THC-O-acetate

[(6aR,10aR)-6,6,9-trimethyl-3-pentyl-6a,7,8,10a-tetrahydrobenzo[c]chromen-1-yl] acetate

Overview

THC-O-acetate belongs to Cannabinoids.

Key safety note: The most serious concern specific to THC-O-acetate is a thermal-decomposition hazard when it is vaped or smoked.[2][6]
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.
  • Cannabis-like intoxication, euphoria, relaxation, altered perception and appetite, reported as stronger than an equivalent amount of THC.
  • A markedly delayed onset (often 20–30+ minutes, longer for edibles) that can tempt redosing before the first dose is felt, leading to overshoot.
  • High-dose and adverse effects: anxiety or panic, rapid heartbeat, sedation, nausea/vomiting, confusion. Possible acute or delayed lung injury if vaped (ketene).
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.

Vaped, smoked, or taken orally (edibles/tinctures) as unregulated grey-market products of uncertain concentration. No established safe dose and no medical dosing exists.. There is no standardised or medically validated dose for THC-O-acetate, and grey-market products vary widely in strength and purity. The delayed, ester-dependent onset (especially orally) makes titration difficult and invites dangerous redosing, and vaping or smoking it risks ketene formation: the lowest-risk choice is not to inhale acetate cannabinoids at all. 'Start low, go slow' cannot be applied reliably to an unquantified product.

Dose ranges

Duration

onset

≈20–30+ min (delayed, longer orally)

total

Several hours (THC-like)

after effects

Residual grogginess. Edible over-intake can last many hours

Chemical & Physical Properties
FormulaC23H32O3
Molar mass356.5 g/mol
StateNot reported
Melting pointNot reported
Boiling pointNot reported
DensityNot reported
Vapor pressureNot reported
pKaNot reported
LogP7.1 (predicted, XLogP3)
SolubilityNot reported
Refractive indexNot reported
Identifiers & Synonyms
CAS23132-17-4
CAS (enantiomer)
PubChem CID198013
InChIKeyDEWSJDIJFWQLOA-RTBURBONSA-N
InChIInChI=1S/C23H32O3/c1-6-7-8-9-17-13-20(25-16(3)24)22-18-12-15(2)10-11-19(18)23(4,5)26-21(22)14-17/h12-14,18-19H,6-11H2,1-5H3/t18-,19-/m1/s1
SMILESCCCCCC1=CC2=C([C@@H]3C=C(CC[C@H]3C(O2)(C)C)C)C(=C1)OC(=O)C

Synonyms

  • THC-O
  • ATHC
  • Δ⁹-THC-O-acetate
  • THC acetate ester
  • Dronabinol O-acetate
Pharmacodynamics & Biochemistry

THC-O-acetate (THC-O, ATHC) is a semi-synthetic cannabinoid: the acetate ester of Δ⁹-tetrahydrocannabinol, made by treating Δ⁸- or Δ⁹-THC with acetic anhydride. It is not itself an appreciable cannabinoid-receptor agonist: it is a metabolic prodrug that must be de-acetylated by esterases to release Δ⁹-THC, the active CB1/CB2 partial agonist responsible for the cannabis-like effects. Acetylation raises the molecule's lipophilicity (predicted logP ≈7), which is thought to increase absorption and brain penetration once it is hydrolysed. Because the effect depends on that conversion step, THC-O has a characteristically delayed onset, subjective effects typically begin around 20–30 minutes or later after use, later than THC, and users and vendors describe it as noticeably more potent than THC (commonly quoted as roughly two to three times). Those potency claims are anecdotal: there are no controlled human pharmacokinetic or dose–response studies, and no reliable receptor-binding constants exist for THC-O-acetate itself (its activity is that of the THC liberated from it), so the binding table is left empty rather than populated with fabricated values. THC-O-acetate carries the same two ring-fusion stereocentres as Δ⁹-THC ((6aR,10aR)) and is handled as that single trans isomer. It is a viscous oil rather than a crystalline solid, and does not occur naturally in the cannabis plant. Its defining hazard is not its receptor pharmacology but its thermal chemistry when inhaled (see safety).

Biological targets

  • CB1
  • CB2
Pharmacokinetics
BioavailabilityNot established, acetylation raises lipophilicity and is thought to increase absorption vs THC
TmaxNot reported
Half-lifeNot established for THC-O itself, governed by the Δ⁹-THC released
VdNot reported
Protein bindingNot reported
MetabolismEsterase de-acetylation to Δ⁹-THC, which then follows THC's hepatic CYP metabolism (11-OH-THC, THC-COOH)
ExcretionAs THC metabolites (renal and faecal)
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

The most serious concern specific to THC-O-acetate is a thermal-decomposition hazard when it is vaped or smoked. Like vitamin E acetate, the agent implicated in the 2019 EVALI outbreak of vaping-associated lung injury, the acetate esters of cannabinoids can pyrolyse to ketene, a colourless, highly toxic gas that damages the lungs even at low concentrations. A 2022 study confirmed that vaping Δ⁸-THC acetate, CBN acetate and CBD acetate (including a commercial product) generates ketene in the condensate, so inhaling THC-O products may carry a real risk of acute and delayed lung injury. Beyond this, THC-O shares the acute risks of high-potency THC: pronounced intoxication, anxiety and panic, tachycardia and, particularly with edibles because of the delayed onset that invites redosing, accidental overconsumption with dysphoria, vomiting and, at high doses, psychotic reactions or cannabinoid hyperemesis. It is an almost entirely unregulated grey-market product: purity, dose and contaminants (residual acetic anhydride, reaction by-products, solvents) are not quality-controlled, long-term human data are essentially absent, and its slow, ester-dependent onset and high lipophilicity make effects hard to titrate.[2][6]

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

Alcohol, Benzodiazepines, Opioids Additive impairment and sedation with alcohol, benzodiazepines, opioids and other CNS depressants.[2]
Stimulants (amphetamines, cocaine) As a Δ9-THC prodrug it shares THC's additive tachycardia and blood-pressure changes with stimulants.[2]
Drugs cleared by shared CYP enzymes (e.g. CYP2C9, CYP3A4) Potential interplay with drugs metabolised by hepatic CYP enzymes, via the liberated THC.[2]

Contraindications

Vaping or smoking acetate esters (toxic ketene lung injury) vaping or smoking inhaled acetate cannabinoids risks ketene lung injury.[6]
Pregnancy or breastfeeding[2]
Personal or family history of psychosis, schizophrenia or bipolar disorder personal or strong family history of psychosis.[2]
Cardiovascular disease, hypertension or arrhythmia tachycardia or arrhythmia risk from the liberated THC.[2]
Combining with alcohol or other CNS depressants concurrent alcohol or other CNS depressants.[2]
Usage & Context
  • A grey-market 'hemp-derived' cannabinoid sold since around 2021 in vapes, edibles and tinctures, marketed as a stronger alternative to Δ⁸/Δ⁹-THC, not an approved medicine and not a natural cannabis constituent.
  • Historically investigated by the US Army's Edgewood Arsenal programme (from 1949) as a possible incapacitating agent, and encountered by the DEA as a clandestine THC analogue as early as 1978.
  • Used recreationally for cannabis-like effects. Its appeal is the reported higher potency, but that profile plus the vaping-ketene risk make it a higher-risk way to consume a THC-like drug.
Sources & Evidence

Further Information