generation run 2026-04-26
52 min completedmodel pipeline-v5plan not recordedrun/c553137d…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
none raised on this run
Reproduce
- inputs
- 19 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 | PubChem | 2C-P | 1 | 1 | Primary chemical identity data |
| 2 | OpenAlex | 2C-P dimethoxy propylphenethylamine psychedelic | 3 | 1 | Wagmann directly includes 2C-P in MAO inhibition study; others not directly relevant |
| 3 | ClinicalTrials.gov · absence | 2C-P phenethylamine psychedelic | 0 | 0 | No results |
| 4 | PubMed · absence | 2C-P psychedelic phenethylamine synthesis Shulgin | 0 | 0 | No results found |
| 5 | PubMed | 2C phenethylamine 5-HT2A agonist binding affinity psychedelic receptor | 12 | 6 | These papers provide 5-HT2A/2C class context and potentially 2C-P specific data |
| 6 | PubMed | 2C-P serotonin receptor binding affinity 5-HT2A phenethylamine | 1 | 1 | Relevant to 2C-P receptor pharmacology |
| 7 | PubMed | 2C-P 2,5-dimethoxy-4-propylphenethylamine pharmacology | 3 | 3 | All directly mention 2C-P; Kim 2021 is the primary rodent pharmacology study; Wink 2015 is the primary metabolism study |
| 8 | Google/WebSearch | 2C-P PiHKAL Shulgin synthesis history discovery phenethylamine | 10 | 1 | Historical synthesis and first documentation |
| 9 | Google/WebSearch | 2C-P five cases intoxication Toxicology Reports 2015 | 5 | 1 | Primary clinical case series for 2C-P intoxication |
| 10 | PubMed | PMID 28130544 - Stoller 2017 2C-P case report | 1 | 1 | Only published human pharmacokinetic data for 2C-P |
| 11 | PubMed | 2C-P serotonin receptor binding affinity 5-HT2A phenethylamine - expanded | 12 | 5 | All relevant to 5-HT2A pharmacology of phenethylamines and 2C-P |
| 12 | Google/WebSearch | 2C-P legal status scheduling DEA United States UK Australia | 10 | 2 | Legal scheduling data for multiple jurisdictions |
| 13 | Google/WebSearch | 2C-P PiHKAL Selene Shulgin dose effects 16mg overdose | 10 | 1 | Primary historical source for 2C-P synthesis and self-experimentation data |
| 14 | Canada Gazette / Google | 2C-P Canada Schedule III Controlled Drugs Substances Act phenethylamine 2016 | 5 | 1 | Canadian legal scheduling documentation |
| 15 | PubMed | Gil-Martins 2025 toxicodynamic 2C NBOMe abuse potential | 1 | 1 | Most recent comprehensive review covering 2C-P class pharmacology and abuse potential |
| 16 | Multiple sources | Cross-referencing dose data between PiHKAL, seed data, and clinical case reports | 4 | 1 | Cross-validation of dose/duration data across sources |
| 17 | PubMed | Writing handoff file 01-research-output.md | 1 | 1 | Comprehensive research output written |
| 18 | Google/WebSearch | 2C-P Australia Schedule 9 SUSMP controlled substance | 10 | 0 | Australia status not confirmed - flagged for human review |
| 19 | PubMed | Kolaczynska 2019 4-alkoxy dimethoxyphenethylamine receptor profile | 1 | 1 | SAR comparison data for 4-substituted 2C series relevant to 2C-P potency prediction |
| 20 | PubMed | Luethi 2018 2C-T monoamine receptor interaction profiles | 1 | 1 | 2C-T drugs are structural analogs; binding data provides comparison framework for 2C-P |
62 claims by section — every cited sentence, checked against its source
pharmacology18 · 15 ok
Claim in pharmacology — not_supportednot supportedworking →
This assignment is supported by structural membership in the 2,5-dimethoxyphenethylamine class and confirmed by rodent behavioral studies demonstrating head-twitch responses characteristic of 5-HT₂A activationsupported
DOI-induced tolerance (HTR paradigm) develops rapidly acschemneuro.2c00170
The 5-HT₂A antagonist M100907 fully blocks behavioral effects of 2C-class compounds in rats, confirming receptor dependence.supported
5-HT2A antagonist M100907 completely blocked all behavioral effects of 2C-C, 2C-I, 25C-NBOMe, 25I-NBOMe in rats. Confirms 5-HT2A as primary mediator. j.neuropharm.2018.02.033
The 2,5-dimethoxy scaffold is essential for in vivo 5-HT₂A activation — removal of either methoxy group significantly reduces head-twitch response in mice even when in vitro binding is only modestly attenuatedsupported
Removal of either methoxy significantly reduces in vivo head-twitch response despite modest in vitro effects. 2,5-dimethoxy motif important for in vivo potency. acschemneuro.0c00129
The 4-propyl substituent increases molecular lipophilicity and, consistent with structure-activity relationships across 4-alkoxy-substituted phenethylamines, larger 4-position substituents progressively enhance 5-HT₂A and 5-HT₂C affinity.supported
increasing 4-substituent size increases 5-HT2A/2C affinity fphar.2019.01423
The β-arrestin 2 recruitment assay by Pottie et al. (2020), which characterized 12 2C-X compounds at 5-HT₂A, likely includes 2C-P, but specific potency values were not confirmed from the published abstractpartially supported
SAR study for 30 phenylalkylamine psychedelics: 12 2C-X series including 2C-P (confirmed) s00204-020-02836-w
Class-level data indicate nanomolar-range affinity at 5-HT₂A with partial agonist efficacy.partially supported
Ki at 5-HT2A = 8-1700 nM fphar.2019.01423
Claim in pharmacology — inconclusiveinconclusiveworking →
Weak trace amine-associated receptor 1 (TAAR1) activity has been described for related phenethylaminessupported
phenethylamines bind TAAR1 more than amphetamine analogs fphar.2019.01423
Weak trace amine-associated receptor 1 (TAAR1) activity has been described for related phenethylaminessupported
TAAR1 5-68 nM j.neuropharm.2017.07.012
Monoamine transporter activity (DAT, SERT, NET) is minimal or absent in the 2C phenethylamine class.supported
no significant monoamine transporter activity fphar.2019.01423
Monoamine transporter activity (DAT, SERT, NET) is minimal or absent in the 2C phenethylamine class.supported
no monoamine transporter activity j.neuropharm.2017.07.012
2C-P was among 17 2C-series compounds tested for monoamine oxidase inhibition; across the panel, 13 compounds inhibited MAO-A (IC₅₀ 10–125 µM) and 11 inhibited MAO-B (IC₅₀ 1.7–180 µM)supported
17 2C-series drugs tested including 2C-P. 13 showed MAO-A inhibition, 11 showed MAO-B inhibition. IC50 values ranged 10-125 microM (MAO-A) and 1.7-180 microM (MAO-B). dta.2494
At high doses in rodents, 2C-P modulates dopaminergic signaling: altered D1 and D2 dopamine receptor expression and dopamine transporter phosphorylation were observed in the nucleus accumbens and medial prefrontal cortexsupported
2C-C and 2C-P affected D1/D2 dopamine receptor expression, DAT phosphorylation in nucleus accumbens and medial prefrontal cortex. s00204-021-02980-x
Stoller et al. (2017) estimated an elimination half-life of approximately 19 hours from two blood sample concentrations in a single emergency presentationsupported
Estimated elimination half-life 19 hours from two blood samples. bkw108
Phase I and II metabolic pathways identified in human urine include N-acetylation, deamination (with subsequent reduction to the alcohol or oxidation to the carboxylic acid), mono- and bis-hydroxylation, mono- and bis-O-demethylation at the 2- and/or 5-methoxy positions, and glucuronidation and/or sulfation of hydroxylated or demethylated metabolitessupported
Metabolic pathways: N-acetylation; deamination followed by reduction/oxidation; mono- and bis-hydroxylation; mono- and bis-O-demethylation with glucuronidation/sulfation. s00216-014-8083-2
Claim in pharmacology — inconclusiveinconclusiveworking →
These pathways were characterized by GC-MS and LC-MS(n) analysis of urine following administration of a common user's dose, confirming analytical detectability.supported
Detection in urine confirmed by GC-MS and LC-MS. s00216-014-8083-2
safety15 · 15 ok
Cross-tolerance extends to all 5-HT₂A agonists: LSD, psilocybin, mescaline, and other 2C compounds.partially supported
Cross-tolerance not fully explained by receptor downregulation alone. pmid:1969270
The Stoller (2017) case presented a near-identical symptom profile, with the additional significance of substance misidentification — the patient believed he was consuming 2C-Bsupported
19-year-old male admitted to ED with severe hallucinations, mydriasis, tachycardia, agitation and confusion after ingesting substance sold as 2C-B; LC-MS confirmed 2C-P. bkw108
Tachycardia and hypertension are consistently reported across all published 2C-P casespartially supported
severe hallucinations, mydriasis, tachycardia, agitation and confusion bkw108
Severe cases may involve vasoconstriction and hyperthermiasupported
Comprehensive review covering 5-HT2A-mediated effects of serotonergic psychedelics, vasoconstriction, hyperthermia, seizures. s00204-020-02693-7
High-dose 2C-P produced microglial activation (neuroinflammation) in the striatum, decreased locomotor activity and rotarod performance, and impaired performance on Y-maze, novel object recognition, and passive avoidance tasks in rodentssupported
High doses decreased locomotor activity, motor performance, and memory test scores. High doses induced microglial activation (neuroinflammation) in striatum. s00204-021-02980-x
At doses exceeding the common range, severe agitation, confusion, and distressing hallucinations are documented in clinical casessupported
severe hallucinations, mydriasis, tachycardia, agitation and confusion bkw108
Tolerance to 2C-P's psychedelic effects develops rapidly following a single dose, mediated by 5-HT₂A receptor downregulation in the frontal cortexpartially supported
Daily LSD in rats decreases 5-HT2 binding in cortex within 3 days pmid:1969270
Tolerance to 2C-P's psychedelic effects develops rapidly following a single dose, mediated by 5-HT₂A receptor downregulation in the frontal cortexsupported
DOI-induced tolerance (HTR paradigm) develops rapidly; 5-HT2A receptor downregulation in frontal cortex acschemneuro.2c00170
This mechanism is β-arrestin-2-independentsupported
mechanism independent of beta-arrestin-2 acschemneuro.2c00170
Cross-tolerance extends to all 5-HT₂A agonists: LSD, psilocybin, mescaline, and other 2C compounds.partially supported
cross-tolerance observed between DOI and LSD acschemneuro.2c00170
However, rodent data complicate the abuse potential assessment: dose-dependent conditioned place preference in mice and increased self-administration in rats were demonstrated, findings atypical for classical serotonergic psychedelicssupported
2C-C and 2C-P produced conditioned place preference in mice and increased self-administration in rats, suggesting abuse potential. s00204-021-02980-x
The primary interaction risk is serotonin toxicity when 2C-P is combined with other serotonergic agents. 2C-P contributes through direct 5-HT₂A agonism and potential MAO inhibition (IC₅₀ range 1.7–180 µM for MAO-B across the 2C panel).supported
IC50 values ranged 1.7-180 microM (MAO-B). Pharmacological contribution of MAO inhibition cannot be excluded. dta.2494
MAOIs combined with 2C-P present a dual risk: 2C-P itself exhibits MAO inhibition in vitro, and exogenous MAO inhibitors would further potentiate serotonergic activity, substantially increasing serotonin syndrome risk.supported
17 2C-series drugs tested including 2C-P. 13 showed MAO-A inhibition, 11 showed MAO-B inhibition. Pharmacological contribution of MAO inhibition cannot be excluded. dta.2494
The 5-HT₂A antagonist M100907 blocks all behavioral effects of 2C-class compounds in rodents; cyproheptadine or atypical antipsychotics (e.g., quetiapine) may be considered for severe presentations per clinical judgmentsupported
5-HT2A antagonist M100907 completely blocked all behavioral effects of 2C-C, 2C-I, 25C-NBOMe, 25I-NBOMe in rats. j.neuropharm.2018.02.033
Seizure disorders: Serotonergic excess may lower seizure threshold; related 2C compounds have produced seizures in case reports.supported
19-year-old male who insufflated 2C-I developed recurrent seizures, hyperadrenergic state, serotonin syndrome s13181-013-0287-x
summary8 · 8 ok
The 4-propyl substituent confers increased lipophilicity and receptor affinity relative to shorter-chain 2C analogs.supported
increasing 4-substituent size increases 5-HT2A/2C affinity fphar.2019.01423
The evidence base consists of Shulgin's self-experiments, a handful of emergency case reports, one rodent study addressing abuse potential and neurotoxicity, and class-level pharmacological data from the broader 2C series.supported
First published human pharmacokinetic data for 2C-P. bkw108
The evidence base consists of Shulgin's self-experiments, a handful of emergency case reports, one rodent study addressing abuse potential and neurotoxicity, and class-level pharmacological data from the broader 2C series.supported
2C-C and 2C-P produced conditioned place preference in mice and increased self-administration in rats, suggesting abuse potential. High doses induced microglial activation (neuroinflammation) in striatum. s00204-021-02980-x
No substance-specific binding affinity data have been published; class-level structure-activity relationships indicate nanomolar-range 5-HT₂A affinity with increasing potency as 4-position substituent size growssupported
Ki at 5-HT2A = 8-1700 nM; increasing 4-substituent size increases 5-HT2A/2C affinity fphar.2019.01423
Tolerance develops rapidly via 5-HT₂A receptor downregulation and cross-generalizes to other serotonergic psychedelicssupported
Daily LSD in rats decreases 5-HT2 binding in cortex within 3 days; effect dissipates 96h after cessation. Cross-tolerance not fully explained by receptor downregulation alone. pmid:1969270
Tolerance develops rapidly via 5-HT₂A receptor downregulation and cross-generalizes to other serotonergic psychedelicssupported
DOI-induced tolerance (HTR paradigm) develops rapidly; cross-tolerance observed between DOI and LSD; 5-HT2A receptor downregulation in frontal cortex acschemneuro.2c00170
Physical dependence liability is low, though rodent data demonstrate conditioned place preference and self-administration, suggesting reinforcing properties atypical for classical psychedelicssupported
2C-C and 2C-P produced conditioned place preference in mice and increased self-administration in rats, suggesting abuse potential. s00204-021-02980-x
Critical unknowns include human pharmacokinetic parameters beyond a single-case half-life estimate of approximately 19 hours, substance-specific receptor binding affinities, and neurotoxicity thresholds in humans.supported
Estimated elimination half-life 19 hours from two blood samples. First published human pharmacokinetic data for 2C-P. bkw108
receptor-pharmacology7 · 5 ok
DAT, SERT, and NET activity is negligible or absent across the 2C class.supported
no monoamine transporter activity j.neuropharm.2017.07.012
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Across 17 2C-series compounds, MAO-A inhibition IC₅₀ values ranged 10–125 µM and MAO-B inhibition IC₅₀ values ranged 1.7–180 µMsupported
IC50 values ranged 10-125 microM (MAO-A) and 1.7-180 microM (MAO-B). dta.2494
Weak TAAR1 activity has been reported for structurally related phenethylaminessupported
phenethylamines bind TAAR1 more than amphetamine analogs fphar.2019.01423
Weak TAAR1 activity has been reported for structurally related phenethylaminessupported
TAAR1 5-68 nM j.neuropharm.2017.07.012
DAT, SERT, and NET activity is negligible or absent across the 2C class.supported
no significant monoamine transporter activity fphar.2019.01423
comparative-pharmacology5 · 2 ok
The progression from methyl (2C-D) through ethyl (2C-E) to propyl (2C-P) illustrates the structure-activity principle that increasing 4-alkyl chain length enhances potency and prolongs duration, correlating with increased 5-HT₂A affinity.partially supported
increasing 4-substituent size increases 5-HT2A/2C affinity fphar.2019.01423
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Kim et al. (2021) demonstrated conditioned place preference and self-administration for 2C-P in rodents, findings that are unusual for classical serotonergic psychedelicssupported
2C-C and 2C-P produced conditioned place preference in mice and increased self-administration in rats, suggesting abuse potential. s00204-021-02980-x
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
pharmacokinetic-detail4 · 3 ok
The only human pharmacokinetic estimate derives from a single case: an elimination half-life of approximately 19 hours calculated from two plasma concentrationssupported
Estimated elimination half-life 19 hours from two blood samples. First published human pharmacokinetic data for 2C-P. bkw108
Urinary metabolite profiling identified the following biotransformation pathways:supported
Identified phase I and II metabolites of 2C-P. Metabolic pathways: N-acetylation; deamination followed by reduction/oxidation; mono- and bis-hydroxylation; mono- and bis-O-demethylation with glucuronidation/sulfation. s00216-014-8083-2
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Targeted analytical methods — GC-MS, LC-MS(n), and UPLC-MS/MS — reliably identify 2C-P and its metabolites in urine and plasma at concentrations consistent with a common user's dose.supported
Detection in urine confirmed by GC-MS and LC-MS. s00216-014-8083-2
neuroscience2 · 2 ok
The dopaminergic effects observed at high doses in rodents — altered D1/D2 receptor expression and DAT phosphorylation in the nucleus accumbens and medial prefrontal cortex — suggest that 2C-P may engage mesolimbic reward circuitry at doses beyond the typical psychedelic rangesupported
2C-C and 2C-P affected D1/D2 dopamine receptor expression, DAT phosphorylation in nucleus accumbens and medial prefrontal cortex. s00204-021-02980-x
Microglial activation (neuroinflammation) observed in the striatum following high-dose 2C-P administration in rodents indicates possible neurotoxic processes, though the doses employed, the species difference, and the absence of any human neuropathological data prevent extrapolation to human recreational use.supported
High doses induced microglial activation (neuroinflammation) in striatum. Suggests dopaminergic signaling involvement and neurotoxicity at high doses. s00204-021-02980-x
chemistry1 · 1 ok
Across the 2C series, increasing the size and lipophilicity of the 4-substituent correlates with increased 5-HT₂A receptor affinity and prolonged duration of actionpartially supported
increasing 4-substituent size increases 5-HT2A/2C affinity fphar.2019.01423
clinical-evidence1 · 1 ok
A 19-year-old male presented with severe hallucinations, mydriasis, tachycardia, agitation, and confusion after ingesting a substance believed to be 2C-Bsupported
19-year-old male admitted to ED with severe hallucinations, mydriasis, tachycardia, agitation and confusion after ingesting substance sold as 2C-B bkw108
history1 · 1 ok
A 2017 case report from Switzerland documented a 19-year-old male who ingested 2C-P sold as 2C-B, providing the first published pharmacokinetic estimate and highlighting the adulterant risk inherent to unregulated marketssupported
First published human pharmacokinetic data for 2C-P... ingesting substance sold as 2C-B; LC-MS confirmed 2C-P. bkw108