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Ibrutinib is an irreversible Bruton tyrosine kinase inhibitor approved for treatment of Waldenstrom macroglobulinemia, chronic lymphocytic leukemia, and mantle cell lymphoma that increases the risk of bleeding among patients. Platelets from ibrutinib-treated patients exhibit deficiencies in collagen-evoked signaling in suspension; however, the significance of this observation and how it relates to bleeding risk is unclear, as platelets encounter immobile collagen in vivo. We sought to clarify the effects of ibrutinib on platelet function to better understand the mechanism underlying bleeding risk.

Ibrutinib Inhibits Platelet Integrin α IIb β 3 Outside-In Signaling and Thrombus Stability But Not Adhesion to Collagen

Ibrutinib Inhibits Platelet Integrin α _IIb β ₃ Outside-In Signaling and Thrombus Stability But Not Adhesion to Collagen