Cannabidiol is metabolized by cytochrome p450 (CYP) enzymes CYP3A4 and CYP2C19. At clinically relevant concentrations, cannabidiol has the potential to inhibit CYP2C8, CYP2C9, and CYP2C19 and may induce or inhibit CYP1A2 and CYP2B6. Cannabidiol inhibits uridine 5'-diphospho-glucuronosyltransferase (UGT) enzymes UGT1A9 and UGT2B7 6,7.
Cannabidiol is a cannabinoid designated chemically as 2-[(1R,6R)-3-Methyl-6-(1-methylethenyl)-2¬ cyclohexen-1-yl]-5-pentyl-1,3-benzenediol (IUPAC/CAS). Its empirical formula is C21H30O2. The molecular weight of cannabidiol is 314.46. The chemical structure is:
Cannabidiol naturally occurs in the Cannabis plant. Cannabidiol is a white to pale yellow crystalline solid. It is insoluble in water and is soluble in organic solvents.
Cannabidiol may increase serum concentrations of macrolides, calcium channel blockers, benzodiazepines, cyclosporine, sildenafil (and other PDE5 inhibitors), antihistamines, haloperidol, antiretrovirals, and some statins (atorvastatin and simvastatin, but not pravastatin or rosuvastatin) and other drugs metabolized by CYP3A4. Drugs such as ketoconazol, itraconazol, ritonavir, and clarithromycin inhibit this enzyme, leading to slower CBD degradation, and can consequently lead to higher CBD doses that are longer medically active. In contrast, phenobarbital, rifampicin, carbamazepine, and phenytoin induce CYP3A4, causing reduced CBD bioavailability8.