We first identified two groups of healthy donors based on their sensitivity to collagen-induced platelet aggregation inhibition by ibrutinib in vitro. In ibrutinib LS donors the half maximal inhibitory concentration (ICIbrutinib has been shown to affect thrombus formation and stability on a collagen matrix under flowThe management of bleeding risk in patients with cardiovascular disease under dual antiplatelet therapy for primary or secondary prevention treated with Btk inhibitors is of concern in clinical practice.The first-generation Btk inhibitor ibrutinib has revolutionized the therapy of CLL and mantle cell lymphoma but the drug can cause some side effects such as atrial fibrillation and bleeding.We performed a series of assays on two populations of healthy donors characterized by high or low sensitivity to ibrutinib, based on the degree of inhibition of collagen-induced platelet aggregation in PRP achieved by the drug.We provide evidence that one factor contributing to predispose platelets to ibrutinib sensitivity in vitro is the drug efflux pump system. It is noteworthy that acalabrutinib had no impact on platelet aggregation induced by thrombin receptor activating peptide (TRAP), the thromboxane A2 analog U46619 or ADP but did affect to some extent platelet aggregation induced by the GPVI agonist, collagen-related peptide, particularly in the HS group (Online Supplementary Figure S3). Acalabrutinib and other second generation BTK inhibitors are generally better tolerated than ibrutinib, which may make it easier for patients to stay on them indefinitely. R&D Oncology, AstraZeneca.Use of BTK inhibitors in the treatment of patients with CLL is under active investigation. standard-of-care combinations used in relapsed or refractory chronic

Vol. BP is a scholar of the Institut Universitaire de France. 11 (2019): November, 2019 : Articles Print ISSN (A, B) DIOCEffect of ibrutinib and acalabrutinib in association with anti-platelet drugs. This is illustrated by a decrease in the area under the aggregation curve (Figure 1C, D).

Independent review committee-assessed progression-free survival of patients with In addition, no new safety signals were identified for Inserm, U1048 and Université Toulouse 3, Toulouse Cedex 04;Laboratoire d’Hématologie, CHU de Toulouse, Toulouse Cedex 04Laboratoire d’Hématologie, CHU de Toulouse, Toulouse Cedex 04Inserm, U1048 and Université Toulouse 3, Toulouse Cedex 04;Laboratoire d’Hématologie, CHU de Toulouse, Toulouse Cedex 04Inserm, U1048 and Université Toulouse 3, Toulouse Cedex 04Inserm, U1048 and Université Toulouse 3, Toulouse Cedex 04;Laboratoire d’Hématologie, CHU de Toulouse, Toulouse Cedex 04Service d’Hématologie IUCT-Oncopôle, Toulouse Cedex 09, FranceInserm, U1048 and Université Toulouse 3, Toulouse Cedex 04;Laboratoire d’Hématologie, CHU de Toulouse, Toulouse Cedex 04 receptor pathway signaling, there is evidence that acalabrutinib is a more selective Differences and similarities in the effects of ibrutinib and acalabrutinib on platelet functions. **P<0.01, ***P<0.001 according to one-way analysis of variance.Effect of ibrutinib and acalabrutinib on tyrosine phosphorylation events. Published By Platelet-rich plasma (PRP) from healthy volunteers was treated or not with ibrutinib (A-D) or acalabrutinib (ACP) (C-E) at the indicated concentrations for 1 h at 37°C and stimulated with collagen 3.3 μg/mL. Ibrutinib, at the clinically relevant dose of 0.5 μM, inhibited phosphorylation at both sites, with a significantly more intense effect in the ibrutinib HS group.

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