generation run 2026-05-09
70 min completedmodel pipeline-v5plan not recordedrun/3829e61f…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
- sparse_evidence
- safety_data_unverified
- structural_inference
Reproduce
- inputs
- 23 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
27 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed | phencyclidine arylcyclohexylamine sigma receptor dopamine reuptake inhibitor | 1 | 1 | Provides class-level mechanistic context relevant to PCE pharmacology. |
| 2 | PubChem | eticyclidine | 1 | 1 | Core chemical identity data confirmed from PubChem. |
| 3 | PubMed · absence | eticyclidine PCE N-ethyl-1-phenylcyclohexylamine pharmacology | 0 | 0 | No results returned. |
| 4 | UNODC | — | 1 | 1 | Authoritative international scheduling confirmation. |
| 5 | UK Legislation | — | 1 | 1 | Confirms UK legal status. |
| 6 | PubMed | antibodies against arylcyclohexylamines phencyclidine receptor binding specificity | 3 | 1 | Directly references PCE/N-ethyl-1-phenylcyclohexylamine in published pharmacological context. |
| 7 | Wikidoc | — | 1 | 2 | Confirmed key chemical identifiers and historical reference. |
| 8 | OpenAlex | phencyclidine PCP analogs structure activity relationship NMDA binding arylcyclohexylamine | 30 | 4 | Provide class-level pharmacological context (NMDA binding, dissociative mechanism, arylcyclohexylamine SAR) applicable to PCE. |
| 9 | WebSearch | PCE eticyclidine pharmacology history DEA scheduling | 10 | 3 | Web sources confirm historical context not available in PubMed. |
| 10 | ClinicalTrials.gov · absence | eticyclidine PCE dissociative | 0 | 0 | No registered trials. |
| 11 | PubMed | Fetch PMID 8095205 | 1 | 1 | Characterizes PCE as both a drug and a metabolite; provides kinetic constants |
| 12 | Crossref/DOI | Verify DOI 10.1021/jm00303a030 for Kalir et al. 1969 | 1 | 1 | Foundational synthesis paper for arylcyclohexylamines including PCE |
| 13 | PubMed | Fetch PMID 1837152 | 1 | 1 | Provides PK/PD data specifically for PCE including in vivo behavioral potency |
| 14 | PubMed | Fetch PMID 528459 | 1 | 1 | Analytical identification reference for PCE and related compounds |
| 15 | PubMed | Fetch PMID 28830759 | 1 | 1 | Directly characterizes PCE discriminative stimulus and in vivo behavioral effects — key pharmacology paper |
| 16 | PubMed | Fetch PMID 660485 | 1 | 1 | First published identification of PCE as a street drug — key historical paper |
| 17 | PubMed | Fetch PMID 4071555 | 1 | 1 | Relevant to smoked ROA pharmacokinetics; shows CYP induction affects PCE metabolism |
| 18 | PubMed | Fetch PMID 30105474 | 1 | 1 | Authoritative recent review of PCP-class NPS pharmacology including historical context for PCE |
| 19 | PubMed | Fetch PMID 8450474 | 1 | 1 | Directly quantifies PCE CNS effects via CSF concentration |
| 20 | PubMed | Fetch PMID 6673975 | 1 | 1 | Directly characterizes PCE pharmacokinetics in animal model |
| 21 | PubMed | Fetch PMID 7128004 - Perez-Reyes 1982 | 1 | 1 | Relevant to harm reduction and clinical management of PCE intoxication |
| 22 | PubMed | Fetch PMID 20440387 - Bey & Patel 2007 | 1 | 1 | Primary clinical reference for PCP-class pharmacokinetics applicable to PCE |
| 23 | WebSearch | Germany BtMG PCE eticyclidine scheduling | 10 | 1 | German legal status (partially confirmed) |
| 24 | WebSearch | Canada CDSA schedule PCE eticyclidine | 10 | 1 | Canadian legal status |
| 25 | WebSearch | PCE eticyclidine SMILES structure | 10 | 1 | Chemical structure verification |
| 26 | PubMed | Fetch PMID 36555217 - Pelletier 2022 ACH review | 1 | 1 | Most comprehensive modern review of ACH class including PCE |
| 27 | WebSearch | Australia PCE scheduling | 10 | 1 | Australian legal status |
69 claims by section — every cited sentence, checked against its source
safety20 · 7 ok
At PCP-equivalent doses in humans: 2–5 mg produces mild intoxication (cognitive disturbance, numbness, analgesia); 5–25 mg produces dissociative stupor and potential unresponsiveness; doses exceeding 25 mg risk deep coma, seizures, and deathsupported
PCP clinical manifestations by dose (2-5mg mild; 5-25mg stupor/coma; >25mg deep coma/seizures/death). pmid:20440387
PCE is slightly more potent than PCP; acute toxic doses may be proportionally lower.supported
N-ethyl-1-phenylcyclohexylamine (PCE), described as 'one of the most potent arylcyclohexylamines'. pmid:2457075
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Amnesia, delusions, and confusion are expected cognitive complications at strong and heavy doses, consistent with PCP-class pharmacology.supported
Effects: hallucinations, delirium, agitation, rigidity, ataxia, nystagmus, seizures. pmid:26256594
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Seizure disorders — NMDA antagonists lower seizure threshold at high dosessupported
>25mg deep coma/seizures/death. pmid:20440387
Hepatic impairment — PCE is primarily hepatically metabolized; impaired clearance may prolong effects and increase toxicity risksupported
metabolism by hydroxylation then conjugation pmid:26256594
Renal impairment — pH-dependent renal excretion means impaired renal function may slow eliminationsupported
PCP renal clearance is pH-dependent. Alkaline urine reduces excretion; acid urine increases it. pmid:7128004
History of rhabdomyolysis — PCP-class compounds are associated with rhabdomyolysis, particularly at high doses or with physical exertionsupported
Complications include rhabdomyolysis, seizures, hyperthermia. pmid:2201519
pharmacology11 · 9 ok
PCE is a non-competitive, open-channel blocker at the N-methyl-D-aspartate (NMDA) glutamate receptor, binding to the phencyclidine site within the ion channel poresupported
Linear-regression analysis showed marked concordance (R=0.95) between NMDA and PCP-site binding distributions in brain. jneurosci.08-02-00493.1988
Claim in pharmacology — inconclusiveinconclusiveworking →
Beyond NMDA antagonism, PCE acts as a dopamine, noradrenaline, and serotonin reuptake inhibitor and as an agonist at sigma-1 and sigma-2 receptorssupported
it also acts as DA/5-HT/NE reuptake inhibitor and sigma-1/2 and opioid receptor agonist. j.mehy.2013.03.030
Claim in pharmacology — inconclusiveinconclusiveworking →
Weak mu-opioid receptor affinity has been noted as a class property for arylcyclohexylamines, though no direct binding data for PCE at opioid receptors exist.supported
Ketamine affinities at PCP, mu/delta/kappa opioid, sigma, and muscarinic receptors. Highest affinity at PCP site. pmid:8835358
Following a single intravenous dose (1.09 µmol) in rats, approximately 93% of radiolabeled PCP was excreted within one week versus only 65% of radiolabeled PCEsupported
within 1 week ~93% of PCP but ~65% of PCE excreted in rats after i.v. administration. pmid:6673975
Primary hepatic metabolism proceeds via hydroxylation followed by glucuronide conjugationsupported
metabolism by hydroxylation then conjugation pmid:26256594
N-deethylation to phenylcyclohexylamine (PCA) is a major metabolic stepsupported
PCE and PCA are major metabolites of PCDE. 6-compartment model with saturable conversion PCDE→PCE→PCA. pmid:8095205
By structural analogy with 3-MeO-PCP, CYP2B6 is the likely primary cytochrome P450 enzyme, with CYP2D6 contributingsupported
CYP2B6 responsible for aliphatic hydroxylations of 3-MeO-PCP; CYP2C19 and CYP2D6 for O-demethylation. 1570159x14666161018151716
PCE metabolism is inducible by CYP inducers such as 3-methylcholanthrene and cigarette smoke exposure.supported
CYP induction by 3-MC or cigarette smoke enhanced PCE metabolism and conjugated metabolite levels in perfusate. pmid:4071555
Renal excretion of PCP-class compounds is pH-dependent: urinary acidification increases clearance, while alkalinization reduces itsupported
Alkaline urine reduces excretion; acid urine increases it. pmid:7128004
summary9 · 5 ok
N-Ethyl-1-phenylcyclohexan-1-amine (PCE), also known as eticyclidine and by the Parke-Davis development code CI-400, is a synthetic arylcyclohexylamine dissociative with in vivo potency slightly exceeding that of phencyclidine (PCP)supported
N-ethyl-1-phenylcyclohexylamine (PCE), described as 'one of the most potent arylcyclohexylamines'. Relative potency data from anti-PCE-model antibody correlated significantly with PCP receptor binding assays and drug discrimination data. pmid:2457075
Synthesized in the 1960s as part of Parke-Davis's systematic exploration of 1-phenylcycloalkylamine anesthetics, PCE was evaluated for anesthetic potential but abandoned in favor of ketamine, which offered a more manageable therapeutic profilesupported
Covers pharmacology, epidemiology, chemistry, metabolism, and case reports of intoxication. Notes eticyclidine first observed in 1960s, considered too powerful. ijms232415574
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
PCE acts as a non-competitive NMDA receptor channel blocker at the PCP binding site, with secondary activity as a monoamine reuptake inhibitor and sigma receptor agonistsupported
it also acts as DA/5-HT/NE reuptake inhibitor and sigma-1/2 and opioid receptor agonist. j.mehy.2013.03.030
Claim in summary — inconclusiveinconclusiveworking →
Animal drug discrimination studies confirm full PCP-like interoceptive effects, though notably PCE does not produce the locomotor stimulation characteristic of PCPsupported
PCE and PCP both engendered full PCP-lever selection in all subjects. All three ACXs (PCP, PCE, MXE) caused dose-dependent hypothermia in mice. Only PCP (not PCE or MXE) increased locomotor activity. j.neuropharm.2017.08.028
Community reports indicate a significantly elevated rate of psychosis and mania relative to other dissociatives, a pattern without clinical validation but consistent with PCE's high potency and slow metabolic clearancesupported
Slower metabolism and excretion of PCE may account for its higher psychotropic effects. pmid:6673975
pharmacokinetic-detail8 · 8 ok
By analogy with PCP, which has a volume of distribution of approximately 6.2 L/kg in humans, PCE is expected to distribute extensively into tissues including the central nervous systemsupported
Pharmacokinetics: Vd 6.2 L/kg, half-life 17.6h, 90% hepatic metabolism. pmid:20440387
Direct evidence supports enhanced tissue retention: at one week post-administration of a single 1.09 µmol intravenous dose, significantly more radiolabeled compound remained in rat tissues from PCE-treated animals compared with PCP-treated animalssupported
More PCE remained in tissues. Slower metabolism and excretion of PCE may account for its higher psychotropic effects. pmid:6673975
The effective half-life of PCE in humans is unknown but is expected to exceed the 17.6-hour elimination half-life reported for PCP in humans.supported
Pharmacokinetics: Vd 6.2 L/kg, half-life 17.6h, 90% hepatic metabolism. pmid:20440387
Primary metabolism proceeds via aromatic and aliphatic hydroxylation followed by phase II glucuronide conjugationsupported
metabolism by hydroxylation then conjugation pmid:26256594
Hepatic metabolism accounts for approximately 90% of PCP elimination; a similar proportion is expected for PCE.supported
Pharmacokinetics: Vd 6.2 L/kg, half-life 17.6h, 90% hepatic metabolism. pmid:20440387
By structural analogy with 3-MeO-PCP, CYP2B6 is the primary cytochrome P450 isoform responsible for aliphatic hydroxylations, with CYP2D6 contributingsupported
CYP2B6 responsible for aliphatic hydroxylations of 3-MeO-PCP; CYP2C19 and CYP2D6 for O-demethylation. 1570159x14666161018151716
Pretreatment with 3-methylcholanthrene or cigarette smoke exposure significantly enhanced pulmonary PCE metabolism and increased conjugated metabolite concentrations in the perfusatesupported
CYP induction by 3-MC or cigarette smoke enhanced PCE metabolism and conjugated metabolite levels in perfusate. pmid:4071555
Urinary acidification increases the proportion of ionized drug in the renal tubule, reducing reabsorption and accelerating clearance; alkaline urine has the opposite effectsupported
Alkaline urine reduces excretion; acid urine increases it. Clinical implication: vigorous urine acidification and diuresis useful in PCP intoxication treatment. pmid:7128004
receptor-pharmacology6 · 4 ok
PCE binds to the PCP site within the NMDA receptor ion channelsupported
Linear-regression analysis showed marked concordance (R=0.95) between NMDA and PCP-site binding distributions in brain. jneurosci.08-02-00493.1988
Owens et al. described PCE as "one of the most potent arylcyclohexylamines" based on antibody binding studies and receptor interaction profilessupported
N-ethyl-1-phenylcyclohexylamine (PCE), described as 'one of the most potent arylcyclohexylamines'. Relative potency data from anti-PCE-model antibody correlated significantly with PCP receptor binding assays and drug discrimination data. pmid:2457075
This discrepancy between in vitro binding and in vivo potency is partially explained by PCE's slower metabolic clearance, which sustains higher effective CNS concentrations over longer periods.supported
Slower metabolism and excretion of PCE may account for its higher psychotropic effects. pmid:6673975
In PCP-trained rats, PCE produced full PCP-lever selection in all subjects in drug discrimination assays, confirming identical interoceptive effectssupported
PCE and PCP both engendered full PCP-lever selection in all subjects. j.neuropharm.2017.08.028
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
comparative-pharmacology4 · 4 ok
PCE is consistently described as slightly more potent than PCP in vivosupported
N-ethyl-1-phenylcyclohexylamine (PCE), described as 'one of the most potent arylcyclohexylamines'. pmid:2457075
In PCP-trained rats, PCE produced full PCP-lever selection in all subjects in drug discrimination studies, confirming identical interoceptive effectssupported
PCE and PCP both engendered full PCP-lever selection in all subjects. j.neuropharm.2017.08.028
Within one week of intravenous dosing in rats, approximately 93% of radiolabeled PCP but only 65% of radiolabeled PCE was excretedsupported
within 1 week ~93% of PCP but ~65% of PCE excreted in rats after i.v. administration. pmid:6673975
A notable behavioral divergence: PCE and PCP both produce dose-dependent hypothermia in mice, but unlike PCP, PCE does not produce locomotor stimulationsupported
All three ACXs (PCP, PCE, MXE) caused dose-dependent hypothermia in mice. Only PCP (not PCE or MXE) increased locomotor activity. j.neuropharm.2017.08.028
history4 · 2 ok
Claim in history — inconclusiveinconclusiveworking →
PCE and related derivatives were first observed in the 1960s, at approximately the same time as ketaminesupported
Notes eticyclidine first observed in 1960s, considered too powerful. ijms232415574
Claim in history — inconclusiveinconclusiveworking →
Bailey and Legault subsequently published reference spectroscopic data — infrared spectroscopy, mass spectrometry, gas chromatography, and thin-layer chromatography — for N-ethyl-1-phenylcyclohexylamine and related analogs to assist forensic laboratories in identification.supported
Spectroscopic identification of 1-phenylcyclohexylamine and N-methyl, N-ethyl (PCE), N-propyl, N-isopropyl, N-phenylethyl derivatives. Reference IR and MS spectra and GC/TLC data provided. pmid:528459
neuroscience3 · 1 ok
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
The absence of locomotor stimulation observed with PCE — in contrast to PCP — suggests that the balance between NMDA antagonism and dopamine reuptake inhibition may differ quantitatively between the two compounds, potentially reflecting lower dopaminergic engagement or differential regional receptor occupancy in motor circuits.supported
Only PCP (not PCE or MXE) increased locomotor activity. j.neuropharm.2017.08.028
chemistry2 · 0 ok
clinical-evidence1 · 0 ok
Claim in clinical-evidence — inconclusiveinconclusiveworking →
effects-overview1 · 1 ok
PCE produces a dissociative experience characterized by the full spectrum of PCP-class phenomenology — profound bodily dissociation, cognitive disconnection, amnesia, and perceptual distortion — but without the pronounced locomotor stimulation typical of PCPsupported
PCE and PCP both engendered full PCP-lever selection in all subjects...Only PCP (not PCE or MXE) increased locomotor activity. j.neuropharm.2017.08.028