generation run 2026-04-26
56 min completedmodel pipeline-v5plan not recordedrun/1124bd03…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
- no_binding_data
- mu_opioid_unverified
Reproduce
- inputs
- 21 source keys (listed under Sources)
- plan
- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
- streams
- none — agent transcripts are persisted from 2026-09 onward
23 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed · absence | 2-oxo-PCE NMDA antagonist dissociative | 0 | 0 | No results; O-PCE not indexed under that term |
| 2 | PubMed | O-PCE metabolism urine detection new psychoactive substance | 3 | 2 | Most directly relevant O-PCE-specific publications with human data |
| 3 | PubMed | eticyclidone designer ketamine novel psychoactive substance | 15 | 2 | Wallach & Brandt provides class-level context; Roth gives binding data for structurally similar compounds |
| 4 | PubChem | eticyclidone | 1 | 1 | Cross-confirmed alternate name |
| 5 | OpenAlex | deschloro-N-ethyl-ketamine O-PCE pharmacology toxicology | 8 | 3 | Relevant context on arylcyclohexylamine class and closely related compounds |
| 6 | OpenAlex | O-PCE eticyclidone dissociative pharmacology | 1 | 1 | Directly studies O-PCE metabolism |
| 7 | PubMed | O-PCE eticyclidone dissociative pharmacology | 1 | 1 | Directly mentions O-PCE metabolism context |
| 8 | ClinicalTrials.gov · absence | O-PCE eticyclidone dissociative | 0 | 0 | As expected for novel unscheduled RC |
| 9 | PubChem | O-PCE | 1 | 1 | Primary chemical identity source; matches known O-PCE (eticyclidone) structure |
| 10 | UNODC | — | 1 | 2 | Official international chemical database confirmation |
| 11 | PubMed + OpenAlex | Cross-referencing O-PCE papers via citation graph | 8 | 0 | Completeness verification of key O-PCE literature |
| 12 | WebSearch | O-PCE 2-oxo-PCE pharmacology receptor binding Ki NMDA published study | 8 | 0 | Important gap identification - flags need for editorial review |
| 13 | PubMed | O-PCE death fatality case report venlafaxine toxicology | 1 | 1 | Critical safety data - only published fatality case for O-PCE |
| 14 | PubMed · absence | 2-oxo-PCE O-PCE ketamine analogue acute poisoning emergency | 0 | 0 | No new finds |
| 15 | WebSearch | O-PCE 2-oxo-PCE Hong Kong intoxication cluster emergency 2017 2018 | 10 | 1 | Primary clinical toxicology paper |
| 16 | WebSearch | O-PCE eticyclidone legal status scheduling UK US EU 2024 | 10 | 2 | Key legal status data confirmed from multiple web sources |
| 17 | PubMed · absence | deschloro-N-ethyl-ketamine O-PCE Hong Kong acute intoxication | 0 | 0 | All relevant papers already found |
| 18 | WebSearch | O-PCE eticyclidone death fatality toxicology case reports | 10 | 2 | Major clinical case series for O-PCE toxicity |
| 19 | WebSearch | CFSRE O-PCE deschloro-N-ethyl ketamine first detected market 2016 2017 | 10 | 1 | Market emergence timeline |
| 20 | WebSearch | O-PCE deschloroketamine first synthesis history research chemical market appearance | 10 | 2 | Market emergence timeline data |
| 21 | CFSRE | — | 1 | 1 | Physical characterization data |
| 22 | PubMed | ketamine CYP3A4 CYP2B6 metabolism pharmacokinetics | 10 | 4 | CYP metabolism applicable to O-PCE via structural analogy (N-ethyl chain) |
| 23 | PsychonautWiki | — | 1 | 0 | Confirms existing database dose data |
88 claims by section — every cited sentence, checked against its source
safety26 · 20 ok
The case series documented confusion in 60% and abnormal behavior in 44% of presentations.partially supported
confusion 60% j.forsciint.2018.07.014
Concurrent CNS depressant use: Alcohol, opioids, benzodiazepines, and GHB carry additive sedation and respiratory depression risk.supported
Case report: multidrug exposure including O-PCE. j.jpba.2024.116086
The primary acute toxicity data derive from a cluster of 56 poisoning cases in Hong Kongsupported
56 cases of O-PCE acute poisoning in Hong Kong Oct-Nov 2017. j.forsciint.2018.07.014
The convulsion rate is significantly elevated relative to ketamine poisonings and represents a distinguishing safety concern for O-PCE.supported
convulsion 16% j.forsciint.2018.07.014
Standard immunoassay-based ketamine urine drug screens do not detect O-PCEsupported
Standard ketamine immunoassay does NOT cross-react with O-PCE. j.forsciint.2018.07.014
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
One published fatality directly involved O-PCE: a 52-year-old male who had co-ingested O-PCE and venlafaxine, with deschloroketamine also detectedsupported
Fatal case of 52-year-old man who used N-ethyldeschloroketamine (O-PCE) together with venlafaxine. Postmortem blood concentration data provided. Deschloroketamine also detected. bky063
Claim in safety — inconclusiveinconclusiveworking →
Non-fatal DUID blood concentrations ranged from 0.08–0.31 µg/mLsupported
Blood concentrations 0.08-0.31 µg/mL. bkaa038
Larabi and colleagues noted that O-PCE "has been involved in acute intoxications with severe outcomes including death," suggesting additional fatalities exist in forensic databases not yet published in peer-reviewed literaturesupported
O-PCE involved in acute intoxications with severe outcomes including death. dta.3007
A fatal polydrug case involving the closely related compounds 2F-DCK and 3-MeO-PCE was attributed to respiratory depression.supported
Fatal polydrug case with closely related ACH compounds 2F-DCK and 3-MeO-PCE. Respiratory depression primary mechanism. j.forsciint.2021.110852
Hypertension (80%) and tachycardia (40%) were prominent in the acute poisoning case seriessupported
hypertension 80%, tachycardia 40% j.forsciint.2018.07.014
Claim in safety — inconclusiveinconclusiveworking →
Cross-tolerance among NMDA receptor channel blockers has been established in animal models: Lu and colleagues demonstrated cross-tolerance between PCP, ketamine, dizocilpine, and dextrorphan in pigeonssupported
Chronic PCP or CGS 19755 administration produced tolerance and cross-tolerance between PCP, ketamine, dizocilpine (MK-801), dextrorphan, and competitive NMDA antagonists in pigeons. pmid:1432686
The compound appears in chemsex contexts with multi-drug chronic use patterns, suggesting a use profile consistent with psychological reinforcement and potential for compulsive redosing, though no published case report of O-PCE-specific dependence or withdrawal has been identified.supported
Case report: multidrug exposure including O-PCE. j.jpba.2024.116086
Venlafaxine (SNRI): Co-ingestion resulted in the only published O-PCE fatalitysupported
Fatal case of 52-year-old man who used N-ethyldeschloroketamine (O-PCE) together with venlafaxine. bky063
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
CYP2B6 inhibitors (ticlopidine, bupropion) and CYP3A4 inhibitors (azole antifungals, macrolide antibiotics, grapefruit juice) would be expected to increase O-PCE plasma exposure via reduced metabolic clearance. CYP3A4/2B6 inducers (rifampicin, carbamazepine) may reduce exposuresupported
CYP2B6 and CYP3A4 inducers reduce ketamine exposure; inhibitors increase it. jcp.17f11802
A fatal polydrug case involving the related compounds 2F-DCK and 3-MeO-PCE was attributed to respiratory depression.supported
Fatal polydrug case with closely related ACH compounds 2F-DCK and 3-MeO-PCE. Respiratory depression primary mechanism. j.forsciint.2021.110852
Cardiovascular disease: The high prevalence of hypertension (80%) and tachycardia (40%) in acute poisoning presentations makes pre-existing cardiovascular conditions — including uncontrolled hypertension, coronary artery disease, and heart failure — a relative contraindicationsupported
hypertension 80%, tachycardia 40% j.forsciint.2018.07.014
This is consistent with the established cardiovascular contraindication profile of ketamine.supported
Clinical toxicology review of ketamine: pharmacological mechanisms, toxic dose ranges, clinical presentations, management. 15563650.2023.2212125
Seizure disorders: The 16% convulsion rate suggests O-PCE may lower the seizure thresholdsupported
convulsion 16% j.forsciint.2018.07.014
Concurrent SNRI/SSRI use: The fatal interaction with venlafaxine warrants listing serotonin-norepinephrine reuptake inhibitors as a relative contraindication pending mechanistic characterization.supported
Fatal case of 52-year-old man who used N-ethyldeschloroketamine (O-PCE) together with venlafaxine. bky063
Concurrent CNS depressant use: Alcohol, opioids, benzodiazepines, and GHB carry additive sedation and respiratory depression risk.supported
Fatal polydrug case with closely related ACH compounds 2F-DCK and 3-MeO-PCE. Respiratory depression primary mechanism. j.forsciint.2021.110852
pharmacology17 · 14 ok
This mechanism is well-established for the arylcyclohexylamine class: Roth and colleagues demonstrated high-affinity NMDA receptor binding for the structurally related compounds methoxetamine and PCE analogs via the NIMH Psychoactive Drug Screening Program, and the class mechanism has been extensively reviewedsupported
NIMH PDSP profiling of ketamine/PCP analogs. MXE and 3-MeO-PCE are high affinity NMDA ligands. journal.pone.0059334
This mechanism is well-established for the arylcyclohexylamine class: Roth and colleagues demonstrated high-affinity NMDA receptor binding for the structurally related compounds methoxetamine and PCE analogs via the NIMH Psychoactive Drug Screening Program, and the class mechanism has been extensively reviewedsupported
Review of dissociative NPS including beta-keto-arylcyclohexylamines: methoxetamine, deschloroketamine class. 164_2018_148
Roth and colleagues found appreciable sigma receptor binding for PCP analogs, though this was less prominent for ketamine-type analogs with the N-alkylaminocyclohexanone coresupported
MXE and 3-MeO-PCE are high affinity NMDA ligands. PCP analogs show sigma receptor affinity. journal.pone.0059334
Hustveit and colleagues confirmed that ketamine binds sigma receptors, but at substantially lower affinity than at the PCP sitesupported
Ketamine binds to PCP (NMDA), mu/kappa opioid, sigma, and muscarinic receptors. PCP receptor affinity highest. pmid:8835358
Ketamine shows mu- and kappa-opioid receptor binding at higher concentrations, while 3-MeO-PCP — another NMDA-blocking arylcyclohexylamine — showed no interaction with μ-, δ-, or κ-opioid receptors at concentrations up to 10,000 nM in NIMH PDSP screeningpartially supported
Ketamine binds to PCP (NMDA), mu/kappa opioid, sigma, and muscarinic receptors. pmid:8835358
The clinical case series documented by Tang and colleagues demonstrated pronounced sympathomimetic effects consistent with NMDA antagonist pharmacology: hypertension occurred in 80% and tachycardia in 40% of 56 acute poisoning presentationssupported
56 cases of O-PCE acute poisoning in Hong Kong Oct-Nov 2017. Clinical: hypertension 80%, tachycardia 40%. j.forsciint.2018.07.014
Claim in pharmacology — inconclusiveinconclusiveworking →
The only published human pharmacokinetic estimate places the elimination half-life at approximately 5 hours, derived from plasma concentration kinetics over 29.5 hours in a single multidrug exposure case (O-PCE + GHB + 3-MMC + MXE).supported
Case report: multidrug exposure including O-PCE. Elimination half-life ~5 hours. j.jpba.2024.116086
Larabi and colleagues performed the first dedicated metabolic profiling using pooled human liver microsomes (HLMs) and biological specimens from a 43-year-old male user, identifying 15 metabolites via Phase I pathways (N-deethylation, hydroxylation, deamination, oxidation) and Phase II conjugation (N-glucuronidation, O-glucuronidation)supported
First O-PCE metabolic profiling. 15 metabolites. Urine and hair forensic markers identified. dta.3007
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Xu and colleagues confirmed O-PCE metabolism in zebrafish and HLMs, identifying hydroxy-O-PCE as the recommended forensic biomarkersupported
Metabolism of deschloro-N-ethyl-ketamine (O-PCE) and two related ACH compounds via zebrafish and HLMs. 49 metabolites. Hydroxy-O-PCE as biomarker. bkae020
Magny and colleagues annotated 27 metabolites in vivo, including previously unreported Phase II compounds.supported
27 O-PCE metabolites annotated. Elimination half-life ~5 hours. Phase II metabolites not previously reported. j.jpba.2024.116086
By structural analogy with methoxetamine — which shares the same N-ethylaminocyclohexanone core — initial N-deethylation is likely catalyzed by CYP2B6 and CYP3A4supported
MXE (structural analog of O-PCE: same N-ethyl, cyclohexanone core) metabolism. Initial N-deethylation catalyzed by CYP2B6 and CYP3A4. s00216-013-7051-6
Ketamine is also metabolized primarily by CYP3A4 and CYP2B6 to norketamine, with secondary contributions from CYP2C9 and CYP2A6.partially supported
Comprehensive review: ketamine metabolized by CYP3A and CYP2B6 to norketamine. s40262-016-0383-6
Ketamine is also metabolized primarily by CYP3A4 and CYP2B6 to norketamine, with secondary contributions from CYP2C9 and CYP2A6.supported
CYP2B6, CYP3A4, CYP2C9, CYP2A6 involved in ketamine metabolism. bcp.15467
Route-dependent onset differences — insufflated onset of 2–5 minutes versus oral onset of 20–40 minutes — are consistent with significant first-pass metabolism by the oral route, as observed for ketamine (oral bioavailability approximately 17–29%).supported
Poor oral bioavailability. Nasal: rapid Tmax. s40262-016-0383-6
clinical-evidence8 · 5 ok
Theofel and colleagues reported a fatal case in a 52-year-old male who had co-ingested O-PCE and venlafaxinesupported
Fatal case of 52-year-old man who used N-ethyldeschloroketamine (O-PCE) together with venlafaxine. bky063
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Cheng and Dao documented O-PCE in driving-under-the-influence cases in Hong Kong, with blood concentrations ranging from 0.08 to 0.31 µg/mL, accompanied by the metabolite deschloronorketamine at 0.04–0.09 µg/mL.partially supported
4 DUID cases. Blood concentrations 0.08-0.31 µg/mL. Metabolite deschloronorketamine co-detected. bkaa038
Tang and colleagues documented 56 cases of acute poisoning associated with O-PCE in Hong Kong between October and November 2017supported
56 cases of O-PCE acute poisoning in Hong Kong Oct-Nov 2017. j.forsciint.2018.07.014
The convulsion rate of 16% is notably elevated compared to typical ketamine presentations and warrants clinical attention.supported
convulsion 16% j.forsciint.2018.07.014
Claim in clinical-evidence — inconclusiveinconclusiveworking →
A consistent finding across clinical reports is that standard immunoassay-based ketamine urine screens do not cross-react with O-PCEsupported
Standard ketamine immunoassay does NOT cross-react with O-PCE. j.forsciint.2018.07.014
Claim in clinical-evidence — inconclusiveinconclusiveworking →
history8 · 8 ok
In 2019, Theofel and colleagues reported the first and, as of 2026, only published fatality directly involving O-PCE: a 52-year-old male who had co-ingested O-PCE and venlafaxine (an SNRI antidepressant)supported
Fatal case of 52-year-old man who used N-ethyldeschloroketamine (O-PCE) together with venlafaxine. bky063
Larabi and colleagues noted that O-PCE "has been involved in acute intoxications with severe outcomes including death," the plural phrasing suggesting additional fatalities beyond the single published case, likely recorded in forensic databases or EMCDDA early warning reports not yet captured in indexed peer-reviewed literature.supported
O-PCE involved in acute intoxications with severe outcomes including death. dta.3007
The earliest confirmed detections of O-PCE in drug seizures and driving-under-the-influence-of-drugs (DUID) cases occurred in Hong Kong in October 2017supported
First detected October 2017 in HK. 31 seizure cases (52 items) + 4 DUID cases. bkaa038
Seized samples appeared as powdery or crystalline solids largely indistinguishable from ketamine; approximately 69% contained O-PCE as the sole active substance, while 19% were mixed with ketaminepartially supported
Often mixed with or misrepresented as ketamine. bkaa038
In December 2017, Chong and colleagues published the earliest peer-reviewed clinical report in the Hong Kong Medical Journal, identifying O-PCE as a new emerging street drug.supported
Early report identifying 2-oxo-PCE as an emerging ketamine analogue in Hong Kong. hkmj177089
The cases demonstrated that users were frequently unaware they had ingested O-PCE rather than ketamine, and that the higher potency of O-PCE was producing adverse effects at doses calibrated for ketamine use.partially supported
Often mixed with or misrepresented as ketamine. bkaa038
Larabi and colleagues published the first systematic metabolic profiling in 2021, identifying 15 metabolites via human liver microsomes and biological specimenssupported
First O-PCE metabolic profiling. 15 metabolites. dta.3007
Xu and colleagues extended this work in 2024, confirming O-PCE metabolism in zebrafish and human liver microsomes and identifying hydroxy-O-PCE as a recommended forensic biomarkersupported
Metabolism of deschloro-N-ethyl-ketamine (O-PCE) and two related ACH compounds via zebrafish and HLMs. Hydroxy-O-PCE as biomarker. bkae020
summary8 · 7 ok
Claim in summary — inconclusiveinconclusiveworking →
O-PCE first appeared on research chemical markets around 2016, with the earliest peer-reviewed report published in December 2017 from Hong Kongpartially supported
Early report identifying 2-oxo-PCE as an emerging ketamine analogue in Hong Kong. hkmj177089
The published evidence base consists entirely of forensic toxicology case series, postmortem analyses, and in vitro metabolic profilingsupported
First O-PCE metabolic profiling. 15 metabolites. O-PCE involved in acute intoxications with severe outcomes including death. Urine and hair forensic markers identified. dta.3007
The published evidence base consists entirely of forensic toxicology case series, postmortem analyses, and in vitro metabolic profilingsupported
Case report: multidrug exposure including O-PCE. 27 O-PCE metabolites annotated. Elimination half-life ~5 hours. j.jpba.2024.116086
As an arylcyclohexylamine, O-PCE is presumed to act primarily through open-channel blockade of the NMDA receptor at the phencyclidine binding site, consistent with published binding data for structurally related compounds including methoxetamine and PCE analogssupported
NIMH PDSP profiling of ketamine/PCP analogs. MXE and 3-MeO-PCE are high affinity NMDA ligands. journal.pone.0059334
Acute toxicity data from a 56-case poisoning cluster in Hong Kong documented convulsions in 16% of presentations — notably elevated for a ketamine-class compound — alongside hypertension (80%) and tachycardia (40%)supported
56 cases of O-PCE acute poisoning in Hong Kong Oct-Nov 2017. Clinical: impaired consciousness 84%, hypertension 80%, confusion 60%, convulsion 16%, tachycardia 40%. j.forsciint.2018.07.014
One published fatality involved co-ingestion with venlafaxine; the interaction mechanism is uncharacterizedsupported
Fatal case of 52-year-old man who used N-ethyldeschloroketamine (O-PCE) together with venlafaxine. bky063
Standard ketamine immunoassays do not detect O-PCE, creating a diagnostic blind spot in emergency settingssupported
Standard ketamine immunoassay does NOT cross-react with O-PCE. j.forsciint.2018.07.014
comparative-pharmacology6 · 5 ok
Notably, a fatal polydrug case involving the related compounds 2F-DCK and 3-MeO-PCE was attributed to respiratory depression, a risk shared across the arylcyclohexylamine class at sufficient doses.supported
Fatal polydrug case with closely related ACH compounds 2F-DCK and 3-MeO-PCE. Blood concentrations, tissue distribution. Respiratory depression primary mechanism. j.forsciint.2021.110852
Binding values are approximate, drawn from separate publications under varying assay conditions.supported
NIMH PDSP profiling of ketamine/PCP analogs. journal.pone.0059334
Binding values are approximate, drawn from separate publications under varying assay conditions.supported
Ketamine binds to PCP (NMDA), mu/kappa opioid, sigma, and muscarinic receptors. Kappa agonism in guinea pig ileum. pmid:8835358
In the Hong Kong poisoning cluster, users calibrating their doses to ketamine were adversely affected by O-PCE's higher potencypartially supported
Often mixed with or misrepresented as ketamine. bkaa038
The 16% convulsion rate in the O-PCE case series stands in contrast to ketamine, which is rarely associated with convulsions at recreational doses and possesses anticonvulsant properties in some contextssupported
convulsion 16% j.forsciint.2018.07.014
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
pharmacokinetic-detail6 · 6 ok
Magny and colleagues monitored plasma concentrations over 29.5 hours in a patient admitted to the ICU following multidrug exposure (O-PCE + GHB + 3-MMC + MXE), estimating an elimination half-life of approximately 5 hourssupported
Case report: multidrug exposure including O-PCE. Elimination half-life ~5 hours. j.jpba.2024.116086
Larabi et al. (2021) identified 15 metabolites using pooled HLMs and clinical specimenssupported
First O-PCE metabolic profiling. 15 metabolites. dta.3007
Xu et al. (2024) confirmed these pathways in zebrafish and HLMs, identifying hydroxy-O-PCE as the recommended analytical biomarker for forensic detection.supported
Metabolism of deschloro-N-ethyl-ketamine (O-PCE) and two related ACH compounds via zebrafish and HLMs. 49 metabolites. Hydroxy-O-PCE as biomarker. bkae020
Methoxetamine (same N-ethylaminocyclohexanone core): N-deethylation catalyzed by CYP2B6 and CYP3A4supported
Initial N-deethylation catalyzed by CYP2B6 and CYP3A4. s00216-013-7051-6
Ketamine (N-methylaminocyclohexanone): N-demethylation to norketamine primarily via CYP3A4 and CYP2B6, with secondary contributions from CYP2C9 and CYP2A6partially supported
Comprehensive review: ketamine metabolized by CYP3A and CYP2B6 to norketamine. s40262-016-0383-6
Ketamine (N-methylaminocyclohexanone): N-demethylation to norketamine primarily via CYP3A4 and CYP2B6, with secondary contributions from CYP2C9 and CYP2A6supported
CYP2B6, CYP3A4, CYP2C9, CYP2A6 involved in ketamine metabolism. bcp.15467
chemistry3 · 0 ok
neuroscience3 · 2 ok
Claim in neuroscience — inconclusiveinconclusiveworking →
This mechanism accounts for the sympathomimetic effects (hypertension, tachycardia) documented in the O-PCE case series.supported
hypertension 80%, tachycardia 40% j.forsciint.2018.07.014
The elevated convulsion rate (16%) observed with O-PCE is neurologically noteworthysupported
convulsion 16% j.forsciint.2018.07.014
receptor-pharmacology2 · 2 ok
The most relevant published binding data derive from Roth and colleagues, who characterized the receptor profiles of methoxetamine, 3-MeO-PCP, 4-MeO-PCP, and related compounds at the NIMH Psychoactive Drug Screening Programsupported
NIMH PDSP profiling of ketamine/PCP analogs. MXE and 3-MeO-PCE are high affinity NMDA ligands. journal.pone.0059334
MXE — which shares the same N-ethylaminocyclohexanone core as O-PCE — demonstrated high-affinity NMDA receptor binding and lower but measurable affinity at sigma, serotonin transporter (SERT), norepinephrine transporter (NET), and dopamine transporter (DAT) sitespartially supported
MXE and 3-MeO-PCE are high affinity NMDA ligands. PCP analogs show sigma receptor affinity. journal.pone.0059334
effects-overview1 · 1 ok
The elevated convulsion rate documented in clinical data distinguishes its safety profile from the relatively benign acute toxicity of ketamine.supported
convulsion 16% j.forsciint.2018.07.014