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New Experimental Drug Reduces Tissue Damage Following Myocardial Infarction and Minimizes the Risk of Bleeding

Researchers at Washington University and St. Louis based APT Therapeutics Inc., show that a novel drug known as APT102 significantly reduced tissue damage to heart muscle following experimental myocardial infarction and minimized the risk of bleeding during follow-up treatments. The research team at Washington University was led by Dr. Dana Abendschein.

Myocardial infarction causes damage to heart muscle. Once the blood clot that causes a heart attack is removed from the artery, molecules from dead and dying cells mix with blood coursing through the reperfused artery. One of these molecules, adenosine triphosphate (ATP), is inflammatory; while another, adenosine diphosphate (ADP), triggers more clotting. APT102 is a genetically engineered version of the human protein apyrase, which transforms ATP and ADP into adenosine monophosphante, which is a benign molecule. Another enzyme changes this molecule into adenosine, which is beneficial for the heart.

“APT102, has the potential to change the paradigm for how heart attack patients initially are treated,” said senior author Dana Abendschein, PhD, associate professor of medicine and of cell biology and physiology at Washington Universtiy. “This also may be a better way to treat strokes caused by or associated with a blood clot.”

The study, which was funded by a National Institutes of Health (NIH) Small Business Innovation Research Grant and by APT Therapeutics, Inc., the developer of APT102, is available online in Science Translational Medicine (online Aug. 6, 2014).

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