CAMK2G and hydrops fetalis: Achieving an IC50 in the low nanomolar range for in vitro binding, this drug was shown to therapeutically inhibit CaMKII in isolated cardiomyocytes from CaMKIIδC-overexpressing mice with HF by reducing SR Ca2+ leak, improving SR Ca2+ loading and Ca2+ transient amplitude, and restoring myocyte fractional shortening.