Roy R. Hantgan
Cardiovascular disease is the leading cause of death in our society, and the major culprit is a blood clot formed by the unwarranted activation of the clotting cascade. While cardiologists can often restore normal blood flow through by widening the blocked artery and inserting a stent to keep it open, this approach require powerful anti-platelet drugs that can themselves cause hemorrhagic or thrombotic problems.
Research in my laboratory focuses on understanding, at the molecular level, how a class of these drugs --- integrin antagonists --- recognize their target receptor and how that interaction actually alters its structure and function. Our biophysical approach to translational research is designed to hasten the development of a new generation of safer and more effective integrin-targeted therapies.
As Director of the Macromolecular Interactions Core Laboratory, I also strive to make an array of biotechnologies “user-friendly” to my colleagues here at the medical school, at Wake Forest University, and to the wider national and international research community.
Modeling integrin antagonists binding to their target aIIbb3 receptor. From Hantgan et al., Journal of Thrombosis and Haemostasis, 5: 542-550 (2007).
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