Omni Bio Pharmaceutical, Inc. announced important results from new studies of its recombinant molecule, Fc-AAT. Reduced infarct size by nearly 50% relative to each control agent; almost fully prevented reduction of Left Ventricular Ejection Fraction (LVEF), a measure of cardiac contractility; was comparable to the effects of plasma-derived AAT but did so with a 40 times lower dose; and was comparable to another recombinant Fc-AAT construct that had been engineered not to have neutrophil elastase inhibitory activity. The study concluded that recombinant Fc-AAT reduces inflammatory myocardial injury following ischemia-reperfusion in the mouse leading to preservation of viable myocardium and systolic function independent of its elastase inhibitory function.

AAT is the most abundant circulating serine protease inhibitor in the body and an acute phase reactant. Systemic deficiency in AAT due to genetic mutations can result in debilitating liver failure and chronic lung disease such as emphysema. Lifelong treatment with plasma-derived AAT, intravenously administered, is indicated for such patients.

Recent evidence suggests that AAT plays an important role in modulating immunity, inflammation and apoptosis. AAT protects various cell types from cell death, inhibits caspases-1 and -3 activity and has been shown to be effective in a wide variety of animal models of human disease, including diabetes, graft versus host disease (rejection reactions following bone marrow or other transplantation procedures), refractory gout, myocardial infarction and inflammatory bowel disease.