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Medically reviewed by Last updated on Aug 24, 2020.

Common Name(s): Cannabidiol, Cannabidiol oil, CBD, Epidiolex

Clinical Overview


Note: This monograph specifically discusses cannabidiol (CBD), a chemical constituent of the cannabis plant (Cannabis sativa L.). For more information regarding clinical uses (including those for CBD in combination with tetrahydrocannabinol [THC]), interactions, adverse reactions, and toxicology associated with C. sativa plant, see the Cannabis monograph.

CBD has been evaluated for use in epilepsy, particularly as an adjuvant to standard therapy in resistant forms. Use in the management of various CNS disorders, as well as other conditions (eg, diabetes, graft-vs-host disease [GVHD], inflammatory bowel disease) has also been investigated. Clinical trials are ongoing.


Epilepsy (treatment-resistant forms): CBD dosages of 10 mg/kg/day and 20 mg/kg/day for 14 days have been used in clinical trials. Systematic reviews of randomized controlled trials report a variety of CBD dosages and treatment durations. Graft-vs-host disease: CBD 300 mg/day orally starting 7 days before transplantation until day 30 was used in a phase 2 clinical study. Schizophrenia: CBD dosages have ranged from 600 mg/day to 1,000 mg/day orally for up to 6 weeks in randomized controlled trials.


Contraindications have not been identified.


Avoid use. Information regarding safety and efficacy in pregnancy and lactation is lacking.


Few case reports exist of interactions in which CBD is solely implicated.

Adverse Reactions

Information regarding adverse effects specifically attributed to CBD is limited. Seizure aggravation, leading to treatment withdrawal, has been reported. Information regarding cardiovascular effects is unclear.


Information specific to CBD is limited. Most data are derived from studies related to preparations from whole cannabis plant material.

Scientific Family

  • Cannabaceae


CBD is a chemical constituent of the cannabis plant Cannabis sativa L. Species ascribed to the Cannabis genus include C. sativa, Cannabis indica, and Cannabis ruderalis; however, disagreement exists regarding distinct classification of these species.Gloss 2015 Variants of C. sativa such as Charlotte's Web cannabis, cultivated specifically to be low in THC and high in CBD content, have been described.Jikomes 2018


The chemical structure of CBD and other major phytocannabinoids was elucidated in the 1960s, with the first clinical use of cannabidiol in epilepsy reported in the literature in 1974.Friedman 2017, Russo 2017

Federal and state laws in the United States are not synchronized with respect to the medical use of cannabis or cannabinoid medicines.Mead 2017 CBD as monotherapy is being evaluated for applications in seizures and other disorders. CBD/THC ("nabiximols" [ie, Sativex]) as an orobuccal spray is approved for multiple sclerosis spasticity in more than 20 countries, including Canada and the United Kingdom, and is being studied in phase 3 clinical trials in the United States.NIH 2018, O'Connell 2017


CBD is a chemical constituent of C. sativa L. Cannabidiol (2-[(1R,6R)-3-methyl-6-prop-1-en-2-ylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol) is distinct from the more than 100 other cannabinoid compounds, such as cannabinol, cannabigerol, and cannabivarin, found in lower concentrations in the plant.Morales 2017, NCBI 2018

Uses and Pharmacology

The uses described in the following sections focus on CBD specifically. See also Cannabis monograph for further information regarding potential uses of other cannabinoids.

CBD acts as an antagonist or partial antagonist at endogenous cannabinoid receptors (both CB1 and CB2 receptor types as well as other G-protein-coupled receptors [GPCRs]) by inhibiting full binding of direct ligands, and may act primarily at allosteric receptor sites. CBD acts as a modulator of receptor activation, influencing the endogenous cannabinoid system by potentiating intrinsic anandamide-mediated neurotransmission and regulating other cerebral neurotransmitters and receptors. It also modulates activity of various transient receptor potential channels and glycine receptors involved within and without the endocannabinoid system. Anti-inflammatory and antioxidant properties have been described.Gaston 2017, Grant 2018, Martinez-Pinilla 2017, Pertwee 2008, Tzadok 2016

CNS effects

Antinociceptive effects

Animal data

Results from experiments conducted in animals and reviews of animal data suggest anti-inflammatory and antinociceptive effects of CBD in conditions such as arthritis,Hammell 2016 chronic neuropathic pain,Lötsch 2018, Mücke 2018 and osteoarthritis pain.O'Brien 2018

Clinical data

Few studies have investigated, or are currently investigating, the effect of CBD alone on pain; most rely on CBD/THC combination preparations.Mücke 2018, NIH 2018 High-quality clinical evidence for the use of CBD in neuropathic pain is lacking,Mücke 2018 with one clinical study suggesting improvement in quality-of-life scores, including a physical discomfort measure as part of the Parkinson Disease Questionnaire (PDQ-39), in patients with Parkinson disease.Chagas 2014

A bias towards reporting positive findings exists both within individual clinical studies, as well as within systematic reviews of CBD use for pain management.Häuser 2018, Lötsch 2018

Parkinson disease

Clinical data

Clinical trials evaluating CBD alone in the management of motor symptoms in Parkinson disease are being conducted.NIH 2018 In a small study, patients with Parkinson disease (N=21) received CBD 75 mg/day, CBD 300 mg/day, or placebo for 6 weeks. There were no significant differences concerning motor and general symptoms; however, in Parkinson disease patients without psychiatric comorbidities, significant improvement in measures related to quality of life were observed with the higher CBD dosage compared to placebo.Chagas 2014

In a case series of Parkinson disease patients with rapid eye movement (REM) sleep behavior disorder, CBD 75 mg/day and 300 mg/day for 6 weeks resulted in a reduction in the frequency of REM sleep behavior disorder–related events. Further research is needed.Chagas 2014


Clinical data

Several phase 1 and phase 2 clinical trials have evaluated CBD as an antipsychotic intervention, with no net effects reported in some, and publication of results pending for others.Boggs 2018, NIH 2018

In one phase 2 trial, men and women 18 to 50 years of age with schizophrenia (N=42) were randomized to receive CBD or amisulpride, each starting at 200 mg/day and increased to 200 mg 4 times per day (800 mg/day) within the first week. After 4 weeks of treatment, both CBD and amisulpride treatment resulted in significant clinical improvement in psychotic symptoms, as evidenced by a reduction in Positive and Negative Syndrome Scale (PANSS) total score (P<0.001), among other measures. Compared to amisulpride, CBD was well tolerated and was associated with fewer extrapyramidal symptoms, less weight gain, and a lower incidence of sexual dysfunction.Leweke 2012

A study of 36 stable antipsychotic-treated patients with schizophrenia showed no improvement in PANSS or MATRICS Consensus Cognitive Battery scores with CBD 600 mg/day for 2 weeks compared to placebo.Boggs 2018

In another multicenter, randomized, controlled trial, patients with schizophrenia (N=43) received CBD 1,000 mg/day or placebo in addition to their existing antipsychotic medication. After 6 weeks, the CBD group had lower levels of positive psychotic symptoms (treatment difference in PANSS positive score, −1.4). Patients receiving CBD also showed greater improvements in cognitive performance and overall functioning, but differences between groups were not statistically significant.McGuire 2018


The exact mechanism by which CBD exerts its anticonvulsant activity is unknown. The antiseizure activity of THC seems to be mediated to an important extent by its partial agonist action on the CB1 receptor, whereas CBD has very weak affinity for the CB1 and CB2 receptors, indicating its antiseizure activity is mediated by other mechanisms; various targets have been investigated to explain CBD's anticonvulsant properties, including transient receptor potential channels, voltage-gated potassium and sodium channels, and certain GPCRs (such as GPR55), among others.Gaston 2017, Perucca 2017

Clinical data

Few moderate- or high-quality clinical trials (randomized controlled trials with a low risk of bias) have been conducted.Perucca 2017, Stockings 2018, Wong 2017 A number of open-label studies conducted by the manufacturers of the CBD preparation Epidiolex have contributed to knowledge surrounding the safety profile of CBD for treatment-resistant epilepsy.Neale 2017, O'Connell 2017, Wong 2017 Retrospective analyses of case reports or clinical data, generally supportive of efficacy of CBD alone or in combination with THC in treatment-resistant seizures, have also been reviewed in the literature.Neale 2017, O'Connell 2017, Perucca 2017, Stockings 2018, Wong 2017

A meta-analysis of data from 2 prospective clinical trials (N=291) (Devinsky et al and Thiele et al) reported CBD 20 mg/kg/day as adjunctive therapy is more likely than placebo to produce a greater than 50% reduction in seizures (relative risk [RR], 1.74; 95% CI, 1.24 to 2.43); number needed to treat (NNT) was 8 for one person to achieve a 50% reduction in seizures.Stockings 2018 A further clinical study by the same group of researchers reports significant findings for both 10 mg/kg/day and 20 mg/kg/day dosages evaluating the same outcome measure (odds ratio for a greater than 50% reduction in seizures in the CBD 20 mg/kg/day group vs placebo was 3.85 [95% CI, 1.75 to 8.47; P<0.001]; and odds ratio for the CBD 10 mg/kg/day group vs placebo was 3.27 [95% CI, 1.47 to 7.26; P=0.003]).Devinsky 2018 These studies included both pediatric and adult patients with Dravet and Lennox-Gastaut syndromes. Seizure aggravation, leading to treatment withdrawal of some participants, was reported.Perucca 2017

It should be noted that studies report a high placebo effect, and findings from open-label design studies must be interpreted with caution. Seizures were reduced in 63% of participants in the placebo arm in one trial of predominantly pediatric Lennox-Gastaut syndrome patients; a meta-analysis of studies in patients with treatment-resistant focal epilepsy found a placebo response of almost 20% in children and 10% in adults.Rosenberg 2015 Further clinical studies are being conducted, with publication of trial findings pending.NIH 2018


Clinical data

Limited studies have evaluated the efficacy of CBD alone in generalized social anxiety disorder (1 study) and psychosis (2 studies). A review deemed the studies to be of lower quality or with potential for bias.Whiting 2015 Clinical trials evaluating CBD alone in the management of Prader-Willi Syndrome are being conducted.NIH 2018

Studies are lacking regarding use of CBD alone in Tourette syndrome or tics.NIH 2018


The role of the endocannabinoid system in energy metabolism has been investigated, with emerging evidence showing CBD may slow beta-cell damage in type 1 diabetes mellitus.Di Marzo 2011, Mastinu 2018

Animal data

Limited experiments in nonobese diabetic mice treated with CBD demonstrated reductions in incidence and manifestations of type 1 diabetes.Di Marzo 2011, Zuardi 2008

Clinical data

The CB1 receptor antagonist rimonabant has been evaluated in clinical trials of obese patients with and without comorbidities (dyslipidemia and/or type 2 diabetes) and has demonstrated reductions in hemoglobin A1c (HbA1c) levels; however, use was suspended in 2008 by the European Medicines Agency when documentation of psychiatric adverse effects (worsening anxiety and depression) showed that the benefits no longer outweighed the risks.Di Marzo 2011 Focus is now on other cannabinoid CB1 antagonists, including the less well studied tetrahydrocannabivarin (THCV), the propyl homologue of THC.

In one small randomized, double-blind, placebo-controlled study (N=62), patents with noninsulin–treated type 2 diabetes received CBD, THCV, a combination of CBD and THCV, or placebo for 13 weeks. CBD and THCV were well tolerated. THCV decreased fasting plasma glucose and improved pancreatic beta cell function, adiponectin, and apolipoprotein A. CBD decreased resistin and increased glucose-dependent insulinotropic peptide. However, the primary end point (change in HDL cholesterol) was not affected by treatment with CBD, THCV, or combination treatment.Jadoon 2016 More research is needed.

Graft-vs-host disease

Animal and in vitro data

Effects of CBD on T cells, cytokines, and other modulators of inflammation have been demonstrated in vitro and in animal models. Insufficient data exist.NIH 2018, Yeshurun 2015

Clinical data

Limited clinical studies evaluating use of CBD alone have been conducted. A small phase 2 study of 48 transplant patients examined effects of CBD on development of GVHD. In addition to GVHD standard prophylaxis (cyclosporine and methotrexate), CBD 300 mg/day was given orally, starting 7 days before transplantation until day 30. No patients developed GVHD during treatment with CBD. Following discontinuation of treatment, 8 patients developed GVHD. It was determined that addition of CBD to GVHD prophylaxis resulted in low cumulative incidence rates of GVHD by day 100.NIH 2018, Yeshurun 2015 Further studies are needed.

Inflammatory bowel disease

Animal and in vitro data

Cannabinoids have been shown to decrease macroscopic inflammation, myeloperoxidase activity, and peristalsis, and to ameliorate inflammation in rodent studies.Naftali 2013, Wallace 2013 CBD demonstrated anti-inflammatory activity in inflamed colonic tissue of inflammatory bowel disease explants.Couch 2017

Clinical data

A small clinical study (N= 20) evaluating CBD 10 mg orally or placebo twice daily in patients with moderately active Crohn disease reported no effect, possibly due to a lack of effect by CBD, the low CBD dose used, and/or the small number of participants.Naftali 2017 Further clinical studies in Crohn disease and inflammatory bowel disease are being conducted, with publication of results pending.NIH 2018

Multiple sclerosis:

Clinical data

Clinical studies evaluating CBD alone in the management of multiple sclerosis are limited, with most studies using commercially available CBD/THC combination preparations.NIH 2018, Nielsen 2018


A phase 1 clinical study is being conducted by Johns Hopkins University to describe the pharmacokinetics of oral and vaporized CBD.Johns Hopkins University 2018

Epilepsy (treatment-resistant forms)

CBD dosages of 10 mg/kg/day and 20 mg/kg/day for 14 days have been used in clinical trials.Devinsky 2018 Systematic reviews of randomized controlled trials report a wide variety of CBD dosages and treatment durations.Stockings 2018, Wong 2017

Graft-vs-host disease

CBD 300 mg/day orally starting 7 days before transplantation until day 30 was used in a phase 2 clinical study.Yeshurun 2015


CBD dosages have ranged from 600 mg/day to 1,000 mg/day orally for up to 6 weeks in randomized controlled trials.Boggs 2018, Leweke 2012, McGuire 2018

Pregnancy / Lactation

Avoid use. Information regarding safety and efficacy of CBD in pregnancy and lactation is limited. The endocannabinoid system plays an role in regulation of fertility; cannabis use and/or disruptions to the endocannabinoid system have demonstrated negative effects on reproduction.Dekker 2012, Karasu 2011, Lewis 2012


The cannabinoids THC and CBD are both metabolized by the cytochrome P450 (CYP-450) enzyme system.Gaston 2017, Tran 2017 CBD has been shown to both inhibit (CYP2C19, CYP2D6, CYP2C9, and CYP3 enzymes), and induce members of the CYP2B family in animal models.Gaston 2017 CBD may also be an inhibitor of certain transporter systems.Perucca 2017 Case reports are minimal.

Cilostazol: CYP2C19 inhibitors may increase the serum concentration of cilostazol. Consider therapy modification.Pletal January 2015, Suri 1999

Citalopram: CYP2C19 inhibitors (moderate) may increase the serum concentration of citalopram. Consider therapy modification.Bondolfi 1996, Celexa August 2011, Mailling 2005, Priskorn 1997, Rocha 2010, Rochat 1997

Clobazam: Cannabidiol may increase serum concentrations of the active metabolite(s) of clobazam. Cannabidiol may increase the serum concentration of clobazam. Monitor therapy. This interaction is only expected with the oral administration of cannabidiol.Epidiolex June 2018, Gaston 2017, Geffrey 2015, Jiang 2013, Onfi December 2016 CBD is well-documented to interact with clobazam, a 2C19 substrate, resulting in increased clobazam levels.Geffrey 2015

Clopidogrel: CYP2C19 inhibitors (moderate) may decrease serum concentrations of the active metabolite(s) of clopidogrel. Consider therapy modification.Brandt 2007, Collet 2009, Fontana 2008, Frere 2008, Gilard 2008, Gilard 2006, Giusti 2009, Hulot 2006, Juurlink 2009, Kim 2008, Mega 2009, Pezalla 2008, Plavix May 2009, Sibbing 2009, Simon 2009, Small 2008, Trenk 2008

CNS depressants: Cannabidiol may enhance the CNS depressant effect of CNS depressants. Monitor therapy.Epidiolex June 2018, Sativex March 2015, Sativex March 2012

CYP2C19 inducers (strong): CYP2C19 inducers (strong) may decrease the serum concentration of cannabidiol. Monitor therapy.Epidiolex June 2018, Jiang 2011, Stott 2013

CYP2C19 inhibitors (moderate): CYP2C19 inhibitors (moderate) may increase the serum concentration of cannabidiol. Monitor therapy.Epidiolex June 2018

CYP2C19 inhibitors (strong): CYP2C19 inhibitors (strong) may increase the serum concentration of cannabidiol. Monitor therapy.Epidiolex June 2018

CYP2C19 substrates (high risk with Inhibitors): CYP2C19 inhibitors (moderate) may decrease the metabolism of CYP2C19 substrates (high risk with inhibitors). Monitor therapy.Bjornsson 2003

CYP3A4 inducers (strong): CYP3A4 inducers (strong) may decrease the serum concentration of cannabidiol. Monitor therapy.Epidiolex June 2018, Jiang 2011, Stott 2013

CYP3A4 inhibitors (moderate): CYP3A4 inhibitors (moderate) may increase the serum concentration of cannabidiol. Monitor therapy.Epidiolex June 2018, Stott 2013, Watanabe 2007

CYP3A4 inhibitors (strong): CYP3A4 inhibitors (strong) may increase the serum concentration of cannabidiol. Monitor therapy.Epidiolex June 2018, Stott 2013, Watanabe 2007

Flibanserin: CYP2C19 Inhibitors (moderate) may increase the serum concentration of flibanserin. Monitor therapy.Addyi August 2015

Tacrolimus: One case report described an interaction with the Epidiolex product and tacrolimus, resulting in tacrolimus toxicity.Leino 2018

Valproate Products: Valproate products may enhance the hepatotoxic effect of cannabidiol. This interaction has only been documented with the oral administration of cannabidiol. Monitor therapy.Epidiolex June 2018, Gaston 2017

Warfarin: Cannabidiol may increase the serum concentration of warfarin. Monitor therapy.Grayson 2017, Yamaori 2012 CBD has been noted to interact with warfarin, resulting in a need for decreased warfarin dosages.Grayson 2017

Adverse Reactions

Seizure aggravation, leading to treatment withdrawal, has been reported in studies of patients with treatment-resistant seizure syndromes. Overall, CBD is generally well tolerated, with mild effects, including drowsiness, reported.Perucca 2017

A systematic review found no effect on blood pressure or heart rate under control conditions, either with acute or chronic CBD administration. However, in models of stress, acute CBD significantly reduced blood pressure and heart rate that had been increased by the stress.Sultan 2017 In animal studies, CBD significantly increased cerebral blood flow.Sultan 2017


Information specific to CBD is limited. Most data are derived from studies related to preparations from whole cannabis plant material.

Index Terms

  • Cannabis indica
  • Cannabis ruderalis
  • Cannabis sativa


Addyi (flibanserin) [prescribing information]. Raleigh, NC: Sprout Pharmaceuticals Inc; August 2015.
Bjornsson TD, Callaghan JT, Einolf HJ, et al. The conduct of in vitro and in vivo drug-drug interaction studies: A PhRMA perspective. J Clin Pharmacol. 2003;43(5):443-469.12751267
Boggs DL, Surti T, Gupta A, et al. The effects of cannabidiol (CBD) on cognition and symptoms in outpatients with chronic schizophrenia a randomized placebo controlled trial. Psychopharmacology (Berl). 2018;235(7):1923-1932.29619533
Bondolfi G, Chautems C, Rochat B, et al. Non-response to citalopram in depressive patients: Pharmacokinetic and clinical consequences of a fluvoxamine augmentation. Psychopharmacology (Berl). 1996;128(4):421-425.8986013
Brandt JT, Close SL, Iturria SJ, et al. Common polymorphisms of CYP2C19 and CYP2C9 affect the pharmacokinetic and pharmacodynamic response to clopidogrel but not prasugrel. J Thromb Haemost. 2007;5(12):2429-2436.17900275
Celexa (citalopram) [prescribing information]. St. Louis, MO: Forest Laboratories, Inc; August 2011.
Chagas MH, Eckeli AL, Zuardi AW, et al. Cannabidiol can improve complex sleep-related behaviours associated with rapid eye movement sleep behavior disorder in Parkinson's disease patients: a case series. J Clin Pharm Ther. 2014;39(5):564-566.24845114
Chagas MH, Zuardi AW, Tumas V, et al. Effects of cannabidiol in the treatment of patients with Parkinson's disease: an exploratory double-blind trial. J Psychopharmacol. 2014;28(11):1088-1098.25237116
Collet JP, Hulot JS, Pena A, et al. Cytochrome P450 2C19 polymorphism in young patients treated with clopidogrel after myocardial infarction: A cohort study. Lancet. 2009;373(9660):309-317.19108880
Couch DG, Tasker C, Theophilidou E, Lund JN, O’Sullivan SE. Cannabidiol and palmitoylethanolamide are anti-inflammatory in the acutely inflamed human colon. Clin Sci (Lond). 2017;131(21):2611-2616.28954820
Dekker GA, Lee SY, North RA, McCowan LM, Simpson NA, Roberts CT. Risk factors for preterm birth in an international prospective cohort of nulliparous women. PLoS One. 2012;7(7):e39154.22815699
Devinsky O, Cross JH, Laux L, et al. Cannabidiol in Dravet syndrome study group. Trial of cannabidiol for drug-resistant seizures in the Dravet syndrome. N Engl J Med. 2017;376(21):2011-2020.28538134
Devinsky O, Patel AD, Cross JH, et al; GWPCARE3 Study Group. Effect of cannabidiol on drop seizures in the Lennox-Gastaut syndrome. N Engl J Med. 2018;378(20):1888-1897.29768152
Di Marzo V, Piscitelli F, Mechoulam R. Cannabinoids and endocannabinoids in metabolic disorders with focus on diabetes. Handb Exp Pharmacol. 2011;(203):75-104.21484568
Epidiolex (cannabidiol) oral solution [prescribing information]. Carlsbad, CA: Greenwich Biosciences Inc; June 2018.
Fontana P, Senouf D, Mach F. Biological effect of increased maintenance dose of clopidogrel in cardiovascular outpatients and influence of the cytochrome P450 2C19*2 allele on clopidogrel responsiveness. Thromb Res. 2008;121(4):463-468.17681590
Frere C, Cuisset T, Morange PE, et al. Effect of cytochrome P450 polymorphisms on platelet reactivity after treatment with clopidogrel in acute coronary syndrome. Am J Cardiol. 2008;101(8):1088-1093.18394438
Friedman D, Sirven JI. Historical perspective on the medical use of cannabis for epilepsy: Ancient times to the 1980s. Epilepsy Behav. 2017;70(pt B):298-301.28089286
Gaston TE, Bebin EM, Cutter GR, Liu Y, Szaflarski JP; UAB CBD Program. Interactions between cannabidiol and commonly used antiepileptic drugs. Epilepsia. 2017;58(9):1586-1592.28782097
Gaston TE, Friedman D. Pharmacology of cannabinoids in the treatment of epilepsy. Epilepsy Behav. 2017;70(pt B):313-318.28087250
Geffrey AL, Pollack SF, Bruno PL, Thiele EA. Drug-drug interaction between clobazam and cannabidiol in children with refractory epilepsy. Epilepsia. 2015;56(8):1246-1251.26114620
Gilard M, Arnaud B, Cornily JC, et al. Influence of omeprazole on the antiplatelet action of clopidogrel associated with aspirin: The randomized, double-blind OCLA (Omeprazole Clopidogrel Aspirin) study. J Am Coll Cardiol, 2008;51(3):256-260.18206732
Gilard M, Arnaud B, Le Gal G, Abgrall JF, Boschat J. Influence of omeprazol on the antiplatelet action of clopidogrel associated to aspirin. J Thromb Haemost. 2006;4(11):2508-2509.16898956
Giusti B, Gori AM, Marcucci R, et al. Relation of cytochrome P450 2C19 loss-of-function polymorphism to occurrence of drug-eluting coronary stent thrombosis. Am J Cardiol. 2009;103(6):806-811.19268736
Gloss D. An overview of products and bias in research. Neurotherapeutics. 2015;12(4):731-734.26202343
Grant KS, Petroff R, Isoherranen N, Stella N, Burbacher TM. Cannabis use during pregnancy: Pharmacokinetics and effects on child development. Pharmacol Ther. 2018;182:133-151.28847562
Grayson L, Vines B, Nichol K, Szaflarski JP; UAB CBD Program. An interaction between warfarin and cannabidiol, a case report. Epilepsy Behav Case Rep. 2017;9:10-11.29387536
Hammell DC, Zhang LP, Ma F, et al. Transdermal cannabidiol reduces inflammation and pain-related behaviours in a rat model of arthritis. Eur J Pain. 2016;20(6):936-948.26517407
Häuser W, Petzke F, Fitzcharles MA. Efficacy, tolerability and safety of cannabis-based medicines for chronic pain management—An overview of systematic reviews. Eur J Pain. 2018;22(3):455-470.29034533
Hulot JS, Bura A, Villard E, et al. Cytochrome P450 2C19 loss-of-function polymorphism is a major determinant of clopidogrel responsiveness in healthy subjects. Blood. 2006;108(7):2244-2247.16772608
Jadoon KA, Ratcliffe SH, Barrett DA, et al. Efficacy and safety of cannabidiol and tetrahydrocannabivarin on glycemic and lipid parameters in patients with type 2 diabetes: A randomized, double-blind, placebo-controlled, parallel group pilot study. Diabetes Care. 2016;39(10):1777-1786.27573936
Jiang R, Yamaori S, Okamoto Y, Yamamoto I, Wantanabe K. Cannabidiol is a potent inhibitor of the catalytic activity of cytochrome P450 2C19. Drug Metab Pharmacokinet. 2013;28(4):332-338.23318708
Jiang R, Yamaori S, Takeda S, Yamamoto I, Watanabe K. Identification of cytochrome P450 enzymes responsible for metabolism of cannabidiol by human liver microsomes. Life Sci. 2011;89(5-6):165-170.21704641
Jikomes N, Zoorob M. The cannabinoid content of legal cannabis in Washington State varies systematically across testing facilities and popular consumer products. Sci Rep. 2018;8(1):4519.29540728
Johns Hopkins University. The pharmacokinetics and pharmacodynamics of oral and vaporized cannabidiol. website. Updated July 16, 2018. Accessed August 14, 2018.
Juurlink DN, Gomes T, Ko DT, et al. A population-based study of the drug interaction between proton pump inhibitors and clopidogrel. CMAJ. 2009;180(7):713-718.19176635
Karasu T, Marczylo TH, Maccarrone M, Konje JC. The role of sex steroid hormones, cytokines and the endocannabinoid system in female fertility. Hum Reprod Update. 2011;17(3):347-361.21227997
Kim KA, Park PW, Hong SJ, Park JY. The effect of CYP2C19 polymorphism on the pharmacokinetics and pharmacodynamics of clopidogrel: A possible mechanism for clopidogrel resistance. Clin Pharmacol Ther. 2008;84(2):236-242.18323861
Leino A, Emoto C, Fukuda T, Privitera M, Vinks A, Alloway R. Evidence of a clinically significant drug-drug interaction between cannabidiol and tacrolimus: A case report [abstract]. 2018 Meeting of American Transplant Congress; June 3, 2018; Cincinnati, OH. Abstract B331.
Leweke FM, Piomelli D, Pahlisch F, et al. Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia. Transl Psychiatry. 2012;2:e94.22832859
Lewis SE, Rapino C, Di Tommaso M, et al. Differences in the endocannabinoid system of sperm from fertile and infertile men. PLoS One. 2012;7(10):e47704.23082196
Lötsch J, Weyer-Menkhoff I, Tegeder I. Current evidence of cannabinoid-based analgesia obtained in preclinical and human experimental settings. Eur J Pain. 2018;22(3):471-484.29160600
Malling D, Poulsen MN, Sogaard B. The effect of cimetidine or omeprazole on the pharmacokinetics of escitalopram in healthy subjects. Br J Clin Pharmacol. 2005;60(3):287-290.16120067
Martinez-Pinilla E, Varani K, Reyes-Resina I, et al. Binding and signaling studies disclose a potential allosteric site for cannabidiol in cannabinoid CB2 receptors. Front Pharmacol. 2017;8:744.29109685
Mastinu A, Premoli M, Ferrari-Toninelli G. Cannabinoids in health and disease: pharmacological potential in metabolic syndrome and neuroinflammation [published online ahead of print March 30, 2018]. Horm Mol Biol Clin Investig.29601300
McGuire P, Robson P, Cubala WJ, et al. Cannabidiol (CBD) as an adjunctive therapy in schizophrenia: A multicenter randomized controlled trial. Am J Psychiatry. 2018;175(3):225-231.29241357
Mead A. The legal status of cannabis (marijuana) and cannabidiol (CBD) under U.S. law. Epilepsy Behav. 2017;70(Pt B):288-291.28169144
Mega JL, Close SL, Wiviott SD, et al. Cytochrome P-450 polymorphisms and response to clopidogrel. N Engl J Med. 2009;360(4):354-362.19106084
Morales P, Hurst DP, Reggio PH. Molecular targets of the phytocannabinoids-A complex picture. Prog Chem Org Nat Prod. 2017;103:103-131.28120232
Mücke M, Phillips T, Radbruch L, Petzke F, Häuser W. Cannabis-based medicines for chronic neuropathic pain in adults. Cochrane Database Syst Rev. 2018;3:CD012182.29513392
Naftali T, Bar-Lev Schleider L, Dotan I, Lansky EP, Sklerovsky Benjaminov F, Konikoff FM. Cannabis induces a clinical response in patients with Crohn's disease: a prospective placebo-controlled study. Clin Gastroenterol Hepatol. 2013;11(10):1276-1280.e1.23648372
Naftali T, Mechulam R, Marii A, et al. Low-dose cannabidiol is safe but not effective in the treatment for Crohn's disease, a randomized controlled trial. Dig Dis Sci. 2017;62(6):1615-1620.28349233
National Center for Biotechnology Information. PubChem Compound Database. Cannabidiol: Compound summary for CID=644019. Accessed August 31, 2018.
National Institute of Health. Cannabidiol. website. Accessed July 2018.
Neale M. Efficacy and safety of cannabis for treating children with refractory epilepsy. Nurs Child Young People. 2017;29(7):32-37.29115760
Nielsen S, Germanos R, Weier M, et al. The use of cannabis and cannabinoids in treating symptoms of multiple sclerosis: A systematic review of reviews. Curr Neurol Neurosci Rep. 2018;18(2):8.29442178
O'Brien M, McDougall JJ. Cannabis and joints: scientific evidence for the alleviation of osteoarthritis pain by cannabinoids. Curr Opin Pharmacol. 2018;40:104-109.29635215
O'Connell BK, Gloss D, Devinsky O. Cannabinoids in treatment-resistant epilepsy: A review. Epilepsy Behav. 2017;70(pt B):341-348.28188044
Onfi (clobazam) [prescribing information]. Deerfield, IL: Lundbeck; December 2016.
Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin. Br J Pharmacol. 2008;153(2):199-215.17828291
Perucca E. Cannabinoids in the treatment of epilepsy: hard evidence at last? J Epilepsy Res. 2017;7(2):61-76.29344464
Pezalla E, Day D, Pulliadath I. Initial assessment of clinical impact of a drug interaction between clopidogrel and proton pump inhibitors. J Am Coll Cardiol. 2008;52(12):1038-1039.18786491
Plavix (clopidogrel) [prescribing information]. Bridgewater, NJ: Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership; May 2009.
Pletal (cilostazol) [prescribing information]. Rockville, MD: Otsuka America Pharmaceutical, Inc.; January 2015.
Priskorn M, Larsen F, Segonzac A, et al. Pharmacokinetic interaction study of citalopram and cimetidine in healthy subjects. Eur J Clin Pharmacol. 1997;52(3):241-242.9218934
Rocha A, Coelho EB, Sampaio SA, et al. Omeprazole preferentially inhibits the metabolism of (+)-(S)-citalopram in healthy volunteers. Br J Clin Pharmacol. 2010;70(1):43-51.20642546
Rochat B, Amey M, Gillet M, et al. Identification of three cytochrome P450 isozymes involved in N-demethylation of citalopram enantiomers in human liver microsomes. Pharmacogenetics. 1997;7(1):1-10.9110356
Rosenberg EC, Tsien RW, Whalley BJ, Devinsky O. Cannabinoids and epilepsy. Neurotherapeutics. 2015;12(4):747-768.26282273
Russo EB. Cannabis and epilepsy: An ancient treatment returns to the fore. Epilepsy Behav. 2017;70(pt B):292-297.27989385
Sativex (tetrahydrocannabinol and cannabidiol) oromucosal spray [summary of product characteristics]. Cambridge, UK: GW Pharma Ltd; March 2015.
Sativex (tetrahydrocannabinol and cannabidiol) buccal spray [product monograph]. Toronto, Ontario, Canada: Bayer Inc; March 2012
Sibbing D, Stegherr J, Latz W, et al. Cytochrome P450 2C19 loss-of-function polymorphism and stent thrombosis following percutaneous coronary intervention. Eur Heart J. 2009;30(8):916-922.19193675
Simon T, Verstuyft C, Mary-Krause M, et al; French Registry of Acute ST-Elevation and Non-ST-Elevation Myocardial Infarction (FAST-MI) Investigators. Genetic determinants of response to clopidogrel and cardiovascular events. N Engl J Med. 2009;360(4):363-375.19106083
Small DS, Farid NA, Payne CD, et al. Effects of the proton pump inhibitor lansoprazole on the pharmacokinetics and pharmacodynamics of prasugrel and clopidogrel. J Clin Pharmacol. 2008;48(4):475-484.18303127
Stockings E, Zagic D, Campbell G, et al. Evidence for cannabis and cannabinoids for epilepsy: a systematic review of controlled and observational evidence. J Neurol Neurosurg Psychiatry. 2018;89(7):741-753.29511052
Stott C, White L, Wright S, Wilbraham D, Guy G. A phase I, open-label, randomized, crossover study in three parallel groups to evaluate the effect of rifampicin, ketoconazole, and omeprazole on the pharmacokinetics of THC/CBD oromucosal spray in healthy volunteers. Springerplus. 2013;2(1):236.23750331
Sultan SR, Millar SA, England TJ, O’Sullivan SE. A systematic review and meta-analysis of the haemodynamic effects of cannabidiol. Front Pharmacol. 2017;8:81.28286481
Suri A, Bramer SL. Effect of omeprazole on the metabolism of cilostazol. Clin Pharmacokinet. 1999;37 Suppl 2:53-59.10702887
Tran K, Spry C. CADTH rapid response report: summary with critical appraisal. The use of medical cannabis with other medications: A review of safety and guidelines. Published April 19, 2017. Accessed August 14, 2018.
Trenk D, Hochholzer W, Fromm MF, et al. Cytochrome P450 2C19 681G>A polymorphism and high on-clopidogrel platelet reactivity associated with adverse 1-year clinical outcome of elective percutaneous coronary intervention with drug-eluting or bare-metal stents. J Am Coll Cardiol. 2008;51(20):1925-1934.18482659
Tzadok M, Uliel-Siboni S, Linder I, et al. CBD-enriched medical cannabis for intractable pediatric epilepsy: The current Israeli experience. Seizure. 2016;35:41-44.26800377
Wallace JL, Flannigan KL, McKnight W, Wang L, Ferraz JG, Tuitt D. Pro-resolution, protective and anti-nociceptive effects of a cannabis extract in the rat gastrointestinal tract. J Physiol Pharmacol. 2013;64(2):167-175.23756391
Watanabe K, Yamaori S, Funahashi T, Kimura T, Yamamoto I. Cytochrome P450 enzymes involved in the metabolism of tetrahydrocannabinols and cannabinol by human hepatic microsomes. Life Sci. 2007;80(15):1415-1419.17303175
Whiting PF, Wolff RF, Deshpande S, et al. Cannabinoids for medical use: A systematic review and meta-analysis [published correction appears in JAMA. 2016;315(14):1522; JAMA. 2015;314(5):520; JAMA. 2015;314(8):837; JAMA. 2015;314(21):2308]. JAMA. 2015;313(24):2456-2473.26103030
Wong SS, Wilens TE. Medical cannabinoids in children and adolescents: A systematic review. Pediatrics. 2017;140(5).29061872
Yamaori S, Koeda K, Kushihara M, Hada Y, Yamamoto I, Watanabe K. Comparison in the in vitro inhibitory effects of major phytocannabinoids and polycyclic aromatic hydrocarbons contained in marijuana smoke on cytochrome P450 2C9 activity. Drug Metab Pharmacokinet. 2012;27(3):294-300.22166891
Yeshurun M, Shpilberg O, Herscovici C, et al. Cannabidiol for the prevention of graft-versus-host-disease after allogeneic hematopoietic cell transplantation: results of a phase II study. Biol Blood Marrow Transplant. 2015;21(10):1770-1775.26033282
Zuardi AW. Cannabidiol: from an inactive cannabinoid to a drug with wide spectrum of action. Rev Bras Psiquiatr. 2008;30(3):271-280.18833429


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