Disclosed are methods of determining cardiac toxicity of a compound of interest, wherein a heart or cardiac cell of a mammal may be contacted a compound of interest and peak levels of one or more indicators of cardiac energetics after administration of the compound may be detected using 31P NMR before and after exposure to a compound known to stress the heart or cardiac cell. Detection of the indicators of cardiac energetics may be combined with other indicators of cardiac function such as, for example, contractility, relaxation, heart rate, and/or conduction velocity to arrive at a profile capable of predicting the cardiotoxicity of potential therapeutics.
