Δ⁹-THC (Tetrahydrocannabinol)

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

Overview

Δ⁹-THC (Tetrahydrocannabinol) belongs to Cannabinoids.

Key safety note: Δ⁹-THC has no documented fatal overdose in humans and does not depress breathing the way opioids do, but it is far from harmless.[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.
  • Typical effects include euphoria, relaxation, altered perception of time and sound, heightened appetite ('the munchies'), talkativeness and, at higher doses, mild sensory or perceptual distortions.
  • Common unwanted effects are impaired short-term memory and concentration, slowed reaction time and coordination, dry mouth, red eyes and a faster heart rate. Anxiety, panic and paranoia are more likely at high doses, in inexperienced users, or with high-potency products.
  • Onset and intensity depend strongly on route: inhaled effects begin within seconds to minutes and last a few hours, whereas oral/edible effects are delayed 30–120 minutes and last much longer (up to ~10 hours): a mismatch that frequently leads to accidental overconsumption.
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.

Inhaled (smoked or vaporised), Oral (edibles, oil, capsules). Doses are given as milligrams of Δ⁹-THC and vary enormously with tolerance, product potency and route. These are commonly cited reference ranges, not a safe or recommended dose. The most important harm-reduction point is edibles: onset is delayed 30–120 minutes, so redosing before the effects are felt is the classic cause of an overwhelming, hours-long experience. Start low, wait for full effects, and treat high-potency concentrates with extra caution.

Dose ranges

Threshold

≈0.4 mg inhaled · 1 mg oral

Light

0.4–2 mg inhaled · 2.5–5 mg oral

Common

2–4 mg inhaled · 5–10 mg oral

Strong

4–10 mg inhaled · 10–25 mg oral

Heavy

10 mg + inhaled · 25 mg + oral

Duration

onset

Inhaled seconds–minutes, oral 20–60 min

peak

Inhaled 15–45 min, oral 1–2 h

total

Inhaled 2.5–5 h, oral 4–10 h

after effects

Inhaled up to ~3 h. Oral 6–12 h

Chemical & Physical Properties
FormulaC21H30O2
Molar mass314.5 g/mol
StateLiquid (resinous oil, amorphous, light yellow to golden)
Melting pointNo sharp melting point (resinous oil)
Boiling point≈200 °C at 0.02 mmHg (high vacuum), decomposes before boiling at atmospheric pressure
DensityNot reported
Vapor pressureNot reported
pKa10.6
LogP≈5.6 (XLogP3), experimental log Kow ≈6.97
SolubilityPractically insoluble in water (~2.8 mg/L at 23 °C), Soluble in alcohol, acetone and fixed oils
Refractive indexNot reported
Identifiers & Synonyms
CAS1972-08-3
CAS (enantiomer)
PubChem CID16078
InChIKeyCYQFCXCEBYINGO-IAGOWNOFSA-N
InChIInChI=1S/C21H30O2/c1-5-6-7-8-15-12-18(22)20-16-11-14(2)9-10-17(16)21(3,4)23-19(20)13-15/h11-13,16-17,22H,5-10H2,1-4H3/t16-,17-/m1/s1
SMILESCCCCCC1=CC(=C2[C@@H]3C=C(CC[C@H]3C(OC2=C1)(C)C)C)O

Synonyms

  • Delta-9-THC
  • Δ⁹-THC
  • Delta-9-tetrahydrocannabinol
  • Δ⁹-tetrahydrocannabinol
  • THC
  • Dronabinol
  • Marinol
  • Syndros
Pharmacodynamics & Biochemistry

Δ⁹-THC is the principal psychoactive constituent of cannabis. It is a partial agonist at the CB1 and CB2 cannabinoid receptors (human Ki ≈ 41 nM and ≈ 36 nM). CB1 receptors are densely expressed throughout the central nervous system, and their activation produces THC's characteristic effects on mood, perception, memory, appetite, coordination and pain, while CB2 (mainly on immune cells) mediates peripheral and immunomodulatory actions. Because it is a partial rather than full agonist there is a ceiling on receptor activation: one reason cannabis does not cause the fatal respiratory depression seen with opioids. Beyond the classical CB receptors, Δ⁹-THC interacts weakly with several other targets (GPR55, GPR18, TRP channels and glycine receptors), but these are low-affinity and of uncertain clinical importance. Its major metabolite 11-hydroxy-THC is itself an active cannabinoid and is produced in larger amounts after oral dosing (hepatic first-pass metabolism): part of why edibles feel stronger and longer-lasting than the same dose smoked.

Biological targets

  • CB1
  • CB2

Binding & functional measurements

TargetMeasurementSpecies
GPR55pEC50 8.1Human
CB1 receptorKi 20 nMHuman
CB2 receptorKi 52 nMHuman
GPR18pEC50 6Human
glycine receptor α2 subunitpEC50 6Human
glycine receptor α1 subunitpEC50 5.5Human
glycine receptor α3 subunitpEC50 5.3Human
CB1 receptorEC50 250 nM
Emax 51 ± 3%
Human
CB1 receptorEC50 167 nMMouse
CB1 receptorKi 15 nMMouse
CB2 receptorEC50 1,157 nM
Emax 13%
Human
Pharmacokinetics
BioavailabilityInhaled ~25% (10–35%), oral ~6–20% (extensive first-pass)
TmaxInhaled peak ~3–10 min, oral ~1–2 h (up to 4–6 h)
Half-lifeTerminal ≈25–36 h, prolonged in chronic heavy users (adipose storage)
Vd~10 L/kg (highly lipophilic, sequestered in fat)
Protein binding97–99%
MetabolismHepatic CYP2C9/CYP3A4 (also CYP2C19) → active 11-hydroxy-THC → inactive 11-nor-9-carboxy-THC (THC-COOH)
Excretion~55–80% faecal, ~20% renal (glucuronides and THC-COOH)
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

Δ⁹-THC has no documented fatal overdose in humans and does not depress breathing the way opioids do, but it is far from harmless. Acute risks are impaired driving and coordination, intense anxiety, panic or paranoia, and a raised heart rate that can strain a vulnerable cardiovascular system. High-potency products or predisposition can precipitate transient psychosis. Edibles are a common cause of accidental overconsumption because their onset is delayed. Regular heavy use can lead to dependence (roughly 1 in 10 users, more with early-onset daily use) and can trigger cannabinoid hyperemesis syndrome (cyclic severe vomiting). Use in adolescence, pregnancy or breastfeeding, and by people with a personal or family history of psychosis, carries added risk.[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

Alcohol, Benzodiazepines, Opioids Additive sedation, dizziness and impairment. Alcohol can also raise peak THC blood levels.[2]
Stimulants (amphetamines, cocaine) Additive tachycardia and blood-pressure effects, so caution in cardiovascular disease.[2]
CYP3A4 inhibitors (ritonavir, azole antifungals, macrolides, grapefruit) Strong inhibitors (some antifungals, ritonavir) raise THC levels, while reduced-function CYP2C9 variants also markedly increase oral exposure, and THC can in turn affect drugs such as warfarin.[2]
CYP3A4 inducers (rifampicin, carbamazepine) Inducers such as rifampicin lower THC levels.[2]

Contraindications

Personal or family history of psychosis, schizophrenia or bipolar disorder personal or family history of psychosis or schizophrenia.[2]
Cardiovascular disease, hypertension or arrhythmia severe or unstable cardiovascular disease.[2]
Pregnancy or breastfeeding[2]
Known hypersensitivity to the drug hypersensitivity to cannabinoids.[2]
Usage & Context
  • The main intoxicant in cannabis, used recreationally worldwide for euphoria and relaxation by smoking, vaporising or ingestion.
  • Medically, synthetic Δ⁹-THC is marketed as dronabinol, as the sesame-oil capsule Marinol (FDA-approved 1985) and the oral solution Syndros (2016), and, as the analogue nabilone, is approved for chemotherapy-induced nausea and vomiting refractory to conventional antiemetics and for AIDS-related appetite loss. The THC:CBD spray nabiximols (Sativex) is approved for multiple-sclerosis spasticity, and herbal medical cannabis is prescribed for chronic pain, spasticity and other indications in many countries. In the US these pharmaceutical forms are less tightly scheduled than herbal THC: Marinol is Schedule III and Syndros/generic dronabinol Schedule II, while cannabis-derived THC remains Schedule I.
  • The potency of recreational cannabis has risen markedly over recent decades, which raises the effective dose and the associated risks of anxiety, dependence and psychosis.
Sources & Evidence
  1. PubChem: Δ⁹-THC / dronabinol (CID 16078) — identifiers & experimental properties
  2. Wikipedia: Tetrahydrocannabinol (pharmacology, pharmacokinetics, medical use & safety) CC BY-SA 4.0
  3. IUPHAR/BPS Guide to PHARMACOLOGY: Δ⁹-tetrahydrocannabinol (ligand 2424) — receptor binding data CC BY-SA 4.0
  4. PsychonautWiki: THC — recreational dosage & duration CC BY-SA 4.0
  5. DEA Diversion Control Division: Controlled Substance Schedules (THC/marijuana are Schedule I)
  6. GOV.UK: Controlled drugs list — cannabis and THC are Class B (Misuse of Drugs Act 1971) OGL v3.0
  7. Konsumcannabisgesetz (KCanG) — Gesetze im Internet: adult non-medical cannabis since 1 April 2024 (possession limits, home cultivation, cannabis clubs)
  8. Medizinal-Cannabisgesetz (MedCanG) — Gesetze im Internet: medical cannabis framework
  9. Federal Register: limited medical-marijuana rescheduling, effective 28 April 2026
  10. Felder CC, Joyce KE, Briley EM, et al. (1995). Comparison of the pharmacology and signal transduction of the human cannabinoid CB1 and CB2 receptors. Mol Pharmacol 48:443-50.

    PMID 7565624

  11. Showalter VM, Compton DR, Martin BR, et al. (1996). Evaluation of binding in a transfected cell line expressing a peripheral cannabinoid receptor (CB2): identification of cannabinoid receptor subtype selective ligands. J Pharmacol Exp Ther 278:989-99.

    PMID 8819477

  12. Ryberg E, Larsson N, Sjögren S, et al. (2007). The orphan receptor GPR55 is a novel cannabinoid receptor. Br J Pharmacol 152:1092-101.

    PMID 17876302 · doi:10.1038/sj.bjp.0707460

  13. McHugh D, Page J, Dunn E, et al. (2012). Δ(9) -Tetrahydrocannabinol and N-arachidonyl glycine are full agonists at GPR18 receptors and induce migration in human endometrial HEC-1B cells. Br J Pharmacol 165:2414-24.

    PMID 21595653 · doi:10.1111/j.1476-5381.2011.01497.x

  14. Alexander SP (2012). So what do we call GPR18 now?. Br J Pharmacol 165:2411-3.

    PMID 22014123 · doi:10.1111/j.1476-5381.2011.01731.x

  15. PubChem (CID 16078, experimental properties) & Merck Index. No experimental density or vapour-pressure value at standard conditions is reported (vapour pressure is very low, only high-temperature research measurements exist).

Further Information