The aptamer ARC1779 is a potent and specific inhibitor of von Willebrand Factor-mediated ex vivo platelet function in ST-elevation and non-ST-elevation acute myocardial infarction

The von Willebrand Inhibitor ARC1779 Reduces Cerebral Embolization After Carotid Endarterectomy

“…9 It inhibits ex vivo platelet aggregation in myocardial infarction. 10 One might expect ARC1779 to reduce thrombus formation on activated atherosclerotic plaque and reduce subsequent cerebral embolization. However, this has not yet been shown in humans.…”

Assessment of platelets and the endothelium in patients presenting with acute coronary syndromes – is there a future?

“…And indeed preclinical testing of experimental VWF antagonists has shown promising results in various models of ischaemia and some of them are now entering early clinical trials (18,29,31,32).…”

Antigen and substrate withdrawal in the management of autoimmune thrombotic disorders

“…78 It has been proposed that the balance between ADAMTS13 activity and VWF can be restored, even in the presence of ADAMTS13 autoantibodies, using N-acetylcysteine, which reduces the VWF intra-A1 and intersubunit disulfide bonds, thereby altering the mean size and platelet adhesive function of VWF multimers in vitro and in vivo 79 ( Figure 3B). Alternatively, acute episodes of TTP might be attenuated by pharmacologic inhibition of the interaction of platelet GPIb with the A1 domain of VWF using an anti-VWF aptamer (eg, ARC1779) 80,81 or nanobody (eg, ALX-0081) [82][83][84] (Figure 3C). A continuous infusion of ARC1779 suppressed VWF activity and led to a rise in platelet counts in patients with hereditary TTP.…”