The enzymes and transporters that set cannabinoid and drug exposure: six CYP isoforms, phase-2 glucuronidation and sulfonation, P-glycoprotein efflux, and the mechanism rules that generalise where an interaction pairs list cannot.
11 pages · 86 citations (12 without a resolved identifier, marked on the page) · updated 2026-09-27
What this section is, and what it is not
Education and harm reduction. Not medical, legal or financial advice. Every factual claim carries a source; contested and single-source claims are marked as such on the page.
The boundary. This section teaches separation, purification, formulation, dosing arithmetic and analytical chemistry with real parameters, because withholding that detail from someone who will proceed anyway is the harm this library exists to prevent. It does not publish preparative routes for converting one cannabinoid into a more intoxicating one; those are described structurally and cited to the literature, without procedures.
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Why cytochrome P450 is the axis on which most substance interactions turn, why inhibition and induction produce opposite clinical disasters, and why a mechanism table generalises to substances nobody has typed into a list yet.
11 sections · enzyme
The single most important drug-metabolising enzyme in the body, expressed in both liver and small intestine, implicated in roughly half of marketed drugs, inducible through the pregnane X receptor, and inhibited by everything from a glass of grapefruit juice to a ritonavir booster.
9 sections · enzyme
The warfarin and phenytoin enzyme, and the enzyme that does most of the work on Δ9-THC. Strongly polymorphic, with reduced-function alleles that lower warfarin dose requirement and raise THC exposure severalfold.
5 sections · enzyme
The clopidogrel-activation and proton-pump-inhibitor enzyme, strongly polymorphic with poor-metaboliser frequencies far higher in East and South-East Asian populations, and the enzyme at the centre of the best-documented cannabinoid drug interaction in the literature: cannabidiol and clobazam.
5 sections · enzyme
The most polymorphic drug-metabolising enzyme in the human genome and the one that is essentially not inducible. It handles a quarter of prescribed drugs including most antidepressants, antipsychotics and several opioid prodrugs, and the population spans from no functional enzyme to gene duplications.
6 sections · enzyme
The caffeine, clozapine and theophylline enzyme, and the only major isoform whose most important inducer is a behaviour rather than a drug. Smoke induces it through the aryl hydrocarbon receptor, which means quitting smoking is itself an interaction.
6 sections · enzyme
The ethanol and small-molecule enzyme, regulated by protein stabilisation rather than by transcription alone, and the enzyme that turns paracetamol into the metabolite that destroys livers. The one isoform where kava has a confirmed in-vivo human inhibitory effect.
5 sections · enzyme
The conjugation step most interaction tables ignore, and the dominant route of cannabinoid elimination. UGT enzymes attach glucuronic acid to a phenol, alcohol or carboxylic acid, and the resulting glucuronides are both the reason cannabinoids leave the body and the reason a urine drug test can detect them for weeks.
5 sections · enzyme
The low-capacity, high-affinity conjugation pathway. Because its cofactor pool is small and easily depleted, a large phenolic load from food or a botanical can saturate sulfation and change the metabolic fate of an unrelated substrate — and for the allylbenzenes, sulfonation is the step that makes a metabolite reactive rather than safe.
4 sections · enzyme
An ATP-driven efflux pump that throws substrates back out of cells. In the gut it limits absorption; at the blood-brain barrier it limits brain entry. The two consequences are separate, and an agent that inhibits P-glycoprotein and CYP3A4 together moves exposure far more than either mechanism alone predicts.
6 sections · target
An explainer for the live mechanism-based interaction checker. It reasons over documented mechanism axes rather than over a list of substance pairs, which is why it reaches plants and novel compounds that pairs databases do not — and why a clean result means no documented interaction in this dataset, never safety.
6 sections · tool