Delta-8-THC
Delta-8-THC at a glance
Naturally occurring
Psychoactive
Cannabinoid type
Discovery year
Also known as
Molecular formula
C21H30O2
CB1 receptor interaction
CB2 receptor interaction
What is Delta-8-THC?
Delta-8-THC is an intoxicating phytocannabinoid and positional isomer of Delta-9-THC. It occurs naturally in cannabis, but generally only in small amounts, while most commercial Delta-8-THC is produced semi-synthetically from CBD. It is generally considered around 0.5× as psychoactively potent as Delta-9-THC.
Delta-8-THC has the same five-carbon (pentyl) side chain and molecular formula as Delta-9-THC, but its double bond is positioned at carbon 8 instead of carbon 9. This small structural change alters its chemical stability and biological activity. The naturally occurring form normally referred to as Delta-8-THC is trans-(6aR,10aR)-Delta-8-THC. Other stereoisomers also exist, including cis-Delta-8-THC, although these are much less commonly encountered.
Commercial Delta-8-THC is generally produced by acid-catalysed isomerisation of hemp-derived CBD and supplied as a clear to amber, viscous distillate. Incomplete conversion or purification can leave other cannabinoids and reaction by-products in the material. Delta-8-THC is more chemically stable than Delta-9-THC and more resistant to degradation.
Delta-8-THC was isolated from cannabis in 1966 and has been studied intermittently since then. Commercial interest increased sharply after 2018, particularly because hemp-derived CBD became widely available as a precursor for Delta-8-THC production. Research is more developed than for many newer semi-synthetic cannabinoids, but controlled human data on its effects, safety and pharmacokinetics remain limited.
How Delta-8-THC works in the human body
Delta-8-THC activates both cannabinoid receptors, producing confirmed intoxicating and cognitive effects in humans. Controlled oral research suggests roughly 0.5x the potency of Delta-9-THC under the tested conditions. Its metabolism produces the psychoactive metabolite 11-OH-Delta-8-THC. It is not found naturally in the human body. It
CB1 receptor
The main cannabinoid receptor in the brain, responsible for THC’s intoxicating effects, is activated by Delta-8-THC as a partial agonist. In one human-receptor binding study, Delta-8-THC had approximately 4.3x weaker CB1 binding affinity than Delta-9-THC, while another direct comparison found approximately 7.7x weaker binding. These differences between studies show that exact binding values depend strongly on the experimental method, but the overall evidence consistently indicates weaker CB1 binding than Delta-9-THC.
Binding affinity does not directly determine psychoactive potency. In a controlled 2025 human oral study, 20 mg Delta-8-THC produced significantly weaker subjective, cognitive, psychomotor and cardiovascular effects than 20 mg Delta-9-THC, while 40 mg Delta-8-THC produced effects broadly comparable to 20 mg Delta-9-THC. This supports an approximate psychoactive potency of 0.5x Delta-9-THC under the tested oral conditions.
CB1 activation reduces neurotransmitter release in the brain and contributes to Delta-8-THC’s confirmed intoxicating effects, including altered perception, cognitive impairment and impaired psychomotor performance.
CB2 receptor
The main cannabinoid receptor in the immune system, involved in regulating immune cell activity and inflammatory responses. Delta-8-THC binds to CB2 and acts as a partial agonist. One study found Delta-8-THC approximately 3.5x stronger in CB2 binding than Delta-9-THC, while another found it approximately 1.2x weaker.
Activation of CB2 could potentially influence immune-cell activity and inflammatory signalling. However, no controlled human study has demonstrated that a specific immune or anti-inflammatory effect of Delta-8-THC is caused by CB2 activation, so these effects remain pharmacologically likely rather than clinically confirmed.
Metabolism
Delta-8-THC is converted to 11-OH-Delta-8-THC, followed by further oxidation to Delta-8-THC-COOH. 11-OH-Delta-8-THC is pharmacologically active in animal studies and can enter the brain. With the oral study (read above, CB1) in mind, 11-OH-Delta-8-THC is thought likely to be 0,5x as potent as it’s 11-OH-Delta-9-THC isomer.
Controlled human research found substantially lower concentrations of 11-OH-Delta-8-THC after Delta-8-THC than concentrations of 11-OH-Delta-9-THC after an equivalent Delta-9-THC dose. This reduced formation of the active metabolite may partly contribute to the lower oral potency of Delta-8-THC compared to Delta-9-THC.
Human safety status
Severe toxicity has also occurred after very high accidental doses, particularly in young children. However, many poison-centre reports involve commercial products with uncertain purity or composition, limiting attribution specifically to Delta-8-THC. Repeated and long-term human safety remain insufficiently studied, but research has not found harm in humans at normal doses .
Delta-8-THC interactions with other compounds
Important disclaimer
This information is provided for educational and technical reference only. Interaction data can change as new research becomes available and may be incomplete or outdated. The real relevance of any interaction depends strongly on dose, route of administration, timing, formulation and individual metabolism. Readers should do their own research and consult a qualified healthcare professional before making decisions involving medicines, alcohol, nicotine, cannabinoids or other compounds. Elementra's products and information are intended for research, production and technical use only and are not intended for human consumption.
Cannabinoids
CBD
Animal study
Analgesic effect increases in combination
CBD and Delta-8-THC produced stronger effects together than either compound alone in a rat vapor study. A mixture containing 60 mg CBD and 20 mg Delta-8-THC produced a significantly stronger analgesic response than the same doses given separately, and some mixtures also altered locomotor activity. This observed combination effect is separate from CBD’s reported negative allosteric modulation of CB1 receptors, which can reduce cannabinoid receptor signalling through a different mechanism. The interaction has not yet been confirmed in humans.
Common substances
Nicotine
Enzyme study
Nicotine exposure is predicted to increase about 2.9x
Delta-8-THC directly inhibits CYP2A6, the main enzyme responsible for converting nicotine into cotinine. Laboratory testing with human liver microsomes found potent inhibition, and pharmacokinetic modelling predicted that 10 mg oral Delta-8-THC could increase total nicotine exposure about 2.9x. The predicted interaction varies with CYP2A6 genetics and has not yet been confirmed in a controlled human interaction study.
Medicines
Warfarin
Enzyme study
Warfarin exposure is predicted to increase
Delta-8-THC directly inhibits CYP2C9-mediated warfarin metabolism in human liver microsomes. Pharmacokinetic modelling predicted approximately 1.6x greater warfarin exposure with 10 mg oral Delta-8-THC, increasing to about 3.1x at 40 mg. Because warfarin has a narrow therapeutic range, this could increase its anticoagulant effect and bleeding risk, but the predicted exposure changes have not yet been confirmed in humans.
Diclofenac
Enzyme study
Diclofenac exposure is predicted to increase
Delta-8-THC directly inhibits CYP2C9-mediated diclofenac metabolism in human liver microsomes. Pharmacokinetic modelling predicted approximately 2.3x greater diclofenac exposure after 10 mg oral Delta-8-THC, rising to about 4.5x at 40 mg. These estimates suggest a potentially substantial pharmacokinetic interaction, although the magnitude has not yet been confirmed in humans.
Midazolam
Enzyme study
Midazolam exposure is predicted to increase
Delta-8-THC directly inhibits CYP3A4-mediated breakdown of midazolam in human liver microsomes. Pharmacokinetic modelling predicted approximately 2.3x greater midazolam exposure with 10 mg oral Delta-8-THC and about 3.9x with 40 mg. This could prolong or strengthen midazolam effects, but the predicted interaction has not yet been confirmed in a controlled human study.
Pentobarbital
Animal study
Pentobarbital-induced sleep lasts longer
Delta-8-THC prolonged pentobarbital-induced sleep in mice. In one experiment, adding 5 mg/kg intravenous Delta-8-THC made the sleeping period approximately 2.5x longer than in mice receiving pentobarbital without Delta-8-THC. This demonstrates a pharmacological interaction in animals, but the mechanism and relevance in humans have not yet been established.
Phenobarbital
Animal study
Seizure protection increases
Delta-8-THC produced an additive anticonvulsant effect when combined with phenobarbital in a mouse seizure model, meaning the combination provided greater seizure protection than either treatment alone at the tested doses. This demonstrates a pharmacological interaction in animals, but whether a similar interaction occurs in humans is unknown.
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