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Cannabidiol.

Cannabidiol (CBD) is a naturally occurring cannabinoid constituent of cannabis, which is either derived from marijuana or industrial hemp. It was discovered in 1940 and initially thought not to be medically active. Cannabidiol can be taken into the body in multiple different ways, including by inhalation of cannabis smoke or vapor, as an aerosol spray into the cheek, and by mouth. It may be supplied as an oil containing only CBD as the active ingredient (no added THC or terpenes), a full-plant CBD-dominant hemp extract oil, capsules, dried cannabis, a prescription liquid solution, or a topical cream.

Cannabidiol (CBD) is one of more than 80 active cannabinoid chemicals in the marijuana plant.1 Unlike the main psychoactive cannabinoid in marijuana, tetrahydrocannabinol (THC), CBD does not produce euphoria or intoxication.^2,3,4 CBD can be derived from marijuana or hemp also known as industrial hemp, which contains little to no THC. Cannabinoids have their effect mainly by interacting with specific receptors on cells in the brain and body: the CB1 receptor, found on neurons and glial cells in various parts of the brain, and the CB2 receptor, found mainly in the body’s immune system. The euphoric effects of THC are caused by its activation of CB1 receptors. CBD has a very low affinity for these receptors (100 fold less than THC), and when it binds it produces little to no effect. Cannabidiol is a negative allosteric modulator of the cannabinoid CB1 receptor5. There is also growing evidence that CBD acts on other brain signaling systems and that these actions may be important contributors to its therapeutic effects.⁴

Metabolism

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.

Description

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.

Drug Interactions

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.

References.

Borgelt et al. The pharmacologic and clinical effects of medical cannabis. Pharmacotherapy (Review) 33 (2): 195–209 (2013).
Martin-Santos et al. Acute effects of a single, oral dose of d9-tetrahydrocannabinol (THC) and cannabidiol (CBD) administration in healthy volunteers. Curr Pharm Des. 2012;18(32):4966-79.
Fusar-Poli et al. Distinct Effects of Δ9-Tetrahydrocannabinol and Cannabidiol on Neural Activation During Emotional Processing. Arch Gen Psychiatry. 2009;66(1):95-105.
Winton-Brown et al. Modulation of Auditory and Visual Processing by Delta-9-Tetrahydrocannabinol and Cannabidiol: an fMRI Study. Neuropsychopharmacology. 2011 Jun;36(7):1340-8
R B Laprairie, A M Bagher, M E M Kelly, E M Denovan‐Wright. Br J Pharmacol. 2015 Oct; 172(20): 4790–4805. Published online 2015 Oct 13. doi: 10.1111/bph.13250 PMCID: PMC4621983
Yamaori et al 2011. Potent inhibition of human cytochrome P450 3A isoforms by cannabidiol: role of phenolic hydroxyl groups in the resorcinol moiety. Life Sci 2011 Apr 11;88(15-16):730-6
Stout and Cimino 2014. Exogenous cannabinoids as substrate inhibitors and inducers of humandrug metabolizing enzymes ; a systemic review. Drug Metab Rev 2014 Feb;46(1):86-95
Fugh-Berman et al. Medical Cannabis Adverse Effects & Drug Interactions Presentation by: Govt of the District of Columbia Department of Health (DOH) 2015 www.doh.dc.gov

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