Caldaret is an intracellularCa²⁺handling modulator that acts through reverse modeNa⁺/Ca²⁺exchangerinhibition.

Na⁺/Ca²⁺exchanger^[1]

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, 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].

256.32

C₁₁H₁₆N₂O₃S

133804-44-1

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

DMSO : 4.81 mg/mL(18.77 mM;ultrasonic and warming and adjust pH to 3 with HCl and heat to 60℃)