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.
Effects
- 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
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
≈0.4 mg inhaled · 1 mg oral
0.4–2 mg inhaled · 2.5–5 mg oral
2–4 mg inhaled · 5–10 mg oral
4–10 mg inhaled · 10–25 mg oral
10 mg + inhaled · 25 mg + oral
Duration
Inhaled seconds–minutes, oral 20–60 min
Inhaled 15–45 min, oral 1–2 h
Inhaled 2.5–5 h, oral 4–10 h
Inhaled up to ~3 h. Oral 6–12 h
Chemical & Physical Properties
| Formula | C21H30O2 |
| Molar mass | 314.5 g/mol |
| State | Liquid (resinous oil, amorphous, light yellow to golden) |
| Melting point | No sharp melting point (resinous oil) |
| Boiling point | ≈200 °C at 0.02 mmHg (high vacuum), decomposes before boiling at atmospheric pressure |
| Density | Not reported |
| Vapor pressure | Not reported |
| pKa | 10.6 |
| LogP | ≈5.6 (XLogP3), experimental log Kow ≈6.97 |
| Solubility | Practically insoluble in water (~2.8 mg/L at 23 °C), Soluble in alcohol, acetone and fixed oils |
| Refractive index | Not reported |
Identifiers & Synonyms
| CAS | 1972-08-3 |
| CAS (enantiomer) | |
| PubChem CID | 16078 |
| InChIKey | CYQFCXCEBYINGO-IAGOWNOFSA-N |
| InChI | InChI=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 |
| SMILES | CCCCCC1=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
| Target | Measurement | Species |
|---|---|---|
| GPR55 | pEC50 8.1 | Human |
| CB1 receptor | Ki 20 nM | Human |
| CB2 receptor | Ki 52 nM | Human |
| GPR18 | pEC50 6 | Human |
| glycine receptor α2 subunit | pEC50 6 | Human |
| glycine receptor α1 subunit | pEC50 5.5 | Human |
| glycine receptor α3 subunit | pEC50 5.3 | Human |
| CB1 receptor | EC50 250 nM Emax 51 ± 3% | Human |
| CB1 receptor | EC50 167 nM | Mouse |
| CB1 receptor | Ki 15 nM | Mouse |
| CB2 receptor | EC50 1,157 nM Emax 13% | Human |
Pharmacokinetics
| Bioavailability | Inhaled ~25% (10–35%), oral ~6–20% (extensive first-pass) |
| Tmax | Inhaled peak ~3–10 min, oral ~1–2 h (up to 4–6 h) |
| Half-life | Terminal ≈25–36 h, prolonged in chronic heavy users (adipose storage) |
| Vd | ~10 L/kg (highly lipophilic, sequestered in fat) |
| Protein binding | 97–99% |
| Metabolism | Hepatic 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
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
US: Product-dependent: Schedule I / III or hemp exception. UK: Class B. DE: KCanG-regulated (since 2024)
Interactions & Contraindications
Drug interactions
Contraindications
No interactions or contraindications listed.
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
- PubChem: Δ⁹-THC / dronabinol (CID 16078) — identifiers & experimental properties
- Wikipedia: Tetrahydrocannabinol (pharmacology, pharmacokinetics, medical use & safety) CC BY-SA 4.0
- IUPHAR/BPS Guide to PHARMACOLOGY: Δ⁹-tetrahydrocannabinol (ligand 2424) — receptor binding data CC BY-SA 4.0
- PsychonautWiki: THC — recreational dosage & duration CC BY-SA 4.0
- DEA Diversion Control Division: Controlled Substance Schedules (THC/marijuana are Schedule I)
- GOV.UK: Controlled drugs list — cannabis and THC are Class B (Misuse of Drugs Act 1971) OGL v3.0
- Konsumcannabisgesetz (KCanG) — Gesetze im Internet: adult non-medical cannabis since 1 April 2024 (possession limits, home cultivation, cannabis clubs)
- Medizinal-Cannabisgesetz (MedCanG) — Gesetze im Internet: medical cannabis framework
- Federal Register: limited medical-marijuana rescheduling, effective 28 April 2026
- 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
- 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
- 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
- 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
- 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
- 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).