Calcium sensitizer agents are a class of inotropic agents in the treatment of decompensated heart failure. Levosimendan is a short half-life calcium sensitizer used as pharmacological inotropic support in acute decompensated heart failure. The cardiovascular effects of Levosimendan mediate mainly by two mechanisms of action: (i) calcium sensitization via binding to the Ca2+-saturated troponin C (cTnC) in cardiomyocytes; and (ii) opening of the ATP-sensitive potassium channels on the sarcolemma and mitochondria. Levosimendan reduces peripheral vascular resistance, and enhances the contractility of the failing heart, without significantly increasing myocardial oxygen uptake. After oral administration, OR-1896 is the active metabolite of Levosimendan.

OR-1896 is a long-lasting metabolite of Levosimendan sharing the pharmacological properties of the parent compound. Levosimendan has an elimination half-life of 1-1.5 h. However, the half-life of OR-1896 is about 75 to 80 hours allowing cardiovascular effects to persist up to 7 to 9 days after discontinuation of a 24-hour infusion of Levosimendan. The pharmacokinetics of Levosimendan is unaltered in subjects with severe renal impairment or with moderate hepatic impairment, whereas the elimination of OR-1896 prolongs. In particular, OR-1896 exhibits comparable hemodynamic effects to those of Levosimendan via Ca2+-sensitization. Furthermore, both Levosimendan and OR-1896 are highly selective inhibitors of the phosphodiesterase (PDE) III isoform. OR-1896 inhibits PDE activity and increases cAMP levels at concentrations giving positive inotropic responses (PIRs). Moreover, oral treatment with OR-1896 prevents post-infarct heart failure and cardiac remodeling in spontaneously diabetic Goto-Kakizaki rats.

All in all, OR-1896, a calcium sensitizer, is efficient in the prevention of post-infarct heart failure and cardiac remodeling in type 2 diabetes.

Reference:
Papp Z, et al. Levosimendan: molecular mechanisms and clinical implications: consensus of experts on the mechanisms of action of Levosimendan. Int J Cardiol. 2012 Aug 23;159(2):82-7.