generation run 2026-04-27
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19 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed | phencyclidine PCP discovery history synthesis clinical anesthetic | 1 | 1 | Key historical review covering PCP discovery and development |
| 2 | WebSearch | phencyclidine PCP pharmacokinetics half-life volume distribution | 10 | 2 | Confirmed PK data from multiple sources |
| 3 | PubMed | phencyclidine pharmacokinetics metabolism half-life human | 10 | 3 | Primary human PK data: half-life 7-46h (mean 21h), Vd 6.2 L/kg, oral bioavailability 72% |
| 4 | PubMed | phencyclidine PCP intoxication clinical features treatment | 3 | 3 | Clinical toxicology data and management |
| 5 | WebSearch | phencyclidine PCP legal status Schedule II UK Canada Australia | 10 | 3 | Legal status by jurisdiction |
| 6 | PubMed · absence | phencyclidine PCP overdose toxicity case report emergency | 0 | 0 | No direct results; searched broader terms |
| 7 | ACNP | — | 1 | 1 | Authoritative pharmacology reference |
| 8 | OpenAlex | phencyclidine PCP NMDA antagonist schizophrenia model psychosis | 10 | 3 | Landmark papers on PCP schizophrenia model and NMDA mechanisms |
| 9 | PubMed | phencyclidine PCP receptor binding NMDA pharmacology | 12 | 2 | Key structural and pharmacological papers on PCP-NMDA interaction |
| 10 | StatPearls/NCBI Bookshelf | — | 1 | 1 | Current clinical reference for PCP intoxication management |
| 11 | WebSearch | phencyclidine PCP history Parke-Davis 1956 Sernyl anesthetic scheduling | 10 | 1 | Key dates and names for PCP history |
| 12 | PubChem | phencyclidine | 1 | 1 | Core chemical identity data for PCP |
| 13 | ClinicalTrials.gov · absence | phencyclidine PCP dissociative | 0 | 0 | PCP has no current therapeutic applications; no registered trials |
| 14 | PubMed | phencyclidine PCP reinforcement tolerance self-administration animal | 4 | 3 | Animal model data for PCP dependence, tolerance, and withdrawal |
| 15 | PubMed | phencyclidine PCP schizophrenia humans administration effects | 3 | 3 | Core clinical evidence for PCP effects in humans, especially psychotomimetic effects |
| 16 | PubMed | individual paper fetches | 5 | 5 | Core PK data and pharmacology citations |
| 17 | PubMed | phencyclidine toxicity LD50 ethanol combination lethality | 3 | 3 | Toxicity data: LD50, drug interactions, specific adverse effects |
| 18 | multiple | PCP kappa opioid receptor agonism evidence | 3 | 0 | Flagging discrepancy between brief pharmacological class and literature evidence |
| 19 | WebSearch | phencyclidine melting point physical properties pKa logP | 10 | 2 | Physical/chemical property data for chemical identity section |
79 claims by section — every cited sentence, checked against its source
pharmacology21 · 11 ok
Primary intoxication lasts 4–8 hours at recreational doses, though symptoms can persist up to 48 hours in overdose and psychosis can last days to weeks after high-dose exposure.partially supported
In healthy volunteers, PCP can induce symptoms that mimic schizophrenia, lasting from a few days to more than a week. pmid:12206280
Claim in pharmacology — inconclusiveinconclusiveworking →
Binding affinities at the NMDA PCP site vary by assay and tissue preparation: Ki = 50–100 nM in [³H]MK-801 radioligand assays, Ki = 100.8 nM in dark Agouti rat brain membranes, and Ki = 313 nM using [³H]dizocilpine on rat striatal tissuesupported
PCP inhibited [3H]MK-801 binding with Ki of 100.8 nM. pmid:15240177
Binding affinities at the NMDA PCP site vary by assay and tissue preparation: Ki = 50–100 nM in [³H]MK-801 radioligand assays, Ki = 100.8 nM in dark Agouti rat brain membranes, and Ki = 313 nM using [³H]dizocilpine on rat striatal tissuesupported
Phencyclidine had a high affinity for D2High with a Ki of 2.7 nM, in contrast to its low affinity for the NMDA receptor, with a Ki of 313 nM as labeled by [3H]dizocilpine on rat striatal tissue. pmid:15852061
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Beyond NMDA antagonism, PCP displays unexpectedly high affinity for the high-affinity state of the dopamine D2 receptor (D2High) at Ki = 2.7 nM — substantially exceeding its NMDA affinity in the same assay system (Ki = 313 nM)supported
Phencyclidine had a high affinity for D2High with a Ki of 2.7 nM, in contrast to its low affinity for the NMDA receptor, with a Ki of 313 nM as labeled by [3H]dizocilpine on rat striatal tissue. pmid:15852061
Seeman and colleagues proposed a "combined hyperdopamine and hypoglutamate" theory of PCP psychosis, arguing that D2 agonism makes a major contribution to psychotomimetic effects alongside NMDA antagonismsupported
Phencyclidine had a high affinity for D2High with a Ki of 2.7 nM, in contrast to its low affinity for the NMDA receptor, with a Ki of 313 nM as labeled by [3H]dizocilpine on rat striatal tissue. pmid:15852061
In a primate PET study, PCP at 0.5 mg/kg IV decreased [¹¹C]-cocaine binding by 25.5%, consistent with competitive DAT interactionsupported
PCP (0.5 mg/kg) decreased [11C]-cocaine binding by 25.5%, consistent with a competitive interaction at the DAT. pmid:12888780
Claim in pharmacology — not_supportednot supportedworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Human pharmacokinetic parameters derive primarily from radiolabelled studies by Cook and colleagues in the early 1980s.supported
[3H]-PCP given IV (0.1 or 1 mg) or oral (1 mg) to male subjects. pmid:7075111
Human pharmacokinetic parameters derive primarily from radiolabelled studies by Cook and colleagues in the early 1980s.supported
Weighted mean apparent terminal half-life 17.6h in 16 subjects (range up to 2+ days). Vd 6.2 L/kg. pmid:6852275
Approximately 75% of the dose converts to polar metabolites eliminated renally; ~9% is excreted as unchanged parent drugpartially supported
Renal clearances average 9% of total clearance. Plasma binding ~65%. pmid:7075111
Claim in pharmacology — inconclusiveinconclusiveworking →
Specific CYP isoenzyme contributions have not been definitively characterised for PCP itself, though structural analogues 3-MeO-PCP and 4-MeO-PCP are metabolised primarily by CYP3A4, CYP2D6, and CYP2C19, suggesting these isoenzymes are likely relevant.supported
In silico ADME profiling of PCP analogues. Metabolic liability assigned primarily to CYP3A4, CYP2D6 and CYP2C19. s00204-025-04283-x
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
This inverse relationship with biotransformation rate suggests sex-dependent CYP activitysupported
Female rats appeared more sensitive to PCP. Half-life of PCP in brain and plasma was longer in female rats. pmid:6538506
safety16 · 14 ok
In silico estimates for rat oral LD50 range from 200–630 mg/kgsupported
Rat oral LD50 estimates: ~200-630 mg/kg. s00204-025-04242-6
In silico modelling predicts hERG IC50 of approximately 4.9–12.3 µM, suggesting potential QT-prolongation risk at high plasma concentrationssupported
hERG IC50 ~4.9-12.3 µM (QT-prolongation risk). s00204-025-04242-6
The PCP-ethanol interaction is particularly well-characterised: synergistic motor incoordination at modest doses, with ~20% reduction in LD50 in micesupported
Low doses of ethanol reduced LD50 of PCP by ~20%. Synergism (potentiation) of motor incoordination with ethanol. pmid:3834927
In mice, the IV LD50 (24-hour) is 57 µmol/kg (males) and 76 µmol/kg (females)supported
PCP acute LD50 (IV, 24h): 57 µmol/kg males, 76 µmol/kg females (mice). pmid:7132580
This interaction is proposed to explain the high rate of drowning and accidental death when PCP and alcohol are used together.supported
Moderate doses of PCP + moderate doses of ethanol could result in total loss of motor ability, explaining prevalence of accidental deaths (especially drowning). pmid:3834927
Animal data demonstrate compensatory upregulation of NMDA receptor subunit NR1 after chronic exposure, a change that may underlie sensitisation phenomena and vulnerability to psychotic relapse.supported
Chronic PCP (20 mg/kg, 5 days) increased locomotor activity following PCP challenge after 3-8 days withdrawal. NMDA function enhanced by ~77% in striatum. pmid:10029241
In healthy volunteers, it induces both positive symptoms (hallucinations, paranoia, thought disorder) and negative symptoms (emotional withdrawal, anhedonia, motor retardation) — a dual profile that distinguishes it from amphetamine-induced psychosis, which generates only positive symptoms.supported
PCP induces a psychotomimetic state that closely resembles schizophrenia, incorporating both positive and negative symptoms, formal thought disorder, and neuropsychological deficits. pmid:1654746
Prolonged psychosis: Can persist for days to weeks after a single high-dose exposure — far exceeding the pharmacokinetic half-lifesupported
In healthy volunteers, PCP can induce symptoms that mimic schizophrenia, lasting from a few days to more than a week. pmid:12206280
Symptom exacerbation in schizophrenia: Administration to patients with existing psychotic disorders specifically recreates each patient's characteristic psychotic symptomspartially supported
Ketamine induced dose-related increase in psychotic symptoms in both normal volunteers and schizophrenic patients. 70% of patients reported exacerbation of positive symptoms. pmid:11557159
Claim in safety — not_supportednot supportedworking →
In animal models, chronic PCP administration produces a complex pattern: behavioural sensitisation (augmented locomotor response on re-challenge) rather than simple tolerance, accompanied by compensatory NMDA receptor upregulation (NR1 subunit; ~77% increase in striatal NMDA-stimulated dopamine release)supported
Chronic PCP (20 mg/kg, 5 days) increased locomotor activity following PCP challenge after 3-8 days withdrawal. NMDA function enhanced by ~77% in striatum. pmid:10029241
PCP shows positive reinforcement in animal self-administration modelssupported
CP-101 606 (NR2B antagonist) produced PCP-like discriminative stimulus effects in rats and monkeys and showed reinforcing properties. NMDA NR2B subunit plays a role in PCP-like abuse potential. pmid:17989511
Continuous PCP infusion in rats (11 days via osmotic pump) followed by pump removal produced disruption of food-maintained operant responding consistent with a withdrawal syndrome; methoxetamine dose-dependently reversed these effects.supported
PCP withdrawal studies: disruption of food-maintained operant responding when pumps delivering continuous PCP removed. MXE dose-dependently reversed withdrawal effects. j.neuropharm.2017.08.028
Claim in safety — inconclusiveinconclusiveworking →
Psychotic disorders and schizophrenia: PCP specifically exacerbates characteristic psychotic symptoms in individuals with established psychotic illness. Any personal or family history of psychosis substantially increases risk of prolonged psychotic reactions.supported
Ketamine induced dose-related increase in psychotic symptoms in both normal volunteers and schizophrenic patients. 70% of patients reported exacerbation of positive symptoms. pmid:11557159
Relative contraindications include bipolar disorder (risk of manic exacerbation), pre-existing anxiety disorders (agitation and panic are common), and concurrent use of medications metabolised by CYP3A4, CYP2D6, or CYP2C19 (potential metabolic interaction based on structural analogy with PCP analogues).supported
In silico ADME profiling of PCP analogues. Metabolic liability assigned primarily to CYP3A4, CYP2D6 and CYP2C19. s00204-025-04283-x
neuroscience8 · 8 ok
Sex-dependent neuropharmacology: Female rats show greater sensitivity to PCP's behavioural effects and different PK profiles. Are there parallel sex differences in humans, and do they have clinical significance for PCP toxicity?supported
Study assessed sex differences in PCP-induced activity in rats. Female rats appeared more sensitive to PCP. Half-life of PCP in brain and plasma was longer in female rats. pmid:6538506
Their functional silencing produces a paradoxical increase in glutamate release from disinhibited pyramidal neurons, activating downstream AMPA and kainate receptors and driving aberrant excitatory signalling.supported
Low doses of ketamine increase glutamate outflow in PFC; AMPA/kainate receptor antagonism blocks ketamine-induced dopamine release and cognitive impairment. jneurosci.17-08-02921.1997
The glutamate surge secondary to interneuron disinhibition drives increased dopamine release in the prefrontal cortex and striatum via glutamate-dopamine interactionssupported
AMPA/kainate receptor antagonism blocks ketamine-induced dopamine release and cognitive impairment. jneurosci.17-08-02921.1997
This effect operates in parallel with PCP's direct actions at D2High receptors (Ki = 2.7 nM) and DAT (demonstrated in vivo by PET)supported
PCP (0.5 mg/kg) decreased [11C]-cocaine binding by 25.5%, consistent with a competitive interaction at the DAT. Results suggest PCP may be exerting some direct effects through the DAT. pmid:12888780
PCP's capacity to reproduce positive symptoms, negative symptoms, and cognitive deficits of schizophrenia in healthy volunteers — a feat unmatched by any other pharmacological agent — provided the empirical foundation for the NMDA hypofunction hypothesissupported
PCP induces a psychotomimetic state that closely resembles schizophrenia, incorporating both positive and negative symptoms, formal thought disorder, and neuropsychological deficits. pmid:1654746
PCP's capacity to reproduce positive symptoms, negative symptoms, and cognitive deficits of schizophrenia in healthy volunteers — a feat unmatched by any other pharmacological agent — provided the empirical foundation for the NMDA hypofunction hypothesissupported
Administration of noncompetitive NMDA/glutamate receptor antagonists, such as phencyclidine (PCP) and ketamine, to humans induces a broad range of schizophrenic-like symptomatology, findings that have contributed to a hypoglutamatergic hypothesis of schizophrenia. s0893-133x(98)00060-8
Subunit selectivity and regional effects: Do PCP's effects differ across NMDA receptor subtypes (GluN2A vs GluN2B vs GluN2C/D) in a way that produces region-specific neural disruption? Cryo-EM data show PCP binds within the channel pore of GluN1-GluN2B receptors, but comparative data across all subtypes in functional systems are incomplete.supported
Here, we monitor the binding of three clinically important channel blockers: phencyclidine, ketamine, and memantine in GluN1-2B NMDARs at local resolutions of 2.5-3.5Å. s41594-022-00772-0
Mechanisms of prolonged psychosis: PCP intoxication can produce psychotic states lasting days to weeks — far exceeding the drug's pharmacokinetic half-life even with lipophilic redistribution. Does prolonged psychosis reflect sustained neural circuit disruption (e.g., persistent interneuron dysfunction), slow receptor unbinding kinetics, or active metabolite contributions?supported
In healthy volunteers, PCP can induce symptoms that mimic schizophrenia, lasting from a few days to more than a week. pmid:12206280
summary8 · 6 ok
Phencyclidine (PCP, 1-(1-phenylcyclohexyl)piperidine) is the prototypical arylcyclohexylamine dissociative, distinguished from its structural descendants — ketamine, methoxetamine, 3-meo-pcp — by unusually high lipophilicity (XLogP 4.22), a long elimination half-life of 17–21 hours, and a primary intoxication duration of 4–8 hours that can extend to days at high doses.partially supported
Apparent terminal phase half-life averaged 21±3 hr (range 7–46 hr). pmid:7075111
Claim in summary — inconclusiveinconclusiveworking →
PCP's principal research significance lies in its role as the pharmacological foundation for the NMDA hypofunction hypothesis of schizophrenia: it remains the only drug class that reliably produces both positive and negative psychotic symptoms in healthy volunteers.supported
PCP induces a psychotomimetic state that closely resembles schizophrenia, incorporating both positive and negative symptoms, formal thought disorder, and neuropsychological deficits. pmid:1654746
PCP acts as a noncompetitive, open-channel blocker at the NMDA receptor (Ki = 50–100 nM at the PCP binding site) and shows unexpectedly high affinity for the D2High dopamine receptor state (Ki = 2.7 nM)partially supported
Phencyclidine had a high affinity for D2High with a Ki of 2.7 nM, in contrast to its low affinity for the NMDA receptor, with a Ki of 313 nM as labeled by [3H]dizocilpine on rat striatal tissue. pmid:15852061
This dual glutamatergic-dopaminergic action produces a dissociative-psychotomimetic profile comprising analgesia, depersonalisation, formal thought disorder, and — at moderate doses — a schizophrenia-mimetic state with hallucinations, emotional withdrawal, and cognitive disruption.supported
PCP induces a psychotomimetic state that closely resembles schizophrenia, incorporating both positive and negative symptoms, formal thought disorder, and neuropsychological deficits. pmid:1654746
Dependence involves dopaminergic reinforcement confirmed by animal self-administration models, though human tolerance and withdrawal characterisation remain sparsepartially supported
CP-101 606 (NR2B antagonist) produced PCP-like discriminative stimulus effects in rats and monkeys and showed reinforcing properties. NMDA NR2B subunit plays a role in PCP-like abuse potential. pmid:17989511
Claim in summary — not_supportednot supportedworking →
Chronic use is associated with compensatory NMDA receptor upregulation (NR1 subunit) and locomotor sensitisation rather than simple tolerancesupported
Chronic PCP (20 mg/kg, 5 days) increased locomotor activity following PCP challenge after 3-8 days withdrawal. NMDA function enhanced by ~77% in striatum. pmid:10029241
clinical-evidence7 · 7 ok
In healthy volunteers, subanesthetic doses of PCP-class compounds produce a state that mimics schizophrenia more faithfully than any other pharmacological model — encompassing positive symptoms (hallucinations, paranoia, thought disorder), negative symptoms (emotional withdrawal, motor retardation, anhedonia), and cognitive deficits (working memory, attention)supported
PCP induces a psychotomimetic state that closely resembles schizophrenia, incorporating both positive and negative symptoms, formal thought disorder, and neuropsychological deficits. pmid:1654746
In healthy volunteers, subanesthetic doses of PCP-class compounds produce a state that mimics schizophrenia more faithfully than any other pharmacological model — encompassing positive symptoms (hallucinations, paranoia, thought disorder), negative symptoms (emotional withdrawal, motor retardation, anhedonia), and cognitive deficits (working memory, attention)supported
Ketamine, a PCP derivative, produces psychotomimetic, perceptual, cognitive, and neuroendocrine responses in healthy human subjects. pmid:8122957
Historical clinical use as the surgical anaesthetic Sernyl was discontinued in 1965 due to emergence psychosis.supported
The history of ketamine and phencyclidine from their development as potential clinical anaesthetics... is reviewed. bph.13222
PCP and the structurally related compound ketamine have been used extensively as pharmacological challenge tools in academic research settings to model schizophrenia in healthy volunteers and to probe symptom exacerbation in patients with established psychotic disorderssupported
PCP induces a psychotomimetic state that closely resembles schizophrenia, incorporating both positive and negative symptoms, formal thought disorder, and neuropsychological deficits. pmid:1654746
Administration of ketamine to patients with schizophrenia exacerbates and specifically recreates each patient's characteristic psychotic symptoms, rather than producing a generic psychotomimetic statepartially supported
Ketamine induced dose-related increase in psychotic symptoms in both normal volunteers and schizophrenic patients. 70% of patients reported exacerbation of positive symptoms. pmid:11557159
Subanesthetic ketamine in schizophrenia patients stimulates psychosis in a dose-dependent manner, with effects including thought disorder, perceptual changes, and negative symptom exacerbationpartially supported
Subanesthetic ketamine (related to PCP) exacerbated positive symptoms in schizophrenic patients without negative symptom exacerbation. 0893-133x(94)00131-i
These studies validated the NMDA hypofunction hypothesis of schizophrenia — the proposal that reduced NMDA receptor function, particularly on GABAergic interneurons, underlies the glutamate/dopamine dysregulation observed in schizophrenic psychosis.supported
Administration of noncompetitive NMDA/glutamate receptor antagonists, such as phencyclidine (PCP) and ketamine, to humans induces a broad range of schizophrenic-like symptomatology, findings that have contributed to a hypoglutamatergic hypothesis of schizophrenia. s0893-133x(98)00060-8
pharmacokinetic-detail6 · 3 ok
The definitive human PK data derive from Cook and colleagues' radiolabelled studies (1982, 1983), in which healthy volunteers received small doses of [³H]-PCP intravenously and orally.supported
[3H]-PCP given IV (0.1 or 1 mg) or oral (1 mg) to male subjects. pmid:7075111
The definitive human PK data derive from Cook and colleagues' radiolabelled studies (1982, 1983), in which healthy volunteers received small doses of [³H]-PCP intravenously and orally.supported
Weighted mean apparent terminal half-life 17.6h in 16 subjects (range up to 2+ days). Vd 6.2 L/kg. pmid:6852275
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
By structural analogy with the closely related compounds 3-MeO-PCP and 4-MeO-PCP — which are primarily metabolised by CYP3A4, CYP2D6, and CYP2C19 — these isoenzymes are likely involvedsupported
In silico ADME profiling of PCP analogues. Metabolic liability assigned primarily to CYP3A4, CYP2D6 and CYP2C19. s00204-025-04283-x
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
receptor-pharmacology5 · 4 ok
Primate PET imaging demonstrated that PCP (0.5 mg/kg IV) reduced [¹¹C]-cocaine binding potential by 25.5%, confirming competitive occupancy at the dopamine transporter in vivosupported
PCP (0.5 mg/kg) decreased [11C]-cocaine binding by 25.5%, consistent with a competitive interaction at the DAT. pmid:12888780
Cryo-EM structures at the GluN1-GluN2B NMDA receptor (2.5–3.5 Å resolution) reveal PCP lodged within the channel pore, forming contacts with pore-lining residues that are conserved across NMDA receptor subtypessupported
Here, we monitor the binding of three clinically important channel blockers: phencyclidine, ketamine, and memantine in GluN1-2B NMDARs at local resolutions of 2.5-3.5Å around the binding site using single-particle electron cryo-microscopy. s41594-022-00772-0
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Comparative binding studies across GluN2 subunit compositions show PCP binds GluN2A- and GluN2B-containing NMDA receptors with broadly similar affinity, though functional potency (IC50 in electrophysiology) may differ modestly between subtypes.supported
The pharmacological activities of MK-801, phencyclidine (PCP), dexoxadrol, etoxadrol, (S)- and (R)-ketamine, dextromethorphan, memantine, and amantadine were analyzed under uniform assay conditions. cmdc.201700810
In their model, PCP's psychotic effects arise from combined NMDA hypofunction and direct D2 stimulation — a "hyperdopamine/hypoglutamate" mechanism.supported
Phencyclidine had a high affinity for D2High with a Ki of 2.7 nM, in contrast to its low affinity for the NMDA receptor, with a Ki of 313 nM. pmid:15852061
comparative-pharmacology3 · 2 ok
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Both compounds are use-dependent NMDA channel blockers, but their clinical profiles diverge markedly: ketamine remains a widely used anaesthetic while PCP was withdrawn due to unacceptable emergence reactions.supported
The history of ketamine and phencyclidine from their development as potential clinical anaesthetics through drugs of abuse and animal models of schizophrenia to potential rapidly acting antidepressants is reviewed. bph.13222
Amphetamine-induced psychosis generates only positive symptoms; PCP uniquely reproduces the full triad of positive symptoms, negative symptoms, and cognitive deficitssupported
PCP induces a psychotomimetic state that closely resembles schizophrenia, incorporating both positive and negative symptoms, formal thought disorder, and neuropsychological deficits. pmid:1654746
history3 · 1 ok
Claim in history — inconclusiveinconclusiveworking →
These reactions proved sufficiently common and severe that human clinical use was discontinued in 1965supported
The history of ketamine and phencyclidine from their development as potential clinical anaesthetics... is reviewed. bph.13222
Claim in history — inconclusiveinconclusiveworking →
chemistry1 · 1 ok
This scaffold is shared by ketamine, tiletamine, methoxetamine, and the designer dissociative PCP analogues (3-meo-pcp, 4-meo-pcp, etc.)supported
Dissociative designer drugs primarily act as NMDA receptor antagonists and pose similar health risks as ketamine. PCP cited as parent compound for the dissociative class. s00204-020-02693-7
effects-overview1 · 0 ok
Claim in effects-overview — inconclusiveinconclusiveworking →