O-PCE

# Research Output: O-PCE (Eticyclidone / 2-Oxo-PCE)

**PSX ID:** PSX-0282  
**Research Date:** 2026-04-26  
**Substance Readiness:** Sparse/emerging — primary literature is limited to forensic toxicology and case reports; no controlled clinical pharmacology studies exist.

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## Chemical Identity

| Field | Value | Source |
|---|---|---|
| Preferred name | O-PCE | — |
| IUPAC name | 2-(ethylamino)-2-phenylcyclohexan-1-one | PubChem CID 132989542 [Ref 1] |
| Common synonyms | Eticyclidone; N-ethyldeschloroketamine; 2-Oxo-PCE; 2'-Oxo-PCE; 2-DCNEK | UNODC [Ref 23] |
| CAS number | 4551-92-2 | UNODC [Ref 23]; Cayman Chemical |
| PubChem CID | 132989542 | PubChem [Ref 1] |
| Molecular formula | C₁₄H₁₉NO | PubChem [Ref 1] |
| Molecular weight | 217.31 g/mol | PubChem [Ref 1] |
| InChIKey | IDLSBAANXISGEI-UHFFFAOYSA-N | PubChem [Ref 1] |
| SMILES (canonical) | CCNC1(c2ccccc2)CCCCC1=O | Derived from IUPAC (consistent with PubChem CID) |
| MS identifier | [M+H]⁺ = 218.1539 | CFSRE monograph [Ref 22] |
| Chemical class | Arylcyclohexylamine; β-keto subtype | UNODC [Ref 23] |
| Physical appearance | Powdery/crystalline solid; described as "blood-colored" in one reference | CFSRE [Ref 22]; Cheng & Dao 2020 [Ref 13] |

**Seed data gaps resolved by research:**
- PubChem CID, molecular formula (C₁₄H₁₉NO), molecular weight (217.31), InChIKey, SMILES, and CAS number were all absent in the brief. All have now been confirmed via PubChem [Ref 1] and UNODC [Ref 23].

**Structural relationships:**
- O-PCE is the N-ethyl analog of deschloroketamine (DCK; N-methyl). It is structurally equivalent to ketamine with (a) the 2-chloro group removed from the phenyl ring, and (b) an ethyl (rather than methyl) N-substituent.
- It shares the same N-ethylaminocyclohexanone core as methoxetamine (MXE), differing only in the absence of a 3-methoxy substituent on the phenyl ring.
- Both the DCK family and MXE are reviewed in Wallach & Brandt (2018) [Ref 5].

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## Pharmacology

### Mechanism of Action

No published receptor binding studies exist specifically for O-PCE [confirmed absent from literature; web search 2026-04-26]. All pharmacological characterization is based on structural analogy and class-level data.

**NMDA receptor antagonism** (primary mechanism, strongly inferred):
O-PCE is a β-keto-arylcyclohexylamine sharing structural features with ketamine and methoxetamine. The primary mechanism of action for this class is channel-blocking antagonism at the PCP binding site within the NMDA receptor, as confirmed for closely related compounds (Roth et al. 2013 [Ref 6] demonstrated high-affinity NMDA binding for MXE and PCE analogs via NIMH PDSP; Wallach & Brandt 2018 [Ref 5] reviewed the class). No published Ki or IC₅₀ data exists for O-PCE at NMDA or any other receptor. **FLAG FOR REVIEW: Specific binding affinity data absent.**

**Sigma receptor agonism** (possible, class-based inference):
Roth et al. (2013) [Ref 6] found appreciable sigma receptor affinity for PCP analogs; however, this was less prominent for ketamine-type analogs (N-ethylaminocyclohexanone class). Hustveit et al. (1995) [Ref 26] confirmed ketamine binds sigma receptors, but at lower affinity than the PCP site. No O-PCE-specific sigma binding data exists. **FLAG FOR REVIEW: Sigma agonism in seed data (pharmacological class) lacks substance-specific evidence; it is a class-level inference.**

**Mu-opioid receptor agonism** (uncertain, weakly supported by class data):
Ketamine has reported mu- and kappa-opioid receptor binding at higher concentrations (Hustveit et al. 1995 [Ref 26]). However, 3-MeO-PCP, another NMDA-blocking arylcyclohexylamine, was found NOT to interact with μ-, δ-, or κ-opioid receptors at concentrations up to 10,000 nM (unpublished NIMH PDSP data). For O-PCE specifically, no opioid receptor binding data has been published. **FLAG FOR REVIEW: "Mu-opioid receptor agonist" in seed data pharmacological class is not confirmed by any published study of O-PCE or its closest structural analogs; this may be an overclaim and should be re-evaluated by the generation agent.**

**Cardiovascular and sympathomimetic effects:**
The clinical case series (Tang et al. 2018 [Ref 11]) documented hypertension in 80% and tachycardia in 40% of cases. These are consistent with central sympathomimetic effects attributable to NMDA antagonism, which may reduce GABA-ergic brake on sympathetic tone (as seen with ketamine). Schep et al. (2023) [Ref 19] describe this mechanism for ketamine. No direct adrenergic binding data for O-PCE exists.

### Pharmacokinetics

**Elimination half-life:** ~5 hours in a single human case (Magny et al. 2024 [Ref 1]). This was estimated from plasma concentration kinetics over 29.5 hours following acute multi-drug exposure (context: GHB + 3-MMC + MXE + O-PCE).

**Metabolism (published; primary source):**
Larabi et al. (2021) [Ref 2] performed the first dedicated metabolic profiling of O-PCE using pooled human liver microsomes (HLMs) and biological specimens from a 43-year-old male user. Fifteen metabolites were identified:
- **Phase I pathways:** N-deethylation, hydroxylation, deamination, oxidation
- **Phase II pathways:** N-glucuronidation, O-glucuronidation
- O-PCE was not detectable in urine after metabolism; nine metabolites were recovered from urine
- Urine markers (ranked by abundance): 2-en-PCA-N-Glu (34%), M3 (16%), O-PCA-N-Glu (15.4%), OH-O-PCE (15%), OH-PCE (11.9%)
- Hair marker: OH-PCA (78% of metabolite burden in hair; metabolite-to-parent ratio = 6)

Xu et al. (2024) [Ref 4] confirmed O-PCE (as deschloro-N-ethyl-ketamine) metabolism in zebrafish and HLMs, identifying hydroxy-O-PCE as a recommended biomarker. Total 49 metabolites were identified across three ACH compounds in that study.

Magny et al. (2024) [Ref 1] annotated 27 O-PCE metabolites in vivo, including previously unreported Phase II compounds.

**CYP enzymes involved:**
No direct CYP enzyme data has been published for O-PCE. By structural analogy:
- Methoxetamine (same N-ethylaminocyclohexanone core) has its initial N-deethylation catalyzed by CYP2B6 and CYP3A4 (Meyer et al. 2013 [Ref 17]) — this is the most directly applicable inference
- Ketamine (N-methylaminocyclohexanone) is also metabolized primarily by CYP3A4 and CYP2B6 to norketamine, with secondary contributions from CYP2C9 and CYP2A6 (Peltoniemi et al. 2016 [Ref 16]; Langmia et al. 2022 [Ref 18])
- **FLAG FOR REVIEW:** CYP enzyme identification for O-PCE is inferred; not substance-specific.

**Bioavailability:**
No published data for O-PCE. Insufflated administration produces faster onset (2-5 minutes) vs. oral (20-40 minutes) per community data [Ref 21]. Ketamine's oral bioavailability is low (~17-29%) due to first-pass CYP metabolism; insufflated is significantly higher (Peltoniemi et al. 2016 [Ref 16]).

**Blood concentrations observed:**
- DUID cases (Hong Kong): 0.08–0.31 µg/mL in blood; with metabolite deschloronorketamine at 0.04–0.09 µg/mL (Cheng & Dao 2020 [Ref 13])
- Fatal case (Theofel 2019 [Ref 12]): postmortem blood concentration reported at ~1.2 µg/mL (per Grokipedia compilation [Ref 21]; specific tissue data not fully extracted from cached abstract)

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## History

**1962 (disputed):** One secondary source (Grokipedia [Ref 21]) claims O-PCE was "originally synthesized during pharmaceutical research at Parke-Davis" in 1962. **This claim likely represents a conflation with PCE (eticyclidine, N-ethylphencyclidine)**, which was first synthesized by Maddox et al. at Parke-Davis in 1962 as part of the same research program that produced PCP. PCE (eticyclidine) lacks the 2-oxo (ketone) group that defines O-PCE's structure. **FLAG FOR REVIEW:** No verified primary source establishes O-PCE as a Parke-Davis 1962 compound. This date more plausibly refers to the parent PCE class.

**2016:** O-PCE first appeared on illicit research chemical markets, with initial detection reportedly in France (Grokipedia [Ref 21]; not independently verified by a peer-reviewed primary source).

**October 2017:** First confirmed detection in drug seizures and DUID cases in Hong Kong (Cheng & Dao 2020 [Ref 13]). Seized samples were in powdery or crystalline form, largely indistinguishable from ketamine but with lower purity (similar to ketamine in appearance, ~69% found as sole substance, ~19% mixed with ketamine).

**December 2017:** Earliest published report in peer-reviewed literature — a letter to the Hong Kong Medical Journal (Chong et al. 2017 [Ref 14]) describing O-PCE as a new emerging street drug.

**October–November 2017:** A cluster of 56 acute poisoning cases associated with O-PCE in Hong Kong, reported by Tang et al. (2018) [Ref 11]. This remains the largest published case series for O-PCE toxicity.

**June 2018:** CFSRE (Center for Forensic Science Research and Education) published a toxicology analytical report/monograph on O-PCE (deschloro-N-ethyl-ketamine), documenting its chemical characterization and emergence [Ref 22].

**2019:** A fatal case involving O-PCE and venlafaxine co-ingestion reported by Theofel et al. [Ref 12]. Same year, the German NpSG regulation took effect (July 18, 2019) [Ref 21].

**2020–2024:** Continued forensic characterization. Larabi et al. (2021) [Ref 2] published the first systematic metabolic profiling; Xu et al. (2024) [Ref 4] and Magny et al. (2024) [Ref 1] provided further in vivo and in vitro metabolic data.

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## Subjective Effects

There are no controlled or observational human pharmacology studies describing O-PCE's subjective effects. All available descriptive data derives from (a) clinical case series documenting toxic presentations and (b) community self-reports.

**From clinical case series (Tang et al. 2018 [Ref 11]; n=56; "sole 2-oxo-PCE" subset):**
- Impaired consciousness: 84%
- Hypertension: 80%
- Confusion: 60%
- Abnormal behaviour: 44%
- Tachycardia: 40%
- Convulsion: 16%

These presentations are consistent with the dissociative/NMDA antagonist toxidrome. The convulsion rate (16%) is notably high compared to typical ketamine presentations, though whether this reflects a class-specific property of O-PCE or a population/dosing confound cannot be determined from this data.

**From community reports (user-report-only data; not controlled):**
- Users describe pronounced dissociation reported as more intense and longer-duration than ketamine
- Effects described include: euphoria, analgesia, amnesia, depersonalization, derealization, visual disturbances, motor impairment
- The KnowDrugs harm reduction database [Ref 21] documents the following effect profile consistent with the Psychedex taxonomy: CNS stimulation, dizziness, increased heart rate, motor control loss, nausea, physical euphoria, depersonalization, derealization, cognitive distortions, and memory suppression

**Duration data (community-sourced, consistent with DB):**
- Insufflated onset: 2–5 minutes
- Insufflated total duration: 3–5 hours
- Insufflated aftereffects: 2–12 hours
- Oral onset: 20–40 minutes
- Oral total duration: 3–6 hours
- Oral aftereffects: 4–48 hours

No published controlled duration data exists. These values are drawn from community sources and are consistent across PsychonautWiki and KnowDrugs. **FLAG FOR REVIEW (dose/duration):** Dose and duration data in the brief appear consistent with community consensus; no published study contradicts them.

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## Safety & Toxicity

**LD50:** Not published. No animal toxicity studies for O-PCE have been identified in peer-reviewed literature. **FLAG FOR REVIEW: Exact toxic dosage is unknown — seed data note is accurate.**

**Published fatality:**
Theofel et al. (2019) [Ref 12] reported the first published fatality involving O-PCE (N-ethyldeschloroketamine). The victim was a 52-year-old male who had co-ingested O-PCE and venlafaxine (an SNRI antidepressant). Deschloroketamine was also detected, possibly as an impurity in the consumed product or from prior use. Postmortem analysis confirmed O-PCE across multiple tissue compartments. This represents the only confirmed published O-PCE death in the peer-reviewed literature.

**Note:** Larabi et al. (2021) [Ref 2] specifically states O-PCE "has been involved in acute intoxications with severe outcomes including death" — the plural ("deaths") suggests additional fatalities in forensic databases not yet captured in peer-reviewed papers. **FLAG FOR REVIEW:** There may be additional unpublished or non-indexed fatality cases.

**Acute clinical toxicity (published; n=56):**
Tang et al. (2018) [Ref 11] documented 56 acute poisoning cases:
- Three patients required intensive care admission
- All patients recovered
- Convulsion occurred in 16% — this is significantly elevated for a ketamine-class compound and warrants explicit clinical emphasis
- Standard ketamine urine immunoassay tests do NOT cross-react with O-PCE, creating a significant diagnostic blind spot in emergency settings
- O-PCE was physically indistinguishable from ketamine in seized samples; users may not have known they were ingesting O-PCE rather than ketamine

**Related compound fatalities (contextual):**
Gicquel et al. (2021) [Ref 15] reported a fatal polydrug case involving 2F-DCK (a closely related ACH compound) and 3-MeO-PCE, attributed to respiratory depression.

**Blood concentration reference data:**
- DUID cases (non-fatal): 0.08–0.31 µg/mL (Cheng & Dao 2020 [Ref 13])
- Fatal case: ~1.2 µg/mL (Theofel 2019 [Ref 12], via Grokipedia compilation [Ref 21])
- The gap between DUID and fatal concentrations (~4-fold) is notable, though the fatal case involved polydrug co-ingestion

**Diagnostic note:**
Standard immunoassay-based ketamine testing does not detect O-PCE, and nasal swab samples from Tang et al. (2018) confirmed insufflation as the primary route in that cluster. LC-MS/MS is required for confirmation (Cheng & Dao 2020 [Ref 13]; Pelixo et al. 2024 [Ref 7]).

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## Harm Reduction

No substance-specific harm reduction publications for O-PCE exist. The following is synthesized from clinical case data and class-level evidence:

**Testing and identification:**
- Standard reagent test kits (Marquis, Mecke, Mandelin) have not been formally characterized for O-PCE in peer-reviewed literature; results from these reagents for O-PCE are community-reported only
- Standard ketamine immunoassay does NOT detect O-PCE (Tang et al. 2018 [Ref 11]); laboratory confirmation requires LC-MS/MS or GC-HRMS
- O-PCE is frequently misrepresented as ketamine or deschloroketamine by vendors and may appear indistinguishable in physical form (Cheng & Dao 2020 [Ref 13])
- Fentanyl test strips are irrelevant for this class

**Dosing safety:**
- O-PCE appears more potent than ketamine gram-for-gram (users in HK were "adversely affected by the more potent 2-oxo-PCE" when presuming they had ketamine; Cheng & Dao 2020 [Ref 13])
- Convulsive risk (16% in the clinical series) is higher than typically reported for ketamine
- The aftereffect window (4–48 hours oral) is extended; impairment may persist well beyond the subjective experience

**Contraindications (class-based, not substance-specific):**
- NMDA antagonist class: should be avoided with MAOIs (risk of serotonin syndrome/hypertensive crisis via indirect mechanisms)
- The co-ingestion fatality involved venlafaxine (SNRI) [Ref 12] — the mechanism of this interaction is not established but likely involves combined CNS and/or cardiovascular depression, or possible serotonergic interaction
- CNS depressants (alcohol, benzodiazepines, opioids, GHB) will have additive sedative/respiratory depressant effects; the multidrug case (Magny 2024 [Ref 1]) involved GHB co-ingestion with ICU admission
- Stimulant co-use: the cardiovascular profile (hypertension, tachycardia) may be exacerbated

**Emergency response:**
- Supportive care is the primary management (Tang et al. 2018 [Ref 11])
- Benzodiazepines for agitation/convulsion consistent with ketamine class management
- Alert clinicians that standard ketamine immunoassays will be negative; do not rule out O-PCE based on negative ketamine screen

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## Tolerance & Dependence

**Published data:** No substance-specific tolerance, dependence, or addiction studies exist for O-PCE. The following is inferred from class-level evidence and community data.

**Class-level cross-tolerance:**
Lu et al. (1992) [Ref — see below; not currently in registry] confirmed cross-tolerance between PCP-like NMDA channel blockers (ketamine, dizocilpine, dextrorphan) in pigeons, indicating shared tolerance mechanism. O-PCE would be expected to share cross-tolerance with other dissociative NMDA antagonists (ketamine, PCP, MXE, DXM).

**Community/harm reduction estimates (KnowDrugs [Ref 21]):**
- Tolerance half-life: 3–7 days (seed data value: 5 days — within this range; consistent)
- Zero tolerance: 1–2 weeks (seed data: 1.5 weeks — consistent)
- These estimates are consistent between KnowDrugs and PsychonautWiki/Psychedex

**Dependence:**
Seed data characterizes dependence as "moderate physical, moderate psychological, moderately addictive with high potential for abuse." This is consistent with the dissociative class (ketamine is known to produce psychological dependence and compulsive redosing). No published case report of O-PCE-specific dependence or withdrawal has been identified. The compound appears in chemsex contexts with multi-drug chronic use patterns (Magny 2024 [Ref 1]).

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## Interactions

**Published interaction data:**
1. **Venlafaxine (SNRI):** Co-ingestion resulted in the published fatality (Theofel 2019 [Ref 12]). The mechanism is not established. Possible contributions include: (a) additive CNS depression; (b) serotonergic interaction (ketamine-class compounds have some serotonin transporter activity per Roth et al. 2013 [Ref 6] for related analogs); (c) cardiovascular synergy. **FLAG FOR REVIEW:** This interaction is safety-critical and not mechanistically resolved.

2. **GHB:** Multi-drug exposure in chemsex context (O-PCE + GHB + 3-MMC + MXE) resulted in loss of consciousness and ICU admission (Magny 2024 [Ref 1]). Combined CNS depression mechanism.

3. **Methoxetamine (MXE):** Combined in above case; additive dissociative effects expected.

**Class-level CYP interactions (ketamine inference; applicable to O-PCE via CYP2B6/CYP3A4):**
- **CYP2B6 inhibitors** (e.g., ticlopidine, bupropion): increase O-PCE plasma exposure (Andrade 2017 [Ref 24]; Peltoniemi et al. 2011)
- **CYP3A4 inhibitors** (e.g., grapefruit juice, azole antifungals): may increase exposure to O-PCE, though effect is less consistent for intranasal/insufflated routes
- **CYP3A4/2B6 inducers** (e.g., rifampicin, carbamazepine): may reduce O-PCE plasma levels
- **FLAG FOR REVIEW:** All CYP interactions are inferred from ketamine and MXE data; no O-PCE-specific interaction studies exist.

**MAOIs:** Contraindicated with dissociative NMDA antagonists as a class (risk of serotonin syndrome and hypertensive crisis, though evidence for this specific combination is primarily from case reports for other serotonergic agents). Not verified substance-specifically for O-PCE.

**Opioids, alcohol, benzodiazepines, GHB:** Combined CNS/respiratory depression risk — class-based inference; evidenced by fatality data for related ACH NPS (Gicquel 2021 [Ref 15]).

---

## Legal Status

| Jurisdiction | Status | Details | Source |
|---|---|---|---|
| United Kingdom | **Class B controlled** | Covered under the generic arylcyclohexylamine clause in the Misuse of Drugs Act 1971 (S.I. 2013/239), effective February 26, 2013. Also prohibited under the Psychoactive Substances Act 2016 (supply offense). | [Ref 21] |
| Germany | **Controlled** | Regulated under the NpSG (Neue-psychoaktive-Stoffe-Gesetz), effective July 18, 2019 | [Ref 21] |
| Sweden | **Banned** | Explicitly scheduled | [Ref 21] |
| China | **Controlled** | Classified under narcotics regulations | [Ref 21] |
| Hong Kong | **Banned** | Explicitly controlled; enforcement documented in drug seizure data (Cheng & Dao 2020 [Ref 13]) | [Ref 13, 21] |
| United States | **Not explicitly scheduled** | Not currently listed on the DEA Controlled Substances Schedule. The Federal Analogue Act (21 U.S.C. § 813) may apply if the substance is shown to be intended for human consumption and substantially similar to a Schedule I/II substance. O-PCE would be a plausible analog of ketamine (Schedule III) or PCP (Schedule II). Legal risk is prosecution-context dependent. | [Ref 21] |
| Canada | **Not explicitly scheduled** | Monitored as NPS under the CDSA framework but not formally listed in controlled substance schedules as of research date | [Ref 21] |
| Australia | **Status unclear** | No specific entry found in the Therapeutic Goods (Poisons Standard) instruments through 2025. May be captured under broad analog provisions in state/territory law. **FLAG FOR REVIEW.** | No primary source found |
| International | **Not scheduled** | Not currently subject to UN Convention on Psychotropic Substances | [Ref 21] |

**Note:** The UK MDA generic arylcyclohexylamine clause (S.I. 2013/239, effective Feb 26, 2013) may be the earliest formal scheduling of O-PCE in any jurisdiction, predating its documented emergence on illicit markets. This is relevant context for the history section.

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## Clinical Trials

No clinical trials for O-PCE were identified in a search of ClinicalTrials.gov. This is expected for an unscheduled/scheduled-research-chemical with no approved medical application.

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## Community Feedback Analysis

No community feedback was submitted in Part A2 of the brief for this substance. Standard investigation procedures apply.

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## Gaps & Flags

### Safety-Critical Flags (require human review before publication)

1. **⚠️ No published Ki/IC50 binding data for O-PCE at any receptor.** The seed data lists pharmacological class as "Mu-opioid receptor agonist, NMDA receptor antagonist, Sigma receptor agonist." The NMDA antagonism is well-supported by class-level evidence. The sigma agonism is plausible by class. The mu-opioid receptor agonism is uncertain and may represent an overclaim — it is not supported by substance-specific data or by data from the closest structural analogs. Recommend flagging or qualifying this claim.

2. **⚠️ Fatal interaction with venlafaxine (SNRI)** documented in Theofel (2019). Mechanism is uncharacterized. This interaction should be prominently noted in the harm reduction and interactions sections.

3. **⚠️ Convulsions documented in 16% of acute poisoning cases** (Tang et al. 2018). This is unusually high for a ketamine-class compound. The generation agent should flag this explicitly.

4. **⚠️ Standard ketamine immunoassay does not detect O-PCE.** Clinicians may receive false-negative results on standard drug screens. This diagnostic blind spot has direct emergency medicine implications.

5. **⚠️ LD50 completely unknown.** The exact toxic dose for humans is unpublished. The fatal blood concentration (~1.2 µg/mL in polydrug context) provides a rough upper reference only.

### Data Gaps

6. **No controlled human pharmacology or pharmacokinetic studies.** All human data is from case reports and retrospective forensic case series. Duration, dose-response, bioavailability data is community-derived.

7. **CYP enzyme identification for O-PCE is inferred** from structurally similar compounds (MXE, ketamine). No direct enzyme kinetic studies for O-PCE have been published.

8. **Physical properties** (melting point, aqueous solubility, pKa) not found in peer-reviewed literature. CFSRE describes "blood-colored" appearance; powdery/crystalline solid in seizures. No standardized physical chemistry data available.

9. **Synthesis history uncertain.** The "1962 Parke-Davis" claim likely conflates O-PCE with PCE (eticyclidine), a structurally distinct compound. The actual first synthesis date for O-PCE (the 2-oxo variant) has not been documented in a primary source.

10. **Australia legal status unverified.** Could not confirm specific scheduling through available web searches. Should be verified against the TGA Poisons Standard directly.

11. **US Federal Analogue Act applicability** is context-dependent and should be reviewed by legal counsel. Not a clear-cut case.

12. **"First detected in France 2016"** claim in Grokipedia [Ref 21] is not supported by a primary peer-reviewed citation. The earliest peer-reviewed documentation is Chong et al. (2017) [Ref 14] from Hong Kong. The France 2016 claim may derive from EMCDDA early warning reports not accessible via PubMed; **FLAG FOR REVIEW.**

13. **Multiple fatalities suggested but not documented.** Larabi et al. (2021) [Ref 2] references "acute intoxications with severe outcomes including death" (plural). Only one fatality (Theofel 2019) has been published in the peer-reviewed literature. The additional cases likely exist in forensic databases or EMCDDA early warning reports. **FLAG FOR REVIEW.**

### Structural Analogy Reliance

The following claims in any downstream article MUST be labeled as class-level inference, not substance-specific:
- CYP2B6/CYP3A4 as primary metabolic enzymes
- Mu-opioid receptor activity
- Sigma receptor affinity
- Drug interaction predictions based on CYP modulation
- Tolerance mechanism (shared with other NMDA antagonists)

### Dose/Duration Data Assessment

The existing database values are consistent with community consensus sources (PsychonautWiki, KnowDrugs). No published data contradicts these values. The only adjustable note is the tolerance half-life — the seed data says 5 days; community sources say 3–7 days. 5 days is within the published community range and appears a reasonable central estimate.

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*Research completed: 2026-04-26. All citations numbered per 01-citations-registry.json.*