Caldaret NLT 98%

Caldaret is an intracellular Ca²⁺ handling modulator that acts through reverse mode Na⁺/Ca²⁺ exchanger inhibition. IC50 & Target: Na⁺/Ca²⁺ exchanger^[1] In Vitro: 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]. In Vivo: Caldaret, an intracellular Ca²⁺ handling modulator, limits infarct size of reperfused canine heart. The cardioprotective effect of Caldaret, a novel intracellular Ca²⁺ handling modulator that acts through reverse-mode Na⁺/Ca²⁺ exchanger inhibition and potential sarcoplasmic reticulum (SR) Ca²⁺ uptake enhancement, against reperfusion injury is investigated. Intravenously infused Caldaret (3 or 30 microg/kg per hour) for 30 min at left circumflex (LCX)-reperfusion markedly reduces infarct size (by 51.3% or 71.9%, respectively). The amelioration of intracellular Ca²⁺ handling dysfunction achieved by Caldaret leads to cardioprotective effects against reperfusion injury following prolonged ischemia^[1]. Caldaret (MCC-135) is a new potent compound with beneficial effects in heart failure. In diabetic rats, Caldaret decreases TR80 significantly without significant effect on developed tension (DT). Caldaret has minimal effects on SR Ca²⁺ uptake in normal rats, that is observed as increased SR Ca²⁺ uptake at uptake time of 20 and 30 s at the highest concentration of 10 μM. In diabetic rats, Caldaret increases SR Ca²⁺ uptake all over the range of uptake time. Both initial rate of SR Ca²⁺ uptake and the amount of Ca²⁺ accumulated in the SR with longer uptake time are increased by Caldaret^[2].