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Dissociative

PCP

Also called Angel Dust, Sherman, Sernyl, Wet, Dust, Supergrass, Boat, Tic Tac, Zoom

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Common dose · Oral5–10 mg PW
Onset30–90 minutes PW
Total4–8 hours PW
After-effects4–48 hours PW

Dosage

When sources disagree, both rows are shown as published. Nothing is averaged or merged.

Oral

SourceThresholdLightCommonStrongHeavy
PsychonautWiki1 mg PW3–5 mg PW5–10 mg PW10–15 mg PW15 mg+ Heavy doses may result in psychosis and mania.[14] PW
TripSit–2–5 mg TS5–10 mg TS10–15 mg+ TS–

Smoked

SourceThresholdLightCommonStrongHeavy
PsychonautWiki1 mg PW2–4 mg PW4–8 mg PW8–12 mg PW12 mg+ Heavy doses may result in psychosis and mania.[14] PW

Insufflated

SourceThresholdLightCommonStrongHeavy
PsychonautWiki1 mg PW2–4 mg PW4–8 mg PW8–15 mg PW15 mg+ Heavy doses may result in psychosis and mania.[14] PW
TripSit–2–4 mg TS4–8 mg TS8–15 mg+ TS–

NOTE: Be cautious with dosing, this drug is known to cause mania. TS

TripSit dose text

TripSit's factsheet also states its doses as text.

Oral Light: 2-5mg Common: 5-10mg Strong: 10-15mg+ | Insufflated Light: 2-4mg Common: 4-8mg Strong: 8-15mg+ | NOTE: Be cautious with dosing, this drug is known to cause mania. TS

What dose are you on? (self-reported, unverified)
Read this first. These numbers come from anonymous visitors typing in a box. Nobody checks them. People misjudge, mistype, troll, or take untested products of unknown strength. They are not a dose guide and never override the sourced table above. They exist only so the sourced ranges can be compared with what people say they take. If you are deciding what to take, use the sourced table, start low, and read the risks section.
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Duration

Route · sourceOnsetCome-upPeakOffsetTotalAfter-effects
Oral · PsychonautWiki30–90 minutes PW40–120 minutes PW2–3 hours PW1–2 hours PW4–8 hours PW4–48 hours PW
Smoked · PsychonautWiki2–20 minutes PW20–40 minutes PW2–3 hours PW1–2 hours PW4–6 hours PW4–48 hours PW
Insufflated · PsychonautWiki3–30 minutes PW30–90 minutes PW2–3 hours PW1–2 hours PW4–6 hours PW4–48 hours PW

TripSit factsheet

Onset
2-20 minutes TS
Duration
4-6 hours TS
Aftereffects
12-24 hours TS

Mixing

Acute combinations: what happens when these are taken close together. Entries backed by a medical journal or agency are listed first.

Backed by medical journals

Awaiting sourcePeer-reviewed reports on acute combinations, from PubMed and the journals the harm reduction sites cite.

Other documented combinations

  • Dangerous 2C-T-x PW
  • Dangerous ΑMT PW
  • Dangerous 5-MeO-xxT PW
  • Dangerous DXM PW
  • Dangerous GHB - Details of this combination are not well understood but PCP generally interacts in an unpredictable manner. PW
  • Dangerous GBL - Details of this combination are not well understood but PCP generally interacts in an unpredictable manner. PW
  • Dangerous Tramadol PW
  • Dangerous MAOIs - Little information exists about this combination. PW
  • Unsafe DOx - Details of this combination are not well understood but PCP generally interacts in an unpredictable manner. PW
  • Unsafe Amphetamines - This combination can easily lead to hypermanic states. PW
  • Unsafe MDMA - This combination can easily lead to hypermanic states. PW
  • Unsafe Cocaine - This combination can easily lead to hypermanic states. PW
  • Unsafe Alcohol - Details of this combination are not well understood but PCP generally interacts in an unpredictable manner. PW
  • Unsafe Benzodiazepines - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position. Memory blackouts are likely. PW
  • Unsafe SSRIs - Details of this combination are not well understood but PCP generally interacts in an unpredictable manner. PW
  • Uncertain MXE - There are no reports available about this combination. PW
  • Uncertain Caffeine - Details of this combination are not well understood but PCP generally interacts in an unpredictable manner. PW
  • Uncertain Opioids - PCP can reduce opioid tolerance, increasing the risk of overdose. PW

TripSit combination chart

TripSit rates each pairing. Only pairings with a number carry a citation from TripSit. See the whole chart, with TripSit's note for every pairing.

Dangerous

2c-t-x TS5-meo-xxt TSamt TSdextromethorphan TSghb/gbl TSmaois TStramadol TS

Unsafe

Caution

Low Risk & Synergy

Risks and toxicity

The long-term use of PCP may lead to schizophrenia-like psychotic episodes, severe lasting memory loss, disorganized thinking, depression, weight loss, liver abnormalities and rhabdomyolysis (skeletal muscle breakdown).[15] PW

It is very strongly recommended that one use extreme caution and harm reduction practices when using this substance. For example, PW

  • Users should avoid taking the drug multiple days in a row or becoming addicted to it as this increases the risk of severe adverse effects. PW
  • The recommended dosage range should not be exceeded as high doses can trigger adverse effects. PW
  • Users should start with extremely low doses and work their way up as slowly as possible. Volumetric liquid dosing should preferably be used due to the drug's potency; most standard milligram scales cannot accurately weigh out doses below 10-15mg. PW
  • Compulsive redosing before one has fully sobered up is not recommended and can result in too high of a dose. PW

Psychosis

PCP has been reported to cause psychosis and mania at a significantly higher rate than other dissociatives such as ketamine, diphenidine, or MXE. Multiple scientific papers describe states of psychosis, mania, and/or delirium occurring after moderate to large doses of the drug were ingested. PW

In one initial human trial, it was reported that one-sixth of the patients who had received anesthetic doses experienced acute psychosis. In some cases, it took up to a week or more to resolve. Similar results (although less severe) were reported during trials using subanesthetic doses of PCP for pain relief.[16][17] PW

Due to the risk of psychosis, it is not recommended to combine this substance with other substances, especially stimulants, psychedelics, or other dissociatives like MXE and DXM. PW

Neurological effects

Some studies found that, like other NMDA receptor antagonists, PCP can cause brain damage called Olney's lesions in rats. 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.[18][19] PW

One unpublished study by Frank Sharp reportedly showed no damage by the NMDA antagonist ketamine (a similar drug) far beyond recreational doses but its validity is controversial since it was never published.[20] PW

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. It also induces symptoms in humans that mimic schizophrenia.[21][22] PW

Urinary tract effects

In terms of its long-term health effects when used repeatedly and excessively for extended periods of time, PCP seems to exhibit almost identical bladder and urinary tract problems to those produced by ketamine. PW

  • Urinary frequency - Urinary frequency is the need to empty the bladder every few minutes. PW
  • Urinary urgency - This can be described as a sudden, compelling need to urinate. PW
  • Urinary pressure - This is experienced as a constant sensation of fullness in the bladder that is unrelieved by urination. PW
  • Pelvic and bladder pain - Pain can develop suddenly and severely, particularly as the bladder fills with urine. PW
  • Hematuria - Hematuria is visible blood in the urine. PW
  • Incontinence - This is the uncontrolled leakage of urine. PW

Dependence and abuse potential

The chronic use of PCP can be considered highly addictive with a high potential for adverse side effects such as psychosis. In comparison to other dissociatives, PCP has been reported to be more addictive than MXE, diphenidine, ephenidine, and ketamine. PW

When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage. There have been multiple reports across the internet of people becoming seriously addicted daily users of this substance so serious precautions and considerations should be taken before trying this substance. PW

Tolerance to many of the effects of PCP develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). PCP presents cross-tolerance with all dissociatives, meaning that after the consumption of PCP, all dissociatives will have a reduced effect. PW

Testing

Awaiting sourceReagent reactions and test kit guidance from a harm reduction testing service.

Effects

Awaiting sourceSubjective and physical effects from PsychonautWiki or TripSit.

Overview

Phencyclidine (also known as PCP, Angel Dust, Sherm, and Sernyl) is a classical dissociative substance of the arylcyclohexylamine class. It is one of the oldest and most notorious dissociatives, known for its potent effects and reputation as an established "street drug" (along with cocaine and heroin). It produces its effects by blocking the NMDA receptor.[1][2][3] PW

A strong dissociative drug. PCP works primarily as an NMDA receptor antagonist. Also referred to as "wet" or "angel dust". Best known for stories of the strange and sometimes violent behaviour of those under its influence, though it is likely these are only in overdose cases. TS

Phencyclidine or phenylcyclohexyl piperidine (PCP), also known in its use as a street drug as angel dust among other names, is a dissociative anesthetic mainly used recreationally for its significant mind-altering effects. PCP may cause hallucinations, distorted perceptions of sounds, and psychotic 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.[4–8] WP

Adverse effects may include paranoia, addiction, and an increased risk of suicide, as well as seizures and coma in cases of overdose. Flashbacks may occur despite stopping usage. Chemically, PCP is a member of the arylcyclohexylamine class. PCP works primarily as an NMDA receptor antagonist.[5][6][7][9][10] WP

PCP is most commonly used in the US. While usage peaked in the US in the 1970s, between 2005 and 2011, an increase in visits to emergency departments as a result of the drug occurred. As of 2022, in the US, about 0.7% of 12th-grade students reported using PCP in the prior year, while 1.7% of people in the US over age 25 reported using it at some point in their lives.[6][11][12][13] WP

History

History

Phencyclidine was initially discovered in 1926 by Arthur Kötz and his student Paul Merkel as a product of a Grignard reaction of 1-piperidinocyclohexancarbonitrile.[23] WP

It was again synthesized in 1956 by chemist H Victor Maddox and brought to market as an anesthetic medication by pharmaceutical company Parke-Davis, now a subsidiary of Pfizer. Its use in humans was disallowed in the US in 1965 due to the high rates of side effects, while its use in animals was disallowed in 1978. Moreover, ketamine was discovered and was better tolerated as an anesthetic.[4][10][23–27] WP

PCP is classified as a schedule II drug in the US. Derivatives of PCP have been sold for recreational and non-medical use.[4][28] WP

Pharmacology

Pharmacodynamics

PCP is well known for its primary action on the NMDA receptor, an ionotropic glutamate receptor. As such, PCP is a non-competitive 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 and colleagues. Other NMDA receptor antagonists include ketamine, tiletamine, dextromethorphan, nitrous oxide, and dizocilpine (MK-801).[28][52][55–59] WP

Research also indicates that PCP inhibits nicotinic acetylcholine receptors (nAChRs) among other mechanisms. Analogues of PCP exhibit varying potency at nACh receptors and NMDA receptors. Findings demonstrate that presynaptic nAChRs and NMDA receptor interactions influence the postsynaptic maturation of glutamatergic synapses and consequently impact synaptic development and plasticity in the brain. These effects can lead to inhibition of excitatory glutamate activity in certain brain regions such as the hippocampus and cerebellum 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.[7][60–64] WP

PCP, like ketamine, also acts as a potent dopamine D₂^High receptor partial agonist in rat brain homogenate and has affinity for the human cloned D₂^High receptor. 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.[52][65][66] WP

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. However, PCP has little affinity for the human monoamine transporters, including the dopamine transporter (DAT). Instead, its inhibition of monoamine reuptake may be mediated by interactions with allosteric sites on the monoamine transporters. 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.[46][47][67] WP

Studies on rats indicate that PCP interacts indirectly with opioid receptors (endorphin and enkephalin) to produce analgesia.[68] WP

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). 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. These results suggest that PCP is a highly selective ligand of the NMDAR and σ₂ receptor. However, PCP may also interact with allosteric sites on the monoamine transporters to produce inhibition of monoamine reuptake.[46] WP

Mechanism of action

Phencyclidine is a noncompetitive NMDA receptor antagonist that blocks the activity of the NMDA receptor to cause anaesthesia and analgesia without causing cardiorespiratory depression. 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 inhibits the NMDA receptor by binding to the specific PCP binding site located within the ion channel. The PCP binding site is near the magnesium blocking site, which may explain the similar inhibitory effects. Binding at the PCP site is mediated by two non-covalent interactions within the receptor: hydrogen bonding and hydrophobic interaction. Binding is also controlled by the gating mechanism of the ion channel. Because the PCP site is located within the ion channel, a coagonist such as glycine must bind and open the channel for PCP to enter, bind to the PCP site, and block the channel.[69–74] WP

Pharmacokinetics

PCP is both water- and lipid-soluble and is therefore distributed throughout the body quickly. 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.[70][72] WP

When smoked, some of the compound is broken down by heat into 1-phenylcyclohexene (PC) and piperidine. WP

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.[70] WP

Receptor binding · Wikipedia

Phencyclidine

SiteKᵢ (nM)ActionSpecies
NMDA (N-Methyl-D-aspartate receptor) (PCP₁)59AntagonistHuman[46–49] WP
MOR (μ-Opioid receptor)>10,000ND (No data)Human[46][48][49] WP
DOR (δ-Opioid receptor)>10,000ND (No data)Human[46][48][49] WP
KOR (κ-Opioid receptor)>10,000ND (No data)Human[46][48][49] WP
NOP (Nociceptin receptor)>10,000ND (No data)Human[46][48][49] WP
σ₁>10,000AgonistGuinea pig[46][48][49][50] WP
σ₂136AgonistRat[46][48][49] WP
D₂>10,000ND (No data)Human[46][48][49] WP
D₂^High2.7–4.3; 144 (EC₅₀)Partial AgonistRat/human; Human[3][48][49][51][52] WP
5-HT2A>10,000ND (No data)Human[46][48][49] WP
5-HT2A^High≥5,000Partial AgonistRat[3][48][49][53] WP
SERT (Serotonin transporter)2,234InhibitorHuman[46][48][49] WP
NET (Norepinephrine transporter)>10,000InhibitorHuman[46][48][49] WP
DAT (Dopamine transporter)>10,000InhibitorHuman[46][48][49] WP
PCP (Phencyclidine)₂154agonistHuman[47][48][49] WP
[³H]5-HT (Serotonin) uptake1,424 (IC₅₀)InhibitorRat[48][49][54] WP
[³H]NIS (Nisoxetine) binding16,628 (IC₅₀)InhibitorRat[48][49][54] WP
[³H]DA (Dopamine) uptake347 (IC₅₀)InhibitorRat[48][49][54] WP
[³H]CFT (WIN-35428) binding1,547 (IC₅₀)InhibitorRat[48][49][54] WP

Chemistry

Formula
C17H25N PC
CAS number
77-10-1 PC
Molar mass (g/mol)
243.4 PC
IUPAC name (computed by PubChem)
1-(1-phenylcyclohexyl)piperidine PC
SMILES
C1CCC(CC1)(C2=CC=CC=C2)N3CCCCC3 PC
InChIKey
JTJMJGYZQZDUJJ-UHFFFAOYSA-N PC
PubChem CID
6468

User reports

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Listings

Erowid Experience Vault listing TS

Link as published on TripSit's factsheet.

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Awaiting sourceShort summaries of the most-read reports, each linked, saying only what the report says.

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Awaiting sourceTrip report threads and this substance's discussion forum.
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Reddit reddit.com

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Pop culture

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References

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