Summary

Warning

Consider Alternative:
  • CYP2C19 inhibitors and cannabidiol (CBD) can affect the conversion of clopidogrel to its active metabolite, leading to a potential loss of efficacy that might increase the risk of ischemic events.

Consider discontinaution of CBD product or use of another antiplatelet agent such as aspirin or another P2Y12 inhibitor. Monitor patient for ischemic events.

Clopidogrel is a prodrug that requires metabolism from cytochrome P450 2C19 (CYP2C19) to become an active drug. Concurrent use of clopidogrel and CYP2C19 inhibitors, such as cannabidiol (CBD), may potentially lead to significant decreases in active clopidogrel levels which can lead to ischemic events as result of a decrease in clopidogrel activity.

Preferred managment options can include discontinuation of the CYP2C19 inhibitor(s) or use of another antiplatelet agent (see the "Alternative Options" box). Patients should be monitored for signs of an ischemic event.

  • This is when two or more drugs react with each other and cause unwanted side effects.
  • Concurrent use of clopidogrel and CYP2C19 inhibitors, including CBD, could potentially lead to an unexpected loss of clopidogrel efficacy.
Literature

CYP2C19 is an important enzyme for the effectiveness of clopidogrel. A boxed warning for Plavix (clopidogrel) states “Effectiveness of Plavix depends on activation to an active metabolite by the cytochrome P450 (CYP) system, principally CYP2C19.” In addition, poor metabolizers (patients with poor functionality of CYP2C19) have been shown to have higher cardiovascular event rates following ACS or PCI than patients with normal CYP2C19 functionality. As a result, CYP2C19 inhibition of clopidogrel metabolism can cause significant issues for any patients using clopidogrel as a part of their treatment regimen.1

According to the product labeling for Epidiolex (prescription cannabidiol, CBD), CBD is a potent inhibitor of CYP2C19.2,3 One in-vivo study supports the effect on CYP2C19 activity by using substrate concentrations of 60 μM (S)-mephenytoin, 2 μM omeprazole, and 4 μM 3-O-Methylfluorescein. CBD showed concentration dependent inhibition with IC50 values of 8.70 μM, 1.55 μM, and 1.79 μM respectively.4 In another study that examined the interaction between CBD and clobazam in 13 children with refractory epilepsy, CBD was found to increase levels of clobazam, a CYP2C19 and CYP3A4 substrate, leading to the reduction of clobazam dose in 10 subjects who experienced side effects potentially from concurrent use with CBD. In addition, levels of clobazam were found to be increased 60 ± 80% and levels of nCLB, an active metabolite of clobazam, were found to be increased 500 ± 300%. Similarly, to clobazam, nCLB is also metabolized by CYP3A4 and CYP2C19. Although it is possible the nCLB levels could be caused by CYP3A4 inhibition, the study reports that poor metabolizers of CYP2C19 see a fivefold higher plasma level than extensive metabolizers in nCLB levels, supporting previous studies concerning CBD’s ability to inhibit CYP2C19.5 Due to the ability of cannabinoids to potently inhibit CYP2C19, concurrent use with clopidogrel should be done with caution.

  1. Plavix (clopidogrel) [prescribing information]. Bridgewater, NJ: Sanofi-Aventis US LLC; September 2022. Clopidogrel Prescribing Information.
  2. Epidiolex (cannabidiol) [prescribing information]. Palo Alto, CA: Jazz Pharmaceuticals Inc; January 2023. Epidiolex Prescribing Information.
  3. Brown, P. (rep.). Application Number: 210365Orig1s000, Non-Clinical Review. https://www.accessdata.fda.gov/drugsatfda_docs/nda/2018/210365Orig1s000PharmR.pdf Center for Drug Evaluation and Research: Non-Clinical Review of Cannabidiol.
  4. Jiang R, Yamaori S, Okamoto Y, Yamamoto I, Watanabe K. Cannabidiol is a potent inhibitor of the catalytic activity of cytochrome P450 2C19. Drug Metab Pharmacokinet. 2013;28(4):332-338. doi:10.2133/dmpk.dmpk-12-rg-129 Pubmed PMID: 23318708
  5. 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. doi:10.1111/epi.13060 Pubmed PMID: 26114620

Authorship:

  • Author: Dr. Kojo Abanyie with input from Dr. Daniel Malone, Dr. Lorenzo Villa-Zapata, Dr. Xiaotong Li
  • Email: koa27@pitt.edu
  • Date: September 17, 2023

Funding acknowledgement:

  • This project was funded in part by grants U54 AT008909 from the National Center for Complimentary and Integrative Health (NCCIH), U18 HS027099, R01HS025984 and R21HS023826 from the Agency for Healthcare Research and Quality (AHRQ). Any opinions, findings, and conclusions or recommendations expressed on the site are those of the site maintainers and do not necessarily reflect the views of the funding agencies.