generation run 2026-04-26
74 min completedmodel pipeline-v5plan not recordedrun/143aea9b…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
- sparse_evidence
- safety_data_gap
Reproduce
- inputs
- 22 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
20 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | ClinicalTrials.gov · absence | 3-HO-PCP hydroxyphencyclidine | 0 | 0 | No trials registered |
| 2 | PubMed | 3-HO-PCP new psychoactive substance NPS analytical detection mass spectrometry | 1 | 1 | Critical pharmacokinetic data: plasma protein binding, metabolism, in vivo concentrations |
| 3 | PubMed | phencyclidine PCP analog designer drug dissociative market emergence | 3 | 1 | Wallach & Brandt provides historical context for PCP analog NPS market; 3-MeO-PCP papers provide class context for 3-HO-PCP |
| 4 | OpenAlex | 3-HO-PCP 3-hydroxyphencyclidine dissociative | 5 | 2 | Both are relevant review papers covering dissociative NPS class |
| 5 | PubChem | 3-HO-PCP | 1 | 1 | Primary chemical identity verification |
| 6 | PubMed | 3-HO-PCP 3-hydroxyphencyclidine pharmacology | 1 | 1 | Primary case report of 3-HO-PCP toxicity; direct relevance |
| 7 | PubMed | 3-hydroxyphencyclidine NMDA opioid receptor binding | 1 | 1 | Foundational receptor binding localization study for 3-HO-PCP |
| 8 | PubMed | 3-hydroxyphencyclidine sigma receptor binding affinity | 2 | 2 | Early pharmacological characterization of 3-HO-PCP binding sites in rat brain |
| 9 | HandWiki | 3-HO-PCP pharmacology history legal status | 1 | 3 | Secondary source with referenced primary data; binding values consistent across multiple sources |
| 10 | WebSearch | 3-HO-PCP binding affinity Ki mu opioid NMDA receptor pharmacology | 10 | 1 | Critical pharmacological data not available in PubMed searches; verified across multiple web sources |
| 11 | WebSearch | 3-HO-PCP legal status scheduling US UK controlled substance | 10 | 1 | Legal status not available in PubMed; web sources provide jurisdiction-specific information |
| 12 | WebSearch | 3-HO-PCP history first synthesis research chemical market appearance year | 10 | 1 | History of synthesis and market emergence not in PubMed; web aggregation of primary sources |
| 13 | WebSearch | WHO ECDD 47th 3-OH-PCP critical review scheduling recommendation 2024 | 10 | 2 | Regulatory milestone: WHO reviewing for international scheduling in 2024 |
| 14 | WebSearch | 3-HO-PCP Canada Australia Germany scheduling controlled | 10 | 3 | Comprehensive multi-jurisdiction legal status |
| 15 | Multiple | 3-HO-PCP binding affinities verification across sources | 5 | 1 | Values consistent across multiple sources; marked as web_retrieved due to inability to verify original primary paper directly |
| 16 | PubMed · absence | 3-MeO-PCP metabolism human hepatocytes CYP enzyme hydroxyl metabolite 3-OH-PCP | 0 | 0 | Query too specific; pivoted to broader metabolism search |
| 17 | ClinicalTrials.gov · absence | 3-HO-PCP hydroxyphencyclidine | 0 | 0 | Confirmed no ongoing clinical development |
| 18 | PubMed | dissociative drug psychosis NMDA antagonist schizophrenia model | 6 | 1 | Mechanism of psychosis risk from NMDA antagonism; relevant to 3-HO-PCP psychological hazard |
| 19 | PubMed | phencyclidine metabolism cytochrome P450 CYP liver human hydroxylation | 2 | 2 | Critical for understanding metabolic pathway and CYP enzyme interactions for 3-HO-PCP |
| 20 | PubMed | PCP analog forensic urine immunoassay cross-reactivity detection | 2 | 1 | Important for harm reduction: standard drug screens likely to miss 3-HO-PCP |
70 claims by section — every cited sentence, checked against its source
safety18 · 17 ok
The only analytically confirmed case of severe acute toxicity involved co-ingestion of 3-HO-PCP with N-ethylhexedrone in the United Kingdomsupported
We describe an analytically confirmed case of acute toxicity related to the use of both 3-hydroxyphencyclidine and N-ethylhexedrone. s13181-019-00734-x
A postmortem forensic case reported a blood concentration of 0.095 mg/kg 3-HO-PCP in a deceased individual, though multiple other substances were co-detected and causation was not established.supported
Blood concentrations: 0.013 mg/kg (living) and 0.095 mg/kg (deceased). dta.2807
The combination of NMDA receptor antagonism with intrinsic μ-opioid agonism (Ki ≈ 39–60 nM) creates a compound risk for respiratory depression beyond what either pharmacological mechanism alone producespartially supported
Dual NMDA and opioid interactions as synergistic mechanism. appi.ajp.20240378
Rhabdomyolysis and acute kidney injury have been documented in the PCP analog class (3-methyl-PCP), establishing rhabdomyolysis as a plausible class risksupported
First confirmed case of 3-methyl-PCP (novel arylcyclohexylamine) with rhabdomyolysis and acute kidney injury. s13181-026-01122-y
Standard urine immunoassay PCP screens detect only approximately 20% of PCP structural analogs, making 3-HO-PCP likely to produce a false-negative result on standard clinical drug testingsupported
DRI Phencyclidine enzyme assay detected 20% of PCP analogs at 100 mcg/mL. bku133
Confirmatory identification requires liquid chromatography–high-resolution mass spectrometry (LC-HRMS).supported
3-HO-PCP detected in law enforcement seizure and forensic samples in Denmark... using high resolution mass spectrometry dta.2807
NMDA antagonists are capable of inducing positive symptoms (hallucinations, paranoia), negative symptoms (emotional withdrawal, psychomotor retardation), and formal thought disorder — a symptom cluster that models aspects of schizophrenia.supported
PCP induces psychotomimetic state resembling schizophrenia, with both positive (hallucinations, paranoia) and negative symptoms (emotional withdrawal, motor retardation), formal thought disorder, and neuropsychological deficits. pmid:1654746
NMDA antagonists are capable of inducing positive symptoms (hallucinations, paranoia), negative symptoms (emotional withdrawal, psychomotor retardation), and formal thought disorder — a symptom cluster that models aspects of schizophrenia.supported
NMDA receptor antagonists (dissociative anesthetics) can replicate full range of psychotic, negative, cognitive symptoms of schizophrenia. sbs076
Dissociative-type psychological dependence: Abuse potential via the mesolimbic dopamine pathway is documented for PCP analogs including 4-MeO-PCP, PCA, and 4-F-PCP.supported
4-MeO-PCP and 3-MeO-PCMo (PCP analogs) produce rewarding/reinforcing effects via mesolimbic dopamine pathway. s00213-019-05412-y
Dissociative-type psychological dependence: Abuse potential via the mesolimbic dopamine pathway is documented for PCP analogs including 4-MeO-PCP, PCA, and 4-F-PCP.supported
PCA (PCP analog) induces CPP and self-administration in rodents via dopaminergic system. j.neuint.2021.104962
Alcohol: Additive CNS depression documented in PCP analog intoxication cases.supported
Two young men in comatose state (Glasgow score 3), respiratory acidosis, anisocoria, hypothermia after 3-MeO-PCP + alcohol. j.forsciint.2016.12.028
Co-ingestion of 3-HO-PCP with N-ethylhexedrone (a synthetic cathinone stimulant) produced severe toxicity in the only analytically confirmed UK case reportsupported
We describe an analytically confirmed case of acute toxicity related to the use of both 3-hydroxyphencyclidine and N-ethylhexedrone. s13181-019-00734-x
By analogy with 3-MeO-PCP (CYP2B6/2C19/2D6) and PCP (CYP3A4):supported
CYP2B6 responsible for aliphatic hydroxylations; CYP2C19 and CYP2D6 for O-demethylation. 1570159x14666161018151716
By analogy with 3-MeO-PCP (CYP2B6/2C19/2D6) and PCP (CYP3A4):supported
CYP3A plays major role in PCP biotransformation in human liver microsomes. pmid:9152594
Claim in safety — inconclusiveinconclusiveworking →
Benzodiazepines remain first-line for agitation and psychomotor symptoms, consistent with standard NPS treatment guidelines.supported
Pharmacotherapy primarily consisted of benzodiazepines (62.7%), neuroleptics, muscle relaxants. fpsyt.2021.669921
History of psychotic disorders or schizophrenia: NMDA receptor antagonism is psychotomimetic and can precipitate or exacerbate psychotic episodessupported
PCP induces psychotomimetic state resembling schizophrenia, with both positive (hallucinations, paranoia) and negative symptoms. pmid:1654746
History of psychotic disorders or schizophrenia: NMDA receptor antagonism is psychotomimetic and can precipitate or exacerbate psychotic episodessupported
NMDA receptor antagonists (dissociative anesthetics) can replicate full range of psychotic, negative, cognitive symptoms of schizophrenia. sbs076
pharmacology13 · 9 ok
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
3-HO-PCP is a confirmed metabolite of 3-MeO-PCP, produced by aromatic O-demethylation of the 3-methoxy groupsupported
CYP2C19 and CYP2D6 for O-demethylation. Multiple aliphatic hydroxylations, aromatic hydroxylation, O-demethylation, and glucuronidation identified. 1570159x14666161018151716
By analogy with structurally related PCP analogs (4-MeO-PCP, 3-MeO-PCMo, PCA, 4-F-PCP), which produce reward and reinforcement via the mesolimbic dopamine pathway, dopaminergic involvement in 3-HO-PCP's rewarding effects is probable but unconfirmed for this specific compound .supported
4-MeO-PCP and 3-MeO-PCMo (PCP analogs) produce rewarding/reinforcing effects via mesolimbic dopamine pathway. s00213-019-05412-y
By analogy with structurally related PCP analogs (4-MeO-PCP, 3-MeO-PCMo, PCA, 4-F-PCP), which produce reward and reinforcement via the mesolimbic dopamine pathway, dopaminergic involvement in 3-HO-PCP's rewarding effects is probable but unconfirmed for this specific compound .supported
PCA (PCP analog) induces CPP and self-administration in rodents via dopaminergic system; altered DA, TH, D1R, D2R expression in NAc and VTA. j.neuint.2021.104962
All available human data derive from a single forensic analytical study using law enforcement seizure and casework samples from Denmark.supported
3-HO-PCP detected in law enforcement seizure and forensic samples in Denmark. dta.2807
The unbound plasma fraction is 0.72 ± 0.09, indicating that approximately 28% of circulating 3-HO-PCP is protein-boundsupported
Plasma protein binding unbound fraction 0.72±0.09. dta.2807
This relatively high free fraction facilitates CNS distribution, consistent with a postmortem brain-to-blood ratio of approximately 1.5.supported
Brain concentration 1.5-fold higher than postmortem blood. dta.2807
Four metabolites have been identified after in vitro incubation with pooled human hepatocytes: a piperidine-hydroxyl metabolite (aliphatic hydroxylation), an N-dealkyl carboxylic acid metabolite (piperidine ring-opened; the dominant urinary metabolite in deconjugated urine), an O-glucuronide conjugate, and an O-sulfate conjugate (detected in vitro but not in vivo).partially supported
Four metabolites identified in vitro: piperidine-hydroxyl, N-dealkyl-COOH, O-glucuronidated, O-sulfate-conjugated. N-dealkylated-COOH metabolite was main metabolite in urine. dta.2807
By class analogy, PCP is primarily metabolized by CYP3A4, while 3-MeO-PCP undergoes aliphatic hydroxylation via CYP2B6 and O-demethylation via CYP2C19 and CYP2D6. 3-HO-PCP metabolism likely involves CYP2B6 and CYP3A4/5, but this is class inference only .supported
CYP3A plays major role in PCP biotransformation in human liver microsomes. pmid:9152594
By class analogy, PCP is primarily metabolized by CYP3A4, while 3-MeO-PCP undergoes aliphatic hydroxylation via CYP2B6 and O-demethylation via CYP2C19 and CYP2D6. 3-HO-PCP metabolism likely involves CYP2B6 and CYP3A4/5, but this is class inference only .supported
CYP2B6 responsible for aliphatic hydroxylations; CYP2C19 and CYP2D6 for O-demethylation. 1570159x14666161018151716
neuroscience7 · 5 ok
Glutamate hypothesis of psychosis: NMDA receptor hypofunction — whether induced pharmacologically by PCP-type compounds or occurring endogenously — produces positive symptoms (hallucinations, paranoia), negative symptoms (withdrawal, flattened affect), and cognitive disorganization that model aspects of schizophrenia. 3-HO-PCP's high NMDA affinity (Ki ≈ 30 nM) and additional opioid activity may produce a psychotomimetic profile qualitatively distinct from ketamine or PCP, though this has not been systematically studied.supported
PCP induces psychotomimetic state resembling schizophrenia, with both positive (hallucinations, paranoia) and negative symptoms (emotional withdrawal, motor retardation), formal thought disorder, and neuropsychological deficits. pmid:1654746
Glutamate hypothesis of psychosis: NMDA receptor hypofunction — whether induced pharmacologically by PCP-type compounds or occurring endogenously — produces positive symptoms (hallucinations, paranoia), negative symptoms (withdrawal, flattened affect), and cognitive disorganization that model aspects of schizophrenia. 3-HO-PCP's high NMDA affinity (Ki ≈ 30 nM) and additional opioid activity may produce a psychotomimetic profile qualitatively distinct from ketamine or PCP, though this has not been systematically studied.supported
NMDA receptor antagonists (dissociative anesthetics) can replicate full range of psychotic, negative, cognitive symptoms of schizophrenia. NMDA receptor hypofunction hypothesis. sbs076
NMDA receptor blockade reduces excitatory glutamatergic transmission, particularly at GABAergic interneurons in cortical microcircuits, producing a net disinhibition of pyramidal neurons and disrupting the normal pattern of cortico-thalamo-cortical information flow.supported
Parvalbumin-positive cortical GABAergic neuron downregulation, pyramidal dendritic dysgenesis. sbs076
Claim in neuroscience — inconclusiveinconclusiveworking →
Autoradiographic mapping of [³H]3-OH-PCP binding sites in rat brain reveals highest density in the hippocampal formation (CA1 stratum radiatum and oriens, dentate gyrus), with high binding in superficial cortical layers, amygdala, and thalamuspartially supported
High densities in CA1 hippocampus, outer layers of cortex. pmid:8884223
Claim in neuroscience — inconclusiveinconclusiveworking →
Incentive salience (wanting vs liking): Dopaminergic reward pathway involvement, documented for PCP analogs, suggests 3-HO-PCP may produce both liking (hedonic, mediated by opioid activity) and wanting (motivational, mediated by mesolimbic dopamine), potentially conferring higher abuse liability than compounds that engage only one system.supported
4-MeO-PCP and 3-MeO-PCMo (PCP analogs) produce rewarding/reinforcing effects via mesolimbic dopamine pathway. Alteration of accumbal CREB, deltaFosB, and BDNF levels. s00213-019-05412-y
pharmacokinetic-detail7 · 6 ok
All quantitative human pharmacokinetic data for 3-HO-PCP derive from a single forensic analytical study using law enforcement seizures and casework samples from Denmark — not controlled clinical trialssupported
3-HO-PCP detected in law enforcement seizure and forensic samples in Denmark. dta.2807
The unbound fraction (fu) was determined as 0.72 ± 0.09, indicating moderate plasma binding (~28% bound)supported
Plasma protein binding unbound fraction 0.72±0.09. dta.2807
Four metabolites were identified after incubation with pooled human hepatocytes:supported
Four metabolites identified in vitro: piperidine-hydroxyl, N-dealkyl-COOH, O-glucuronidated, O-sulfate-conjugated. dta.2807
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
PCP: primarily CYP3A4supported
CYP3A plays major role in PCP biotransformation in human liver microsomes. pmid:9152594
3-MeO-PCP: CYP2B6 for aliphatic hydroxylations; CYP2C19 and CYP2D6 for O-demethylation (producing 3-HO-PCP as a metabolite)supported
CYP2B6 responsible for aliphatic hydroxylations; CYP2C19 and CYP2D6 for O-demethylation. 1570159x14666161018151716
Postmortem brain-to-blood concentration ratio was approximately 1.5, indicating moderate-to-good CNS penetration consistent with the compound's lipophilicity and high unbound fraction.supported
Brain concentration 1.5-fold higher than postmortem blood. dta.2807
receptor-pharmacology7 · 7 ok
The trend is consistent with autoradiographic and radioligand displacement studies that used [³H]3-OH-PCP to map NMDA/PCP receptor distributionsupported
Quantitative autoradiography of [3H]3-OH-PCP binding in rat brain. pmid:8884223
The trend is consistent with autoradiographic and radioligand displacement studies that used [³H]3-OH-PCP to map NMDA/PCP receptor distributionsupported
Binding of a novel radioligand, [3H]3-OH-PCP, to NMDA receptor-coupled and -uncoupled PCP sites was investigated in rat brain. pmid:7620917
Autoradiographic studies using [³H]3-OH-PCP in rat brain established a binding distribution closely corresponding to [³H]TCP and [³H]MK-801 binding sites:supported
Distribution consistent with [3H]TCP and [3H]MK-801 binding sites. pmid:7620917
Autoradiographic studies using [³H]3-OH-PCP in rat brain established a binding distribution closely corresponding to [³H]TCP and [³H]MK-801 binding sites:supported
Regional distribution corresponds to [3H]TCP and [3H]MK-801 binding sites. pmid:8884223
The binding pattern confirmed that 3-OH-PCP binds to NMDA/PCP ion-channel complexes in preference to sigma sitessupported
suggesting 3-OH-PCP binds to NMDA/PCP ion-channel complexes in preference to sigma sites. pmid:7620917
MK-801 strongly inhibited [³H]3-OH-PCP binding, and glutamate/glycine/polyamine site antagonists displaced it similarly to [³H]MK-801.partially supported
Strongly inhibited by MK-801. Binding site similar/identical to PCP site labeled by [3H]TCP and [3H]MK-801. pmid:8884223
In early receptor characterization work using rat brain membrane preparations, [³H]PCP-3-OH labeled both a high-affinity component shared with (+)[³H]SKF 10047 (a sigma ligand) and a lower-affinity, PCP-selective component unaffected by guanine nucleotidessupported
[3H]PCP-3-OH used as prototypical ligand for labeling sigma- and PCP-receptor subtypes. Low affinity [3H]PCP-3-OH binding representing PCP-selective site unaffected by GTP. pmid:2834673
history6 · 5 ok
Claim in history — not_supportednot supportedworking →
By 1988, Itzhak and colleagues had adopted tritium-labeled 3-HO-PCP ([³H]3-OH-PCP, also designated [³H]PCP-3-OH) as a radioligand to characterize sigma and PCP receptor binding sites in rat brain membranessupported
[3H]PCP-3-OH used as prototypical ligand for labeling sigma- and PCP-receptor subtypes. pmid:2834673
By 1988, Itzhak and colleagues had adopted tritium-labeled 3-HO-PCP ([³H]3-OH-PCP, also designated [³H]PCP-3-OH) as a radioligand to characterize sigma and PCP receptor binding sites in rat brain membranessupported
3-HO-PCP ([3H]PCP-3-OH) used as radioligand to label sigma and PCP binding sites in rat brain membranes. pmid:2893238
Through the 1990s, autoradiographic studies using [³H]3-OH-PCP mapped the brain distribution of NMDA/PCP ion-channel complexes, confirming binding preference for NMDA sites over sigma sites.supported
Distribution consistent with [3H]TCP and [3H]MK-801 binding sites, suggesting 3-OH-PCP binds to NMDA/PCP ion-channel complexes in preference to sigma sites. pmid:7620917
Through the 1990s, autoradiographic studies using [³H]3-OH-PCP mapped the brain distribution of NMDA/PCP ion-channel complexes, confirming binding preference for NMDA sites over sigma sites.supported
Regional distribution corresponds to [3H]TCP and [3H]MK-801 binding sites. Binding site similar/identical to PCP site labeled by [3H]TCP and [3H]MK-801. pmid:8884223
Law enforcement seizures followed — analytically confirmed detections were reported in Denmark and the United Kingdom.partially supported
3-HO-PCP detected in law enforcement seizure and forensic samples in Denmark. dta.2807
summary5 · 4 ok
First synthesized in 1978 as part of PCP structure-activity relationship studies, 3-HO-PCP served primarily as a pharmacological radioligand for NMDA/PCP receptor characterization throughout the 1980s and 1990spartially supported
[3H]PCP-3-OH used as prototypical ligand for labeling sigma- and PCP-receptor subtypes. pmid:2834673
First synthesized in 1978 as part of PCP structure-activity relationship studies, 3-HO-PCP served primarily as a pharmacological radioligand for NMDA/PCP receptor characterization throughout the 1980s and 1990spartially supported
3-HO-PCP ([3H]PCP-3-OH) used as radioligand to label sigma and PCP binding sites in rat brain membranes. pmid:2893238
Claim in summary — inconclusiveinconclusiveworking →
The dual NMDA/opioid profile creates compound respiratory depression risk beyond what either mechanism produces alone — a substance-specific hazard not shared by most dissociativespartially supported
Dual NMDA and opioid interactions as synergistic mechanism. appi.ajp.20240378
All documented serious adverse events involved polydrug exposure. μ-Opioid agonism predicts physical dependence liability with repeated use, while NMDA antagonism carries psychotomimetic risk including hallucinations, paranoia, and formal thought disordersupported
PCP induces psychotomimetic state resembling schizophrenia, with both positive (hallucinations, paranoia) and negative symptoms (emotional withdrawal, motor retardation), formal thought disorder, and neuropsychological deficits. pmid:1654746
comparative-pharmacology3 · 2 ok
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
3-MeO-PCP (3-methoxyphencyclidine) is the O-methylated structural analog and metabolic precursor of 3-HO-PCP — aromatic O-demethylation of 3-MeO-PCP produces 3-HO-PCP as a human metabolitesupported
CYP2C19 and CYP2D6 for O-demethylation. Multiple aliphatic hydroxylations, aromatic hydroxylation, O-demethylation, and glucuronidation identified. 1570159x14666161018151716
Both ketamine and 3-HO-PCP act as uncompetitive NMDA receptor channel blockers, but they differ substantially in potency (3-HO-PCP Ki ≈ 30 nM vs ketamine Ki ≈ 800–2,500 nM at the MK-801 site), opioid activity (3-HO-PCP has intrinsic MOR agonism; ketamine's opioid interactions are indirect and debated), and duration (3-HO-PCP 4–6 hours oral vs ketamine 1–2 hours)partially supported
Argues ketamine pharmacology should be redefined to include opioid receptors. Dual NMDA and opioid interactions as synergistic mechanism. appi.ajp.20240378
chemistry2 · 2 ok
This 3-hydroxyl substitution is pharmacologically consequential: it confers substantial μ-opioid receptor affinity absent in the parent compound, and it is the product of aromatic O-demethylation of 3-MeO-PCP. 3-HO-PCP is thus both a standalone research chemical and a confirmed human metabolite of 3-MeO-PCP.supported
CYP2C19 and CYP2D6 for O-demethylation. Multiple aliphatic hydroxylations, aromatic hydroxylation, O-demethylation, and glucuronidation identified. 1570159x14666161018151716
The phenolic hydroxyl group renders 3-HO-PCP susceptible to phase II conjugation reactions (glucuronidation, sulfation) that the methoxy analog 3-MeO-PCP does not undergo directly.supported
Four metabolites identified in vitro: piperidine-hydroxyl, N-dealkyl-COOH, O-glucuronidated, O-sulfate-conjugated. dta.2807
clinical-evidence2 · 2 ok
Dunlop et al. (2020) reported an analytically confirmed case of severe toxicity following co-ingestion of 3-HO-PCP and N-ethylhexedrone (a synthetic cathinone stimulant) in the United Kingdomsupported
We describe an analytically confirmed case of acute toxicity related to the use of both 3-hydroxyphencyclidine and N-ethylhexedrone. s13181-019-00734-x
Davidsen et al. (2020) reported forensic casework including one deceased individual with a blood concentration of 0.095 mg/kg 3-HO-PCPsupported
Blood concentrations: 0.013 mg/kg (living) and 0.095 mg/kg (deceased). dta.2807