IC50 in the 10 nM range for CaMKIIδ/γ with weaker potency against CaMKIIα/β and relatively weak inhibition against hERG, Kv4.3, Nav1.5, and Cav1.2. In vivo oral delivery restored contractility in genetic mouse model of dilated cardiomyopathy with minimal drug delivery to the brain. Limitations: Potential inhibition of other kinases associated with cardiac remodeling. Effects on electrical remodeling are not defined. Additional detail needed on acquired disease states like pressure overload. The gene discussed is CACNA1C; the disease is dilated cardiomyopathy.