Benefit

Technology Description

Thrombotic cardiovascular diseases (CVDs) impose a significant health and economic burden, costing over $407 billion annually in the United States. While platelets are essential for normal blood clotting after an injury, their abnormal activation—such as during the rupture of atherosclerotic plaques—can lead to thrombotic events like heart attacks or strokes. Current antiplatelet drugs have several limitations including bleeding risks, developed resistance, and variable response. There is a critical need for new therapeutic interventions that can inhibit platelet function without causing severe bleeding risk.

Dr. Chauhan and his team have developed a novel method of inhibiting platelet function and preventing thrombosis. By targeting a key enzyme that contributes to human platelet activation, they are able to significantly reduce platelet aggregation and dense granule secretion in human cells. Pharmacological inhibition of this enzyme using a small molecule reduces obesity associated platelet hyperactivity in human platelets. Importantly in vivo work demonstrates that targeting this enzyme does not affect bleeding, and the small molecule is well tolerated in wild type mice. Overall, this new intervention offers a method of targeting thrombosis without affecting bleeding, resulting in a safer more efficacious treatment. 

UIRF Case No. 2025-075

Stage of Development

The small molecule has been tested in human platelets from lean and obese patients, with significant supporting data generated using an mutant murine model.