Caldaret HCl is an intracellular Ca2+ modulator that regulates calcium homeostasis at the sarcoplasmic reticulum and cell membrane, and can be used to study acute myocardial infarction and heart failure.

Caldaret (MCC-135) is demonstrated to restore Ca2+-ATPase activity of the sarcoplasmic reticulum (SR) isolated from the myocardium acutely exposed to ischemia and reperfusion in vitro[2].

Caldaret is a modulator of intracellular Ca2+ handling that limits infarct size in reperfused canine hearts; its cardioprotective effects against reperfusion injury were investigated through inhibition of the reverse mode Na+/Ca2+ exchanger and potential sarcoplasmic reticulum (SR) Ca2+ uptake enhancement. Intravenous infusion of Caldaret (3 or 30 μg/kg/hour) for 30 minutes during left circumflex artery (LCX) reperfusion significantly reduced infarct size (by 51.3% or 71.9%, respectively). Caldaret improves the dysfunction of intracellular Ca2+ handling, thereby exerting cardioprotective effects against reperfusion injury after prolonged ischemia [1]. Caldaret (MCC-135) is a novel potent compound with beneficial effects in heart failure. In diabetic rats, Caldaret significantly reduced TR80 but had no significant effect on developed tension (DT). Caldaret had minimal effects on SR Ca2+ uptake in normal rats, with the highest concentration of 10 μM resulting in an increase in SR Ca2+ uptake at uptake times of 20 and 30 seconds. In diabetic rats, Caldaret increased SR Ca2+ uptake over the entire uptake time range. Caldaret increased both the initial rate of SR Ca2+ uptake and the amount of Ca2+ accumulated in the SR during longer uptake times. [1]