Improvement of Cardiomyocyte Function by a Novel Pyrimidine-Based CaMKII-Inhibitor

摘要

ObjectivePathologically increased activity of Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) and the associated Ca²⁺-leak from the sarcoplasmic reticulum are recognized to be important novel pharmacotherapeutic targets in heart failure and cardiac arrhythmias. However, CaMKII-inhibitory compounds for therapeutic use are still lacking. We now report on the cellular and molecular effects of a novel pyrimidine-based CaMKII inhibitor developed towards clinical use.