Prolongation of the QT interval of the heart’s electrical cycle is a potential adverse effect carried by a wide variety of drugs prescribed for various conditions. This effect has been linked to increased susceptibility of torsades de pointes (TdP) and fatal arrhythmias. The Totah lab hypothesizes that one factor may involve an enzyme known as Cytochrome P450 2J2 (CYP2J2), known to be present in the heart and responsible for metabolizing endogenous arachidonic acid into epoxyeicosatrienoic acid (EET) isomers. EETs are physiologically important, especially in the heart, because of their role in providing several protective properties such as vasodilation. Consequently, interference of this enzyme’s activity through xenobiotic inhibition could contribute to QT-prolongation and potentially fatal cardiotoxicity. Here, the activity and inhibition of CYP2J2 are being investigated in four specific models: recombinant enzyme, transgenic mouse hearts, human heart tissue, and human cardiomyocytes through the use of various assays and mass spectroscopy. CYP2J2 expression in each of the models is also being quantified through immunoblotting. Drugs such as pimozide (an anti-psychotic) and danazol (a modified testosterone), which are associated with QT-prolongation, have experimentally inhibited CYP2J2 activity by as much as 50% and 80%, respectively. The results of this research are expected to increase the understanding of CYP2J2’s role in the heart, and the potential role of this isozyme in QT-prolongation and other fatal heart conditions..