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Targeting von Willebrand factor as a novel anti-platelet therapy; Application of ARC1779, an Anti-vWF aptamer, against thrombotic risk

Excessive activation of platelets is a causative factor for thrombotic diseases such as acute coronary syndrome or stroke, and various anti-platelet drugs were developed. Aspirin and clopidogrel have been used as gold standards for anti-platelet therapies, however, their clinical limitations includi...

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Bibliographic Details
Published in:Archives of pharmacal research 2012, 35(10), , pp.1693-1699
Main Author: Bae, Ok-Nam
Format: Article
Language:English
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Summary:Excessive activation of platelets is a causative factor for thrombotic diseases such as acute coronary syndrome or stroke, and various anti-platelet drugs were developed. Aspirin and clopidogrel have been used as gold standards for anti-platelet therapies, however, their clinical limitations including bleeding problem have increased the demand driving development of novel anti-platelet drugs with new targets. Among several activating pathways leading to platelet aggregation, the interaction between von Willebrand factor (vWF) and glycoprotein Ib, which mainly occurs under high shear stress in arterioles, is recently suggested to be a new promising target. The anti-thrombotic efficacy of anti-vWF agents, such as ARC1779, has been proved in several preclinical and clinical studies. Here, we will discuss the potential benefits of targeting vWF as a novel antiplatelet therapy, providing an insight into the role of vWF in increased thrombotic risk.
ISSN:0253-6269
1976-3786
DOI:10.1007/s12272-012-1000-3