Glycoprotein (GP) VI plays a major role in thrombosis but not haemostasis, making it a promising antithrombotic target. The primary role of GPVI on the surface of platelets is a signalling receptor for collagen, which is one of the most potent thrombotic sub-endothelial components that is exposed by atherosclerotic plaque rupture. Inhibition of GPVI has therefore been investigated as a strategy for treatment and prevention of atherothrombosis, such as during stroke and acute coronary syndromes. A range of specific GPVI inhibitors have been characterised and 2 of these inhibitors, glenzocimab and revacept, have completed phase II clinical trials in ischemic stroke. In this review, we summarise mechanisms of GPVI activation and the latest progress of clinically tested GPVI inhibitors, including their mechanisms of action. By focussing on what is known about GPVI activation, we also discuss whether alternate strategies could also be used to target GPVI.
Keywords: Anti-platelet; Glycoprotein VI; Revacept; arterial thrombosis; glenzocimab.
© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.