.
“fen SAI kluh deen”
*aka ‘PCP’*
(ain’t no ‘day at the beach’…)
.
.
(or “Phenyl Cyclo-hexyl Piperidine”)
(PCP)
.
“angel dust”
.
-as of [13 APRIL 2024]–
.
-a ‘dissociative hallucinogenic drug’ used for its ‘mind-altering effects’-
.
PCP may cause hallucinations, distorted perceptions of sounds, and violent behavior
As a recreational drug, it is typically smoked, but may be taken by mouth, snorted, or injected
It may also be mixed with cannabis or tobacco
Adverse effects may include seizures, coma, addiction, and an increased risk of suicide
Flashbacks may occur despite stopping usage
Chemically, PCP is a member of the arylcyclohexylamine class,
and pharmacologically, it is a dissociative anesthetic.[5][10][11]
PCP works primarily as an NMDA receptor antagonist.[10]
PCP is most commonly used in the United States
While usage peaked in the US in the 1970s,[13] between 2005 and 2011 an increase in visits to emergency departments as a result of the drug occurred
As of 2017 in the United States, about 1% of people in grade 12 reported using PCP in the prior year while 2.9% of those over the age of 25 reported using it at some point in their lives.[14]
Recreational uses[edit]
Illicit PCP in several forms seized by the DEA.
Phencyclidine is used for its ability to induce a dissociative state
.
Effects
Behavioral effects can vary by dosage.
Low doses produce
a numbness in the extremities
and intoxication,
characterized by
staggering,
unsteady gait,
slurred speech,
bloodshot eyes,
and loss of balance
.
Moderate doses (5–10 mg intranasal, or 0.01–0.02 mg/kg intramuscular or intravenous) will produce analgesia and anesthesia. High doses may lead to convulsions.[16] The drug is often illegally produced under poorly controlled conditions; this means that users may be unaware of the actual dose they are taking.[17]
Psychological effects include severe changes in body image, loss of ego boundaries, paranoia, and depersonalization. Psychosis, agitation and dysphoria, hallucinations, blurred vision, euphoria, and suicidal impulses are also reported, as well as occasional aggressive behavior.[18][19]: 48–49 [16] Like many other drugs, PCP has been known to alter mood states in an unpredictable fashion, causing some individuals to become detached, and others to become animated. PCP may induce feelings of strength, power, and invulnerability as well as a numbing effect on the mind.[6]
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 unusual and often limited to individuals with reputations for aggression regardless of drug use.[19]: 48 Although uncommon, events of PCP-intoxicated individuals acting in an unpredictable fashion, possibly driven by their delusions or hallucinations, have been publicized.[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 medicinal use in the 1950s and 1960s, however, and reports of physical violence on PCP have often been shown to be unfounded.[21][22]
Recreational doses of the drug also occasionally appear to induce a psychotic state, with emotional and cognitive impairment that resembles a schizophrenic episode.[23][24] Users generally report feeling detached from reality.[25]
Symptoms are summarized by the mnemonic device RED DANES: rage, erythema (redness of skin), dilated pupils, delusions, amnesia, nystagmus (oscillation of the eyeball when moving laterally), excitation, and skin dryness.[26]
Addiction[edit]
PCP is self-administered and induces ΔFosB expression in the D1-type medium spiny neurons of the nucleus accumbens,[2][27] and accordingly, excessive PCP use is known to cause addiction.[2] 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.[2] PCP has been shown to produce conditioned place aversion and conditioned place preference in animal studies.[28]
Schizophrenia[edit]
A 2019 review found that the transition rate from a diagnosis of hallucinogen-induced psychosis (which included PCP) to that of schizophrenia was 26%. This was lower than cannabis-induced psychosis (34%) but higher than amphetamine (22%), opioid (12%), alcohol (10%) and sedative (9%) induced psychoses. In comparison, the transition rate to schizophrenia for “brief, atypical and not otherwise specified” psychosis was found to be 36%.[29]
Methods of administration[edit]
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.[citation needed]
PCP can be ingested through smoking. “Fry” or “sherm” are street terms for marijuana or tobacco cigarettes that are dipped in PCP and then dried.[30]
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[edit]
Management of PCP intoxication mostly consists of supportive care – controlling breathing, circulation, and body temperature – and, in the early stages, treating psychiatric symptoms.[31][32][33] Benzodiazepines, such as lorazepam, are the drugs of choice to control agitation and seizures (when present). Typical antipsychotics such 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.[31][32] If an antipsychotic is given, intramuscular haloperidol has been recommended.[33][34][35]
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.[31][32][33] 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), a not-unusual manifestation of PCP toxicity.[31][32]
Pharmacology[edit]
Pharmacodynamics[edit]
Phencyclidine[36][37]
Site Ki (nM) Action Species Ref
NMDA 44–59 Antagonist Human [38][39]
MOR >10,000 ND Human [38]
DOR >10,000 ND Human [38]
KOR >10,000 ND Human [38]
NOP >10,000 ND Human [38]
σ1 >10,000 Agonist Guinea pig [38][40]
σ2 136 Agonist Rat [38]
D2 >10,000 ND Human [38]
D2High 2.7–4.3
144 (EC50) Agonist Rat/human
Human [41][42]
[43]
5-HT2A >10,000 ND Human [38]
5-HT2AHigh ≥5,000 Agonist? Rat [42][44]
SERT 2,234 Inhibitor Human [38]
NET >10,000 Inhibitor Human [38]
DAT >10,000 Inhibitor Human [38]
PCP2 154 ND Human [39]
[3H]5-HT uptake 1,424 (IC50) Inhibitor Rat [45]
[3H]NIS binding 16,628 (IC50) Inhibitor Rat [45]
[3H]DA uptake 347 (IC50) Inhibitor Rat [45]
[3H]CFT binding 1,547 (IC50) Inhibitor Rat [45]
Values are Ki (nM). The smaller the value, the more strongly the drug binds to the site.
PCP is well known for its primary action on the NMDA receptor, an ionotropic glutamate receptor, in rats and in rat brain homogenate.[46][43] 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[47] and colleagues.[48] Other NMDA receptor antagonists include ketamine,[49] tiletamine,[50] dextromethorphan,[51] 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[52] and NMDA receptors.[53] 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.[54] These effects can lead to inhibition of excitatory glutamate activity in certain brain regions such as the hippocampus[55] and cerebellum[56] 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.[9]
PCP, like ketamine, also acts as a potent dopamine D2High receptor partial agonist in rat brain homogenate[43] and has affinity for the human cloned D2High receptor.[57] 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.[58]
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.[59] However, PCP has little affinity for the human monoamine transporters, including the dopamine transporter (DAT).[38] Instead, its inhibition of monoamine reuptake may be mediated by interactions with allosteric sites on the monoamine transporters.[38] PCP is notably a high-affinity ligand of the PCP site 2 (Ki = 154 nM), a not-well-characterized site associated with monoamine reuptake inhibition.[39]
Studies on rats indicate that PCP interacts indirectly with opioid receptors (endorphin and enkephalin) to produce analgesia.[60]
A binding study assessed PCP at 56 sites including neurotransmitter receptors and transporters and found that PCP had Ki values of >10,000 nM at all sites except the dizocilpine (MK-801) site of the NMDA receptor (Ki = 59 nM), the σ2 receptor (PC12) (Ki = 136 nM), and the serotonin transporter (Ki = 2,234 nM).[38] The study notably found Ki values of >10,000 nM for the D2 receptor, the opioid receptors, the σ1 receptor, and the dopamine and norepinephrine transporters.[38] These results suggest that PCP is a highly selective ligand of the NMDAR and σ2 receptor.[38] However, PCP may also interact with allosteric sites on the monoamine transporters to produce inhibition of monoamine reuptake.[38]
Mechanism of action[edit]
Phencyclidine is an NMDA receptor antagonist that blocks the activity of the NMDA receptor to cause anaesthesia and analgesia without causing cardiorespiratory depression.[61][18] NMDA is an excitatory receptor in the brain, when activated normally the receptor acts as an ion channel and there is an influx of positive ions through the channel to cause nerve cell depolarisation. Phencyclidine enters the ion channel and binds, reversibly and non-competitively, inside the channel pore to block the entry of positive ions to the cell, thereby inhibiting cell depolarisation.[61][62]
Neurotoxicity[edit]
Some studies found that, like other NMDA receptor antagonists, PCP can cause a kind of brain damage called Olney’s lesions in rats.[63][64] Studies conducted on rats showed that high doses of the NMDA receptor antagonist dizocilpine caused reversible vacuoles to form in certain regions of the 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 structurally similar drug, far beyond recreational doses,[65] 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.[66] It also induces symptoms in humans that mimic schizophrenia.[67] 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.[68] PCP-induced augmentation of dopamine release may link the NMDA and dopamine hypotheses of schizophrenia.[69]
Pharmacokinetics[edit]
PCP is metabolized into PCHP, PPC and PCAA. The drug is metabolized 90% by oxidative hydroxylation in the liver during the first pass. Metabolites are glucuronidated and excreted in the urine. Nine percent of ingested PCP is excreted in its unchanged form.[18]
When smoked, some of the compound is broken down by heat into 1-phenylcyclohexene (PC) and piperidine.
Conversion of PCP into PC and piperidine by heat.
The time taken before the effects of PCP manifest is dependent on the route of administration. The onset of action for inhalation occurs in 2–5 minutes, whereas the effects may take 15 to 60 minutes when ingested orally.[18]
Chemistry[edit]
PCP is an arylcyclohexylamine.
Analogues[edit]
Possible analogues of PCP
Fewer than 30 different analogs of PCP were reported as being used on the street during the 1970s and 1980s, mainly in the United States.[48] Only of a few of these compounds were widely used including rolicyclidine (PCPy), eticyclidine (PCE), and tenocyclidine (TCP).[48] Less common analogs include 3-HO-PCP, 3-MeO-PCMo, and 3-MeO-PCP.
The generalized structural motif required for PCP-like activity is derived from structure-activity relationship studies of PCP derivatives. 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 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 analogs of PCP under the Federal Analog Act and are hence illegal drugs if sold for human consumption.[70][71]
History[edit]
PCP was initially made in 1926 and brought to market as an anesthetic medication in the 1950s.[11][72][73][74] Its use in humans was disallowed in the United States in 1965 due to the high rates of side effects, while its use in animals was disallowed in 1978.[1][11][75] Moreover, ketamine was discovered and was better tolerated as an anesthetic.[75] PCP is classified as a schedule II drug in the United States.[1] A number of derivatives of PCP have been sold for recreational and non-medical use.[48]
Society and culture[edit]
Regulation[edit]
PCP is a Schedule II substance in the United States and its ACSCN is 7471.[76] Its manufacturing quota for 2014 was 19 grams.[77]
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.[78]
Frequency of use[edit]
PCP began to emerge as a recreational drug in major cities in the United States in 1960s.[8] 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 least once fell from 13% in 1979 to less than 3% in 1990.[19]: 46–49
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^ Giannini AJ, Nageotte C, Loiselle RH, Malone DA, Price WA (1984). “Comparison of chlorpromazine, haloperidol and pimozide in the treatment of phencyclidine psychosis: DA-2 receptor specificity”. Journal of Toxicology. Clinical Toxicology. 22 (6): 573–9. doi:10.3109/15563658408992586. PMID 6535849.
^ Rothman RB, Reid AA, Monn JA, Jacobson AE, Rice KC (Dec 1989). “The psychotomimetic drug phencyclidine labels two high affinity binding sites in guinea pig brain: evidence for N-methyl-D-aspartate-coupled and dopamine reuptake carrier-associated phencyclidine binding sites”. Molecular Pharmacology. 36 (6): 887–96. PMID 2557536.
^ Castellani S, Giannini AJ, Adams PM (1982). “Effects of naloxone, metenkephalin, and morphine on phencyclidine-induced behavior in the rat”. Psychopharmacology. 78 (1): 76–80. doi:10.1007/BF00470593. PMID 6815700. S2CID 21996319.
^ Jump up to: a b “Phencyclidine”. www.drugbank.ca. Retrieved 28 January 2019.
^ Johnson KM, Jones SM (April 1990). “Neuropharmacology of phencyclidine: basic mechanisms and therapeutic potential”. Annual Review of Pharmacology and Toxicology. 30 (1): 707–50. doi:10.1146/annurev.pa.30.040190.003423. PMID 2160793.
^ Olney JW, Labruyere J, Price MT (Jun 1989). “Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs”. Science. 244 (4910): 1360–2. Bibcode:1989Sci…244.1360O. doi:10.1126/science.2660263. PMID 2660263.
^ Hargreaves RJ, Hill RG, Iversen LL (1994). “Neuroprotective NMDA antagonists: the controversy over their potential for adverse effects on cortical neuronal morphology”. Brain Edema IX. Acta Neurochirurgica. Supplementum. Vol. 60. pp. 15–9. doi:10.1007/978-3-7091-9334-1_4. ISBN 978-3-7091-9336-5. PMID 7976530.
^ Jansen, Karl. Ketamine: Dreams and Realities. MAPS, 2004. ISBN 0-9660019-7-4
^ Reynolds LM, Cochran SM, Morris BJ, Pratt JA, Reynolds GP (March 2005). “Chronic phencyclidine administration induces schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in rat brain”. Schizophrenia Research. 73 (2–3): 147–52. doi:10.1016/j.schres.2004.02.003. PMID 15653257. S2CID 1651693.
^ Murray JB (May 2002). “Phencyclidine (PCP): a dangerous drug, but useful in schizophrenia research”. The Journal of Psychology. 136 (3): 319–27. doi:10.1080/00223980209604159. PMID 12206280. S2CID 20334137.
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External links[edit]
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
“Phencyclidine”. Drug Information Portal. U.S. National Library of Medicine.
en.wikipedia.org /wiki/Phencyclidine
Phencyclidine
Contributors to Wikimedia projects32-41 minutes 11/26/2001
DOI: 10.1046/j.1460-9568.1999.00858.x, Show Details
Phencyclidine
Phencyclidine structure.svg
Phencyclidine-from-xtal-3D-balls.png
Clinical data
Trade names Sernyl, Sernylan (both discontinued)
Other names CI-395; Phenylcyclohexylpiperidine; “Angel dust”[1]
AHFS/Drugs.com phencyclidine
Addiction
liability Variable reported from low to high[2][3][4]
Routes of
administration Smoking, injection, snorted, by mouth[5][6]
Drug class NMDA receptor antagonists; General anesthetics; Dissociative hallucinogens[5]
ATC code
None
Legal status
Legal status
AU: S9 (Prohibited substance)
CA: Schedule I
DE: Anlage I (Authorized scientific use only)
UK: Class A
US: Schedule II
Pharmacokinetic data
Metabolism Oxidative hydroxylation in liver by CYP450 enzymes, glucuronidation
Metabolites PCHP, PPC, PCAA
Onset of action 2–60 min[7]
Elimination half-life 7–46 hours
Duration of action 6–48 hours[7]
Excretion Urine
Identifiers
show
IUPAC name
CAS Number
77-10-1 check
PubChem CID
6468
IUPHAR/BPS
4282
DrugBank
DB03575 check
ChemSpider
6224 check
UNII
J1DOI7UV76
KEGG
C07575 check
ChEBI
CHEBI:8058 ☒
ChEMBL
ChEMBL275528 check
CompTox Dashboard (EPA)
DTXSID6023446 Edit this at Wikidata
ECHA InfoCard 100.150.427 Edit this at Wikidata
Chemical and physical data
Formula C17H25N
Molar mass 243.394 g·mol−1
3D model (JSmol)
Interactive image
Melting point 46.5 °C (115.7 °F)
Boiling point 136 °C (277 °F)
show
SMILES
show
InChI
Data page
Phencyclidine (data page)
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