibit CYP2D6 below 100µM. j.toxlet.2015.11.013
Concurrent MAOI use — critical serotonin syndrome risk given SERT substrate properties of the DiPT class.supported
All tryptamines show substrate (not blocker) behavior at both transporters. s00702-009-0308-8
Cardiac conditions — 4-OH-DiPT's 5-HT₂B agonism represents an unstudied risk for individuals with pre-existing valvular disease or conditions sensitive to serotonergic cardiac effects.supported
near full agonist at 5-HT2A/2B/2C s41386-023-01744-8
pharmacology10 · 9 ok
Human hepatocyte metabolism data confirm that the sole first-generation metabolite is 4-OH-DiPT, formed by ester hydrolysis of the acetate group; all subsequent metabolites derive from this intermediatepartially supported
Primary pathway: ester hydrolysis to 4-OH-DiPT. N-oxidation and N-dealkylation. Biomarkers: 4-OH-DiPT, 4-OH-iPT, 4-OH-DiPT-N-oxide. metabo12080705
Recommended forensic biomarkers for confirming 4-AcO-DiPT consumption are 4-OH-DiPT, 4-OH-iPT (N-deisopropylated metabolite), and 4-OH-DiPT-N-oxide.supported
Biomarkers: 4-OH-DiPT, 4-OH-iPT, 4-OH-DiPT-N-oxide. metabo12080705
Kelly et al. (2024) profiled 4-OH-DiPT at all 12 human serotonin GPCRs, identifying strongest agonist activity at 5-HT₂A, 5-HT₂B, and 5-HT₂C receptors, with comparable activity at both mouse and human receptor orthologspartially supported
Profiled 4-OH-DiPT at all 12 human 5-HT GPCRs; near full agonist at 5-HT2A/2B/2C. s41386-023-01744-8
Multiple tryptamine psychedelics including diisopropyl-substituted analogs also target 5-HT₁A; at high doses, 5-HT₁A agonism attenuates the 5-HT₂A-mediated head twitch response in mice.partially supported
Multiple serotonin receptors targeted including 5-HT1A. acsptsci.2c00222
Claim in pharmacology — inconclusiveinconclusiveworking →
4-OH-DiPT and DiPT interact with the serotonin transporter (SERT) and partially with the norepinephrine transporter (NET) — a pattern similar to MDMA but distinct from LSD and mescaline, which do not interact with SERTsupported
4-OH-DiPT and DiPT interacted with SERT and partially NET. Binding affinity correlated with psychoactive dose in humans. j.euroneuro.2016.05.001
Cozzi et al. (2009) demonstrated that DiPT (the N,N-diisopropyl backbone) is a SERT substrate (not a blocker): K_I for SERT = 2.32 ± 0.46 µM; K_I for VMAT2 = 19 ± 3.1 µMsupported
DiPT KI for SERT = 2.32 ± 0.46 µM; VMAT2 = 19 ± 3.1 µM. All tryptamines show substrate (not blocker) behavior at both transporters. s00702-009-0308-8
For 4-OH-DiPT, plasma half-life was approximately 40 minutes after subcutaneous administration of RE104 (a glutarate ester prodrug) in ratssupported
Half-life of 4-OH-DiPT 40 min after s.c. RE104 in rats. acschemneuro.4c00058
Shulgin reported 4-OH-DiPT duration as 2–3 hours oral; the 3–4 hour total duration observed with 4-AcO-DiPT is consistent with additional lag time from prodrug hydrolysis.supported
Short duration (2-3h) psychedelic effects. acschemneuro.4c00058
DiPT-class compounds inhibit CYP2D6 at IC₅₀ values below 100 µM in vitrosupported
DiPTs inhibit CYP2D6 below 100µM. j.toxlet.2015.11.013
summary10 · 8 ok
It occupies a distinctive niche within the 4-substituted tryptamine series: brief total duration (3–4 hours oral), moderate potency (common dose 15–30 mg oral), and rapid onset (15–40 minutes) — making it among the shortest-acting members of its structural class.supported
Short duration (2-3h) psychedelic effects. acschemneuro.4c00058
Claim in summary — inconclusiveinconclusiveworking →
4-AcO-DiPT undergoes hepatic ester hydrolysis to 4-OH-DiPT as its sole first-generation metabolite. 4-OH-DiPT acts as a near-full agonist at the 5-HT₂A receptor, with additional agonism at 5-HT₂B and 5-HT₂C, and interacts with SERT and NET — a transporter profile more reminiscent of MDMA than classical psychedelicspartially supported
Primary pathway: ester hydrolysis to 4-OH-DiPT. Phase II: glucuronidation, sulfation. N-oxidation and N-dealkylation. metabo12080705
4-AcO-DiPT undergoes hepatic ester hydrolysis to 4-OH-DiPT as its sole first-generation metabolite. 4-OH-DiPT acts as a near-full agonist at the 5-HT₂A receptor, with additional agonism at 5-HT₂B and 5-HT₂C, and interacts with SERT and NET — a transporter profile more reminiscent of MDMA than classical psychedelicspartially supported
Profiled 4-OH-DiPT at all 12 human 5-HT GPCRs; near full agonist at 5-HT2A/2B/2C. s41386-023-01744-8
4-AcO-DiPT undergoes hepatic ester hydrolysis to 4-OH-DiPT as its sole first-generation metabolite. 4-OH-DiPT acts as a near-full agonist at the 5-HT₂A receptor, with additional agonism at 5-HT₂B and 5-HT₂C, and interacts with SERT and NET — a transporter profile more reminiscent of MDMA than classical psychedelicssupported
All novel tryptamines were partial or full 5-HT2A agonists. 4-OH-DiPT and DiPT interacted with SERT and partially NET. j.euroneuro.2016.05.001
In mice, 4-OH-DiPT activates basolateral amygdala GABAergic interneurons via 5-HT₂A receptors, suppressing learned fear responses.supported
Activated BLA interneurons via 5-HT2A to enhance GABAergic inhibition. Enhanced fear extinction in mice dose-dependently. s41386-023-01744-8
No LD₅₀ or controlled toxicity data exist for 4-AcO-DiPT or 4-OH-DiPT in any species. 4-OH-DiPT demonstrates strong 5-HT₂B agonism — a receptor target associated with cardiac valvulopathy under chronic activation — representing an unstudied riskpartially supported
near full agonist at 5-HT2A/2B/2C s41386-023-01744-8
Tolerance operates through 5-HT₂A receptor downregulation, though rodent data for DiPT show attenuated tolerance development compared to phenethylamine hallucinogenssupported
Tolerance to psychedelic HTR involves 5-HT2A receptor downregulation; not observed with non-psychedelic 5-HT2A agonists. acschemneuro.2c00170
Tolerance operates through 5-HT₂A receptor downregulation, though rodent data for DiPT show attenuated tolerance development compared to phenethylamine hallucinogenssupported
DIPT and DPT do NOT develop tolerance to HTR with daily dosing in mice (unlike DOI/2C-T-7). jpet.114.219337
Claim in summary — inconclusiveinconclusiveworking →
neuroscience6 · 6 ok
Kelly et al. (2024) provided the most mechanistically detailed neuroscience data relevant to 4-AcO-DiPTsupported
Profiled 4-OH-DiPT at all 12 human 5-HT GPCRs; near full agonist at 5-HT2A/2B/2C. Enhanced fear extinction in mice dose-dependently. Activated BLA interneurons via 5-HT2A to enhance GABAergic inhibition. s41386-023-01744-8
This interneuron-mediated inhibition of BLA output is proposed as the cellular mechanism by which 4-OH-DiPT suppresses learned fear: in a fear extinction paradigm, 4-OH-DiPT dose-dependently reduced freezing to conditioned cues, with greater potency in female mice than male mice.supported
Enhanced fear extinction in mice dose-dependently. Activated BLA interneurons via 5-HT2A to enhance GABAergic inhibition. Sex differences in potency (female > male). s41386-023-01744-8
The 5-HT₂A receptor is densely expressed on layer V pyramidal neurons in the prefrontal cortex — the primary cellular trigger for psychedelic effects. 4-OH-DiPT's additional interactions with SERT and NET may produce entactogenic-type neural effects (reduced amygdala fear responses, enhanced prefrontal-limbic connectivity) overlaid on classical psychedelic phenomenology.supported
All novel tryptamines were partial or full 5-HT2A agonists. 4-OH-DiPT and DiPT interacted with SERT and partially NET. j.euroneuro.2016.05.001
The 5-HT₂A receptor is densely expressed on layer V pyramidal neurons in the prefrontal cortex — the primary cellular trigger for psychedelic effects. 4-OH-DiPT's additional interactions with SERT and NET may produce entactogenic-type neural effects (reduced amygdala fear responses, enhanced prefrontal-limbic connectivity) overlaid on classical psychedelic phenomenology.supported
All tryptamines show substrate (not blocker) behavior at both transporters. s00702-009-0308-8
No direct neuroplasticity data exist for 4-OH-DiPT, but the antidepressant-like effects observed with RE104 in the rat forced swim test — persisting 1 week post-administration — are consistent with structural plasticity rather than acute pharmacological action.supported
Significant antidepressant effect in forced swim test at 1 week. acschemneuro.4c00058
What accounts for the sex difference in fear extinction potency (greater in female mice) observed by Kelly et al. (2024)? Estrogen-dependent modulation of 5-HT₂A receptor expression or downstream signaling may be involved.supported
Sex differences in potency (female > male). s41386-023-01744-8
pharmacokinetic-detail6 · 6 ok
Dinger et al. (2016) demonstrated CYP2D6 inhibition by tryptamines of the diisopropyltryptamine class at IC₅₀ values below 100 µM in vitrosupported
DiPTs inhibit CYP2D6 below 100µM. j.toxlet.2015.11.013
Caspar et al. (2018) identified CYP enzyme involvement in the metabolism of related N,N-diisopropyltryptamine compoundssupported
CYP1A2, CYP2C19, CYP2D6, CYP3A4 involved in hydroxylation and N-dealkylation. dta.2197
Bryson et al. (2024) reported a plasma half-life of approximately 40 minutes for 4-OH-DiPT following subcutaneous administration of RE104 (a glutarate ester prodrug) in ratssupported
Half-life of 4-OH-DiPT 40 min after s.c. RE104 in rats. acschemneuro.4c00058
Malaca et al. (2022) definitively mapped the metabolic pathway of 4-AcO-DiPT using human hepatocyte incubationsupported
First dedicated 4-AcO-DiPT human hepatocyte metabolism study. metabo12080705
This pathway parallels that of other 4-acetoxy tryptamines: Zhai et al. (2022) demonstrated that 4-AcO-DMT undergoes predominant hydrolysis to psilocin via the same mechanism.supported
hydrolysis to psilocin is most abundant pathway. dta.3255
In the absence of formal pharmacokinetic studies, duration estimates for oral 4-AcO-DiPT are triangulated from three sources: (1) Shulgin's TiHKAL report of 2–3 hours total for 4-OH-DiPT oral, (2) the approximately 40-minute rat plasma half-life from Bryson et al. (2024) — consistent with a short-acting compound, and (3) community-sourced data reporting 3–4 hours total for 4-AcO-DiPTsupported
Half-life of 4-OH-DiPT 40 min after s.c. RE104 in rats. Short duration (2-3h) psychedelic effects. acschemneuro.4c00058
receptor-pharmacology6 · 6 ok
Kelly et al. (2024) provided the most comprehensive receptor characterization of 4-OH-DiPT, profiling functional activity at all 12 human serotonin GPCRs. 4-OH-DiPT demonstrated near-full agonist activity at 5-HT₂A, with strong agonism at 5-HT₂B and 5-HT₂Csupported
Profiled 4-OH-DiPT at all 12 human 5-HT GPCRs; near full agonist at 5-HT2A/2B/2C. s41386-023-01744-8
Rickli et al. (2016) characterized 4-OH-DiPT binding and functional pharmacology at 5-HT₂A, 5-HT₂B, SERT, and NETsupported
Investigated binding affinities at human monoamine receptors for DiPT, 4-OH-DiPT... All novel tryptamines were partial or full 5-HT2A agonists. 4-OH-DiPT and DiPT interacted with SERT and partially NET. j.euroneuro.2016.05.001
Specific Ki and EC₅₀ values for 4-OH-DiPT at individual receptors are reported in the full-text tables of this paper and in Kozell et al. (2023), but were not accessible via API during research; full-text consultation is recommended for numeric binding data.supported
21 substituted tryptamines tested at 5-HT1A, 5-HT2A, 5-HT2C and SERT. jpet.122.001454
Kozell et al. (2023) measured pharmacological activity of 21 substituted tryptamines at 5-HT₂A, 5-HT₂C, 5-HT₁A, and SERT, finding that 4-substituted compounds showed high selectivity for 5-HT₂A.supported
21 substituted tryptamines tested at 5-HT1A, 5-HT2A, 5-HT2C and SERT. 4-substituted compounds show high selectivity for 5-HT2AR. jpet.122.001454
Glatfelter et al. (2023) established that 4-acetoxy and 4-propionoxy analogs display somewhat weaker binding affinities than their corresponding 4-hydroxy analogs but retain similar target profiles across serotonin receptor subtypessupported
4-Acetoxy analogs show weaker binding affinities but similar target profiles vs 4-hydroxy compounds. acsptsci.2c00222
Cozzi et al. (2009) characterized DiPT (the N,N-diisopropyl backbone) as a SERT substrate with K_I = 2.32 ± 0.46 µM and a VMAT2 substrate with K_I = 19 ± 3.1 µMsupported
DiPT KI for SERT = 2.32 ± 0.46 µM; VMAT2 = 19 ± 3.1 µM. s00702-009-0308-8
comparative-pharmacology5 · 5 ok
Gatch et al. (2021) systematically compared substituted tryptamines in rat drug discrimination assayssupported
Evaluated hallucinogen-like discriminative stimulus effects of eight novel substituted tryptamines including 4-AcO-DiPT and 4-OH-DiPT in DOM-trained rats. acsptsci.0c00173
Glatfelter et al. (2023) confirmed this pattern at the receptor level: 4-acetoxy and 4-propionoxy analogs display somewhat weaker binding affinities but retain similar target profiles compared to 4-hydroxy compounds.supported
4-Acetoxy analogs show weaker binding affinities but similar target profiles vs 4-hydroxy compounds. acsptsci.2c00222
Bryson et al. (2024) specifically cited 4-OH-DiPT's shorter duration as a pharmacological advantage in clinical contexts — permitting completion of a psychedelic session within a single clinical day without extended monitoring required by longer-acting compounds.supported
Short duration (2-3h) psychedelic effects. acschemneuro.4c00058
Unlike most classical serotonergic psychedelics, the DiPT class interacts with SERT and partially with NET — a profile more reminiscent of MDMA than LSD or mescalinesupported
4-OH-DiPT and DiPT interacted with SERT and partially NET. Binding affinity correlated with psychoactive dose in humans. j.euroneuro.2016.05.001
Cozzi et al. (2009) demonstrated that DiPT is a SERT substrate (K_I = 2.32 ± 0.46 µM), and Rickli et al. (2016) confirmed this interaction for 4-OH-DiPTsupported
DiPT KI for SERT = 2.32 ± 0.46 µM. s00702-009-0308-8
chemistry4 · 2 ok
As an acetate ester, 4-AcO-DiPT is hydrolyzed in vivo to yield 4-OH-DiPT — the pharmacologically active metabolitesupported
Primary pathway: ester hydrolysis to 4-OH-DiPT. metabo12080705
The two isopropyl groups on the amine nitrogen create significant steric bulk compared to smaller N-alkyl tryptamines, contributing to reduced receptor binding potency relative to dimethyl, diethyl, and mixed N-alkyl analogs.supported
N,N-diisopropyl compounds less potent than dimethyl/diethyl analogs. acsptsci.0c00173
Claim in chemistry — inconclusiveinconclusiveworking →
Claim in chemistry — inconclusiveinconclusiveworking →
history4 · 2 ok
Claim in history — inconclusiveinconclusiveworking →
Bryson et al. (2024) confirmed RE104 produces antidepressant-like effects in the rat forced swim test (1 mg/kg subcutaneous, p < 0.001 vs. vehicle at 1 week)partially supported
Significant antidepressant effect in forced swim test at 1 week. acschemneuro.4c00058
Claim in history — inconclusiveinconclusiveworking →
Shulgin continued investigating the diisopropyltryptamine framework, co-authoring Cozzi et al. (2009), which demonstrated that DiPT functions as a substrate (not blocker) at both SERT and VMAT2.supported
All tryptamines show substrate (not blocker) behavior at both transporters. s00702-009-0308-8
clinical-evidence1 · 1 ok
In preclinical work, Bryson et al. (2024) confirmed that RE104 produces antidepressant-like effects in the rat forced swim test (1 mg/kg subcutaneous, p < 0.001 vs. vehicle at 1 week post-administration).partially supported
Significant antidepressant effect in forced swim test at 1 week. acschemneuro.4c00058