3-HO-PCP

3-(1-piperidin-1-ylcyclohexyl)phenol

Overview

3-HO-PCP belongs to Dissociatives / Arylcyclohexylamines.

Key safety note: 3-HO-PCP is extremely potent: oral doses are in the low single-digit milligram range (threshold ≈1 mg, common ≈4–6 mg), so a small volumetric or weighing error can be a large overdose, and it should never be eyeballed.[3][6][2]
Effects
Subjective effects vary. What a substance feels like depends on dose, individual physiology, mindset, and setting. The points below describe commonly reported effects, not guaranteed, uniform, or desirable outcomes.
  • Dose-dependent dissociation: depersonalisation, derealisation and, at higher doses, near-complete disconnection from the body and environment (a dissociative 'hole' with immobilisation).
  • Euphoria and an opioid-like warmth and analgesia that is unusual for a dissociative and reflects its μ-opioid agonism, alongside the expected numbness and detachment.
  • Alternating stimulation and sedation, motor incoordination and slurred, uncoordinated movement.
  • Cognitive and perceptual distortion: internal hallucinations and dream-like states, distorted sense of time and space, anxiety suppression at low doses but confusion, anxiety or psychosis-like states at high doses.
Dosing & duration
Harm-reduction note: These are commonly cited reference ranges, not a recommendation or a “safe” dose. Potency, purity, body chemistry, tolerance, and drug combinations vary widely. Start low, go slow, wait for full effects before redosing, and never assume an unknown product matches these figures. Missing data is not evidence of safety.

Oral, Insufflated. Not a recommendation. 3-HO-PCP has never been studied in controlled human trials, so these are only commonly cited community ranges. It is exceptionally potent, active in the low single-digit milligram range, so it must be dosed by accurate milligram scale or volumetric solution, never eyeballed. A small error is a large overdose. Because it is a genuine opioid agonist as well as a dissociative, redosing and combining it with any other depressant are especially dangerous. Onset is slow (≈60–90 min orally), which frequently leads users to redose too early.

Dose ranges

Threshold

≈1 mg (oral)

Light

≈2–4 mg (oral)

Common

≈4–6 mg (oral)

Strong

≈6–8 mg (oral)

Duration

onset

≈60–90 min (oral)

peak

Not well characterised

total

≈4–6 h (oral)

Chemical & Physical Properties
FormulaC17H25NO
Molar mass259.4 g/mol
StateSolid (usually the hydrochloride salt)
Melting pointNot reported
Boiling pointNot reported
DensityNot reported
Vapor pressureNot reported
pKaNot reported
LogP3.3 (predicted, XLogP3)
SolubilityNot reported
Refractive indexNot reported
Identifiers & Synonyms
CAS79787-43-2
CAS (enantiomer)
PubChem CID133277
InChIKeyAMSXTZUCNOKUEN-UHFFFAOYSA-N
InChIInChI=1S/C17H25NO/c19-16-9-7-8-15(14-16)17(10-3-1-4-11-17)18-12-5-2-6-13-18/h7-9,14,19H,1-6,10-13H2
SMILESC1CCC(CC1)(C2=CC(=CC=C2)O)N3CCCCC3

Synonyms

  • 3-HO-PCP
  • 3-Hydroxyphencyclidine
  • 3-OH-PCP
Pharmacodynamics & Biochemistry

3-HO-PCP (3-hydroxyphencyclidine) is an arylcyclohexylamine dissociative and a high-affinity uncompetitive antagonist of the NMDA glutamate receptor, binding inside the channel at the dizocilpine (MK-801)/PCP site with roughly eight-fold greater potency than PCP itself (Kᵢ ≈30 nM vs. ≈250 nM). This NMDA channel block produces the dissociative anaesthesia, analgesia and depersonalisation shared by the whole PCP/ketamine family. What makes 3-HO-PCP unique among arylcyclohexylamines is that it is also a genuine, potent μ-opioid receptor agonist (Kᵢ ≈39–60 nM, agonist EC50 ≈85 nM), with additional κ-opioid (Kᵢ ≈140 nM) and σ1 (Kᵢ ≈42 nM) affinity and only weak δ-opioid activity. PCP and most other dissociatives are essentially inactive at opioid receptors, so this opioid agonism is a defining and dangerous feature of 3-HO-PCP rather than a footnote. The practical consequence is that 3-HO-PCP behaves partly like an opioid: it can cause opioid-type respiratory depression, its opioid component is reversible by naloxone, and combining it with other central-nervous-system depressants (opioids, benzodiazepines, alcohol, GHB) stacks respiratory depression in a way that plain dissociatives do not.

Biological targets

  • NMDA
  • MOR
  • KOR
  • Sigma-1

Binding & functional measurements

TargetMeasurementSpecies
NMDAKi 30 nMRat
MORKi 50 nMRodent
KORKi 140 nMRodent
Sigma-1Ki 42 nMRodent
DORKi 2,300 nMRodent
Pharmacokinetics
BioavailabilityOral and insufflated (active by both routes)
TmaxSlow onset ≈60–90 min (oral)
Half-lifeNot established in humans (oral effects ≈4–6 h)
VdNot reported
Protein bindingNot reported
MetabolismHepatic. 3-HO-PCP is itself the O-demethylation metabolite of 3-MeO-PCP
ExcretionRenal (presumed)
Toxicology & Safety
Harm-reduction note: Toxicity and risk depend on dose, route, purity, combinations, setting, and individual health factors. Missing harms should never be interpreted as evidence of safety.

Not reported

3-HO-PCP is extremely potent: oral doses are in the low single-digit milligram range (threshold ≈1 mg, common ≈4–6 mg), so a small volumetric or weighing error can be a large overdose, and it should never be eyeballed. Its defining hazard is that, unlike PCP or ketamine, it is a real μ-opioid agonist as well as an NMDA antagonist: it can cause opioid-type respiratory depression, and it is especially dangerous combined with opioids, benzodiazepines, alcohol or other depressants, where respiratory arrest can occur. The opioid component can be reversed by naloxone, but the NMDA/dissociative component cannot. Heavy dissociation brings the usual dissociative dangers: falls and accidents, vomiting with a suppressed gag reflex (aspiration risk), and dangerous behaviour from impaired judgement. The slow, creeping onset tempts redosing, which produces cumulative dissociation and opioid depression. It is reported to be more habit-forming than dissociatives such as ketamine or MXE, and bladder/urinary-tract toxicity seen with chronic dissociative use is a plausible long-term risk. 3-HO-PCP has never been formally studied in humans. The absence of toxicity data must never be read as evidence of safety.[3][6][2]

Legal Status
Legal note: Legal status can change over time and may vary by country, region, formulation, analogue status, prescription context, and enforcement practice. Always confirm with current official sources before relying on this section.
Interactions & Contraindications

Drug interactions

Opioids, Benzodiazepines, Alcohol, GHB / GBL Additive respiratory depression. Because 3-HO-PCP is itself an opioid agonist this combination can be fatal, unlike with plain dissociatives.[3]
Stimulants (amphetamines, cocaine) Mask dissociative impairment, add cardiovascular strain and raise the risk of agitation, psychosis and dangerous behaviour.[6]
Other dissociatives (NMDA antagonists) Additive dissociation, with risk of unintended full anaesthesia and immobilisation.[6]

Contraindications

Combining with alcohol or other CNS depressants concurrent opioids or other CNS depressants (respiratory-depression risk).[3]
Respiratory disease or sleep apnoea[3]
Using alone, with no one present to respond to an overdose opioid-type overdose risk with no one to intervene or give naloxone.[3]
Personal or family history of psychosis, schizophrenia or bipolar disorder personal or family history of psychosis or bipolar disorder.[6]
Pre-existing bladder or urinary-tract disease, or drug-induced cystitis dissociative uropathy risk with repeated use.[6]
Usage & Context
  • Sold online as a 'research chemical' / grey-market dissociative from around 2009 onward. Discussed on drug forums (The Hive, Bluelight) as early as the late 1990s–2000s.
  • First synthesised in the late 1970s–early 1980s during structure–activity studies of phencyclidine. The 3-hydroxy derivative was specifically noted for its opioid character.
Sources & Evidence

Further Information