Mice treated with azapeptide 15 and subjected to myocardial ischemia and reperfusion exhibited a small but significant reduction of mitochondrial-derived reactive oxygen species in saponin-permeabilized cardiomyocyte bundles, preservation of aconitase activity, augmented cyclooxygenase-2 (COX-2) expression and increased AMP-activated protein kinase (AMPK), Akt, and acetyl-CoA carboxylase (ACC) phosphorylation, as well as reduced cytosolic cytochrome c release and caspase 3 activity. This evidence concerns the gene AKT1 and myocardial ischemia.