, Volume 35, Issue 10, pp 1693-1699
Date: 09 Nov 2012

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

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Abstract

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.

Edited by Mi-Kyoung Kwak, College of Pharmacy (Rm 408), The Catholic University of Korea, Bucheon 420-743, Korea Tel: 82-2-2164-6532 E-mail: mkwak@catholic.ac.kr
Ok-Nam Bae Laboratory of Toxicology and Environmental Pathology, College of Pharmacy, Hanyang University
Main Research Areas
Role of endogenous/exogenous risk factors to development of chronic human diseases Target diseases; Stroke (neurovascular unit), diabetes (cardiovascular complications) and acute kidney injury (ischemia/reperfusion)