ArticleJournal of thrombosis and thrombolysis2017
Dabigatran reduces thrombin-induced platelet aggregation and activation in a dose-dependent manner.
Article in Journal of thrombosis and thrombolysis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- An updated meta-analysis of device related thrombus following left atrial appendage closure in patients with atrial fibrillation.Frontiers in cardiovascular medicine · 2022Pooled it
- Antiplatelet effects of oral anticoagulants in patients with atrial fibrillation: ex-vivo studies.Journal of thrombosis and thrombolysis · 2026Article
- Role of Thrombosis in Neurodegenerative Diseases: An Intricate Mechanism of Neurovascular Complications.Molecular neurobiology · 2025Review
- Unbiased high-throughput screening of drug-repurposing libraries identifies small-molecule inhibitors of clot retraction.Blood advances · 2025Article
- Clinical effectiveness and safety comparison between direct oral anticoagulants and warfarin for nonvalvular atrial fibrillation patients following percutaneous left atrial appendage closure operation intervention: a prospective observational study.BMC pharmacology & toxicology · 2025Observational
- The study of platelet aggregation using a microtiter plate reader ‒ methodological considerations.Pharmacological reports : PR · 2024Review
- Ex Vivo Antiplatelet Effects of Oral Anticoagulants.Journal of cardiovascular development and disease · 2024Article
- Targeting PAR4 to Reduce Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Diabetes- versus smoking-related thrombo-inflammation in peripheral artery disease.Cardiovascular diabetology · 2023Review
- Factors Associated with Platelet Activation-Recent Pharmaceutical Approaches.International journal of molecular sciences · 2022Review
- Clinical Efficacy and Safety Comparison of Rivaroxaban and Dabigatran for Nonvalvular Atrial Fibrillation Patients Undergoing Percutaneous Left Atrial Appendage Closure Operation.Frontiers in pharmacology · 2021Article
- The Impact of Dabigatran and Rivaroxaban on Variation of Platelet Activation Biomarkers and DRT Following Percutaneous Left Atrial Appendage Closure.Frontiers in pharmacology · 2021Article
- Thrombin contributes to cancer immune evasion via proteolysis of platelet-bound GARP to activate LTGF-β.Science translational medicine · 2020Article
- Type 2 Diabetes, Atrial Fibrillation, and Direct Oral Anticoagulation.Journal of diabetes research · 2019Review
- Adjunctive dabigatran therapy improves outcome of experimental left-sided Staphylococcus aureus endocarditis.PloS one · 2019Article
- Comparison of Effects of Anti-thrombin Aptamers HD1 and HD22 on Aggregation of Human Platelets, Thrombin Generation, Fibrin Formation, and Thrombus Formation Under Flow Conditions.Frontiers in pharmacology · 2019Article
- First evidence: rivaroxaban and apixaban reduce thrombin-dependent platelet aggregation.Journal of thrombosis and thrombolysis · 2018Observational
- Anticoagulant Activities of Indobufen, an Antiplatelet Drug.Molecules (Basel, Switzerland) · 2018Article
- Impact of Edoxaban on Thrombin-Dependent Platelet Aggregation.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dabigatran is an oral anticoagulant and a reversible inhibitor of thrombin. Further, dabigatran might affect platelet function through a direct effect on platelet thrombin receptors. The aim was to investigate the effect of dabigatran on platelet activation and platelet aggregation. Healthy donor blood was incubated with dabigatran 0, 50, 500 ng/mL, corresponding to the therapeutic range of dabigatran peak plasma concentrations, and 10,000 ng/mL comprising a supra-therapeutic dabigatran plasma level. Platelet aggregation was tested with 96-well aggregometry. Flow cytometry was used to test platelet activation and platelet thrombin receptor expression (SPAN-12 and WEDE-15 expression). Agonists were thrombin, thrombin receptor-activating peptide, protease-activated receptor-4 agonist, collagen, collagen-related peptide, arachidonic acid, and adenosine diphosphate. All concentrations of dabigatran fully inhibited platelet aggregation for thrombin up to 2 IU/mL, while dabigatran did not affect platelet aggregation by other agonists. Platelet activation (percentage of platelets positive for activated GPIIb/IIIa, CD63, P-selectin) was reduced after thrombin stimulation in samples with dabigatran levels ≥500 ng/mL. After stimulation with thrombin, the percentage of activated GPIIb/IIIa-positive platelets was 99.8 ± 0.2% without dabigatran, 14.7 ± 4.7% with 500 ng/mL dabigatran, and 4.2 ± 0.2% with 10,000 ng/mL dabigatran, both p < 0.001 when compared to samples without dabigatran. Also, the receptor expression of GPIIb/IIIa, CD63, and P-selectin were reduced after dabigatran treatment. The expression of thrombin receptors was reduced at dabigatran on ≥ 500 ng/mL. In conclusion, dabigatran exclusively inhibits thrombin-induced platelet activation and aggregation with a dose-dependent response. Platelet stimulation with other agonists was not affected by dabigatran.
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