Skip to main content
Log in

Antiplatelet therapy

The P2Y12 receptor: no active metabolite, no party

  • News & Views
  • Published:

From Nature Reviews Cardiology

View current issue Sign up to alerts

Poor responders to clopidogrel have low levels of circulating active metabolite. However, in vitro experiments have shown that blood platelets from poor responders are fully inhibited by the active metabolite of this prodrug. Impaired platelet inhibition reflects inadequate plasma levels of active metabolites, and not differences in platelet P2Y12 receptor function.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

References

  1. De Miguel, A., Ibanez, B. & Badimón, J. J. Clinical implications of clopidogrel resistance. Thromb. Haemost. 100, 196–203 (2008).

    Article  CAS  Google Scholar 

  2. Wallentin, L. et al. Prasugrel achieves greater and faster P2Y12 receptor-mediated platelet inhibition than clopidogrel due to more efficient generation of its active metabolite in aspirin-treated patients with coronary artery disease. Eur. Heart J. 29, 21–30 (2008).

    Article  CAS  Google Scholar 

  3. Erlinge, D. et al. Patients with poor responsiveness to thienopyridine treatment or with diabetes have lower levels of circulating active metabolite, but their platelets respond normally to active metabolite added ex vivo. J. Am. Coll. Cardiol. 52, 1968–1977 (2008).

    Article  CAS  Google Scholar 

  4. Patrono, C., Baigent, C., Hirsh, J. & Roth, G. Antiplatelet drugs: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 133, 199S–233S (2008).

    Article  CAS  Google Scholar 

  5. Wiviott, S. D. et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N. Engl. J. Med. 357, 2001–2015 (2007).

    Article  CAS  Google Scholar 

  6. Järemo, P., Lindahl, T. L., Fransson, S. G. & Richter, A. Individual variations of platelet inhibition after loading doses of clopidogrel. J. Intern. Med. 252, 233–238 (2002).

    Article  Google Scholar 

  7. Mega, J. L. et al. Cytochrome P-450 polymorphisms and response to clopidogrel. N. Engl. J. Med. 360, 354–362 (2009).

    Article  CAS  Google Scholar 

  8. Santilli, F. et al. Platelet cyclooxygenase inhibition by low-dose aspirin is not reflected consistently by platelet function assays: implications for aspirin “resistance”. J. Am. Coll. Cardiol. 53, 667–677 (2009).

    Article  CAS  Google Scholar 

  9. Freedman, J. E. & Hylek, E. M. Clopidogrel, genetics, and drug responsiveness. N. Engl. J. Med. 360, 411–413 (2009).

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Carlo Patrono.

Ethics declarations

Competing interests

The author declared that he his a consultant for Astra-Zeneca, Bayer, Eli Lilly, Sanofi-Aventis and Servier, has received speakers bureau from Bayer, Eli Lilly and Schering-Plough, and grant/research support from Bayer and Servier.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Patrono, C. The P2Y12 receptor: no active metabolite, no party. Nat Rev Cardiol 6, 271–272 (2009). https://doi.org/10.1038/nrcardio.2009.29

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1038/nrcardio.2009.29

  • Springer Nature Limited

This article is cited by

Navigation