| Identification | Back Directory | [Name]
PHENCYCLIDINE | [CAS]
77-10-1 | [Synonyms]
PCP
C07575
HUMPCP
Phencylidine
PHENCYCLIDINE
PrCP active human
Pcp (phencyclidine)
Phencyclidine (pcp)
prolylcarboxypeptidase
Phencyclidine solution
Pentachlorophenol in methanol
1-(1-PHENYLCYCLOHEXYL)PIPERIDINE
PCP (Phencyclidine) solution
Piperidine, 1-(1-phenylcyclohexyl)-
Methanol(test Phencyclidine(PCP),1.0mg/mL)
1-(1-Phenylcyclohexyl)piperidine solution, PCP solution | [Molecular Formula]
C17H25N | [MDL Number]
MFCD00055598 | [MOL File]
77-10-1.mol | [Molecular Weight]
243.39 |
| Hazard Information | Back Directory | [Uses]
Anesthetic. | [Definition]
ChEBI: A member of the class of piperidines that is piperidine in which the nitrogen is substituted with a 1-phenylcyclohexyl group. Formerly used as an anaesthetic agent, it exhibits both hallucinogenic and neurotoxic effects. | [Brand name]
Sernylan (Parke-Davis). | [General Description]
Phencyclidine was introduced as a dissociative anestheticfor animals. Its close structural relative ketamine is still soused and may be used in humans. In humans,PCP produces a sense of intoxication, hallucinogenic experiencesnot unlike those produced by the anticholinergic hallucinogens,and often, amnesia.
The drug affects many systems, including those of NE,DA, and 5-HT. It has been proposed that PCP (and certainother psychotomimetics) produces a unique pattern of activationof ventral tegumental area dopaminergic neurons.Itblocks glutaminergic N-methyl-D-aspartate receptors.Thisaction is the basis for many of its CNS effects. PCP itself appearsto be the active agent. The psychotic state produced bythis drug is also cited as a better model than amphetaminepsychosis for the psychotic state of schizophrenia. | [Pharmacology]
PCP acts as a biocide through its ability
to uncouple mitochondrial oxidative phosphorylation. | [Safety Profile]
Poison by intraperitoneal route. Experimental reproductive effects. Caution: This is a controlled substance (depressant) listed in the U.S. Code of Federal Regulations, Title 21 Part 1308.12 (1985). The ethylamine, pyrrolidine and thiophene analogs are l | [Enzyme inhibitor]
This piperidine (FWfree-base = 243.39 g/mol; CAS 77-10-1: Symbol: PCP),
commonly known as Angel Dust and systematically as 1- (1-
phenylcyclohexyl) piperidine, is a NMDA (N-methyl-D-aspartate)
antagonist, psychostimulant, s receptor agonist, and frequent drug of abuse
(2-5). Formerly used as a veterinary anesthetic and briefly as a general
anesthetic in humans, phencyclidine is also a powerful hallucinogen. Mode
of Action: NMDA receptors play important roles in mediating excitatory
neurotransmission and are preferentially inhibited by some general
anesthetics. Phencyclidine is similar to ketamine in structure and in many of
its effects; both produce a dissociative state (See Ketamine). Phencyclidine
inhibits activation of NMDA receptors (3-5), inducing schizophrenia-like
symptoms in healthy individuals and exacerbating pre-existing symptoms in
patients with schizophrenia. PCP behavioral effects are strongly dose-
dependent: low doses (3-5 mg) produce intoxication (characteristics:
numbness in the extremities, staggering or unsteady gait, slurred speech,
and bloodshot eyes); moderate doses (e.g., 5–10 mg intranasal or 0.01–0.02
mg/kg IM or IV) produce analgesia and anesthesia; and high doses often
lead to convulsions. Pharmacokinetics & Metabolism: PCP is well absorbed
by all routes of administration, but, in cigarette smoke, about half is
converted to an inactive thermal degradation product. PCP is highly lipid-
soluble, accouting for its tendency to concentrate in fat and brain tissue. The
plasma binding of PCP is 65%, and its t1/2 ranges from 7-46 hours, with a
21-hour average. PCP is extensively metabolized to inactive metabolites by
a variety of metabolic routes. Benzodiazepines decrease PCP’s hypertensive
effects and reverse seizure activity. PCP is also an inhibitor of a number of
cytochrome P450 systems and a suicide inhibitor of nitric-oxide synthase
. However, the inhibition of nitric-oxide synthase is not related to the
psychotomimetic action of phencyclidine. Target (s) : Ca2+-dependent
ATPase; CYP2B1; K+ channels, ATP-sensitive; nitric-oxide
synthase; and NMDA-receptor channel. Phencyclidine is a
powerful, noncompetitive inhibitor of the nicotinic acetylcholine receptor in
a sympathetic nerve cell line, PC-12. In the presence of 1 mM
carbamoylcholine, the rate of the receptor-controlled influx of 22Na+ is
reduced by a factor of 2 by 0.7 μM phencyclidine. | [Metabolic pathway]
When mice and rats are administered phencyclidine
intraperitoneally, several hydroxylated metabolites are
identified in the urine. A new metabolite, 1-phenyl-1-
(1-piperidinyl-3-ol)cyclohexane, is identified in the urine
and liver microsomal preparations. | [Metabolism]
Pentachlorophenolwas metabolized in rats
by conjugation with glucuronic acid and eliminated as
the glucuronide. P450 catalyzed oxidative dechlorination
also occurred to form tetrachlorohydroquinone, and this
was conjugated to form a monoglucuronide representing
27% of the dose administered. Other metabolites
have been reported, including isomeric tetrachlorophenols,
tetrachlorocatechol and tetrachlororesorcinol. Trace
amounts of benzoquinones were also noted.
Metabolites in female rats were tetrachloromonophenols,
diphenols, and hydroquinones. | [Toxicity evaluation]
The toxicology has been addressed in a
recent risk assessment (119). Acutely, pentachlorophenol
was reported to have LD50 values in the rat of 12 mg/kg
(inhalation) and 146 mg/kg (M)–175 mg/kg (F) by oral
gavage. More detailed studies of the toxicology of pentachlorophenol
have been compromised by the toxicity of
impurities present in most of the earlier samples used
in the evaluation process. |
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