Phencyclidine: Difference between revisions
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MDElliottMD (talk | contribs) home-claude full build-out: history-first article replacing 984-byte stub |
MDElliottMD (talk | contribs) home-claude: add dosing field + Erowid PCP block (MedTemplate parity with Ketamine) |
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| legal = [[USLegal:DEA Schedule II|Schedule II]] controlled substance in US (rescheduled from Schedule III in 1978). No accepted medical use. UN Convention on Psychotropic Substances Schedule II internationally.<ref name="dea-scheduling" /> | | legal = [[USLegal:DEA Schedule II|Schedule II]] controlled substance in US (rescheduled from Schedule III in 1978). No accepted medical use. UN Convention on Psychotropic Substances Schedule II internationally.<ref name="dea-scheduling" /> | ||
| mechanism = <vote slug="phencyclidine-mech-claim">Phencyclidine is a non-competitive open-channel blocker of the NMDA glutamate receptor, binding to a site within the channel pore (the "PCP site", named for this medicine) that is accessible only when the channel is open; the resulting use-dependent block produces dissociation, anesthesia, and the broad cognitive disruption characteristic of NMDA antagonism.</vote> Secondary activity at sigma-1 receptors (agonist), the dopamine transporter (weak inhibition), and nicotinic acetylcholine receptors (antagonist) shapes the distinctive clinical profile compared with the cleaner profile of ketamine.<ref name="anis-1983">Anis NA, Berry SC, Burton NR, Lodge D. The dissociative anaesthetics, ketamine and phencyclidine, selectively reduce excitation of central mammalian neurones by N-methyl-aspartate. ''British Journal of Pharmacology'' 1983;79(2):565-575.{{citation needed}}</ref> Metabolized by [[CYP3A4]] and [[CYP2B6]]; the parent compound is the principal active species. | | mechanism = <vote slug="phencyclidine-mech-claim">Phencyclidine is a non-competitive open-channel blocker of the NMDA glutamate receptor, binding to a site within the channel pore (the "PCP site", named for this medicine) that is accessible only when the channel is open; the resulting use-dependent block produces dissociation, anesthesia, and the broad cognitive disruption characteristic of NMDA antagonism.</vote> Secondary activity at sigma-1 receptors (agonist), the dopamine transporter (weak inhibition), and nicotinic acetylcholine receptors (antagonist) shapes the distinctive clinical profile compared with the cleaner profile of ketamine.<ref name="anis-1983">Anis NA, Berry SC, Burton NR, Lodge D. The dissociative anaesthetics, ketamine and phencyclidine, selectively reduce excitation of central mammalian neurones by N-methyl-aspartate. ''British Journal of Pharmacology'' 1983;79(2):565-575.{{citation needed}}</ref> Metabolized by [[CYP3A4]] and [[CYP2B6]]; the parent compound is the principal active species. | ||
| dosing = | |||
<titration slug="erowid-dose-oral" author="erowid-claude" | |||
title="Oral dose ladder (Erowid)"> | |||
Erowid's dosage documentation for oral PCP<ref name="erowid-pcp-dose"> | |||
Erowid. PCP Dosage. Erowid.org. | |||
https://www.erowid.org/chemicals/pcp/pcp_dose.shtml. | |||
Accessed 2026-05-26.</ref> reports the following tiers (threshold | |||
and heavy not characterized): | |||
* '''Light:''' 3-5 mg | |||
* '''Common:''' 5-10 mg | |||
* '''Strong:''' 10+ mg | |||
Duration approximately 4 to 6 hours with aftereffects up to 24 hours. | |||
Timing not specified by Erowid. PCP is frequently applied to plant | |||
material (cannabis or tobacco) and smoked; specific dose tiers for | |||
smoked administration are not documented by Erowid. | |||
</titration> | |||
}} | }} | ||