ArticleThrombosis research2015
The BCR-ABL inhibitor ponatinib inhibits platelet immunoreceptor tyrosine-based activation motif (ITAM) signaling, platelet activation and aggregate formation under shear.
Article in Thrombosis research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed.
- Trial
- Cardiotoxicity of Targeted Therapies in Hematologic Malignancies: From Molecular Mechanisms to Clinical Management.Current treatment options in oncology · 2026Review
- Non-receptor tyrosine kinase signaling pathways and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Distinct endothelial cell toxicities of Abl tyrosine kinase inhibitors lead to arterial thrombosis.Blood vessels, thrombosis & hemostasis · 2026Article
- 40 is the new 50: reducing the need for platelet transfusions prior to lumbar puncture in adults with hematologic malignancies.Haematologica · 2025Article
- Safe platelet count for lumbar puncture: are we being overcautious?Haematologica · 2025Article
- KF1601, a dual inhibitor of BCR::ABL1 and FLT3, overcomes drug resistance in FLT3Molecular cancer · 2025Article
- Pharmacological effects of small molecule BCR-ABL tyrosine kinase inhibitors on platelet function.The Journal of pharmacology and experimental therapeutics · 2025Article
- A Review on Medicinal Approaches of Novel Imatinib Derivatives.Current topics in medicinal chemistry · 2025Review
- Imatinib‑ and ponatinib‑mediated cardiotoxicity in zebrafish embryos and H9c2 cardiomyoblasts.Molecular medicine reports · 2024Article
- Endothelium as a Source of Cardiovascular Toxicity From Antitumor Kinase Inhibitors.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Ponatinib Induces a Procoagulant Phenotype in Human Coronary Endothelial Cells via Inducing Apoptosis.Pharmaceutics · 2024Article
- Review
- Effect of antiplatelet agents and tyrosine kinase inhibitors on oxLDL-mediated procoagulant platelet activity.Blood advances · 2023Article
- Renal Safety Profile of BCR-ABL Tyrosine Kinase Inhibitors in a Real-Life Setting: A Study Based on VigibaseCancers · 2023Article
- Ponatinib-Induced Cerebrovascular Accident (CVA).Cureus · 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
- Prevention of venous thromboembolism in hematologic neoplasms: an expert consensus from SEHH-SETH.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Janus kinase inhibitors ruxolitinib and baricitinib impair glycoprotein-VI mediated platelet function.Platelets · 2022Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundTreatment of chronic myelogenous leukemia (CML) with the BCR-ABL tyrosine kinase inhibitor (TKI) imatinib significantly improves patient outcomes. As some patients are unresponsive to imatinib, next generation BCR-ABL inhibitors such as nilotinib have been developed to treat patients with imatinib-resistant CML. The use of some BCR-ABL inhibitors has been associated with bleeding diathesis, and these inhibitors have been shown to inhibit platelet functions, which may explain the hemostasis impairment. Surprisingly, a new TKI, ponatinib, has been associated with a high incidence of severe acute ischemic cardiovascular events. The mechanism of this unexpected adverse effect remains undefined. OBJECTIVE AND
methodsThis study used biochemical and functional assays to evaluate whether ponatinib was different from the other BCR-ABL inhibitors with respect to platelet activation, spreading, and aggregation. RESULTS AND
conclusionsOur results show that ponatinib, similar to other TKIs, acts as a platelet antagonist. Ponatinib inhibited platelet activation, spreading, granule secretion, and aggregation, likely through broad spectrum inhibition of platelet tyrosine kinase signaling, and also inhibited platelet aggregate formation in whole blood under shear. As our results indicate that pobatinib inhibits platelet function, the adverse cardiovascular events observed in patients taking ponatinib may be the result of the effect of ponatinib on other organs or cell types, or disease-specific processes, such as BCR-ABL+cells undergoing apoptosis in response to chemotherapy, or drug-induced adverse effects on the integrity of the vascular endothelium in ponatinib-treated patients.
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