3-HO-PCE

# Research Output: 3-HO-PCE (3-Hydroxyeticyclidine)

**Research date:** 2026-05-10  
**Provenance ID:** 6e531558-e471-4159-b83e-bd9e8ac52161  
**Substance readiness:** Sparse/emerging (< 0.3) — most pharmacological data inferred from structural analogs

---

## Chemical Identity

### PubChem-Verified Data (CID 137332171)

| Property | Value | Source |
|---|---|---|
| PubChem CID | 137332171 | PubChem API [api_verified] |
| Systematic (IUPAC) name | 3-[1-(ethylamino)cyclohexyl]phenol | PubChem API |
| Molecular formula | C₁₄H₂₁NO | PubChem API |
| Molecular weight | 219.32 g/mol | PubChem API |
| InChIKey (PubChem) | MIKNPNLBFHVMKK-UHFFFAOYSA-N | PubChem API |

**SMILES:** The PubChem API did not return SMILES for CID 137332171. From the IUPAC name, the canonical SMILES can be derived as: `CCNC1(c2cccc(O)c2)CCCCC1`. This should be independently verified.

**CAS number:** UNRESOLVED — see Gaps & Flags. Vendor sources cite 2243815-20-3 and 79295-51-5; the NMS Labs CFSRE monograph (2019) listed the CAS as unavailable at time of publication.

### Seed Data Comparison

The brief's seed data lists the systematic name as `3-[1-(ethylamino)cyclohexyl]phenol`, which is **confirmed** by PubChem. Molecular formula (C₁₄H₂₁NO) and molecular weight (219.32) are confirmed. SMILES, InChIKey, and PubChem CID were empty in the brief — all have now been identified. 

**⚠️ InChIKey discrepancy:** The PubChem API returns InChIKey `MIKNPNLBFHVMKK-UHFFFAOYSA-N`, but web-retrieved sources (vendor sites) cite `LMRZSZMXPXJCQF-UHFFFAOYSA-N`. The PubChem API result should be treated as authoritative; the vendor-site InChIKey may correspond to a different tautomer, salt form, or data error. **Flag for editorial verification.**

### Structure and Classification

3-HO-PCE consists of a cyclohexane ring bearing two substituents at C1: an ethylamine group (N-H, secondary amine) and a phenyl ring hydroxylated at the 3-position. It is the N-ethyl analog of 3-hydroxyphencyclidine (3-HO-PCP), and the 3-hydroxy analog of eticyclidine (PCE). Within the arylcyclohexylamine class, this substitution pattern is pharmacologically significant: the 3-hydroxyl on the phenyl ring specifically confers mu-opioid receptor affinity not present in the parent compound PCE (Itzhak et al. 1981 [Ref 10]).

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## Pharmacology

### Mechanism of Action Overview

3-HO-PCE has no published receptor binding data (Ki or EC50). Its pharmacological profile is inferred from structural analogs and class membership. The compound is expected to act via three principal mechanisms:

1. **NMDA receptor antagonism** — the class-defining mechanism of all arylcyclohexylamines
2. **Mu-opioid receptor agonism** — specifically conferred by the 3-hydroxy phenyl substitution, as demonstrated for 3-HO-PCP
3. **Sigma-1 receptor agonism** — documented across PCP-type compounds

### NMDA Receptor Antagonism

All arylcyclohexylamines act as uncompetitive antagonists at the PCP/dizocilpine site within the NMDA receptor ion channel (Martin & Lodge 1988 [Ref 9]). The compound 3-MeO-PCE — the N-ethyl analog differing only in having a methoxy rather than hydroxy group at the 3-position — was confirmed as a high-affinity NMDA receptor ligand via NIMH Psychoactive Drug Screening Program (PDSP) binding assays (Roth et al. 2013 [Ref 2]).

For 3-HO-PCP (the N-piperidyl 3-hydroxy compound and closest pharmacological reference): NMDA Ki = 30 nM, representing ~8-fold higher affinity than PCP itself (NMDA Ki ~250 nM) (Suzuki et al. 1995 [Ref 11]). The autoradiographic distribution of [³H]3-OH-PCP binding in rat brain was consistent with NMDA/PCP ion-channel complex binding rather than sigma site binding (Suzuki et al. 1995 [Ref 11]).

**No published NMDA Ki data exists for 3-HO-PCE specifically.** By structural analogy to 3-HO-PCP, NMDA antagonism is expected at low nanomolar concentrations.

### Mu-Opioid Receptor Agonism

The 3-hydroxy substitution on the phenyl ring of arylcyclohexylamines is uniquely associated with opioid receptor activity. This was first established by Itzhak et al. (1981 [Ref 10]):

- 3-HO-PCP (PCP-3-OH) produces dose-dependent, **naloxone-reversible** inhibition of guinea pig ileum electrical stimulation
- Unlike PCP, 3-HO-PCP shows opioid antagonist activity in the mouse vas deferens bioassay
- 3-HO-PCP has high affinity for [³H]morphine binding sites; PCP does not
- The mediation of both alpha- and mu-opioid receptors in these effects was discussed

For 3-HO-PCP, published Ki values include: mu-opioid receptor (MOR) Ki = 39–60 nM, kappa-opioid receptor (KOR) Ki = 140 nM, sigma-1 receptor Ki = 42 nM / IC50 = 19 nM, delta-opioid receptor Ki = 2,300 nM (low affinity). These are from web-retrieved sources citing published papers; the primary binding studies are Itzhak et al. (1981 [Ref 10]) and subsequent assays.

The opioid component of arylcyclohexylamine pharmacology is clinically significant. Williams et al. (2018 [Ref 16]) demonstrated via randomized crossover study that naltrexone (opioid receptor antagonist) pretreatment blocked ketamine's acute antidepressant effects (though not its dissociative effects), establishing that opioid system activation is mechanistically required for at least some clinical effects of this compound class.

**No published MOR Ki data exists for 3-HO-PCE specifically.** By structural analogy to 3-HO-PCP, mu-opioid agonist activity at low nanomolar concentrations is expected.

### Sigma Receptor Activity

PCP-type compounds, including the 3-methoxy analogs, display appreciable affinity for sigma receptors (Roth et al. 2013 [Ref 2]). The sigma-1 receptor is a ligand-regulated chaperone modulating ion channel activity and neurotransmitter systems (Maurice & Su 2009). Given the 3-HO-PCP Ki = 42 nM at sigma-1, sigma receptor involvement is expected for 3-HO-PCE by structural analogy.

**No published sigma Ki data exists for 3-HO-PCE specifically.**

### Summary: Receptor Profile by Evidence Level

| Receptor | Evidence | Source |
|---|---|---|
| NMDA antagonist | Class inference + close analog (3-MeO-PCE confirmed) | Roth et al. 2013 [Ref 2]; Martin & Lodge 1988 [Ref 9] |
| Mu-opioid agonist | 3-hydroxy analog inference (3-HO-PCP naloxone-reversible) | Itzhak et al. 1981 [Ref 10] |
| Sigma-1 agonist | Class inference (3-HO-PCP Ki = 42 nM) | Roth et al. 2013 [Ref 2] |
| Kappa-opioid | 3-HO-PCP Ki = 140 nM; class-level inference | Web-retrieved data |
| Delta-opioid | 3-HO-PCP Ki = 2,300 nM (low affinity) | Web-retrieved data |

**⚠️ Flag:** All receptor binding data for 3-HO-PCE is inferred by structural analogy. No substance-specific binding studies have been published. This is a safety-critical gap.

### Pharmacokinetics

**No published human pharmacokinetic studies exist for 3-HO-PCE.** The Larabi et al. (2023 [Ref 1]) study identified metabolites but explicitly stated no pharmacokinetic conclusions could be drawn.

**Metabolism (Larabi et al. 2023 [Ref 1]):**
- 15 putative metabolites identified (5 with 2–4 additional isomers, giving 23 detected features)
- **Phase I (12 metabolites):** N-dealkylation (→3-HO-PCA/M4 and M10), deamination (M2a/M2b, M5), and hydroxylation (M3, M6, M9, M11, M12)
- **Phase II (3 metabolites):** O-glucuronidation on phenyl ring or cyclohexane group
- Metabolism closely resembles O-PCE (deschloroketamine), another eticyclidine-family compound
- Overlapping metabolites at m/z 172.08881, 174.10447, and 191.09938 with O-PCE suggest analogous enzymatic pathways

**Detection biomarkers (Larabi et al. 2023 [Ref 1]):**
- Urine (untargeted, eticyclidine family): M2a/M2b at m/z 174.10447
- Hair (untargeted, eticyclidine family): 3-HO-PCA (hydroxy-PCA) at m/z 191.09938
- Urine (targeted, 3-HO-PCE specific): M10 at m/z 241.13141
- Hair (targeted, long-term monitoring): M5 at m/z 192.11503

**CYP enzymes:** Not identified in the Larabi 2023 study. By analogy to ketamine (the most studied arylcyclohexylamine): CYP3A4 and CYP2B6 are the primary enzymes involved in N-dealkylation (Peltoniemi et al. 2016 [Ref 12]; Mössner et al. 2011). CYP2B6 inhibitors (e.g., ticlopidine) and CYP3A inhibitors (e.g., itraconazole) significantly affect ketamine exposure and should be considered interactions (Peltoniemi et al. 2011).

**Comparative data from 3-HO-PCP (direct pharmacological analog, Davidsen et al. 2020 [Ref 21]):**
- Plasma protein binding: unbound fraction 0.72 ± 0.09 (relatively high free fraction)
- Four metabolites in hepatocytes: piperidine-hydroxyl, N-dealkyl-COOH, O-glucuronide, O-sulfate conjugates
- Blood concentrations: 0.013 mg/kg (living user) vs. 0.095 mg/kg (deceased, postmortem)
- Brain concentration: 1.5-fold higher than postmortem peripheral blood (CNS penetration documented)

---

## History

### Parent Compound: Eticyclidine (PCE)

Eticyclidine (PCE, CI-400, N-ethyl-1-phenylcyclohexylamine) was developed by Parke-Davis in the 1970s and evaluated for anesthetic potential, but research was discontinued following the clinical development of ketamine, which had more favorable properties. PCE is slightly more potent than phencyclidine (PCP) but has an unpleasant taste and greater tendency to cause nausea, which reduced its appeal (web-retrieved, Wikipedia/Eticyclidine [Ref 15]).

PCE was placed in Schedule I of the US Controlled Substances Act in the 1970s and is listed in Schedule I of the United Nations 1971 Convention on Psychotropic Substances.

### 3-HO-PCP: Structural Precursor

3-Hydroxyphencyclidine (3-HO-PCP) was synthesized in 1978 to investigate the structure-activity relationships of phencyclidine derivatives (Ameline et al. 2023 [Ref 20]). This work established that a hydroxyl group at the 3-position of the phenyl ring confers opioid receptor activity not present in the parent compound.

### 3-HO-PCE: Research Chemical Market Emergence

3-HO-PCE has no precedent in the scientific literature prior to its appearance on the research chemical market. Based on available documentation, 3-HO-PCE emerged on research chemical markets during the 2010s (web-retrieved, history sources). No academic, patent, or regulatory literature identified the compound prior to market emergence.

The first published scientific study on 3-HO-PCE is Larabi et al. (2023 [Ref 1]) in the journal *Metabolites*, which characterized its metabolism and noted that "little is known about its pharmacological properties, metabolism, and toxicity compared to other designer ketamine analogs" at the time of publication.

The compound was designed as an analog of 3-HO-PCP, preserving the 3-hydroxy phenyl group while substituting the N-piperidyl moiety of PCP with the N-ethyl group of PCE (eticyclidine).

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## Subjective Effects

No controlled human studies of 3-HO-PCE's subjective effects exist. The Larabi et al. (2023 [Ref 1]) study characterizes the compound as producing "dissociative, hallucinogenic, and euphoric effects when consumed," based on reports from drug users whose biological samples were analyzed.

The seed effect profile (40 effects, all lacking intensity/frequency values) is derived from community consensus. PsychonautWiki (web-retrieved [Ref 14]) notes the compound should not be confused with 3-HO-PCP, and includes a warning that "redosing may result in dangerous cumulative effects."

**By structural analogy to the arylcyclohexylamine class:**
- Dissociation (cognitive and sensory disconnection from surroundings)
- Analgesia (from opioid component)
- Sedation at moderate-to-high doses
- Perceptual distortions (visual, auditory)
- Amnesia at higher doses
- Euphoria (potentially enhanced by opioid component relative to ketamine)

**Duration (community consensus only [Ref 14]):** 4–6 hours total (oral route). No breakdown of onset/peak/offset from published sources.

---

## Safety & Toxicity

### Toxic Dose and LD50

**No LD50 data exists for 3-HO-PCE.** The toxic dose in humans is unknown (brief seed data confirmed). This is a safety-critical gap.

### Clinical Toxicity: 3-HO-PCP Case Reports (by Analogy)

**Non-fatal toxicity (Dunlop et al. 2020 [Ref 19]):** An analytically confirmed case of 3-HO-PCP acute toxicity in a 56-year-old male who presented to the emergency department with:
- Hyperthermia (39.9°C)
- Sinus tachycardia (150 beats per minute)
- Reduced consciousness
- Ocular clonus
- Vertical nystagmus
- Co-ingestion of cathinone N-ethylhexedrone contributed sympathomimetic and serotonergic features

Treatment: cooled intravenous fluids and benzodiazepines. Patient discharged after 25 hours with full recovery.

**Fatal intoxication (Ameline et al. 2023 [Ref 20]):** A 38-year-old male with known drug addiction was found dead at home with 3-OH-PCP and 5-MeO-DMT powders. Peripheral blood 3-OH-PCP concentration: 524 ng/mL — the highest reported in the published literature at the time. Polydrug co-ingestion included nordiazepam, methylphenidate, amisulpride, methadone, and benzoylecgonine, all at concentrations consistent with recreational abuse. Cause of death: polydrug toxicity with 3-OH-PCP as primary dissociative agent.

**Reference blood concentrations from Davidsen et al. 2020 [Ref 21]:** 3-HO-PCP blood concentrations: 0.013 mg/kg in a living user and 0.095 mg/kg in a deceased individual (postmortem). Brain concentration was 1.5-fold higher than postmortem blood.

### Fatal Toxicity: 3-MeO-PCE Case Report (N-ethyl Analog)

**Gicquel et al. (2021 [Ref 4]):** A 42-year-old male polydrug user was found dead with powders of 2F-DCK, 3-MeO-PCE, and 5-MeO-DMT. Blood concentration of 3-MeO-PCE: 90 µg/L (peripheral), 66 µg/L (vitreous). Death attributed primarily to **respiratory depression** from 2F-DCK in the context of polydrug use. 3-MeO-PCE contributed to CNS and respiratory depression. Co-ingested drugs included cannabis, cocaine, and amphetamine; hair analysis showed months of NPS polydrug use.

This case establishes that N-ethyl arylcyclohexylamines (the same structural class as 3-HO-PCE) can contribute to fatal respiratory depression, especially in polydrug contexts.

### Class-Level Adverse Event Pattern

From 2-oxo-PCE (O-PCE/deschloroketamine) cluster cases (Tang et al. 2018 [Ref 8]):
- Impaired consciousness: 84%
- Confusion: 60%
- Abnormal behaviour: 44%
- Hypertension: 80%
- Tachycardia: 40%
- Convulsion: 16%

Rhabdomyolysis and acute kidney injury have been documented with arylcyclohexylamine derivatives (Deutsch et al. 2026 [Ref 7]).

### NMDA Antagonist-Induced Neurotoxicity

NMDA receptor antagonists including phencyclidine and ketamine produce a schizophrenia-like psychosis in humans and neurotoxicity in adult rat brain (Farber et al. 1996). This is a class-level safety concern for 3-HO-PCE. Antipsychotics (particularly clozapine-like agents) can prevent NMDA antagonist neurotoxicity.

### Critical Risk Factor: Dual Opioid + NMDA Mechanism

The combination of opioid receptor agonism and NMDA receptor antagonism in a single compound represents a qualitatively distinct and underappreciated risk profile. The opioid component (naloxone-reversible, as demonstrated for 3-HO-PCP) raises the concern of **respiratory depression** at doses where the NMDA component alone might not cause significant respiratory compromise. This risk is compounded by the absence of standard opioid immunoassay detection for novel arylcyclohexylamines.

**⚠️ Safety-critical flag:** The toxic dose range for 3-HO-PCE is completely unknown. All dose/safety data for this compound is either community-reported or inferred from structural analogs. The opioid component makes this compound potentially more dangerous than ketamine or PCE alone.

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## Harm Reduction

### Testing and Identification

Standard immunoassay opioid panels do not detect arylcyclohexylamine opioids (Gicquel et al. 2021 [Ref 4]). Standard PCP immunoassays may not cross-react with 3-HO-PCE. High-resolution mass spectrometry (HRMS) is required for identification and quantification. The Larabi 2023 study (PMID 36984871) provides reference metabolite targets.

Hair analysis methods validated for phencyclidine-type substances (Li et al. 2023 [Ref 24]) can detect related arylcyclohexylamines with LOD 0.25–2 pg/mg.

### Harm Reduction Principles

The following are class-level harm reduction inferences (no 3-HO-PCE-specific guidance is published):
- **Avoid polydrug use**, particularly with other CNS depressants (opioids, benzodiazepines, alcohol, 2F-DCK and other ketamine analogs) — all fatal/severe cases involved polydrug contexts
- **Do not redose** — cumulative effects noted by community sources (PsychonautWiki [Ref 14])
- **Monitor respiratory rate** — opioid component adds respiratory depression risk not present with ketamine
- **Have naloxone available** — opioid agonist component is naloxone-reversible (Itzhak et al. 1981 [Ref 10])
- **Hyperthermia risk** — documented in 3-HO-PCP case; avoid hot environments and maintain hydration
- **Do not use alone** — no recovery possible if respiratory compromise occurs without witness

### Emergency Management

Based on class-level data and the 3-HO-PCP case (Dunlop et al. 2020 [Ref 19]):
- Supportive care is first-line
- Benzodiazepines for agitation/seizures
- Cooling measures for hyperthermia
- **Consider naloxone** given the documented mu-opioid agonist activity of the 3-hydroxy class (naloxone reversed effects in Itzhak 1981 [Ref 10])
- Standard NMDA antagonist immunoassays will not confirm exposure; HRMS required

---

## Tolerance & Dependence

**No published tolerance or dependence data exists for 3-HO-PCE specifically.**

The brief seed data (community consensus) characterizes:
- Physical dependence: moderate
- Psychological dependence: moderate
- Formation: "moderately addictive with a moderate potential for adverse side effects such as psychosis"
- Tolerance buildup: with prolonged and repeated use
- Tolerance half-life: approximately 5.5 days
- Full tolerance reset: approximately 1.5 weeks
- Cross-tolerance: with other dissociatives

These values are consistent with the class-level pattern for NMDA antagonists. The additional mu-opioid component of 3-HO-PCE (unlike ketamine) may confer higher physical dependence liability than pure NMDA antagonists, as mu-opioid receptor agonism is associated with physical dependence and withdrawal.

**⚠️ Flag:** Tolerance/dependence parameters in the database (5.5-day half-life, 1.5-week full reset) are not sourced from published pharmacokinetic data and represent community-derived estimates. The opioid component of 3-HO-PCE could make these figures inaccurate and potentially dangerous if users under-estimate dependence risk.

Dextromethorphan, which shares NMDA antagonism and sigma-1 agonism (without opioid activity) with this compound class, has been documented to produce dependence, psychosis, and withdrawal (Miller 2005).

---

## Interactions

**No published drug interaction data exists for 3-HO-PCE specifically.**

The following are class-level inferences and represent safety-critical information:

### High-Risk Interactions (opioid component)

- **CNS depressants (opioids, benzodiazepines, alcohol, barbiturates):** Additive/synergistic respiratory depression. Documented in all fatal cases involving 3-HO-PCP and 3-MeO-PCE. **This is the highest-risk interaction category** given the polydrug deaths documented.
- **Other opioid agonists (fentanyl, heroin, methadone):** Risk of fatal respiratory depression from additive opioid receptor engagement.
- **Other NMDA antagonists (ketamine, 2F-DCK, MXE, nitrous oxide):** Additive CNS depression and dissociation.
- **Tramadol:** Seizure risk (serotonin syndrome + lowered seizure threshold).

### CYP Enzyme Interactions (by ketamine class analogy)

By analogy to ketamine (Peltoniemi et al. 2016 [Ref 12]):
- **CYP2B6 inhibitors (ticlopidine):** May significantly increase exposure (2.4-fold increase documented with oral S-ketamine).
- **CYP3A4 inhibitors (itraconazole, ketoconazole):** May increase exposure.
- **CYP inducers (rifampicin):** May decrease exposure and duration.

**⚠️ Flag:** No 3-HO-PCE-specific interaction studies have been published. All interaction risk assessments are class-level inferences from ketamine and 3-HO-PCP data.

---

## Legal Status

### United States

**Eticyclidine (PCE)** — the direct parent compound — is a DEA Schedule I controlled substance. It is listed in 21 CFR § 1308.11 as N-Ethyl-1-phenylcyclohexylamine (PCE), under hallucinogenic substances.

**3-HO-PCE is not explicitly listed** in the DEA Controlled Substances Act schedules. However, under the **Federal Analogue Act (21 U.S.C. § 813)**, substances substantially similar in structure or pharmacology to Schedule I or II substances are treated as Schedule I for purposes of human consumption. Given that 3-HO-PCE is structurally and pharmacologically similar to both PCE (Schedule I) and PCP (Schedule I), prosecution as a controlled substance analogue is plausible.

The related compound 3-methoxyphencyclidine (3-MeO-PCP) was placed in Schedule I by DEA final order effective March 2026 (Federal Register, 2026-05618), demonstrating active scheduling of hydroxyphenyl/methoxyphenyl arylcyclohexylamine analogs.

### United Kingdom

The **Psychoactive Substances Act 2016** (PSA 2016) creates a blanket prohibition on the supply, production, and import/export of psychoactive substances in the UK, with exceptions only for specified exempt substances (alcohol, tobacco, caffeine, medicinal products). 3-HO-PCE, as a psychoactive substance not on any exempt list, is **prohibited under the PSA 2016.**

There is no indication that 3-HO-PCE is specifically listed under the Misuse of Drugs Act 1971, meaning it falls under the broader PSA 2016 framework rather than the MDA.

### Canada

**Phencyclidine (PCP)** is Schedule I under Canada's Controlled Drugs and Substances Act (CDSA). PCE (eticyclidine) is not identified in current CDSA schedules accessed. The status of 3-HO-PCE under the CDSA is not definitively established from available sources. Canada's CDSA does not contain a structural analogue provision equivalent to the US Federal Analogue Act, but Health Canada may provide status determinations on request.

### Australia

**Phencyclidine** is listed as a Schedule 9 prohibited substance in Australia's Standard for the Uniform Scheduling of Medicines and Poisons (SUSMP/Poisons Standard). 3-HO-PCE is not identified as specifically listed in the Poisons Standard from available search results. Status under state/territory drug laws varies.

### European Union

No EU-wide specific scheduling of 3-HO-PCE was identified. Individual member states may schedule under national NPS blanket-ban legislation (e.g., Germany's Neue-psychoaktive-Stoffe-Gesetz, NpSG). The EMCDDA/EUDA early warning system did not return specific alerts for 3-HO-PCE.

### International

**Eticyclidine (PCE)** is listed in Schedule I of the United Nations 1971 Convention on Psychotropic Substances. This creates scheduling obligations for all signatory nations for PCE; 3-HO-PCE as a derivative may be covered depending on national implementation of the Convention.

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## Clinical Trials

No registered clinical trials involving 3-HO-PCE were identified in a search of ClinicalTrials.gov. This was expected given the compound's status as an unscheduled research chemical with no established medical application and no pre-clinical safety data.

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## Community Feedback Analysis

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

---

## Gaps & Flags

### Safety-Critical Gaps

1. **⚠️ No published receptor binding (Ki/EC50) data for 3-HO-PCE.** The entire pharmacological profile (opioid agonism, NMDA antagonism, sigma activity) rests on structural analogy to 3-HO-PCP and class membership. Generation agent must label all receptor affinity data as inferred by analogy, not measured.

2. **⚠️ Toxic dose completely unknown.** No LD50, no minimum toxic dose, no human overdose concentration data specific to 3-HO-PCE. The database entry "toxic dosage unknown" is confirmed correct. Do not propose a toxic dose range.

3. **⚠️ Opioid component: naloxone relevance.** The mu-opioid agonist activity (inferred from 3-HO-PCP) has direct emergency management implications — naloxone may be indicated in overdose. This is not documented in any harm reduction guidance specific to 3-HO-PCE and must be framed carefully as inference.

4. **⚠️ No human pharmacokinetic data.** Half-life, bioavailability, Tmax, volume of distribution — all unknown for 3-HO-PCE. Database tolerance values (5.5-day half-life) are community-derived estimates without published pharmacokinetic basis.

### Chemical Identity Gaps

5. **InChIKey discrepancy:** PubChem API returns `MIKNPNLBFHVMKK-UHFFFAOYSA-N`; web vendor sources cite `LMRZSZMXPXJCQF-UHFFFAOYSA-N`. Editorial resolution needed before populating the InChIKey field. The PubChem API result is preferred.

6. **CAS number unresolved.** Vendor sources cite 2243815-20-3 and 79295-51-5; NMS Labs CFSRE monograph (2019) listed CAS as unavailable. These conflicting values should not be published without verification.

7. **SMILES string absent from PubChem API response.** Derived SMILES from IUPAC name: `CCNC1(c2cccc(O)c2)CCCCC1` — requires database verification.

### Data Reliance on Structural Analogy

8. **All pharmacology inferred from analogs.** The two primary reference points are 3-HO-PCP (N-piperidyl version, with published opioid Ki data) and 3-MeO-PCE (N-ethyl version with methoxy rather than hydroxy, with published NMDA data). Neither is identical to 3-HO-PCE.

9. **Dose/duration data from community consensus only.** The oral dose ranges (threshold 5 mg through heavy 25+ mg) and 4–6 hour duration are from PsychonautWiki community aggregation [Ref 14]. No controlled dosing study supports these figures. However, these match the seed data in the brief and no community feedback has contested them — propose with appropriate confidence framing.

10. **Tolerance/dependence parameters community-derived.** The 5.5-day half-life and 1.5-week full reset values in the database lack published pharmacokinetic support and may be inaccurate, particularly given the compound's opioid component.

### Legal Status Gaps

11. **Legal status in Canada and Australia is uncertain** for 3-HO-PCE specifically. The parent compounds (PCP, PCE) are scheduled, but 3-HO-PCE's coverage depends on jurisdiction-specific analog/derivative provisions.

### Other Gaps

12. **No published synthesis route for 3-HO-PCE.** Only market emergence data available.

13. **Stereochemistry:** The brief notes no stereochemistry data. The compound has a chiral center at C1 of the cyclohexane ring (same as PCP/PCE). Whether racemic mixtures or specific enantiomers are sold on the research chemical market, and whether enantiomers differ in pharmacological activity, is undocumented for 3-HO-PCE.

14. **Melting point, solubility, and physical properties:** Not found in published sources. The NMS Labs CFSRE monograph (December 2019) may contain analytical characterization data, but the PDF was not accessible in text form.