Phencyclidine

Phencyclidine (PCP), also known as angel dust among other names, is a drug used
Phencyclidine
for its mind-altering effects.[5] PCP may cause hallucinations, distorted perceptions
of sounds, and violent behavior.[7][8] As a recreational drug, it is typically smoked,
but may be taken by mouth, snorted, or injected.[7][4] It may also be mixed with
cannabis or tobacco.[5]

Adverse effects may include seizures, coma, addiction, and an increased risk of
suicide.[7] Flashbacks may occur despite stopping usage.[8] Chemically, PCP is a
member of the arylcyclohexylamine class, and pharmacologically, it is a dissociative
anesthetic.[9][10] PCP works primarily as anNMDA receptor antagonist.[9]

PCP is most commonly used in the United States.[11] While usage peaked there in
the 1970s,[12] between 2005 and 2011 an increase in visits to emergency
departments as a result of the drug occurred.[7] As of 2017 in the United States about
1% of people in grade twelve reported using PCP in the prior year while 2.9% of
[13]
those over the age of 25 reported using it at some point in their life.

PCP was initially made in 1926 and brought to market as ananesthetic medication in
the 1950s.[10][14] Its use in humans was disallowed in the United States in 1965 due
to the high rates of side effects while its use in other animals was disallowed in
Clinical data
1978.[5][15][10] Moreover, ketamine was discovered and was better tolerated as an
Trade names Sernyl, Sernylan
anesthetic.[15] PCP is currently illegal in the United States where it is classified as a
schedule II drug.[5] A number of derivatives of PCP have been sold for recreational
(both
and non-medical use.[16]
discontinued)
Synonyms Phenylcyclohexyl
piperidine, Angel
dust, animal
Contents tranquilizer,
Recreational uses embalming fluid,
Effects wack[5]
Addiction
AHFS/Drugs.com phencyclidine
Methods of administration
Addiction Variable reported
Management of intoxication
liability from low to
Pharmacology
Pharmacodynamics high[1][2][3]
Pharmacokinetics Routes of Smoking,
administration injection, snorted,
Chemistry
Analogues by mouth[4]
Usage ATC code None
History
Legal status
Regulation
Legal status AU: S9
References
(Prohibited)
External links
CA: Schedule I

DE: Anlage I
Recreational uses (Authorized
 scientific use
only)
Effects
UK: Class A
Behavioral effects can vary by dosage. Low doses produce a numbness in the
US: Schedule II
extremities and intoxication, characterized by staggering, unsteady gait, slurred
speech, bloodshot eyes, and loss of balance. Moderate doses (5–10 mg intranasal, or Pharmacokinetic data
0.01–0.02 mg/kg intramuscular or intravenous) will produce analgesia and Onset of action 2–60 min[6]
anesthesia. High doses may lead to convulsions.[17] The drug is often illegally Elimination 7–46 hours
produced under poorly-controlled conditions; this means that users may be unaware half-life
of the actual dose they are taking.[18] Duration of 6–48 hours[6]
action
Psychological effects include severe changes in body image, loss of ego boundaries, Identifiers
paranoia, and depersonalization. Hallucinations, euphoria, and suicidal impulses are
IUPAC name
also reported, as well as occasional aggressive behavior.[19]:48–49[17] Like many
other drugs, PCP has been known to alter mood states in an unpredictable fashion,
CAS Number 77-10-1
causing some individuals to become detached, and others to become animated. PCP PubChem CID 6468
may induce feelings of strength, power, and invulnerability as well as a numbing
IUPHAR/BPS 4282
effect on the mind.[4]
DrugBank DB03575
Studies by the Drug Abuse Warning Network in the 1970s show that media reports
of PCP-induced violence are greatly exaggerated and that incidents of violence are ChemSpider 6224
unusual and often limited to individuals with reputations for aggression regardless of UNII J1DOI7UV76
drug use.[19]:48 Although uncommon, events of PCP-intoxicated individuals acting
KEGG C07575
in an unpredictable fashion, possibly driven by their delusions or hallucinations,
have been publicized. One example is the case of Big Lurch, a former rapper with a ChEBI CHEBI:8058
history of violent crime, who was convicted of murdering and cannibalizing his
ChEMBL CHEMBL275528
roommate while under the influence of PCP.[20] Other commonly cited types of
incidents include inflicting property damage and self-mutilation of various types,
such as pulling one's own teeth.[19]:48[20] These effects were not noted in its ECHA InfoCard 100.150.427
medicinal use in the 1950s and 1960s however, and reports of physical violence on Chemical and physical data
PCP have often been shown to be unfounded.[21][22]
Formula C17H25N
Recreational doses of the drug also occasionally appear to induce a psychotic state Molar mass 243.39 g·mol−1
that resembles a schizophrenic episode, sometimes lasting for months at a time.[23] 3D model Interactive image
.[24]
Users generally report feeling detached from reality (JSmol)
SMILES
Symptoms are summarized by the mnemonic device RED DANES: rage, erythema
(redness of skin), dilated pupils, delusions, amnesia, nystagmus (oscillation of the InChI
[25]
eyeball when moving laterally), excitation, and skin dryness. See also: data page
(what is this?) (verify)

Addiction
PCP is self-administered and induces ΔFosB expression in the D1-type medium spiny neurons of the nucleus accumbens,[1][26] and
accordingly, excessive PCP use is known to causeaddiction.[1] PCP's rewarding and reinforcing effects are at least partly mediated by
blocking the NMDA receptors in the glutamatergic inputs to D1-type medium spiny neurons in the nucleus accumbens.[1] PCP has
been shown to produceconditioned place aversionand conditioned place preferencein animal studies.[27]

Methods of administration
PCP comes in both powder and liquid forms (PCP base is dissolved most often in
ether), but typically it is sprayed onto leafy material
such as cannabis, mint, oregano, tobacco, parsley, or ginger leaves, then smoked.
 PCP can be ingested through smoking. "Fry" is a street term for marijuana
[28]
or tobacco cigarettes that are dipped in PCP and then dried.
PCP hydrochloride can be insufflated (snorted), depending upon the
purity.
The free base is quite hydrophobic and may be absorbed through skin
and mucus membranes (often inadvertently).

Management of intoxication
Management of PCP intoxication mostly consists of supportive care – controlling
breathing, circulation, and body temperature – and, in the early stages, treating
psychiatric symptoms.[29][30][31] Benzodiazepines, such as lorazepam, are the drugs
Illicit PCP in several forms seized
of choice to control agitation and seizures (when present). Typical antipsychotics such by the DEA.
as phenothiazines and haloperidol have been used to control psychotic symptoms, but
may produce many undesirable side effects – such as dystonia – and their use is
therefore no longer preferred; phenothiazines are particularly risky, as they may lower the seizure threshold, worsen hyperthermia,
and boost the anticholinergic effects of PCP.[29][30] If an antipsychotic is given, intramuscular haloperidol has been
recommended.[31][32][33]

Forced acid diuresis (with ammonium chloride or, more safely, ascorbic acid) may increase clearance of PCP from the body, and was
somewhat controversially recommended in the past as a decontamination measure.[29][30][31] However, it is now known that only
around 10% of a dose of PCP is removed by the kidneys, which would make increased urinary clearance of little consequence;
furthermore, urinary acidification is dangerous, as it may induce acidosis and worsen rhabdomyolysis (muscle breakdown), which is
.[29][30]
not an unusual manifestation of PCP toxicity

Pharmacology

Pharmacodynamics
PCP is well known for its primary action on the NMDA receptor, an ionotropic glutamate receptor, in rats and in rat brain
homogenate.[44][41] As such, PCP is an NMDA receptor antagonist. The role of NMDAR antagonism in the effect of PCP, ketamine,
and related dissociative agents was first published in the early 1980s by David Lodge[45] and colleagues.[16] Other NMDA receptor
antagonists include ketamine,[46] tiletamine,[47] dextromethorphan,[48] nitrous oxide, and dizocilpine (MK-801).

Research also indicates that PCP inhibits nicotinic acetylcholine receptors (nAChRs) among other mechanisms. Analogues of PCP
exhibit varying potency at nACh receptors[49] and NMDA receptors.[50] Findings demonstrate that presynaptic nAChRs and NMDA
receptor interactions influence postsynaptic maturation of glutamatergic synapses and consequently impact synaptic development and
plasticity in the brain.[51] These effects can lead to inhibition of excitatory glutamate activity in certain brain regions such as the
hippocampus[52] and cerebellum[53] thus potentially leading to memory loss as one of the effects of prolonged use. Acute effects on
the cerebellum manifest as changes in blood pressure, breathing rate, pulse rate, and loss of muscular coordination during
intoxication.[8]

PCP, like ketamine, also acts as a potent dopamine D2High receptor partial agonist in rat brain homogenate[41] and has affinity for the
human cloned D2High receptor.[54] This activity may be associated with some of the other more psychotic features of PCP
intoxication, which is evidenced by the successful use of D2 receptor antagonists (such as haloperidol) in the treatment of PCP
psychosis.[55]

In addition to its well explored interactions with NMDA receptors, PCP has also been shown to inhibit dopamine reuptake, and
thereby leads to increased extracellular levels of dopamine and hence increased dopaminergic neurotransmission.[56] However, PCP
has little affinity for the human monoamine transporters, including the dopamine transporter (DAT).[36] Instead, its inhibition of
monoamine reuptake may be mediated by interactions with allosteric sites on the monoamine transporters.[36] PCP is notably a high-
affinity ligand of the PCP site 2 (Ki = 154 nM), a
not-well-characterized site associated with Phencyclidine[34][35]
monoamine reuptake inhibition.[37] Site Ki (nM) Action Species Ref
[36][37]
Studies on rats indicate that PCP interacts indirectly NMDA 44–59 Antagonist Human
with opioid receptors (endorphin and enkephalin) to MOR >10,000 ND Human [36]

produce analgesia.[57] [36]

DOR >10,000 ND Human

A binding study assessed PCP at 56 sites including KOR >10,000 ND Human [36]

neurotransmitter receptors and transporters and NOP >10,000 ND Human [36]

found that PCP had Ki values of >10,000 nM at all
σ1 >10,000 Agonist Guinea pig [36][38]
sites except the dizocilpine (MK-801) site of the
[36]
NMDA receptor (Ki = 59 nM), the σ2 receptor σ2 136 Agonist Rat
(PC12) (Ki = 136 nM), and the serotonin transporter D >10,000 ND Human [36]
2
(Ki = 2,234 nM).[36] The study notably found Ki
2.7–4.3 Rat/human [39][40]
High
values of >10,000 nM for the D2 receptor, the D2 144 (EC50)
Agonist
Human [41]
opioid receptors, the σ1 receptor, and the dopamine
5-HT2A >10,000 ND Human [36]
and norepinephrine transporters.[36] These results
suggest that PCP is a highly selective ligand of the 5-HT2AHigh ≥5,000 Agonist? Rat [40][42]

NMDAR and σ2 receptor.[36] However, PCP may SERT 2,234 Inhibitor Human [36]
also interact with allosteric sites on the monoamine
NET >10,000 Inhibitor Human [36]
transporters to produce inhibition of monoamine
DAT >10,000 Inhibitor Human [36]
reuptake.[36]
PCP2 154 ND Human [37]

Neurotoxicity [3H]5-HT uptake 1,424 (IC50) Inhibitor Rat [43]

Some studies found that, like other NMDA receptor [3H]NIS binding 16,628 (IC50) Inhibitor Rat [43]

antagonists, PCP can cause a kind of brain damage

[3H]DA uptake 347 (IC50) Inhibitor Rat [43]
called Olney's lesions in rats.[58][59] Studies
3 1,547 (IC50) [43]
conducted on rats showed that high doses of the [ H]CFT binding Inhibitor Rat
NMDA receptor antagonist dizocilpine caused Values are K (nM). The smaller the value, the more strongly the drug
i
reversible vacuoles to form in certain regions of the binds to the site.
rats' brains. All studies of Olney's lesions have only
been performed on non-human animals and may not apply to humans. One unpublished study by Frank Sharp reportedly showed no
damage by the NDMA antagonist, ketamine, a similar drug, far beyond recreational doses,[60] but due to the study never having been
published, its validity is controversial.

PCP has also been shown to cause schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate levels in the rat
brain, which are detectable both in living rats and upon necropsy examination of brain tissue.[61] It also induces symptoms in humans
that mimic schizophrenia.[62] PCP not only produced symptoms similar to schizophrenia, it also yielded electroencephalogram
changes in the thalamocortical pathway (increased delta decreased alpha) and in the hippocampus (increase theta bursts) that were
similar to those in schizophrenia.[63] PCP induced augmentation of dopamine release may link the NMDA and DA hypothesis of
schizophrenia.[64]

Pharmacokinetics
PCP is metabolized intoPCHP, PPC and PCAA.

When smoked, some of the compound is broken down by heat into1-phenylcyclohexene (PC) and piperidine.
 Conversion of PCP into PC and piperidine by heat.

Chemistry
PCP is an arylcyclohexylamine.

Analogues
Fewer than 30 different analogues of PCP were reported as being used on the street
during the 1970s and 1980s, mainly in the United States.[16] The best known of these
are rolicyclidine (PCPy or 1-(1-phenylcyclohexyl)pyrrolidine); eticyclidine (PCE or
N-ethyl-1-phenylcyclohexylamine); and tenocyclidine (TCP or 1-(1-(2-
thienyl)cyclohexyl)piperidine).[65] Only of a few of these compounds were widely
used.[16]

The generalized structural motif required for PCP-like activity is derived from
structure-activity relationship studies of PCP derivatives, and summarized in the
illustration (right). All of these derivatives are likely to share some of their
psychoactive effects with PCP itself, although a range of potencies and varying
mixtures of anesthetic, dissociative and stimulant effects are known, depending on the
Possible analogues of PCP
particular drug and its substituents. In some countries such as the United States,
Australia, and New Zealand, all of these compounds would be considered controlled
substance analogues of PCP, and are hence illegal drugs if sold for human consumption, even though many of them have never been
made or tested.[66][67]

Other analogues of PCP include3-HO-PCP, 3-MeO-PCMo, and 3-MeO-PCP.

Usage
PCP began to emerge as a recreational drug in major cities in the United States in 1960s.[7] In 1978, People magazine and Mike
Wallace of 60 Minutes called PCP the country's "number one" drug problem. Although recreational use of the drug had always been
relatively low, it began declining significantly in the 1980s. In surveys, the number of high school students admitting to trying PCP at
[19]:46–49
least once fell from 13% in 1979 to less than 3% in 1990.

History
It is commonly mistakenly reported that PCP was first synthesized in 1926.[68] This early synthesis, in fact, refers to the PCP
intermediate PCC.[16] PCP was actually discovered by Victor Maddox, a chemist at Parke-Davis in Michigan, while investigating
synthetic analgesic agents. Although unexpected, PCP was identified as potentially interesting, and as such, was submitted for
pharmacological testing. The promising results of these pharmacological investigations led to the rapid development of PCP. It was
approved for use as an investigational drug under the brand names Sernyl and Sernylan in the 1950s as an anesthetic, but because of
its long terminal half-life and adverse side effects, such as hallucinations, mania, delirium, and disorientation, it was removed from
the market in 1965 and limited to veterinary use.[16][69][70]

Regulation
PCP is a Schedule II substance in the United States and itsACSCN is 7471.[71] Its manufacturing quota for 2014 was 19 grams.[72]

It is a Schedule I drug by the Controlled Drugs and Substances act in Canada, a List I drug of the Opium Law in the Netherlands, and
a Class A substance in the United Kingdom.[73]

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External links
Erowid.org – PCP Information
National Institute of Drug Abuse InfoFacts: PCP (Phencyclidine)
Drugs and Human Performance Fact Sheets on Phencyclidine
Phencyclidine and Ketamine: A View From the Street-1981 article on the use and effects of PCP

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