THC — Delta-9-Tetrahydrocannabinol

Pharmacology, therapeutic effects, pharmacokinetics, adverse effects and GMP significance of delta-9-THC for healthcare professionals and cannabis manufacturers.

Cannabinoid Library🕐 3 minGary McPolin · ECI
Gary McPolin
Founder, European Cannabis Institute · Senior CQV and GMP Consultant · 20+ years pharmaceutical manufacturing
Last reviewed: June 2026 · EU GMP Annex 1 (2022) aligned
Clinical Disclaimer

This page is an educational summary and does not constitute clinical guidance or a recommendation for use. Prescribing, dosing and treatment decisions should be made on the basis of individual patient assessment, current clinical guidelines and the treating healthcare professional's judgement.

What is THC?

Delta-9-tetrahydrocannabinol (THC) is the primary psychoactive cannabinoid in Cannabis sativa. It is responsible for the intoxicating effects of cannabis and is the primary pharmacologically active component in authorised cannabis-based medicinal products including Sativex (nabiximols).

Pharmacology

THC acts as a partial agonist at CB1 and CB2 receptors. CB1 agonism in the CNS produces both psychoactive effects (euphoria, cognitive impairment) and therapeutic effects (analgesia, antiemesis, appetite stimulation, muscle relaxation). THC also activates TRPV1 channels contributing to analgesia through a CB-receptor-independent mechanism.

Pharmacokinetics

Oral: Bioavailability 4–20%, variable; substantially increased by high-fat meal. Onset 1–3 hours. Extensive first-pass metabolism to active 11-OH-THC.
Inhalation: Bioavailability 10–35%. Onset minutes. Duration 2–4 hours.
Metabolism: CYP2C9 and CYP3A4. Active metabolite: 11-OH-THC. Urinary metabolite: THC-COOH (detected in drug screening).
Interactions: Inhibits CYP2C9 — clinically significant warfarin interaction (elevated INR). Monitor anticoagulation closely.

Therapeutic Applications

Neuropathic pain: Multiple RCTs demonstrating statistically significant pain reduction. NNT ~8–15 for 30% pain reduction.
CINV: Strongest evidence. Nabilone and dronabinol approved in several jurisdictions.
MS spasticity: Sativex approved in multiple EU countries. Significant patient-reported spasticity reduction.
Appetite stimulation: CB1 hypothalamic activation — useful in HIV wasting and cancer cachexia.

Adverse Effects

  • Tachycardia, postural hypotension (fall risk in elderly)
  • Cognitive impairment, sedation, dizziness
  • Anxiety, paranoia, acute psychosis (rare; higher risk in predisposed individuals)
  • Driving impairment — advise patients accordingly
  • Cannabis use disorder with chronic use (~9% of all users)

Contraindications

Active or history of psychosis; severe cardiovascular disease; pregnancy and breastfeeding; children and adolescents (except specific authorised paediatric indications); concurrent CNS depressants without dose adjustment.

GMP Significance

Cross-contamination: THC residues on shared equipment are a patient safety risk. Cleaning validation acceptance limits must be based on the pharmacological intoxication threshold — more stringent than standard PDE-based limits.
Stability marker: THC degrades to CBN under oxidative conditions. CBN specification in finished products serves as a stability indicator.
Decarboxylation: THCA→THC requires validated temperature-time parameters with CBN as an in-process control parameter.

See the Cannabis Glossary for definitions of related cultivation, extraction and quality terms.

References

  • Gaoni Y, Mechoulam R. Isolation, Structure and Partial Synthesis of an Active Constituent of Hashish. J Am Chem Soc. 1964.
  • Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids. Br J Pharmacol. 2008.
  • GW Pharmaceuticals. Sativex Summary of Product Characteristics.
  • EU GMP Annex 1 (2022) — Contamination Control Strategy.
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