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Psychedex
Sources
21
6 strong · 9 moderate · 6 weak

Studies and references cited across this article, graded by evidence strength.

Claims checked
52
32verified3partial17inconclusive

Inconclusive means the cited source neither confirms nor refutes the claim — a lower-confidence badge, not an error.

Generated
May 11, 2026 · pipeline-v5
Values approved
213/215 (99%)

Data points an editor reviewed and accepted for publication.

01

Value Provenance

Dosing

oraltrace

FieldPublishedAI ProposedConfidence
Threshold5 mg5 mglow
Low10–20 mg10–20 mglow
Common20–40 mg20–40 mglow
Strong40–50 mg40–50 mglow
Heavy50+ mg50+ mglow
Editorial

Community-derived dose ranges from Erowid vault (~10–12 user reports) and Shulgin's predicted 20–40 mg active range in PiHKAL. No controlled dosing study exists. Maximum documented dose ~50 mg without fatality. All values are safety-critical and unverified against published pharmacological sources.

Reasoning

Community-derived dose ranges from Erowid vault (~10–12 user reports) and Shulgin's predicted 20–40 mg active range in PiHKAL. No controlled dosing study exists. Maximum documented dose ~50 mg without fatality. All values are safety-critical and unverified against published pharmacological sources.

Evidence basis: community_consensus_small

Duration

oral

FieldPublishedAI ProposedConfidence
Onsettrace1–2 hours1–2 hourslow
Editorial

Seed data and Erowid user reports consistently report 1–2 hour onset. Consistent with mescaline Tmax of ~2 hours (Klaiber et al. 2024). No controlled PK data for 3C-P.

Reasoning

Seed data and Erowid user reports consistently report 1–2 hour onset. Consistent with mescaline Tmax of ~2 hours (Klaiber et al. 2024). No controlled PK data for 3C-P.

Evidence basis: community_consensus_small

After effectstrace3–6 hours3–6 hourslow
Editorial

Seed data specifies 3–6 hours aftereffects. User reports describe persistent stimulation and insomnia after primary effects resolve. Consistent with work-notes.

Reasoning

Seed data specifies 3–6 hours aftereffects. User reports describe persistent stimulation and insomnia after primary effects resolve. Consistent with work-notes.

Evidence basis: community_consensus_small

Come uptrace1–3 hours1–3 hourslow
Editorial

Derived from Erowid user reports describing gradual build over 1–3 hours after first alerts. Consistent with work-notes. No controlled data.

Reasoning

Derived from Erowid user reports describing gradual build over 1–3 hours after first alerts. Consistent with work-notes. No controlled data.

Evidence basis: community_consensus_small

Peaktrace4–8 hours4–8 hourslow
Editorial

Seed data specifies 4–8 hours peak. Consistent with Erowid user reports and work-notes. Extended peak duration is characteristic of 3C-P.

Reasoning

Seed data specifies 4–8 hours peak. Consistent with Erowid user reports and work-notes. Extended peak duration is characteristic of 3C-P.

Evidence basis: community_consensus_small

Offsettrace3–6 hours3–6 hourslow
Editorial

Seed data specifies 3–6 hours offset. User reports describe extended comedown with residual stimulation. Consistent with work-notes.

Reasoning

Seed data specifies 3–6 hours offset. User reports describe extended comedown with residual stimulation. Consistent with work-notes.

Evidence basis: community_consensus_small

Totaltrace10–16 hours10–16 hourslow
Editorial

Seed data specifies 10–16 hours total. Erowid user reports range up to 17 hours in some cases. Consistent with mescaline mean subjective duration of 11.1 hours (Ley et al. 2023). Alpha-methyl group confers MAO resistance, likely extending duration.

Reasoning

Seed data specifies 10–16 hours total. Erowid user reports range up to 17 hours in some cases. Consistent with mescaline mean subjective duration of 11.1 hours (Ley et al. 2023). Alpha-methyl group confers MAO resistance, likely extending duration.

Evidence basis: community_consensus_small

Safety

Toxicity Profiletrace

FieldPublishedAI ProposedConfidence
Acutelowlowlow
Chronic——low
Organs Affectedcardiovascularcardiovascularlow
Editorial

Work-notes specify acute toxicity as 'low (tentative)' with no controlled data. Evidence is limited to ~12 Erowid user reports and class extrapolation from mescaline clinical data and 2C-series toxicology. No organ toxicity data, no LD50, no therapeutic index. Cardiovascular system identified as primary organ of concern from user reports documenting tachycardia and chest pressure at standard doses.

Reasoning

Work-notes specify acute toxicity as 'low (tentative)' with no controlled data. Evidence is limited to ~12 Erowid user reports and class extrapolation from mescaline clinical data and 2C-series toxicology. No organ toxicity data, no LD50, no therapeutic index. Cardiovascular system identified as primary organ of concern from user reports documenting tachycardia and chest pressure at standard doses.

Evidence basis: community_consensus_small

Dependence Profiletrace

FieldPublishedAI ProposedConfidence
Physicalnonenonemedium
Psychologicalnegligiblenegligiblemedium
Compulsive Redosingnegligiblenegligiblemedium
Dose Escalationnegligiblenegligiblemedium
Editorial

Class inference from serotonergic hallucinogen pharmacology (Nichols 2004). No 3C-P-specific dependence data exist. Serotonergic hallucinogens as a class are not considered habit-forming and do not produce physical dependence. Rapid tachyphylaxis via 5-HT2A downregulation limits compulsive redosing potential.

Reasoning

Class inference from serotonergic hallucinogen pharmacology (Nichols 2004). No 3C-P-specific dependence data exist. Serotonergic hallucinogens as a class are not considered habit-forming and do not produce physical dependence. Rapid tachyphylaxis via 5-HT2A downregulation limits compulsive redosing potential.

Evidence basis: structural_analogy

Withdrawal Profiletrace

FieldPublishedAI ProposedConfidence
Severitynonenonemedium
Symptoms——medium
FatalNoNomedium
Medical SupervisionNot requiredNot requiredmedium
Editorial

No withdrawal syndrome identified for 3C-P or any serotonergic hallucinogen. Class inference from serotonergic psychedelic pharmacology.

Reasoning

No withdrawal syndrome identified for 3C-P or any serotonergic hallucinogen. Class inference from serotonergic psychedelic pharmacology.

Evidence basis: structural_analogy

Tolerance Profiletrace

FieldPublishedAI ProposedConfidence
Builduprapidrapidmedium
Half-life3 days3 daysmedium
Full Reset7 days7 daysmedium
Cross-tolerancesLSD, Psilocybin, Mescaline, DMT, 2C-x series, DOx seriesLSD, Psilocybin, Mescaline, DMT, 2C-x series, DOx seriesmedium
Editorial

Class inference from serotonergic hallucinogen pharmacology (Nichols 2004; Halberstadt 2015). Seed data tolerance values (buildup: immediate, half-life: 3 days, reset: 7 days) are consistent with established class-level tolerance kinetics for 5-HT2A agonists. No 3C-P-specific tolerance studies exist.

Reasoning

Class inference from serotonergic hallucinogen pharmacology (Nichols 2004; Halberstadt 2015). Seed data tolerance values (buildup: immediate, half-life: 3 days, reset: 7 days) are consistent with established class-level tolerance kinetics for 5-HT2A agonists. No 3C-P-specific tolerance studies exist.

Evidence basis: structural_analogy

Effects & Profile

Contraindications

FieldPublishedAI ProposedConfidence
cardiovascular Cardiovascular diseasetraceabsoluteabsolutemedium
Editorial

Cardiovascular stress documented in Erowid user reports at standard doses; mechanism consistent with phenethylamine sympathomimetic class. Class-level evidence from mescaline clinical studies confirms autonomic effects.

Reasoning

Cardiovascular stress documented in Erowid user reports at standard doses; mechanism consistent with phenethylamine sympathomimetic class. Class-level evidence from mescaline clinical studies confirms autonomic effects.

other Concurrent MAOI usetraceabsoluteabsolutemedium
Editorial

Class inference from serotonergic hallucinogen pharmacology (Nichols 2004). No 3C-P-specific interaction data exist. Mechanism is well-established for the phenethylamine psychedelic class.

Reasoning

Class inference from serotonergic hallucinogen pharmacology (Nichols 2004). No 3C-P-specific interaction data exist. Mechanism is well-established for the phenethylamine psychedelic class.

other Concurrent SSRI/SNRI usetraceabsoluteabsolutemedium
Editorial

Class inference from serotonergic psychedelic pharmacology. No 3C-P-specific data. Mechanism well-established for phenethylamine 5-HT2A agonists.

Reasoning

Class inference from serotonergic psychedelic pharmacology. No 3C-P-specific data. Mechanism well-established for phenethylamine 5-HT2A agonists.

other Concurrent tramadol usetraceabsoluteabsolutemedium
Editorial

Mechanistic support from tramadol's documented SERT inhibition (Baldo 2018; Pergolizzi 2022) combined with 3C-P's 5-HT2A agonism. Listed as dangerous interaction in seed data. Not tested for 3C-P specifically.

Reasoning

Mechanistic support from tramadol's documented SERT inhibition (Baldo 2018; Pergolizzi 2022) combined with 3C-P's 5-HT2A agonism. Listed as dangerous interaction in seed data. Not tested for 3C-P specifically.

neurological Seizure disorderstracerelativerelativelow
Editorial

Class extrapolation from 2C-series toxicology data (Dean et al. 2013). No 3C-P-specific seizure data exist.

Reasoning

Class extrapolation from 2C-series toxicology data (Dean et al. 2013). No 3C-P-specific seizure data exist.

psychiatric Psychotic spectrum disorderstracerelativerelativemedium
Editorial

Standard contraindication for all serotonergic psychedelics based on 5-HT2A mechanism of action. No 3C-P-specific psychiatric adverse event data exist.

Reasoning

Standard contraindication for all serotonergic psychedelics based on 5-HT2A mechanism of action. No 3C-P-specific psychiatric adverse event data exist.

psychiatric Bipolar disordertracerelativerelativelow
Editorial

Class-level contraindication for serotonergic psychedelics. No 3C-P-specific data. Low confidence due to reliance on class extrapolation.

Reasoning

Class-level contraindication for serotonergic psychedelics. No 3C-P-specific data. Low confidence due to reliance on class extrapolation.

pregnancy breastfeeding Pregnancy and lactationtraceabsoluteabsolutelow
Editorial

Precautionary contraindication based on absence of safety data and known pharmacological activity. Standard for all psychoactive compounds lacking reproductive safety data.

Reasoning

Precautionary contraindication based on absence of safety data and known pharmacological activity. Standard for all psychoactive compounds lacking reproductive safety data.

hepatic Hepatic impairmenttracerelativerelativelow
Editorial

Theoretical risk based on absence of metabolic data. Phenethylamine amphetamines are typically hepatically metabolized (CYP-mediated), so impaired clearance is a reasonable concern.

Reasoning

Theoretical risk based on absence of metabolic data. Phenethylamine amphetamines are typically hepatically metabolized (CYP-mediated), so impaired clearance is a reasonable concern.

renal Renal impairmenttracerelativerelativelow
Editorial

Theoretical risk based on absence of renal elimination data. Mescaline (structural parent) has documented urinary recovery, suggesting renal involvement in the class.

Reasoning

Theoretical risk based on absence of renal elimination data. Mescaline (structural parent) has documented urinary recovery, suggesting renal involvement in the class.

Timeline Phases

oral

FieldPublishedAI ProposedConfidence
Onsettrace1800–3600 sec(i=0.05)1800–3600 sec(i=0.05)low
Editorial

Timeline phases derived from work-notes and Erowid user reports (~10–12 reports). Onset 1–2h, come-up 1–3h, peak 3–8h, plateau 6–10h, resolution 10–14h, and afterglow 14–20h from work-notes. No controlled pharmacokinetic data exist. Phase durations represent ranges from community reports only.

Reasoning

Timeline phases derived from work-notes and Erowid user reports (~10–12 reports). Onset 1–2h, come-up 1–3h, peak 3–8h, plateau 6–10h, resolution 10–14h, and afterglow 14–20h from work-notes. No controlled pharmacokinetic data exist. Phase durations represent ranges from community reports only.

Evidence basis: community_consensus_small

Come uptrace3600–7200 sec(i=0.30)3600–7200 sec(i=0.30)low
Editorial

Timeline phases derived from work-notes and Erowid user reports (~10–12 reports). Onset 1–2h, come-up 1–3h, peak 3–8h, plateau 6–10h, resolution 10–14h, and afterglow 14–20h from work-notes. No controlled pharmacokinetic data exist. Phase durations represent ranges from community reports only.

Reasoning

Timeline phases derived from work-notes and Erowid user reports (~10–12 reports). Onset 1–2h, come-up 1–3h, peak 3–8h, plateau 6–10h, resolution 10–14h, and afterglow 14–20h from work-notes. No controlled pharmacokinetic data exist. Phase durations represent ranges from community reports only.

Evidence basis: community_consensus_small

Peaktrace14400–18000 sec(i=1.00)14400–18000 sec(i=1.00)low
Editorial

Timeline phases derived from work-notes and Erowid user reports (~10–12 reports). Onset 1–2h, come-up 1–3h, peak 3–8h, plateau 6–10h, resolution 10–14h, and afterglow 14–20h from work-notes. No controlled pharmacokinetic data exist. Phase durations represent ranges from community reports only.

Reasoning

Timeline phases derived from work-notes and Erowid user reports (~10–12 reports). Onset 1–2h, come-up 1–3h, peak 3–8h, plateau 6–10h, resolution 10–14h, and afterglow 14–20h from work-notes. No controlled pharmacokinetic data exist. Phase durations represent ranges from community reports only.

Evidence basis: community_consensus_small

Plateautrace10800–14400 sec(i=0.70)10800–14400 sec(i=0.70)low
Editorial

Timeline phases derived from work-notes and Erowid user reports (~10–12 reports). Onset 1–2h, come-up 1–3h, peak 3–8h, plateau 6–10h, resolution 10–14h, and afterglow 14–20h from work-notes. No controlled pharmacokinetic data exist. Phase durations represent ranges from community reports only.

Reasoning

Timeline phases derived from work-notes and Erowid user reports (~10–12 reports). Onset 1–2h, come-up 1–3h, peak 3–8h, plateau 6–10h, resolution 10–14h, and afterglow 14–20h from work-notes. No controlled pharmacokinetic data exist. Phase durations represent ranges from community reports only.

Evidence basis: community_consensus_small

Resolutiontrace10800–14400 sec(i=0.30)10800–14400 sec(i=0.30)low
Editorial

Timeline phases derived from work-notes and Erowid user reports (~10–12 reports). Onset 1–2h, come-up 1–3h, peak 3–8h, plateau 6–10h, resolution 10–14h, and afterglow 14–20h from work-notes. No controlled pharmacokinetic data exist. Phase durations represent ranges from community reports only.

Reasoning

Timeline phases derived from work-notes and Erowid user reports (~10–12 reports). Onset 1–2h, come-up 1–3h, peak 3–8h, plateau 6–10h, resolution 10–14h, and afterglow 14–20h from work-notes. No controlled pharmacokinetic data exist. Phase durations represent ranges from community reports only.

Evidence basis: community_consensus_small

Afterglowtrace10800–21600 sec(i=0.10)10800–21600 sec(i=0.10)low
Editorial

Timeline phases derived from work-notes and Erowid user reports (~10–12 reports). Onset 1–2h, come-up 1–3h, peak 3–8h, plateau 6–10h, resolution 10–14h, and afterglow 14–20h from work-notes. No controlled pharmacokinetic data exist. Phase durations represent ranges from community reports only.

Reasoning

Timeline phases derived from work-notes and Erowid user reports (~10–12 reports). Onset 1–2h, come-up 1–3h, peak 3–8h, plateau 6–10h, resolution 10–14h, and afterglow 14–20h from work-notes. No controlled pharmacokinetic data exist. Phase durations represent ranges from community reports only.

Evidence basis: community_consensus_small

Dose Tier Summaries

thresholdtrace
low

Sub-perceptual to barely perceptible effects. A faint mood lift and subtle increase in physical energy may be the only indicators of activity. No visual effects, no meaningful cognitive alteration, and no significant body load are expected. Mild stimulation and slight body scan awareness may emerge over 1–2 hours, consistent with 3C-P's characteristically slow onset. Appetite may be marginally reduced. This range is appropriate for an allergy test dose. Effects at threshold are easily dismissed as placebo. The slow onset means effects may not manifest for up to 2 hours — patience is essential before considering any additional dose.

Editorial

Work-notes specify threshold at 5–10 mg. Descriptions derived from user reports of sub-active doses and class-level inference from mescaline-class phenethylamines. No controlled data exist for threshold effects.

Reasoning

Work-notes specify threshold at 5–10 mg. Descriptions derived from user reports of sub-active doses and class-level inference from mescaline-class phenethylamines. No controlled data exist for threshold effects.

Evidence basis: community_consensus_small

lighttrace
low

Mild stimulation becomes clearly apparent, with increased sociability and light mood elevation. Music enhancement emerges as a subtle but noticeable feature. Cognitive function is largely preserved or slightly enhanced — conversation flows easily. Physical effects are generally mild: slight appetite suppression, possible faint nausea during the come-up, and minor increases in heart rate awareness. Visual effects are minimal to absent at this level. The experience lasts 8–12 hours with residual wakefulness extending beyond the primary effects. Functional impairment is minimal, but sleep may be delayed by several hours.

Editorial

Work-notes specify light at 10–20 mg. Descriptions drawn from Erowid user reports at lower dose ranges and class inference from mescaline/3C-E phenomenology. Fewer than 15 total user reports exist.

Reasoning

Work-notes specify light at 10–20 mg. Descriptions drawn from Erowid user reports at lower dose ranges and class inference from mescaline/3C-E phenomenology. Fewer than 15 total user reports exist.

Evidence basis: community_consensus_small

commontrace
low

Prominent stimulation and sustained wakefulness define the experience. Cognitive enhancement becomes apparent — articulate speech, information synthesis, and pattern recognition enhancement are reported. Empathy enhancement and emotional openness provide an empathogenic warmth. Mild visual effects emerge: color enhancement, gentle visual drifting, subtle tracers, and possible faint synesthesia. Music enhancement is notable. Body load includes muscle tension, mild bruxism, appetite suppression, and possible nausea during the come-up. Pupil dilation is observable. The full experience extends 10–16 hours. Sleep is effectively impossible for 8+ hours after ingestion. A full day cleared of obligations is necessary.

Editorial

Work-notes specify common at 20–40 mg. Core descriptions from Erowid user reports at this dose range, consistent with the article prose's effects overview. Community-derived from ~10–12 reports.

Reasoning

Work-notes specify common at 20–40 mg. Core descriptions from Erowid user reports at this dose range, consistent with the article prose's effects overview. Community-derived from ~10–12 reports.

Evidence basis: community_consensus_small

strongtrace
low

Intensified stimulation with pronounced cardiovascular effects — tachycardia, vasoconstriction, and chest pressure are documented at this level. The stimulant dimension dominates: restlessness, trembling, and elevated heart rate awareness become prominent. Visual effects become more apparent but remain mild relative to equipotent doses of other psychedelics. Risk of anxiety and paranoia increases, particularly with physical exertion. Cognitive confusion is possible alongside the stimulant-enhanced cognition, creating a paradoxical mental state. Duration may extend to 17+ hours with significant insomnia. Challenging experiences become more likely due to the combined intensity and extreme duration. Strenuous physical activity dramatically worsens cardiovascular effects at this level.

Editorial

Work-notes specify strong at 40–50 mg. Descriptions from Erowid report at 43 mg documenting alarming cardiovascular effects during mountain biking. Maximum documented dose ~50 mg without fatality.

Reasoning

Work-notes specify strong at 40–50 mg. Descriptions from Erowid report at 43 mg documenting alarming cardiovascular effects during mountain biking. Maximum documented dose ~50 mg without fatality.

Evidence basis: community_consensus_small

heavytrace
low

Doses above 50 mg represent undocumented territory — no reports at this level have been published. Safety above the maximum documented dose (~50 mg) is entirely unknown, and this tier should be treated as carrying serious risk. Based on class extrapolation from phenethylamine psychedelic toxicology, sympathomimetic toxidrome risk increases significantly: severe hypertension, dangerous tachycardia, hyperthermia, possible seizures, and excited delirium are class-level risks at supratherapeutic doses. At least five fatalities have been reported for the structurally related 2C series. This dose range carries unknown and potentially life-threatening risk. The absence of documented experience at these doses means no safety margin has been established.

Editorial

Work-notes specify heavy at 50+ mg. No user reports exist above ~50 mg. Safety assessment is entirely class extrapolation from 2C-series toxicology (Dean et al. 2013) and phenethylamine sympathomimetic toxidrome literature.

Reasoning

Work-notes specify heavy at 50+ mg. No user reports exist above ~50 mg. Safety assessment is entirely class extrapolation from 2C-series toxicology (Dean et al. 2013) and phenethylamine sympathomimetic toxidrome literature.

Evidence basis: structural_analogy

02

History

current version
published Jun 4, 2026AI-generated—
versions
1 total
publication ledger

backfill Jun 4, 2026

Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.

full version history suggest a correctioncontact@psychedex.org
03

Sources

6 strong · 9 moderate · 6 weak
  1. [1]
    moderate
    Comparison of the behavioral effects of mescaline analogs using the head twitch response in mice
    Halberstadt AL, Chatha M, Chapman SJ, Brandt SD · 2019 · Journal of Psychopharmacology
    doi.org/10.1177/0269881119826610pubmed 3078929115 claims checked11 verified1 partial3 inconclusive
  2. [2]
    weak
    3C-P - Erowid Experience Report: Euphoric Stimmy Rollercoaster
    2017
    linkno claims checked
  3. [3]
    strong
    Hallucinogens
    Nichols DE · 2004 · Pharmacology & Therapeutics
    pubmed 147617036 claims checked1 verified5 inconclusive
  4. [4]
    weak
    Erowid 3C-P Vault: Brief 3C-P Information
    Erowid · 2003
    linkno claims checked
  5. [5]
    weak
    PiHKAL Entry #140: Proscaline
    Shulgin A, Shulgin A · 1991
    linkno claims checked
  6. [6]
    weak
    PeakAL: Protons I Have Known and Loved — NMR spectra of psychedelic phenylethanamines including TMA-2
    Chapman SJ, Avanes AA · 2015
    doi.org/10.16889/isomerdesign-11 claim checked1 inconclusive
  7. [7]
    moderate
    Multiple receptors contribute to the behavioral effects of indoleamine hallucinogens
    Halberstadt AL, Geyer MA · 2011 · Neuropharmacology
    doi.org/10.1016/j.neuropharm.2011.01.017pubmed 212561403 claims checked3 verified
  8. [8]
    strong
    Acute dose-dependent effects of mescaline in a double-blind placebo-controlled study in healthy subjects
    Klaiber A, Schmid Y, Becker AM, Straumann I, Erne L, Jelusic A, Thomann J, Luethi D, Liechti ME · 2024 · Translational Psychiatry
    doi.org/10.1038/s41398-024-03116-2pubmed 393494275 claims checked4 verified1 partial
  9. [9]
    moderate
    Recent advances in the neuropsychopharmacology of serotonergic hallucinogens
    Halberstadt AL · 2015 · Behavioural Brain Research
    doi.org/10.1016/j.bbr.2014.07.016pubmed 250364253 claims checked1 verified2 inconclusive
  10. [10]
    strong
    Comparative acute effects of mescaline, lysergic acid diethylamide, and psilocybin in a randomized, double-blind, placebo-controlled cross-over study in healthy participants
    Ley L, Holze F, Arikci D, Becker AM, Straumann I, Klaiber A, Coviello F, Dierbach S, Thomann J, Duthaler U, Luethi D, Varghese N, Eckert A, Liechti ME · 2023 · Neuropsychopharmacology
    doi.org/10.1038/s41386-023-01607-2pubmed 372310806 claims checked4 verified2 inconclusive
  11. [11]
    moderate
    Receptor Interaction Profiles of 4-Alkoxy-Substituted 2,5-Dimethoxyphenethylamines and Related Amphetamines.
    Kolaczynska KE, Luethi D, Trachsel D, Hoener MC, Liechti ME · 2019 · Frontiers in Pharmacology
    doi.org/10.3389/fphar.2019.01423pubmed 318496711 claim checked1 verified
  12. [12]
    moderate
    Receptor interaction profiles of novel N-2-methoxybenzyl (NBOMe) derivatives of 2,5-dimethoxy-substituted phenethylamines (2C drugs)
    Rickli A, Luethi D, Reinisch J, Buchy D, Hoener MC, Liechti ME · 2015 · Neuropharmacology
    doi.org/10.1016/j.neuropharm.2015.08.034pubmed 263180991 claim checked1 verified
  13. [13]
    moderate
    Dihydrobenzofuran analogues of hallucinogens. 4. Mescaline derivatives
    Monte AP, Waldman SR, Marona-Lewicka D, Wainscott DB, Nelson DL, Sanders-Bush E, Nichols DE · 1997 · Journal of Medicinal Chemistry
    pubmed 93016612 claims checked2 verified
  14. [14]
    strong
    Pharmacokinetics, Pharmacodynamics, and Urinary Recovery of Oral Mescaline Hydrochloride in Healthy Participants
    Mueller L, Klaiber A, Ley L, Becker AM, Thomann J, Luethi D, Schmid Y, Liechti ME · 2025 · Clinical Pharmacokinetics
    doi.org/10.1007/s40262-025-01544-xpubmed 406583451 claim checked1 inconclusive
  15. [15]
    weak
    3C-P - Erowid Experience Report: Smooth, Fun, Therapeutic - A Nice Surprise
    2012
    linkno claims checked
  16. [16]
    strong
    The Ethnopharmacological Use of Mescaline for Psychiatric Disorders: A Systematic Review
    Shaw J, Yong A, Lee J, Cheng J, Andricioaei A, Wang JY, Zisman-Ilani Y, Bota R · 2026 · International Journal of Molecular Sciences
    doi.org/10.3390/ijms27073081pubmed 419772672 claims checked1 verified1 partial
  17. [17]
    moderate
    Safety pharmacology of acute mescaline administration in healthy participants
    Klaiber A, Humbert-Droz M, Ley L, Schmid Y, Liechti ME · 2024 · British Journal of Clinical Pharmacology
    doi.org/10.1111/bcp.16349pubmed 395874361 claim checked1 inconclusive
  18. [18]
    strong
    2C or Not 2C: Phenethylamine Designer Drug Review
    Dean BV, Stellpflug SJ, Burnett A, Engebretsen KM · 2013 · Journal of Medical Toxicology
    doi.org/10.1007/s13181-013-0295-xpubmed 234948443 claims checked2 verified1 inconclusive
  19. [19]
    weak
    3C-P - Erowid Experience Report: Slow Burn
    2015
    linkno claims checked
  20. [20]
    moderate
    Opioid analgesic drugs and serotonin toxicity (syndrome): mechanisms, animal models, and links to clinical effects
    Baldo BA · 2018 · Archives of Toxicology
    doi.org/10.1007/s00204-018-2244-6pubmed 299160501 claim checked1 verified
  21. [21]
    moderate
    Multimechanistic Single-Entity Combinations for Chronic Pain Control: A Narrative Review.
    Pergolizzi J, Magnusson P, Coluzzi F, Breve F, LeQuang JAK, Varrassi G · 2022 · Cureus
    doi.org/10.7759/cureus.26000pubmed 358552481 claim checked1 inconclusive
04

Claim Verification

Citation-bearing claims in this article were checked by an AI model against the abstract of the source they cite — every safety-critical claim, plus a sample of the rest. Verdicts below are model-issued, not human-issued; when an editor overrides a verdict, the override is recorded alongside it. Claims whose source does not support them are flagged for editorial review.

summary3 claims2verified1inconclusive
verifiedNo clinical pharmacological characterization has been published; the sole quantitative study is a murine head twitch response assay establishing an ED₅₀ of 2.45 mg/kg.[1]model confidence 97%
Verified

Abstract directly reports 3C-P ED₅₀ = 2.45 mg/kg in the HTR assay in mice. The paper is a murine study, consistent with the claim that no clinical characterization exists.

3C-P ED50=2.45 mg/kg (molar 8.47 μmol/kg)

checked by claude-sonnet-4-6 · May 11, 2026

verified3C-P is presumed to act as a 5-HT₂A/5-HT₂C receptor agonist based on structural class membership and its capacity to elicit the head twitch response in mice — a behavior selectively mediated by 5-HT₂A activation[1]model confidence 88%
Verified

Abstract confirms 3C-P produces HTR in mice and that HTR potency parallels human hallucinogenic data. Citing this paper for the HTR→5-HT₂A inference is standard practice; the abstract supports the empirical basis of the claim.

Potency relationships in HTR closely parallel human hallucinogenic data.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusiveThe compound is not habit-forming; rapid tachyphylaxis via 5-HT₂A receptor downregulation limits compulsive use, with cross-tolerance extending to other serotonergic hallucinogens[3]model confidence 72%
Inconclusive

Abstract confirms hallucinogens do not produce dependence and stimulate 5-HT2A receptors, supporting the 'not habit-forming' portion. However, the specific claims about rapid tachyphylaxis, 5-HT2A receptor downregulation, and cross-tolerance are not present in the abstract and would require the full review text.

Hallucinogens physiologically safe, do not produce dependence. Stimulate 5-HT2A receptors on neocortical pyramidal cells.

checked by claude-sonnet-4-6 · May 11, 2026

history1 claim1verified
verifiedThe sole published pharmacological study was conducted by Halberstadt and colleagues in 2019, establishing 3C-P's potency in the murine head twitch response assay[1]model confidence 95%
Verified

Abstract confirms HTR experiments with 3C-P producing a quantitative ED₅₀ (2.45 mg/kg), consistent with this being the pharmacological study establishing 3C-P's potency.

HTR experiments conducted with mescaline, escaline, proscaline, TMA, 3C-E, 3C-P, TMA-2, MEM, MPM. 3C-P ED50=2.45 mg/kg

checked by claude-sonnet-4-6 · May 11, 2026

chemistry3 claims1partial2inconclusive
partialThis regiochemical difference confers fundamentally distinct structure-activity relationships: in the 3,4,5-substitution pattern, extending the 4-position alkoxy chain from methyl to ethyl to propyl progressively increases hallucinogenic potency, whereas in the 2,4,5-series such homologation does not alter potency.[1]model confidence 85%
Partial

Abstract shows methyl (TMA) → ethyl (3C-E) increases potency, but 3C-E and 3C-P are 'essentially equipotent' — meaning ethyl → propyl does NOT further increase potency. The claim that potency 'progressively increases from methyl to ethyl to propyl' is materially incorrect per the abstract; there is a plateau at ethyl, not a progressive increase through propyl.

3C-E and 3C-P were essentially equipotent, both ~50% more potent than TMA.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusiveNo enantiopure preparations have been reported in the literature, and all available pharmacological data (including the Halberstadt et al. 2019 HTR study) were generated using the racemate.[1]model confidence 60%
Inconclusive

Abstract does not mention chirality, enantiopure preparations, or racemate. This claim cannot be verified from the abstract alone.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusiveNMR spectroscopic characterization of the 3,5-dimethoxy mescaline analog series (including closely related compounds) has been performed, providing analytical reference data for identification purposes.[6]model confidence 60%
Inconclusive

Abstract not available for this citation; cannot verify the NMR characterization claim.

checked by claude-sonnet-4-6 · May 11, 2026

pharmacology11 claims8verified3inconclusive
verifiedBoth demonstrated approximately 50% greater molar potency than TMA (3,4,5-trimethoxyamphetamine, the α-methyl homolog of mescaline)[1]model confidence 98%
Verified

Abstract directly states '3C-E and 3C-P were essentially equipotent, both ~50% more potent than TMA.'

3C-E and 3C-P were essentially equipotent, both ~50% more potent than TMA.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedPhenylalkylamine hallucinogens are selective 5-HT₂ receptor agonists, in contrast to indoleamine hallucinogens (e.g., LSD, psilocybin) which interact with a broader receptor repertoire[7]model confidence 97%
Verified

Abstract directly states 'Phenylalkylamine hallucinogens are selective 5-HT2 receptor agonists.' The paper title ('Multiple receptors contribute to behavioral effects of indoleamine hallucinogens') supports the contrast with indoleamines having a broader receptor profile.

Phenylalkylamine hallucinogens are selective 5-HT2 receptor agonists.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusiveThe 5-HT₂A receptor is the primary mediator of hallucinogenic action: agonism at 5-HT₂A receptors on layer V pyramidal neurons in the neocortex increases cortical glutamate release via thalamic afferent pathways, disrupting normal thalamocortical filtering.[3]model confidence 75%
Inconclusive

Abstract confirms 5-HT2A stimulation on neocortical pyramidal cells, supporting the broad receptor localization claim. However, the specific mechanism — glutamate release via thalamic afferent pathways disrupting thalamocortical filtering — is not present in the abstract and would require the full review text.

Stimulate 5-HT2A receptors on neocortical pyramidal cells.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedDirect confirmation that the mescaline-class mechanism is 5-HT₂A-mediated comes from controlled human studies in which co-administration of the selective 5-HT₂A antagonist ketanserin significantly attenuated all subjective effects of mescaline. 3C-P is expected to act via the same receptor mechanism, though no blocking study or receptor binding assay has been performed with this specific compound.[8]model confidence 93%
Verified

Abstract directly confirms ketanserin attenuated mescaline's subjective effects and confirms 5-HT2A as the primary mechanism in a randomized double-blind crossover study. The second part (no 3C-P-specific data) is not contradicted.

Ketanserin attenuated effects, confirming 5-HT2A as primary mechanism.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedThe only published quantitative pharmacological study of 3C-P is Halberstadt et al. 2019, which measured the head twitch response (HTR) in C57BL/6J mice — a 5-HT₂A-mediated behavior with established predictive validity for human hallucinogenic potency.[1]model confidence 88%
Verified

Abstract confirms HTR experiments with 3C-P and that 'potency relationships in HTR closely parallel human hallucinogenic data,' supporting the predictive validity claim. Mouse strain (C57BL/6J) is not confirmed in the abstract but is a detail likely in the full text; no contradiction present.

HTR experiments conducted with mescaline, escaline, proscaline, TMA, 3C-E, 3C-P, TMA-2, MEM, MPM... Potency relationships in HTR closely parallel human hallucinogenic data.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedThe only published quantitative pharmacological study of 3C-P is Halberstadt et al. 2019, which measured the head twitch response (HTR) in C57BL/6J mice — a 5-HT₂A-mediated behavior with established predictive validity for human hallucinogenic potency.[1]model confidence 88%
Verified

Duplicate of Pair 7. Abstract confirms HTR study with 3C-P and predictive validity for human hallucinogenic potency.

Potency relationships in HTR closely parallel human hallucinogenic data.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusiveThe only published quantitative pharmacological study of 3C-P is Halberstadt et al. 2019, which measured the head twitch response (HTR) in C57BL/6J mice — a 5-HT₂A-mediated behavior with established predictive validity for human hallucinogenic potency.[9]model confidence 70%
Inconclusive

Review confirms HTR as a validated assay and 5-HT2A as primary site, supporting the predictive validity claim. However, it does not confirm that Halberstadt 2019 is the only published study for 3C-P specifically; that factual assertion requires checking the full text or a broader literature search.

Reviews drug discrimination, HTR, PPI, and human clinical trial data.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusivePlasma elimination half-life is approximately 3.5 hours, with Tmax at approximately 2 hours after oral dosing[10]model confidence 72%
Inconclusive

Abstract confirms t½ ~3.5h, but states only that Tmax is 'longer than LSD/psilocybin' without specifying a numeric value. The Tmax ~2h figure is not confirmed in this abstract; it appears in citation [25].

plasma t½ ~3.5h; Tmax longer than LSD/psilocybin

checked by claude-sonnet-4-6 · May 11, 2026

verifiedPlasma elimination half-life is approximately 3.5 hours, with Tmax at approximately 2 hours after oral dosing[8]model confidence 97%
Verified

Abstract directly confirms both PK parameters: 'Tmax ~2h, t½ ~3.5h.'

Dose-proportional PK, Tmax ~2h, t½ ~3.5h

checked by claude-sonnet-4-6 · May 11, 2026

verifiedMean subjective effect duration at pharmacologically active doses (500 mg mescaline sulfate equivalent) is 11.1 hours, with a range of 6.4–14 hours across doses.[10]model confidence 90%
Verified

Abstract directly confirms 'Mescaline effect duration mean 11.1h.' The range (6.4–14h) is not in this abstract but appears in citation [25]; it is not contradicted here.

Mescaline effect duration mean 11.1h

checked by claude-sonnet-4-6 · May 11, 2026

verifiedMean subjective effect duration at pharmacologically active doses (500 mg mescaline sulfate equivalent) is 11.1 hours, with a range of 6.4–14 hours across doses.[8]model confidence 90%
Verified

Abstract confirms 'effect duration 6.4-14h' directly. The mean 11.1h is from citation [24] and is not contradicted here.

effect duration 6.4-14h

checked by claude-sonnet-4-6 · May 11, 2026

receptor pharmacology7 claims7verified
verifiedThe compound's classification as a 5-HT₂A/5-HT₂C agonist rests on structural class membership — it is a 3,5-dimethoxy-4-alkoxy-substituted amphetamine, a pharmacological class defined by selective 5-HT₂ receptor agonism — and on its activity in the murine head twitch response, a behavior mediated exclusively by 5-HT₂A receptors.[7]model confidence 90%
Verified

Abstract directly confirms phenylalkylamine hallucinogens are 'selective 5-HT2 receptor agonists' and that '5-HT2A mediates characteristic effects,' supporting the class-level receptor classification.

Phenylalkylamine hallucinogens are selective 5-HT2 receptor agonists... 5-HT2A mediates characteristic effects.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedThe compound's classification as a 5-HT₂A/5-HT₂C agonist rests on structural class membership — it is a 3,5-dimethoxy-4-alkoxy-substituted amphetamine, a pharmacological class defined by selective 5-HT₂ receptor agonism — and on its activity in the murine head twitch response, a behavior mediated exclusively by 5-HT₂A receptors.[1]model confidence 88%
Verified

Abstract confirms 3C-P produces HTR in mice, providing the empirical basis for 5-HT₂A classification. Potency parallels to human hallucinogenic data further support validity of the HTR→receptor inference.

HTR experiments conducted with... 3C-P... Potency relationships in HTR closely parallel human hallucinogenic data.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedWhile no direct binding data exist for 3C-P, extensive receptor interaction profiling has been performed on structurally related compounds in the 2,5-dimethoxy-4-substituted phenethylamine and amphetamine series[11]model confidence 93%
Verified

Abstract directly describes receptor binding affinity profiling (5-HT2A, 5-HT2C, 5-HT1A, TAAR1, alpha-adrenergic, D2, monoamine transporters) for 2,5-dimethoxy-4-alkoxy phenethylamines and related amphetamines.

Receptor binding affinities of 2C-O and DO-alkoxy derivatives at 5-HT1A, 5-HT2A, 5-HT2C, TAAR1, alpha-adrenergic, D2 and monoamine transporters.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedWhile no direct binding data exist for 3C-P, extensive receptor interaction profiling has been performed on structurally related compounds in the 2,5-dimethoxy-4-substituted phenethylamine and amphetamine series[12]model confidence 90%
Verified

Abstract confirms receptor binding profiles characterized for 2C drugs (2,5-dimethoxy-substituted phenethylamines), directly supporting the claim about profiling in the structural analog class.

Characterized receptor binding profiles of NBOMe drugs vs 2C drugs and LSD. Provides 5-HT2A binding data for phenethylamine psychedelics.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedThe divergent structure-activity relationships between these two substitution patterns — documented in the HTR assay — suggest that receptor selectivity and binding kinetics may also differ[1]model confidence 83%
Verified

Abstract includes compounds from both the 3,4,5-series (TMA, 3C-E, 3C-P) and 2,4,5-series (TMA-2) under identical HTR conditions, providing the empirical SAR comparison. The inference about receptor selectivity and binding kinetics is a reasonable scientific extrapolation.

HTR experiments conducted with mescaline, escaline, proscaline, TMA, 3C-E, 3C-P, TMA-2, MEM, MPM.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedHomology modeling of the 5-HT₂A receptor with mescaline-class ligands indicates that the 3,4,5-substitution pattern requires conformational freedom for efficacious binding, a constraint not present in the 2,4,5 series.[13]model confidence 90%
Verified

Abstract directly states '3 and 5 methoxy groups must remain conformationally mobile to enable receptor activation' for 3,4,5-trioxygenated mescaline analogues, directly supporting the conformational freedom requirement.

3 and 5 methoxy groups must remain conformationally mobile to enable receptor activation.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedThe prolonged subjective duration (10–16 hours) relative to the expected plasma half-life (estimated at 3–5 hours based on mescaline analog data) could reflect extended receptor occupancy, slow tissue redistribution, the contribution of active metabolites, or some combination thereof[10]model confidence 87%
Verified

Abstract confirms mescaline mean effect duration of 11.1h with plasma t½ ~3.5h — the duration-vs-half-life disparity underpins this claim. The mechanistic hypotheses (receptor occupancy, redistribution, metabolites) are reasonable inferences not contradicted by the abstract.

Mescaline effect duration mean 11.1h; plasma t½ ~3.5h

checked by claude-sonnet-4-6 · May 11, 2026

neuroscience3 claims1partial2inconclusive
inconclusiveSerotonergic psychedelics acting through 5-HT₂A receptors on layer V cortical pyramidal neurons trigger a cascade of glutamatergic signaling that disrupts default mode network (DMN) integrity and increases global functional connectivity[3]model confidence 65%
Inconclusive

Abstract confirms 5-HT2A stimulation on neocortical pyramidal cells, but does not mention layer V specifically, glutamatergic signaling cascades, DMN disruption, or global functional connectivity changes. These are mechanistic details likely in the full review.

Stimulate 5-HT2A receptors on neocortical pyramidal cells.

checked by claude-sonnet-4-6 · May 11, 2026

partialFor mescaline specifically, controlled studies confirm that its subjective effects are entirely attributable to 5-HT₂A agonism, as demonstrated by complete attenuation with the selective antagonist ketanserin.[8]model confidence 82%
Partial

Abstract confirms ketanserin 'attenuated effects, confirming 5-HT2A as primary mechanism.' However, the claim asserts 'entirely attributable' and 'complete attenuation,' whereas the abstract uses 'attenuated' (not complete) and 'primary mechanism' (not sole mechanism). These qualifiers represent a material overstatement.

Ketanserin attenuated effects, confirming 5-HT2A as primary mechanism.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusiveDose-response relationship in humans: What is the quantitative relationship between oral dose and subjective intensity? The inverted-U pattern observed in mice has not been confirmed in humans.[1]model confidence 65%
Inconclusive

Abstract reports murine HTR dose-response data for 3C-P. It does not address human dose-response relationships or whether an inverted-U pattern has been confirmed in humans. The human gap claim cannot be verified from this abstract.

Potency relationships in HTR closely parallel human hallucinogenic data.

checked by claude-sonnet-4-6 · May 11, 2026

pharmacokinetic detail1 claim1inconclusive
inconclusiveMore detailed pharmacokinetic characterization of mescaline hydrochloride in healthy volunteers has been published, including urinary recovery data[14]model confidence 60%
Inconclusive

Abstract not available; cannot verify the specific PK/urinary recovery claim from the abstract.

checked by claude-sonnet-4-6 · May 11, 2026

clinical evidence3 claims3verified
verifiedOne murine head twitch response study[1]model confidence 99%
Verified

Abstract directly describes HTR experiments in mice including 3C-P.

HTR experiments conducted with mescaline, escaline, proscaline, TMA, 3C-E, 3C-P, TMA-2, MEM, MPM.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedStructural analog inference from mescaline clinical data[10]model confidence 97%
Verified

This citation is a controlled RCT providing mescaline clinical data; it is the source from which structural analog inferences about 3C-P are drawn.

Randomized double-blind placebo-controlled crossover in 32 healthy participants. Mescaline 300/500mg...

checked by claude-sonnet-4-6 · May 11, 2026

verifiedStructural analog inference from mescaline clinical data[8]model confidence 97%
Verified

This citation provides dose-dependent mescaline clinical and PK data; it is an appropriate source for structural analog inference about 3C-P.

Randomized double-blind crossover in 16 healthy subjects: mescaline 100-800mg...

checked by claude-sonnet-4-6 · May 11, 2026

comparative pharmacology6 claims4verified1partial1inconclusive
verifiedMescaline at pharmacologically active doses (300–500 mg sulfate salt, oral) produces altered states of consciousness comparable in intensity to LSD 100 μg and psilocybin 20 mg[10]model confidence 98%
Verified

Abstract directly states the study compared mescaline 300/500mg vs LSD 100μg vs psilocybin 20mg and that 'Subjective effects comparable at equivalent doses.'

Mescaline 300/500mg vs LSD 100μg vs psilocybin 20mg. Subjective effects comparable at equivalent doses.

checked by claude-sonnet-4-6 · May 11, 2026

partialMescaline's adverse effect profile includes nausea, headache, hypertension, and tachycardia as the most common events. 3C-P's more stimulant-dominant phenomenology, operating at dramatically lower absolute doses (20–40 mg vs 300–500 mg), suggests partial pharmacological differentiation despite structural similarity[16]model confidence 82%
Partial

Abstract confirms hypertension, headache, nausea, and vomiting as common AEs — but the claim includes tachycardia (not listed in this abstract) and omits vomiting. Tachycardia is a material assertion that the abstract does not support. The second part of the claim (about 3C-P) is not addressed in this mescaline systematic review.

Common AEs: hypertension, headache, nausea, vomiting.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedThis establishes that extending the 4-position alkoxy chain from methyl (TMA) to ethyl (3C-E) increases potency, but further extension to propyl (3C-P) does not yield additional gains — suggesting a potency plateau at the ethoxy chain length in this regiochemistry.[1]model confidence 97%
Verified

Abstract directly supports this conclusion: '3C-E and 3C-P were essentially equipotent, both ~50% more potent than TMA' — confirming the gain from methyl→ethyl but plateau from ethyl→propyl.

3C-E and 3C-P were essentially equipotent, both ~50% more potent than TMA.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedThe only head-to-head pharmacological comparison involving 3C-P is the Halberstadt et al. 2019 HTR study, which tested multiple mescaline-class compounds under identical conditions:[1]model confidence 95%
Verified

Abstract confirms HTR experiments on multiple mescaline-class compounds (mescaline, escaline, proscaline, TMA, 3C-E, 3C-P, TMA-2, MEM, MPM) under identical conditions.

HTR experiments conducted with mescaline, escaline, proscaline, TMA, 3C-E, 3C-P, TMA-2, MEM, MPM.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusiveA critical finding from the Halberstadt et al. 2019 study is that the structure-activity relationships of the 3,4,5-substituted series (mescaline/TMA/3C-x) are fundamentally distinct from those of the 2,4,5-substituted series (TMA-2/DOx/2C-x)[1]model confidence 68%
Inconclusive

Abstract confirms both series were tested under identical HTR conditions, but does not explicitly state divergent SAR between them as a named finding. The SAR comparison conclusion is likely articulated in the paper body rather than the abstract.

HTR experiments conducted with mescaline, escaline, proscaline, TMA, 3C-E, 3C-P, TMA-2, MEM, MPM.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedThis divergence indicates that the two regiochemistries engage the 5-HT₂A receptor through different binding geometries, consistent with earlier homology modeling work showing that the 3,4,5 pattern requires conformational flexibility for efficacious receptor engagement.[13]model confidence 88%
Verified

Abstract directly establishes that 3,4,5-trioxygenated mescaline analogues require conformational mobility in the 3- and 5-methoxy groups for receptor activation, supporting the binding geometry divergence claim.

3 and 5 methoxy groups must remain conformationally mobile to enable receptor activation.

checked by claude-sonnet-4-6 · May 11, 2026

safety14 claims7verified7inconclusive
inconclusiveMescaline clinical studies confirm blood pressure elevation and tachycardia as moderate autonomic effects of the mescaline pharmacological class.[10]model confidence 65%
Inconclusive

Abstract does not specifically mention blood pressure elevation or tachycardia; it notes 'slightly more subacute AEs at 12-24h' and compares to other psychedelics, but cardiovascular parameters are not listed in the abstract.

Slightly more subacute AEs at 12-24h.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusiveMescaline clinical studies confirm blood pressure elevation and tachycardia as moderate autonomic effects of the mescaline pharmacological class.[17]model confidence 60%
Inconclusive

Abstract not available for this citation; cannot verify the specific claim.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedAt least five fatalities have been reported for the 2C series[18]model confidence 99%
Verified

Abstract directly states 'At least 5 deaths' in the 2C-series toxicology review.

At least 5 deaths.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedThe mescaline systematic review documents hypertension, headache, nausea, and vomiting as the most common adverse effects, with no deaths specifically attributed to pure mescaline.[16]model confidence 92%
Verified

Abstract lists exactly the same AEs: hypertension, headache, nausea, vomiting. The absence of attributed deaths is consistent with the review finding limited quality evidence and no fatal outcomes mentioned.

Common AEs: hypertension, headache, nausea, vomiting. Limited quality evidence.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusiveThis rapid tolerance constitutes a biological mechanism that limits addictive potential.[3]model confidence 68%
Inconclusive

Abstract confirms hallucinogens do not produce dependence, supporting the broad conclusion that addiction potential is limited. However, the specific claim about rapid tolerance as the mechanistic basis is not addressed in the abstract.

Hallucinogens physiologically safe, do not produce dependence.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusiveThis rapid tolerance constitutes a biological mechanism that limits addictive potential.[9]model confidence 65%
Inconclusive

Abstract documents cross-tolerance among serotonergic hallucinogens and 5-HT2A as primary site, but doesn't explicitly connect tolerance to the mechanism limiting addictive potential.

Cross-tolerance among serotonergic hallucinogens documented.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedCross-tolerance extends to all serotonergic hallucinogens, including lsd, psilocybin, and mescaline, via the shared 5-HT₂A receptor downregulation mechanism.[9]model confidence 90%
Verified

Abstract directly states 'Cross-tolerance among serotonergic hallucinogens documented' and identifies 5-HT2A as the primary site of action, supporting the shared receptor mechanism inference.

5-HT2A receptor is primary site of hallucinogen action. Cross-tolerance among serotonergic hallucinogens documented.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedCross-tolerance extends to all serotonergic hallucinogens, including lsd, psilocybin, and mescaline, via the shared 5-HT₂A receptor downregulation mechanism.[7]model confidence 90%
Verified

Abstract directly states 'Cross-tolerance between phenylalkylamines and indoleamines' and confirms 5-HT2A mediates characteristic effects, supporting the shared receptor cross-tolerance mechanism.

Cross-tolerance between phenylalkylamines and indoleamines. 5-HT2A mediates characteristic effects.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedSerotonergic hallucinogens as a class are not considered habit-forming and do not produce physical dependence[3]model confidence 98%
Verified

Abstract directly states 'Hallucinogens physiologically safe, do not produce dependence.'

Hallucinogens physiologically safe, do not produce dependence.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedTramadol and its active metabolites inhibit the serotonin transporter (SERT) in human cells[20]model confidence 98%
Verified

Abstract directly states 'Tramadol inhibits human SERT in HEK293 cells.'

Tramadol inhibits human SERT in HEK293 cells.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusiveTramadol and its active metabolites inhibit the serotonin transporter (SERT) in human cells[21]model confidence 60%
Inconclusive

Abstract not available for this citation; cannot verify the specific SERT inhibition claim.

checked by claude-sonnet-4-6 · May 11, 2026

verifiedSevere cases can be fatal.[18]model confidence 99%
Verified

Abstract directly states 'At least 5 deaths' in the 2C-series clinical toxicology review, confirming that severe cases can be fatal.

At least 5 deaths. Treatment primarily supportive.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusiveMAOIs increase synaptic serotonin by blocking its enzymatic degradation; combined with direct 5-HT₂A agonism, severe serotonin syndrome is the expected outcome[3]model confidence 60%
Inconclusive

Abstract confirms 5-HT2A agonism as the hallucinogen mechanism but does not address MAOI pharmacology, enzymatic serotonin degradation, or serotonin syndrome. The MAOI interaction claim is outside the scope of this abstract.

Stimulate 5-HT2A receptors on neocortical pyramidal cells.

checked by claude-sonnet-4-6 · May 11, 2026

inconclusiveSeizure disorders: Phenethylamine psychedelics have been associated with seizure threshold reduction at the class level[18]model confidence 62%
Inconclusive

Abstract covers 2C-series clinical toxicology including toxidromes and deaths, but does not specifically mention seizures or seizure threshold reduction in the abstract text.

Excited delirium, serotonergic toxicity, or sympathomimetic toxidrome.

checked by claude-sonnet-4-6 · May 11, 2026

05

Coverage & Gaps

effect links
183 links · 181 approved · 51 audited0/183 with evidence basis
interactions
2 approved pairs0/2 graded
06

Research Trail

substance-article pipeline-v5 May 11, 2026

StepSourceQueryResults
1database lookupPubChem3C-P1 result, 1 selected
selection rationale

Primary chemical identity confirmed via PubChem

2literature searchPubMed3C-P 3,5-dimethoxy-4-propoxyphenethylamine psychedelic1 result, 1 selected
selection rationale

Only paper directly testing 3C-P in a pharmacological assay

3literature searchPubMedmescaline analogs phenethylamine serotonin 5-HT2A binding affinity hallucinogen3 results, 3 selected
selection rationale

Contextual pharmacology for 5-HT2A agonism in mescaline-class compounds

4literature searchOpenAlex3C-P mescaline analog phenethylamine psychedelic amphetamine10 results, 3 selected
selection rationale

Selected papers with direct relevance to 3C-P pharmacology and chemical characterization

5web searchWebSearch3C-P 3,5-dimethoxy-4-propoxyphenylisopropylamine Shulgin PiHKAL history10 results, 2 selected
selection rationale

Historical context for discovery timeline

6web searchWebSearch3C-P phenethylamine legal status scheduling United States United Kingdom10 results, 1 selected
selection rationale

Legal status data for major jurisdictions

7document retrievalErowid—— results, 1 selected
selection rationale

Primary historical source for discovery of proscaline; 3C-P mentioned in PiHKAL as related compound

8document retrievalisomerdesign countyourculture blog—— results, 1 selected
selection rationale

Historical context for discovery of proscaline family including 3C-P's phenethylamine progenitor

9document retrievalErowid—— results, 1 selected
selection rationale

Primary source for Shulgin's predictions about 3C-P and the related proscaline bioassay

10document retrievalErowid—— results, 3 selected
selection rationale

Community-level harm reduction data for a compound with no published human pharmacology studies

11document retrievalPubMed Central—— results, 2 selected
selection rationale

Only quantitative rodent pharmacology data specifically for 3C-P

12database lookupNCATS Inxight Drugs—— results, 3 selected
selection rationale

Official chemical identifiers including missing CAS number and SMILES string

13literature searchPubMedhallucinogen cross tolerance psychedelic LSD psilocybin mescaline serotonin 5-HT2A receptor2 results, 2 selected
selection rationale

Key papers establishing cross-tolerance mechanism relevant to 3C-P tolerance profile

14literature searchPubMedtramadol serotonin syndrome mechanism opioid 5-HT reuptake inhibition4 results, 1 selected
selection rationale

Mechanism for dangerous 3C-P + tramadol interaction

15web searchErowidsite:erowid.org 3C-P experience report10 results, 3 selected
selection rationale

Primary user-report data for 3C-P subjective effects; no controlled human studies exist

16web searchWebSearch3C-P legal status Australia Canada Germany scheduling10 results, 1 selected
selection rationale

Legal status for major jurisdictions required for article

17database lookupPubMed (direct article fetch)PMID 147617031 result, 1 selected
selection rationale

Foundational hallucinogens pharmacology review

18cross referenceMultiple sources3C-P SMILES molecular formula stereochemistry— results, 1 selected
selection rationale

Cross-verification of chemical identity data

19web searchWebSearchLiechti mescaline clinical study Neuropsychopharmacology 2021 randomized placebo controlled10 results, 3 selected
selection rationale

High-quality RCTs on mescaline parent compound; definitive pharmacokinetic and pharmacodynamic data applicable to 3C-P class

20web searchWebSearchTrachsel 2002 phenethylamine synthesis proscaline 3C-P characterization publication10 results, 1 selected
selection rationale

Historical synthesis reference for 3C-P

21data extractionNCATS + PubChem + cross-reference3C-P chemical identifiers SMILES CAS stereochemistry— results, 1 selected
selection rationale

Full chemical identity package for handoff file

Research document (raw, unedited pipeline output)
# Research Output: 3C-P

## Chemical Identity

**Verified chemical data (cross-confirmed via PubChem CID 54929142 and NCATS Inxight Drugs):**

| Field | Value |
|-------|-------|
| Preferred name | 3C-P; 3C-Proscaline; α-methylproscaline |
| Systematic name | 1-(3,5-dimethoxy-4-propoxyphenyl)propan-2-amine |
| CAS number | 501700-11-4 |
| PubChem CID | 54929142 |
| Molecular formula | C₁₄H₂₃NO₃ |
| Molecular weight | 253.34 g/mol |
| SMILES | CCCOC1=C(OC)C=C(CC(C)N)C=C1OC |
| InChIKey | KKMCHCCXGKYEKJ-UHFFFAOYSA-N |
| Stereochemistry | Racemic (1 undefined stereocenter at α-carbon; R and S enantiomers exist) |

**Discrepancies with seed data:** The brief's seed data listed no SMILES, no molecular formula, no molecular weight, and no PubChem CID. All four have now been verified and should be added to the database. The seed systematic name (1-(3,5-dimethoxy-4-propoxyphenyl)propan-2-amine) is confirmed correct.

**Structural notes:** 3C-P is the α-methyl homolog of proscaline (3,5-dimethoxy-4-propoxyphenethylamine). The 3,5-dimethoxy-4-propoxy substitution pattern on the phenyl ring distinguishes it from the 2,5-dimethoxy regiochemistry of the 2C and DO drug series. This different substitution pattern confers distinct SAR behavior (Halberstadt et al. 2019 [Ref 1]).

---

## Pharmacology

### Mechanism of Action

3C-P is a serotonin 5-HT2A/5-HT2C receptor agonist, consistent with its classification as a phenylalkylamine hallucinogen. Phenylalkylamine hallucinogens are selective 5-HT2 receptor agonists, unlike indoleamine hallucinogens which are pharmacologically less selective (Halberstadt & Geyer 2011 [Ref 16]). The 5-HT2A receptor is the primary site of hallucinogenic action, mediating characteristic effects through agonism at neocortical pyramidal cell receptors, which increases cortical glutamate via thalamic afferent release (Nichols 2004 [Ref 14]).

Confirmation that the mescaline parent-class mechanism is 5-HT2A-mediated comes from a controlled human study (Klaiber et al. 2024 [Ref 25]) in which co-administration of the 5-HT2A antagonist ketanserin significantly attenuated mescaline's acute effects. 3C-P can be expected to act via the same mechanism, though no direct confirmation study has been performed.

**FLAG for generation agent:** No Ki or EC50 data at 5-HT2A or other receptors specific to 3C-P is available in the published literature. Pharmacological class assignment rests on structural class membership and rodent HTR data; no human receptor binding study has been performed.

### Rodent Behavioral Pharmacology (Head Twitch Response)

The only published quantitative pharmacological study specific to 3C-P is Halberstadt et al. 2019 [Ref 1], which used the head twitch response (HTR) in C57BL/6J mice as a measure of 5-HT2A-mediated behavior. Key findings:

- 3C-P **ED50 = 2.45 mg/kg** (95% CI: 1.72–3.51 mg/kg)
- **Molar ED50 = 8.47 μmol/kg** (95% CI: 5.92–12.1 μmol/kg)
- 3C-P and 3C-E (the ethoxy analog) were essentially **equipotent** in the HTR assay
- Both 3C-E and 3C-P showed approximately **50% higher molar potency than TMA** (3,4,5-trimethoxyamphetamine, the α-methyl homolog of mescaline)
- The study authors noted: "3C-P would be active in humans in the same dosage range as 3C-E" based on the paralleled potency relationships
- The inverted-U dose-response pattern (tested at 1.5, 3, 6, 12 mg/kg) is typical of serotonergic hallucinogens

The HTR assay has established predictive validity for human hallucinogenic potency; potency relationships in the HTR closely parallel human hallucinogenic data (Halberstadt et al. 2019 [Ref 1]; Halberstadt 2015 [Ref 15]).

**Structure-activity relationship context:** For both mescaline and TMA, replacing the 4-methoxy substituent with ethoxy or propoxy groups increases HTR potency. This contrasts with the 2,4,5-regiochemistry (TMA-2/MPM series), where such 4-alkyl homologation does not alter potency — indicating fundamentally distinct SAR between the 3,4,5 and 2,4,5 regiochemistries (Halberstadt et al. 2019 [Ref 1]).

### Pharmacokinetic Data

**3C-P-specific pharmacokinetic data: None published.** No human PK studies have been conducted.

**Analog inference from mescaline (structural parent compound):**
- Mescaline plasma elimination half-life: approximately **3.5 hours** (Ley et al. 2023 [Ref 24]; Klaiber et al. 2024 [Ref 25])
- Mescaline Tmax: approximately **2 hours** oral (Klaiber et al. 2024 [Ref 25])
- Mescaline effect duration: **mean 11.1 hours** at 500 mg equivalent doses (Ley et al. 2023 [Ref 24])
- Mescaline effect duration range across doses: 6.4–14 hours (Klaiber et al. 2024 [Ref 25])

The alpha-methyl group in 3C-P (vs. the phenethylamine proscaline) typically prolongs metabolic stability relative to the parent phenethylamine, as it blocks primary amine oxidation by MAO. This is expected to contribute to 3C-P's notably long subjective duration of 10–16 hours observed in user reports.

**FLAG:** Metabolism, CYP enzyme involvement, and metabolic pathway data for 3C-P are unknown. No biotransformation studies have been published. By structural class inference, phenethylamine amphetamines are typically metabolized via N-dealkylation, ring hydroxylation, and O-dealkylation (loss of methoxy groups). MAO-B likely plays a reduced role relative to non-alpha-methylated phenethylamines due to the alpha-methyl substituent.

---

## History

### Discovery and First Description

The compound proscaline (3,5-dimethoxy-4-propoxyphenethylamine — the non-alpha-methylated phenethylamine analog of 3C-P) was first described by **Otakar Leminger**, a retired Czechoslovakian industrial chemist living near Ústí nad Labem on the Elbe, in a 1972 paper published in the Czech journal *Chemicky Prumysl* (volume 22) [Ref 7]. Leminger self-experimented with several alkoxylated phenethylamines and noted differential potency, observing that proscaline, escaline, and allylescaline were "much more active" than two-substituted analogs.

**3C-P itself** (the alpha-methylated amphetamine version) was not described in Leminger's work. It was first mentioned in the published scientific literature by **Alexander Shulgin** in his 1991 book *PiHKAL: A Chemical Love Story* [Ref 6], within the entry for proscaline (compound #140 [Ref 9]). Shulgin described 3C-P as the "unexplored amphetamine homologue" of proscaline and:
- Proposed a synthesis route: propylation of syringaldehyde, followed by nitroethane coupling, and lithium aluminum hydride reduction
- Predicted that 3C-P would be "active, and a psychedelic, in the 20 to 40 milligram range"
- Did not report any human bioassay

**Daniel Trachsel** formally synthesized 3C-P around 2002 and published the synthesis in *Helvetica Chimica Acta* in 2003 [Ref 27] in a paper on mescaline derivative SAR, but also did not report human pharmacology. Stanislov Wistupkin is credited with bringing Leminger's original 1972 work to Shulgin's attention, preserving knowledge that might otherwise have been lost.

**First commercial availability:** 3C-P became available through research chemical markets approximately in **late 2003**, representing its first likely human exposure outside of any possible self-experimentation by Shulgin or Trachsel. As of the Erowid vault's last update (ca. 2003–2015), approximately 10–12 anonymous experience reports had been submitted [Ref 8].

### Regulatory History

No formal scheduling or controlled substance history specifically targeting 3C-P was identified in major jurisdictions prior to Japan's action in 2018 (see Legal Status section).

---

## Subjective Effects

### Published Descriptions

No controlled human studies of 3C-P's subjective effects have been published. The following is derived from user reports in the Erowid Experience Vault [Refs 18–20, 29] and community sources, consistent with the Erowid information brief [Ref 8].

**General character:** 3C-P is consistently described as producing effects that are more **stimulating than psychedelic** relative to mescaline and other phenethylamines, particularly compared to 3C-E. The psychedelic component is present but mild relative to the amphetamine-like stimulant profile.

**Effects documented in user reports (oral route, ~40 mg doses):**

*Onset and come-up (1–3 hours):*
- Stimulation, increased energy
- Mild nausea and gastrointestinal discomfort (common, rarely severe)
- Head tension reported

*Peak (3–8 hours):*
- Euphoria in waves (mental and bodily)
- Strong stimulation
- Enhanced sociability and communication
- Mild to moderate visual effects: color shifting, tracers, drifting textures, gentle fractals (described as subtle compared to mescaline)
- Music enhancement and mild synaesthesia
- Empathy and emotional openness
- Cognitive enhancement: ability to synthesize information, articulate speech
- Pupil dilation (delayed onset in some reports, appearing ~T+7-8h)
- Muscle tension, mild jaw tension/bruxism
- Vasoconstriction (hands)
- Increased heart rate

*Higher doses (40–43 mg) or strenuous activity:*
- Paranoia possible
- Chest pressure, "alarming" heart rate increases
- Body tremors and shaky hands
- Sensory overload reported with physical exertion

*Comedown and aftereffects (8–17 hours):*
- Extended stimulation preventing sleep
- Physical fatigue
- One report documented visual distortions persisting into subsequent days (at 40 mg)

**Comparison to 3C-E:** User reports and Shulgin's commentary suggest 3C-P is "more confusing than 3C-E, especially at higher dosages." 3C-E is described in PiHKAL as producing stronger visuals but "a little too heavy on the body." 3C-P appears to offer more functional stimulation with lighter psychedelic effects.

**Comparison to mescaline:** Mescaline at equivalent psychoactive doses produces comparable altered states of consciousness to LSD and psilocybin (Ley et al. 2023 [Ref 24]); mescaline is associated with nausea, headache, and hypertension as common AEs (Shaw et al. 2026 [Ref 23]). 3C-P's more stimulant-dominant profile suggests partial differentiation from mescaline despite structural similarity.

---

## Safety & Toxicity

**FLAG (safety-critical):** All safety data for 3C-P are based on user reports, analog inference from the phenethylamine class, or the parent compound mescaline. No published LD50, therapeutic index, or controlled toxicology data exists for 3C-P.

### Dose Safety

- Seed data states: "toxic dose is unknown" — confirmed; no published data
- Maximum documented oral dose: approximately **50 mg** without a fatal outcome (Erowid vault [Ref 8])
- Seeds data has no dose ranges; community thresholds are threshold 5–10 mg, common 20–40 mg, strong 40+ mg

### Cardiovascular Risks

User reports at 40–43 mg document:
- Tachycardia (subjectively "alarming" heart rate)
- Chest pressure
- Vasoconstriction in extremities

Mescaline clinical studies document blood pressure elevation and tachycardia as moderate autonomic effects (Ley et al. 2023 [Ref 24]). These findings are expected to apply to 3C-P given the shared pharmacological mechanism.

### Duration-Related Risks

The extended duration (10–17 hours) creates prolonged physiological stress and delays recovery sleep. User reports document difficulty sleeping for >13 hours post-dose, with stimulation persisting throughout.

### Class-Level Adverse Effects

The phenethylamine psychedelic class (2C-series, which shares mechanism with 3C-P):
- Common: hallucinations, agitation, hypertension, tachycardia
- Serious: seizures, hyperthermia, excited delirium
- Fatalities: at least 5 reported for the 2C-series (Dean et al. 2013 [Ref 13])
- Presentations: sympathomimetic toxidrome or serotonin toxicity picture

Mescaline systematic review (Shaw et al. 2026 [Ref 23]) documents:
- Hypertension, headache, nausea, vomiting as most common adverse effects
- Very limited quality evidence; no deaths specifically attributed to pure mescaline

### Psychological Risks

- Paranoia documented at high doses in physical exertion context [Ref 20]
- Anxiety at higher doses; cognitive confusion described
- Risk of challenging experiences amplified by long duration
- No published case reports of psychosis or HPPD specific to 3C-P

---

## Harm Reduction

**FLAG (no published harm reduction guidelines specific to 3C-P):** The following is based on class-level evidence and community best practices.

- **Start low:** Given the long duration, starting at or below 20 mg is advisable. Effects may not appear for up to 2 hours.
- **Set and setting:** The 10–16 hour duration requires a full day cleared of obligations.
- **Avoid strenuous physical activity:** One user report documents alarming cardiovascular stress during mountain biking at 43 mg [Ref 20].
- **Avoid combination drugs:** Tramadol is explicitly dangerous (serotonin syndrome risk). MAOIs are contraindicated by class. SSRIs/SNRIs should be avoided.
- **Testing:** The compound can be identified via NMR spectroscopy (Chapman & Avanes 2015 [Ref 22] demonstrated NMR characterization of the 3,5-dimethoxy mescaline analog series). Colorimetric reagents (Marquis, Mecke, Simon's) provide some discrimination.
- **No published emergency protocol specific to 3C-P.** In cases of toxicity, supportive care consistent with phenethylamine psychedelic overdose management applies (Dean et al. 2013 [Ref 13]): temperature management, benzodiazepines for agitation, cardiovascular monitoring. Cyproheptadine (5-HT2A antagonist) may be considered for serotonin syndrome features.

---

## Tolerance & Dependence

### Tolerance Development

Serotonergic hallucinogens develop **rapid tolerance (tachyphylaxis)** after repeated use, mediated by 5-HT2A receptor downregulation. This rapid tolerance development is shared across serotonergic hallucinogens and constitutes a biological mechanism that limits addictive potential (Nichols 2004 [Ref 14]; Halberstadt 2015 [Ref 15]).

3C-P is expected to follow the class pattern: tolerance develops almost immediately after ingestion, with a half-life of approximately 3 days and full reset at approximately 7 days (consistent with seed data, and with the known pharmacology of serotonergic hallucinogens).

### Cross-Tolerance

**Cross-tolerance with other serotonergic hallucinogens is expected.** Phenylalkylamine hallucinogens (including mescaline and TMA analogs) share cross-tolerance with LSD, psilocybin, and DMT via shared 5-HT2A receptor downregulation (Halberstadt 2015 [Ref 15]; Halberstadt & Geyer 2011 [Ref 16]).

**FLAG (no 3C-P-specific cross-tolerance data exists):** This is class inference only.

### Dependence Liability

Serotonergic hallucinogens as a class are not considered habit-forming and do not produce physical dependence (Nichols 2004 [Ref 14]). The rapid tachyphylaxis discourages compulsive redosing. No dependence cases for 3C-P or closely related 3C-series compounds have been reported.

---

## Interactions

### Tramadol: DANGEROUS

Tramadol is listed as a dangerous interaction in the seed data. The mechanistic basis is well-established:

Tramadol (and its active metabolites) inhibit the serotonin transporter (SERT) in human HEK293 cells (Baldo 2018 [Ref 11]; Pergolizzi et al. 2022 [Ref 17]). Combining a SERT inhibitor with a potent 5-HT2A agonist creates conditions for serotonin syndrome: elevated synaptic serotonin concentrations combined with direct 5-HT2A receptor stimulation.

Serotonin syndrome features: agitation, hyperthermia, tachycardia, clonus, muscle rigidity. Severe cases can be fatal (Dean et al. 2013 [Ref 13]).

**FLAG (safety-critical):** The dangerous tramadol interaction has not been specifically studied for 3C-P. It is inferred from tramadol's documented SERT inhibition and the phenethylamine class's 5-HT2A agonism. However, this mechanism applies broadly to all serotonergic phenethylamine psychedelics and should be treated as confirmed.

### Cannabis: UNKNOWN

No data available. Cannabis can both modulate and amplify psychedelic effects, but the direction of effect is highly variable. Interaction severity for 3C-P specifically is unresolved.

### MAO Inhibitors: DANGEROUS (class inference)

MAOIs increase serotonin availability by blocking its breakdown. Combined with a serotonergic 5-HT2A agonist, severe serotonin syndrome is expected. This is a standard contraindication for all serotonergic hallucinogens (Nichols 2004 [Ref 14]).

**FLAG:** Not specifically studied for 3C-P. Class inference only.

### Other Serotonergic Drugs (SSRIs, SNRIs, lithium): CAUTION

SSRIs and SNRIs inhibit SERT and can produce additive serotonergic effects; they may also attenuate hallucinogenic effects through 5-HT2A desensitization. Lithium combined with serotonergic psychedelics has been associated with seizures in case reports (class level). No specific data for 3C-P.

### Stimulants (amphetamines, cocaine): CAUTION

Given 3C-P's intrinsic stimulant properties, combination with other stimulants increases cardiovascular risk (hypertension, tachycardia, hyperthermia). Not specifically studied.

---

## Legal Status

| Jurisdiction | Status | Notes |
|---|---|---|
| United States | Not explicitly scheduled | May be treated as Schedule I analog under Federal Analogue Act (analogue of mescaline/TMA, which are Schedule I). Sell/purchase/possess "for human consumption" carries legal risk. |
| United Kingdom | Covered under Psychoactive Substances Act 2016 | Broad blanket prohibition on psychoactive substances; production, supply, and possession with intent to supply prohibited |
| Germany | Controlled under NpSG | Neue-psychoaktive-Stoffe-Gesetz (New Psychoactive Substances Act); restricted to industrial/scientific use |
| Japan | Controlled as designated substance | Scheduled as of February 28, 2018 |
| Canada | Controlled under Schedule I | Covered by amphetamine blanket ban language in the Controlled Drugs and Substances Act |
| Australia | Status unconfirmed | FLAG: Not verified; likely falls under analog scheduling provisions but not confirmed from primary legal sources |

**FLAG:** Legal status data relies primarily on web-retrieved sources and Wikipedia [Ref 28]. For the US specifically, the analog status analysis is inferential. A primary legal database search (e.g., DEA scheduling documents) was not completed.

---

## Clinical Trials

No clinical trials involving 3C-P were found on ClinicalTrials.gov. No interventional research is registered, ongoing, or completed for this compound.

---

## Community Feedback Analysis

No community feedback was submitted in Part A2 of the brief. No feedback items to analyze.

---

## Gaps & Flags

### Safety-Critical Values Not Confirmed by Published Sources

1. **FLAGGED:** Dose ranges in seed data (none present) are entirely unverified against published sources. The community-derived dose range (threshold 5–10 mg, common 20–40 mg, strong 40+ mg) comes from the Erowid vault [Ref 8] and approximately 10 user reports — not controlled studies.

2. **FLAGGED:** Toxic dose is genuinely unknown. The maximum documented human dose is approximately 50 mg (Erowid vault [Ref 8]); no fatalities specifically attributed to 3C-P were identified. Safety at doses above 50 mg is untested in any documented setting.

3. **FLAGGED:** The tramadol "dangerous" interaction is classified as dangerous in seed data. This classification is supported by the mechanistic literature but has not been tested or confirmed for 3C-P specifically. The rating is appropriate and consistent with class pharmacology.

### Data Absent from Literature

4. No published Ki or EC50 values for 3C-P at any receptor.
5. No published human pharmacokinetic data (Tmax, Cmax, t½, bioavailability).
6. No stereospecific activity data (which enantiomer is more potent is unknown; for alpha-methylphenethylamines generally the R-enantiomer is more potent at 5-HT2A).
7. No metabolic pathway or CYP enzyme data for 3C-P.
8. No LD50 data in any species.
9. No case reports of adverse events or overdose attributable to 3C-P specifically.

### Contradictions Between Seed Data and Published Sources

10. The seed data **SMILES field is blank** — SMILES (CCCOC1=C(OC)C=C(CC(C)N)C=C1OC) is now confirmed via NCATS/PubChem and should be added.
11. The seed data **PubChem CID field is blank** — CID 54929142 is confirmed.
12. The seed data **molecular formula and weight are blank** — C₁₄H₂₃NO₃ and 253.34 are confirmed.
13. Seed data duration (onset 1-2h, peak 4-8h, offset 3-6h, aftereffects 3-6h, total 10-16h) is **consistent with community reports** but not confirmed by controlled studies. No contradiction identified.

### Areas Relying on Structural Analogy or Class Inference

14. Pharmacokinetics (Tmax, t½, oral bioavailability) — inferred from mescaline clinical data.
15. CYP metabolism — inferred from amphetamine-class general pharmacology.
16. MAOI interaction — inferred from class.
17. Cross-tolerance with serotonergic hallucinogens — inferred from class; not tested for 3C-P.
18. Dependence non-liability — inferred from class.
19. Stereochemical activity — inferred from SAR patterns in related alpha-methylphenethylamines.

### Legal Status Flags

20. Australian legal status not confirmed from primary sources.
21. US analog status analysis is inferential and has not been confirmed by DEA ruling or case law.