Δ⁸-Tetrahydrocannabinol (delta-8-THC, Δ⁸-THC) is a psychoactive cannabinoid found in the Cannabis plant. It is an isomer of delta-9-tetrahydrocannabinol (delta-9-THC, Δ⁹-THC), the compound commonly known as THC, with which it co-occurs in hemp; natural quantities of ∆⁸-THC found in hemp are low. Psychoactive effects are similar to that of Δ⁹-THC, with central effects occurring by binding to cannabinoid receptors found in various regions of the brain.

Partial synthesis of ∆⁸-THC was published in 1941 by Roger Adams and colleagues at the University of Illinois. After the 2018 United States farm bill was signed, ∆⁸-THC products synthesized from industrial hemp by acid-catalyzed cyclization experienced a rise in popularity; THC products have been sold in licensed recreational cannabis and medical cannabis industries within the United States in California, Pennsylvania, and medicinally licensed in Michigan and Oregon. According to a March 2024 study, 11% of US twelfth graders in the study had used ∆⁸-THC over the past 12 months.

∆⁸-THC is moderately less potent than Δ⁹-THC. This means that while its effects are similar to that of Δ⁹-THC, as both are psychoactive cannabinoids, it would take more ∆⁸-THC to achieve a comparable level of effect.

A 1973 study testing the effects of ∆⁸-THC in dogs and monkeys reported that a single oral dose of 9,000 milligrams per kilogram of body mass (mg/kg) was nonlethal in all dogs and monkeys studied. The same study reported that the median lethal dose of ∆⁸-THC in rats was comparable to that of ∆⁹-THC. Both isomers of THC have been found to cause a transient increase in blood pressure in rats, although the effects of cannabinoids on the cardiovascular system are complex. Animal studies indicate that ∆⁸-THC exerts many of its central effects by binding to cannabinoid receptors found in various regions of the brain, including the cerebral cortex, thalamus, basal ganglia, hippocampus, and cerebellum.

As of 2022, the safety profile, including risks of psychosis and addiction after regular, long-term ∆⁸-THC use was unknown.

As of 2022, there had been at least 104 adverse event reports made for ∆⁸-THC, and at least two deaths associated with ∆⁸-THC products. US national poison control centers received 2,362 exposure cases of Δ⁸-THC products between 1 January 2021 and 28 February 2022; 58% of these exposures involved adults, and 70% thought they required medical care.

The pharmacodynamic profile of ∆⁸-THC is similar to that of ∆⁹-THC. It is a partial agonist of CB₁ and CB₂ cannabinoid receptors with about half the potency of ∆⁹-THC in most but not all measures of biological activity.

The pharmacokinetic profile of ∆⁸-THC is also similar to that of ∆⁹-THC. Following ingestion in humans, hepatic cytochrome P450 enzymes including CYP2C9 and CYP3A4 first convert ∆⁸-THC into 11-hydroxy-Δ⁸-tetrahydrocannabinol (11-OH-Δ⁸-THC). Next, dehydrogenase enzymes convert 11-OH-Δ⁸-THC into 11-nor-Δ⁸-tetrahydrocannabinol-9-carboxylic acid (11-nor-Δ⁸-THC-9-COOH, also known as Δ⁸-THC-11-oic acid). Finally, Δ⁸-THC-11-oic acid undergoes glucuronidation by glucuronidase enzymes to form 11-nor-Δ⁸-tetrahydrocannabinol-9-carboxylic acid glucuronide (Δ⁸-THC-COOH-glu), which is then excreted in the urine.