ArticleAmerican journal of physiology. Cell physiology2016
Oral administration of Bruton's tyrosine kinase inhibitors impairs GPVI-mediated platelet function.
Article in American journal of physiology. Cell physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 75 citations in OpenAlex.
- A pilot study of lower doses of ibrutinib in patients with chronic lymphocytic leukemia.Blood · 2018Trial
- Platelets as Central Modulators of Post-Cardiac Arrest Syndrome: Mechanisms and Therapeutic Implications.Biomolecules · 2026Review
- Platelet activation, aspirin, and cancer: From basic science to clinical trials.Pharmacological reviews · 2026Review
- Simulation of perioperative Ibrutinib withdrawal using a population pharmacokinetic model and sparse clinical concentration data.Cancer chemotherapy and pharmacology · 2025Article
- Current and future landscape of Bruton tyrosine kinase inhibitors in allergy.The Journal of allergy and clinical immunology · 2025Review
- Next-generation Bruton tyrosine kinase inhibitors and degraders in the treatment of B-cell malignancies: advances and challenges.Annals of hematology · 2025Review
- Activation of coagulation FXI promotes endothelial inflammation and amplifies platelet activation in a nonhuman primate model of hyperlipidemia.Research and practice in thrombosis and haemostasis · 2024Article
- Diagnosis and Management of Cardiovascular Effects of Bruton's Tyrosine Kinase Inhibitors.Current cardiology reports · 2023Review
- Chemical degradation of BTK/TEC as a novel approach to inhibit platelet function.Blood advances · 2023Article
- Effect of antiplatelet agents and tyrosine kinase inhibitors on oxLDL-mediated procoagulant platelet activity.Blood advances · 2023Article
- Adenosine 2A Receptor Activation Amplifies Ibrutinib Antiplatelet Effect; Implications in Chronic Lymphocytic Leukemia.Cancers · 2022Article
- Novel Antithrombotic Agents in Ischemic Cardiovascular Disease: Progress in the Search for the Optimal Treatment.Journal of cardiovascular development and disease · 2022Review
- Platelet caspase-1 and Bruton tyrosine kinase activation in patients with COVID-19 is associated with disease severity and reversed in vitro by ibrutinib.Research and practice in thrombosis and haemostasis · 2022Article
- Platelets and tyrosine kinase inhibitors: clinical features, mechanisms of action, and effects on physiology.American journal of physiology. Cell physiology · 2022Review
- Ibrutinib Inhibits BMX-Dependent Endothelial VCAM-1 ExpressionCellular and molecular bioengineering · 2022Article
- Janus kinase inhibitors ruxolitinib and baricitinib impair glycoprotein-VI mediated platelet function.Platelets · 2022Article
- Case Report: Intraocular Hemorrhage in a Primary Vitreoretinal Lymphoma Patient Treated With Zanubrutinib.Frontiers in medicine · 2022Article
- Comparison of inhibitory effects of irreversible and reversible Btk inhibitors on platelet function.EJHaem · 2021Article
- Vascular Impact of Cancer Therapies: The Case of BTK (Bruton Tyrosine Kinase) Inhibitors.Circulation research · 2021Review
- Aspirin and antiplatelet treatments in cancer.Blood · 2021Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The Tec family kinase Bruton's tyrosine kinase (Btk) plays an important signaling role downstream of immunoreceptor tyrosine-based activation motifs in hematopoietic cells. Mutations in Btk are involved in impaired B-cell maturation in X-linked agammaglobulinemia, and Btk has been investigated for its role in platelet activation via activation of the effector protein phospholipase Cγ2 downstream of the platelet membrane glycoprotein VI (GPVI). Because of its role in hematopoietic cell signaling, Btk has become a target in the treatment of chronic lymphocytic leukemia and mantle cell lymphoma; the covalent Btk inhibitor ibrutinib was recently approved by the US Food and Drug Administration for treatment of these conditions. Antihemostatic events have been reported in some patients taking ibrutinib, although the mechanism of these events remains unknown. We sought to determine the effects of Btk inhibition on platelet function in a series of in vitro studies of platelet activation, spreading, and aggregation. Our results show that irreversible inhibition of Btk with two ibrutinib analogs in vitro decreased human platelet activation, phosphorylation of Btk, P-selectin exposure, spreading on fibrinogen, and aggregation under shear flow conditions. Short-term studies of ibrutinib analogs administered in vivo also showed abrogation of platelet aggregation in vitro, but without measurable effects on plasma clotting times or on bleeding in vivo. Taken together, our results suggest that inhibition of Btk significantly decreased GPVI-mediated platelet activation, spreading, and aggregation in vitro; however, prolonged bleeding was not observed in a model of bleeding.
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