represents a novel cardioprotective approach with a unique mechanism of action that addresses key functional maladaptations responsible for the worsening heart failure state." "The beneficial effects of GP531 were remarkably consistent within this study," noted David G. Shand, M.D., Ph.D., Senior Advisor for Clinical and Scientific Affairs. "The findings provide important insights for further evaluation of GP531 in heart failure." Results from these studies should be reported later this year and early next year. Richard Stover, President and CEO of PeriCor Therapeutics, Inc., added, "We are confident that these studies will provide additional insights into this novel approach to improve global myocardial function in patients with heart failure, and we plan to initiate a Phase II study of GP531 in acute decompensated heart failure during the second half of the year."
GP531 is an adenosine regulating agent (ARA) that has been shown to amplify the body's broad-spectrum protective response -- the localized release of endogenous adenosine -- during episodes of cellular stress. Cellular stress, as occurs with ischemia and tissue hypoxia, triggers the breakdown of adenosine triphosphate (ATP). ATP is the key energy molecule of living cells. Endogenous adenosine has been termed a "retaliatory metabolite" that targets multiple pathways of cellular stress and myocardial injury to counter net ATP catabolism and, as such, acts as a key regulator of cellular energetics. Endogenous adenosine protects cells from multiple pathways of injury such as inflammation, apoptosis and necrosis. Endogenous adenosine levels have been shown to be elevated in heart failure patients but not sufficiently to be cardioprotective.
By augmenting a patient's own adenosine release in stressed tissues of the heart and its microvasculature, GP531 may have the potential to protect the heart muscle from further damage, alter the deterioration of
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