generation run 2026-04-25
63 min completedmodel pipeline-v5plan not recordedrun/4467b3b6…Selection
Verification
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- seen / partial
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The model's own caveats
8 further caveats recorded as free text — readable on the working page
Reproduce
- inputs
- 26 source keys (listed under Sources)
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- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
- streams
- none — agent transcripts are persisted from 2026-09 onward
17 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubChem | 3-methoxyphencyclidine | 1 | 1 | Chemical identity confirmation for 3-MeO-PCP |
| 2 | PubMed · absence | 3-MeO-PCP 3-methoxyphencyclidine pharmacology receptor binding | 0 | — | — |
| 3 | OpenAlex | 3-MeO-PCP 3-methoxyphencyclidine pharmacology dissociative | 10 | 5 | Roth 2013 is landmark binding affinity paper; Michely 2016 is key metabolic pathway paper; others provide toxicology and clinical context |
| 4 | PubMed | 3-methoxyphencyclidine toxicity case report adverse effects | 5 | 4 | All directly relevant to 3-MeO-PCP toxicology and case reports |
| 5 | PubMed · absence | 3-methoxyphencyclidine manic episode dissociative hallucinogen NPS | 0 | — | — |
| 6 | PubMed | 3-MeO-PCP fatal death postmortem blood concentration forensic | 4 | 3 | — |
| 7 | WHO ECDD Repository | 3-MeO-PCP ECDD critical review | 1 | — | — |
| 8 | PubMed | methoxyphencyclidine metabolite urine detection forensic toxicology | 4 | 4 | — |
| 9 | WebSearch + Erowid | 3-MeO-PCP legal status scheduling United States United Kingdom controlled substance | 10 | 2 | — |
| 10 | OpenAlex | 3-methoxyphencyclidine psychosis psychiatric symptoms clinical review 2024 | 6 | 2 | — |
| 11 | PubMed | Maddox 1965 synthesis phencyclidine | 1 | — | — |
| 12 | WebSearch | 3-MeO-PCP mu opioid receptor binding affinity pharmacology | 10 | 2 | — |
| 13 | WebSearch | 3-MeO-PCP synthesis history Geneste 1979 research chemical market | 10 | 2 | — |
| 14 | WebSearch | 3-MeO-PCP physical properties melting point CAS 91164-58-8 | 10 | — | — |
| 15 | PubMed | 3-methoxyphencyclidine OR 3-MeO-PCP (broad search) | 20 | 7 | — |
| 16 | WebSearch | 3-MeO-PCP Australia scheduled substance Poisons Standard | 10 | — | — |
| 17 | PubMed / PubChem / OpenAlex / WebSearch compiled | Compilation of all pharmacological, chemical, toxicological, legal, and historical data for 3-MeO-PCP | 31 | 1 | — |
95 claims by section — every cited sentence, checked against its source
safety35 · 32 ok
Multiple fatal cases involved amphetamine co-ingestionsupported
Also diphenhydramine (4.1 mg/L), amphetamine (<0.10 mg/L). Death: combined toxicity. bkw056
3-MeO-PCP is metabolized by CYP2D6, CYP2C19, CYP2B6, and CYP3A4supported
CYP3A4, CYP2D6, CYP2C19 as primary metabolic enzymes. s00204-025-04283-x
Paroxetine and bupropion were co-present in one fatal polysubstance case, though causality cannot be established from a single observation.supported
second for ethanol, bupropion, delorazepam, paroxetine, mitragynine. bkx048
Published postmortem blood concentrations in fatal intoxications span a wide range: approximately 50–3,525 ng/mL (0.05–3.5 mg/L)supported
Fatal 3-MeO-PCP case. Femoral blood: 3525 ng/mL. 20961790.2021.1928821
Copeland et al. reviewed 16 published fatalities as of 2022 and concluded that blood concentrations associated with toxicity and death "remain unclear"supported
First UK fatal case. 15 prior fatal intoxication reports. bkac015
Claim in safety — inconclusiveinconclusiveworking →
In silico estimates from Noga and Jurowski predict rat oral LD₅₀ of approximately 200–630 mg/kg (EPA Category III, moderate acute toxicity) and mouse IV LD₅₀ of approximately 25–59 mg/kgsupported
Rat oral LD50 estimates: ~200-630 mg/kg; mouse IV LD50 ~25-59 mg/kg. Moderate acute oral toxicity (EPA Category III). s00204-025-04242-6
In silico hERG channel inhibition is predicted with IC₅₀ of approximately 4.9–12.3 µM, indicating QT-prolongation risksupported
hERG IC50 ~4.9-12.3 µM (QT-prolongation risk). s00204-025-04242-6
Copeland et al. specifically cautioned against use in exercise or "club drug" settings where elevated heart rate, body temperature, and blood pressure may exacerbate cardiovascular toxicity.supported
Exercise may exacerbate toxicity via elevated HR, body temperature, blood pressure. bkac015
In silico modeling predicts primary organ targets as lung (probability 0.89–0.93), liver (up to 0.91), and blood (up to 0.85), with gastrointestinal involvement also predicted (up to 0.82)partially supported
Organ targets: lungs (0.89-0.93), liver (up to 0.91), blood (up to 0.85). s00204-025-04242-6
Consistent features across published intoxication case reports include coma (Glasgow Coma Scale 3 in severe cases), agitation and delirium during recovery, respiratory acidosis and respiratory depression, hypothermia, mydriasis (including unilateral anisocoria), visual hallucinations and psychosis, and behavioral disinhibition.supported
Glasgow score 3, respiratory acidosis, mydriasis, hypothermia. j.forsciint.2016.12.028
Consistent features across published intoxication case reports include coma (Glasgow Coma Scale 3 in severe cases), agitation and delirium during recovery, respiratory acidosis and respiratory depression, hypothermia, mydriasis (including unilateral anisocoria), visual hallucinations and psychosis, and behavioral disinhibition.supported
Two cases of 3-MeO-PCP intoxication in same patient with literature review. Severe intoxication manifestations characterized. md.0000000000018295
Consistent features across published intoxication case reports include coma (Glasgow Coma Scale 3 in severe cases), agitation and delirium during recovery, respiratory acidosis and respiratory depression, hypothermia, mydriasis (including unilateral anisocoria), visual hallucinations and psychosis, and behavioral disinhibition.supported
Glasgow score 3, respiratory acidosis, mydriasis, hypothermia. j.forsciint.2016.12.028
Consistent features across published intoxication case reports include coma (Glasgow Coma Scale 3 in severe cases), agitation and delirium during recovery, respiratory acidosis and respiratory depression, hypothermia, mydriasis (including unilateral anisocoria), visual hallucinations and psychosis, and behavioral disinhibition.supported
Glasgow score 3, respiratory acidosis, mydriasis, hypothermia. j.forsciint.2016.12.028
Consistent features across published intoxication case reports include coma (Glasgow Coma Scale 3 in severe cases), agitation and delirium during recovery, respiratory acidosis and respiratory depression, hypothermia, mydriasis (including unilateral anisocoria), visual hallucinations and psychosis, and behavioral disinhibition.supported
Clinical and laboratory data of two non-fatal 3-MeO-PCP intoxication cases. bkx009
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
LC-MS/MS is required for analytical confirmation — standard immunoassays are unreliable.supported
3-MeO-PCP showed 1-143% cross-reactivity in all PCP IAs tested. bkz026
Multiple fatal cases involved amphetamine co-ingestionsupported
Polysubstance: 3-MeO-PCP + amphetamine + alcohol. j.jflm.2019.05.011
Substance-induced psychotic disorder (SIP) with persistent symptoms after cessation has been documented: Pepe et al. described a 29-year-old male who developed psychosis with cognitive impairment after small oral doses over two weeks followed by high-dose ingestionsupported
case of 29-year-old man with substance-induced psychotic disorder after small oral doses over 2 weeks then high-dose ingestion. ph17040452
Psychotic symptoms including paranoia, delusions, and hallucinations are documented across multiple case reports.supported
Severe intoxication manifestations characterized. md.0000000000018295
Psychotic symptoms including paranoia, delusions, and hallucinations are documented across multiple case reports.supported
substance-induced psychotic disorder after small oral doses over 2 weeks then high-dose ingestion. ph17040452
Mania-like presentations — characterized by grandiosity, agitation, pressured behavior, and disinhibition — occur at moderate-to-high dosessupported
Severe intoxication manifestations characterized. md.0000000000018295
Mania-like presentations — characterized by grandiosity, agitation, pressured behavior, and disinhibition — occur at moderate-to-high dosessupported
Literature review of 3-MeO-PCP mechanisms and effects. ph17040452
Amnesia is reported, which complicates self-assessment of dose and behavioral risk during the experience.supported
Severe intoxication manifestations characterized. md.0000000000018295
Alcohol co-ingestion features in multiple fatal and non-fatal intoxication casessupported
Two young men brought to hospital comatose after 3-MeO-PCP + alcohol. j.forsciint.2016.12.028
Alcohol co-ingestion features in multiple fatal and non-fatal intoxication casessupported
Polysubstance: 3-MeO-PCP + amphetamine + alcohol. j.jflm.2019.05.011
Synergistic CNS and respiratory depression is the primary mechanism of harm. Opioids present extreme risk: Castro et al. documented a fatality from combined 3-MeO-PCP and O-desmethyltramadol (the active opioid metabolite of tramadol), with additive respiratory depression as the probable mechanism. Benzodiazepines appeared in one fatal polysubstance case (delorazepam); while benzodiazepines are used therapeutically for 3-MeO-PCP-induced agitation, unsupervised combination carries respiratory depression risk.supported
Male found unresponsive; death attributed to combined 3-MeO-PCP and O-desmethyltramadol (opioid). Illustrates danger of combining dissociatives with opioids. s00414-022-02818-w
Synergistic CNS and respiratory depression is the primary mechanism of harm. Opioids present extreme risk: Castro et al. documented a fatality from combined 3-MeO-PCP and O-desmethyltramadol (the active opioid metabolite of tramadol), with additive respiratory depression as the probable mechanism. Benzodiazepines appeared in one fatal polysubstance case (delorazepam); while benzodiazepines are used therapeutically for 3-MeO-PCP-induced agitation, unsupervised combination carries respiratory depression risk.supported
second for ethanol, bupropion, delorazepam, paroxetine, mitragynine. bkx048
No published case reports document serotonin syndrome from 3-MeO-PCP combinations, but the mechanism is pharmacologically plausible.supported
PCP analogues exhibited high affinities for sigma receptors and serotonin transporter. journal.pone.0059334
3-MeO-PCP is metabolized by CYP2D6, CYP2C19, CYP2B6, and CYP3A4partially supported
CYP2B6 responsible for aliphatic hydroxylations; CYP2C19 and CYP2D6 for O-demethylation. 1570159x14666161018151716
Copeland et al. cautioned that physical activity may exacerbate 3-MeO-PCP cardiovascular toxicity through elevated heart rate, body temperature, and blood pressure.supported
Exercise may exacerbate toxicity via elevated HR, body temperature, blood pressure. bkac015
In silico hERG inhibition predicts QT-prolongation risksupported
hERG IC50 ~4.9-12.3 µM (QT-prolongation risk). s00204-025-04242-6
Psychotic disorders and bipolar disorder: 3-MeO-PCP reliably produces psychotomimetic effects and has triggered persistent substance-induced psychotic disordersupported
case of 29-year-old man with substance-induced psychotic disorder after small oral doses over 2 weeks then high-dose ingestion. ph17040452
Hepatic impairment: Hepatic metabolism via CYP2D6, CYP2C19, and CYP2B6 is the primary elimination pathwaysupported
CYP2B6 responsible for aliphatic hydroxylations; CYP2C19 and CYP2D6 for O-demethylation. 1570159x14666161018151716
pharmacology14 · 13 ok
3-MeO-PCP acts as a non-competitive, open-channel blocker of NMDA receptors at the PCP/dizocilpine (MK-801) binding sitesupported
3-MeO-PCP confirmed as high affinity ligand at PCP-site on glutamate NMDA receptor. journal.pone.0059334
With a Ki of 20 nM, it ranks among the most potent NMDA antagonists characterized, exceeded only by dizocilpine (MK-801, Ki = 4.8 nM) and surpassing the parent compound PCPsupported
3-MeO-PCP confirmed as high affinity ligand at PCP-site on glutamate NMDA receptor. journal.pone.0059334
Secondary pharmacological activity includes sigma-1 receptor agonism (Ki = 42 nM), which may contribute to psychotomimetic, analgesic, and stimulant-like properties, and moderate serotonin transporter (SERT) inhibition (Ki = 216 nM), which introduces serotonergic activity relevant to both subjective effects and drug interaction risk.supported
PCP analogues exhibited high affinities for sigma receptors and serotonin transporter. journal.pone.0059334
NMDA receptor inhibition has been independently confirmed using a high-throughput drebrin immunocytochemical assay.supported
High-throughput NMDAR inhibition assay using drebrin as a postsynaptic density marker. Tested phencyclidine analogues including 3-MeO-PCP for NMDAR inhibitory activity. j.vascn.2019.106583
Absorption and distribution: In silico ADME modeling predicts high passive permeability, high gastrointestinal absorption, ready blood-brain barrier penetration, approximately 70–80% plasma protein binding, and a large volume of distribution consistent with extensive tissue partitioning.supported
High passive permeability, high GI absorption, BBB penetrant. Plasma protein binding ~70-80%. Large apparent Vd. s00204-025-04283-x
Metabolism: Metabolic pathways were characterized in rat urine and pooled human liver microsomes by Michely et al.supported
Metabolic fate of 3-MeO-PCP elucidated in rat urine and pooled human liver microsomes. 1570159x14666161018151716
CYP3A4 is also implicatedsupported
CYP3A4, CYP2D6, CYP2C19 as primary metabolic enzymes. s00204-025-04283-x
Key metabolites identified include O-demethyl-3-MeO-PCP, piperidine-OH-3-MeO-PCP, O-demethyl-piperidine-di-OH-3-MeO-PCP, and piperidine-di-OH-3-MeO-PCP.supported
Multiple aliphatic hydroxylations, aromatic hydroxylation, O-demethylation, and glucuronidation identified. 1570159x14666161018151716
Key metabolites identified include O-demethyl-3-MeO-PCP, piperidine-OH-3-MeO-PCP, O-demethyl-piperidine-di-OH-3-MeO-PCP, and piperidine-di-OH-3-MeO-PCP.supported
6 metabolites identified including O-demethyl-3-MeO-PCP. 20961790.2021.1928821
Key metabolites identified include O-demethyl-3-MeO-PCP, piperidine-OH-3-MeO-PCP, O-demethyl-piperidine-di-OH-3-MeO-PCP, and piperidine-di-OH-3-MeO-PCP.supported
metabolites O-demethyl-3-MeO-PCP, piperidine-OH-3-MeO-PCP, and di-OH forms identified. bky097
Poor metabolizers at either locus may experience impaired clearance and elevated plasma concentrations, though this has not been clinically characterized for 3-MeO-PCP.supported
CYP2C19 and CYP2D6 for O-demethylation. 1570159x14666161018151716
Claim in pharmacology — inconclusiveinconclusiveworking →
Forensic detection: Metabolite-to-parent ratios in both blood and urine are consistently below 1.0, meaning metabolite testing does not meaningfully extend the detection window beyond the parent compound.supported
Metabolite:parent ratio always <1. bky097
Forensic detection: Metabolite-to-parent ratios in both blood and urine are consistently below 1.0, meaning metabolite testing does not meaningfully extend the detection window beyond the parent compound.supported
Metabolite:parent ratio <1, so metabolite testing does not extend detection window. 20961790.2021.1928821
pharmacokinetic-detail11 · 10 ok
This interaction has not been studied clinically but is supported by the observation that paroxetine (a potent CYP2D6 inhibitor) was co-present in one fatal polysubstance case.supported
second for ethanol, bupropion, delorazepam, paroxetine, mitragynine. bkx048
All values below derive from in silico modelingsupported
In silico ADME profiling of 3-MeO-PCP and 4-MeO-PCP. s00204-025-04283-x
Michely et al. characterized metabolic pathways using rat urine and pooled human liver microsomes:supported
Metabolic fate of 3-MeO-PCP elucidated in rat urine and pooled human liver microsomes. 1570159x14666161018151716
Phase II conjugation proceeds via glucuronidation.supported
Multiple aliphatic hydroxylations, aromatic hydroxylation, O-demethylation, and glucuronidation identified. 1570159x14666161018151716
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Strong CYP2D6 inhibitors (paroxetine, fluoxetine, bupropion) and CYP2C19 inhibitors (omeprazole, fluvoxamine) may impair 3-MeO-PCP metabolism and elevate plasma concentrationssupported
CYP2C19 and CYP2D6 for O-demethylation. 1570159x14666161018151716
Metabolite-to-parent ratios in both blood and urine are consistently below 1.0supported
Metabolite:parent ratio always <1. bky097
Metabolite-to-parent ratios in both blood and urine are consistently below 1.0supported
Metabolite:parent ratio <1, so metabolite testing does not extend detection window. 20961790.2021.1928821
3-MeO-PCP cross-reacts with commercial PCP immunoassays at rates of 1–143% across five tested assayssupported
3-MeO-PCP showed 1-143% cross-reactivity in all PCP IAs tested. bkz026
LC-MS/MS is the recommended confirmatory methodpartially supported
GC-MS method developed for quantification. bkx048
LC-MS/MS is the recommended confirmatory methodsupported
LC-MS/MS method validated. j.forsciint.2016.12.028
history9 · 7 ok
By mid-decade, 3-MeO-PCP had become one of the most widely distributed novel dissociative substances, with fatal and non-fatal intoxication cases reported across Sweden, Italy, France, the Netherlands, the United Kingdom, and the United States.supported
Sweden: 7 deaths + 1 non-fatal intoxication involving 3-MeO-PCP (March 2014 to June 2016). j.forsciint.2017.02.034
By mid-decade, 3-MeO-PCP had become one of the most widely distributed novel dissociative substances, with fatal and non-fatal intoxication cases reported across Sweden, Italy, France, the Netherlands, the United Kingdom, and the United States.supported
3-MeO-PCP intoxication in two young men: First in vivo detection in Italy. j.forsciint.2016.12.028
By mid-decade, 3-MeO-PCP had become one of the most widely distributed novel dissociative substances, with fatal and non-fatal intoxication cases reported across Sweden, Italy, France, the Netherlands, the United Kingdom, and the United States.supported
First two death cases in Washington State involving 3-MeO-PCP. bkx048
By mid-decade, 3-MeO-PCP had become one of the most widely distributed novel dissociative substances, with fatal and non-fatal intoxication cases reported across Sweden, Italy, France, the Netherlands, the United Kingdom, and the United States.supported
First fatal case in Netherlands. Postmortem blood concentration: 152 µg/L 3-MeO-PCP. j.jflm.2019.05.011
Claim in history — inconclusiveinconclusiveworking →
3-MeO-PCP entered the grey-market research chemical supply approximately in 2010, with broad internet availability beginning in 2011partially supported
3-MeO-PCP appeared on illicit drug market in 2011. j.forsciint.2017.02.034
Claim in history — not_supportednot supportedworking →
The landmark — and to date only comprehensive — receptor binding study was published in 2013 by Roth and colleagues, who screened 3-MeO-PCP against 57 CNS molecular targets through the NIMH Psychoactive Drug Screening Program (PDSP)supported
Pharmacological profiles of ketamine and PCP analogues via NIMH PDSP. journal.pone.0059334
Metabolic pathways were subsequently characterized by Michely et al. using rat urine and pooled human liver microsomes in 2017.supported
Metabolic fate of 3-MeO-PCP elucidated in rat urine and pooled human liver microsomes. 1570159x14666161018151716
summary9 · 9 ok
3-Methoxyphencyclidine (3-MeO-PCP) is a synthetic dissociative of the arylcyclohexylamine class, distinguished by exceptional potency at the NMDA receptor (Ki = 20 nM) — placing it among the most potent NMDA antagonists characterized to date and exceeding the parent compound phencyclidinesupported
3-MeO-PCP confirmed as high affinity ligand at PCP-site on glutamate NMDA receptor. journal.pone.0059334
First synthesized in 1979 by Geneste and colleagues during a structure-activity study of phencyclidine derivatives, 3-MeO-PCP remained an obscure research compound for three decades before appearing on the grey-market research chemical scene around 2010supported
3-MeO-PCP appeared on illicit drug market in 2011. j.forsciint.2017.02.034
Regulatory scheduling culminated in UN Schedule II placement in 2021 and US DEA Schedule I in 2026.supported
3-MeO-PCP added to UN 1971 Convention Schedule II in April 2021. bkac015
3-MeO-PCP acts as a non-competitive, open-channel blocker at the PCP/dizocilpine site of the NMDA receptor (Ki = 20 nM), with secondary sigma-1 receptor agonism (Ki = 42 nM) and moderate serotonin transporter inhibition (Ki = 216 nM)supported
3-MeO-PCP confirmed as high affinity ligand at PCP-site on glutamate NMDA receptor. PCP analogues exhibited high affinities for sigma receptors and serotonin transporter. journal.pone.0059334
Case reports describe a dissociative-psychotomimetic profile: confusion, visual and auditory hallucinations, agitation, mania-like disinhibition, and at higher doses, coma (Glasgow Coma Scale 3)supported
Two cases of 3-MeO-PCP intoxication in same patient with literature review. Severe intoxication manifestations characterized. md.0000000000018295
Case reports describe a dissociative-psychotomimetic profile: confusion, visual and auditory hallucinations, agitation, mania-like disinhibition, and at higher doses, coma (Glasgow Coma Scale 3)supported
Two young men brought to hospital comatose after 3-MeO-PCP + alcohol. Glasgow score 3, respiratory acidosis, mydriasis, hypothermia. j.forsciint.2016.12.028
Multiple fatalities are documented, with postmortem blood concentrations spanning 50–3,525 ng/mL; nearly all cases involve polysubstance usesupported
Fatal 3-MeO-PCP case. Femoral blood: 3525 ng/mL. 20961790.2021.1928821
Multiple fatalities are documented, with postmortem blood concentrations spanning 50–3,525 ng/mL; nearly all cases involve polysubstance usesupported
First UK fatal case. 15 prior fatal intoxication reports. bkac015
In silico modeling predicts cardiotoxicity via hERG inhibition (IC₅₀ ~4.9–12.3 µM) and organ toxicity targeting lungs, liver, and bloodsupported
hERG IC50 ~4.9-12.3 µM (QT-prolongation risk). Organ targets: lungs (0.89-0.93), liver (up to 0.91), blood (up to 0.85). s00204-025-04242-6
comparative-pharmacology4 · 4 ok
3-MeO-PCP and its parent compound PCP share the arylcyclohexylamine scaffold and the same primary mechanism — non-competitive NMDA receptor antagonism at the PCP/MK-801 binding site. 3-MeO-PCP displays higher NMDA receptor affinity (Ki = 20 nM) compared to PCP (Ki ≈ 60 nM), consistent with user reports describing 3-MeO-PCP as active at lower dosessupported
3-MeO-PCP confirmed as high affinity ligand at PCP-site on glutamate NMDA receptor. journal.pone.0059334
A key pharmacological difference is 3-MeO-PCP's sigma-1 receptor agonism (Ki = 42 nM) and moderate SERT inhibition (Ki = 216 nM), which may account for its reportedly more stimulant-like and serotonergically modulated subjective profile compared to PCP.supported
PCP analogues exhibited high affinities for sigma receptors and serotonin transporter. journal.pone.0059334
Roth et al. reported ketamine NMDA Ki values in the range of approximately 500–3,000 nM depending on preparation, compared to 20 nM for 3-MeO-PCP — an approximately 25–150-fold difference in binding affinitysupported
Pharmacological profiles of ketamine and PCP analogues via NIMH PDSP. journal.pone.0059334
Methoxetamine (MXE), another arylcyclohexylamine screened alongside 3-MeO-PCP by Roth et al., showed NMDA Ki of approximately 260 nM — roughly 13-fold less potent than 3-MeO-PCP at the NMDA receptor.supported
The ketamine analogue methoxetamine and 3- and 4-methoxy analogues of phencyclidine are high affinity and selective ligands for the glutamate NMDA receptor. journal.pone.0059334
receptor-pharmacology4 · 1 ok
The definitive receptor binding characterization was performed by Roth et al. using the NIMH Psychoactive Drug Screening Program (PDSP), screening 3-MeO-PCP against 57 CNS molecular targets:supported
Pharmacological profiles of ketamine and PCP analogues via NIMH PDSP. journal.pone.0059334
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
clinical-evidence3 · 2 ok
Copeland et al. reviewed 16 total published fatalities as of 2022 and concluded that blood concentrations associated with toxicity and death "remain unclear"supported
First UK fatal case. 15 prior fatal intoxication reports. bkac015
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Pepe et al. reported FDG PET/CT imaging of a 29-year-old male who developed substance-induced psychotic disorder after repeated oral 3-MeO-PCP administration over two weeks, followed by a high-dose ingestionsupported
case of 29-year-old man with substance-induced psychotic disorder after small oral doses over 2 weeks then high-dose ingestion. FDG PET/CT brain imaging used to characterize neural substrates. ph17040452
neuroscience3 · 3 ok
The sigma-1 receptor agonism (Ki = 42 nM) may modulate NMDA receptor function allosterically and contribute to neuroplasticity and neuroprotective signaling, though the behavioral significance of sigma-1 activation at this occupancy level — independent of NMDA antagonism — is uncertain.supported
PCP analogues exhibited high affinities for sigma receptors. journal.pone.0059334
A single case of FDG PET/CT imaging during 3-MeO-PCP-induced psychotic disorder was published by Pepe et al.supported
FDG PET/CT brain imaging used to characterize neural substrates. ph17040452
The observation that 3-MeO-PCP can produce persistent psychotic symptoms after cessation supports the view that sustained NMDA hypofunction may trigger lasting changes in glutamatergic circuit function.supported
substance-induced psychotic disorder after small oral doses over 2 weeks then high-dose ingestion. ph17040452
chemistry2 · 1 ok
Claim in chemistry — inconclusiveinconclusiveworking →
Chemical identity confirmed via PubChem; CAS numbers confirmed by Jurowski et al. and Gomila et al..supported
ADME profile of phencyclidine (PCP) analogues: emerging dissociative hallucinogens 3-MeO-PCP (CAS: 72242-03-6) and 4-MeO-PCP. s00204-025-04283-x
effects-overview1 · 1 ok
Compared to PCP, the subjective effects are qualitatively similar but achieved at lower doses owing to 3-MeO-PCP's higher NMDA receptor affinity (Ki = 20 nM vs. ~60 nM)supported
3-MeO-PCP confirmed as high affinity ligand at PCP-site on glutamate NMDA receptor. journal.pone.0059334