Saroglitazar Magnesium Inhibitor

Solid. Powder

98.00%

Store at -20 degree C for 3 years powder
-80 degree C for 2 years in solvent

901.42

DMSO: 50mg/mL (55.47mM) Need ultrasonic
H2O: <0.1mg/mL (insoluble)
(<1mg/ml refers to the product slightly soluble or insoluble)

C50H56MgN2O8S2

CCO([Mg+2]1(O(CC)[C@H](C([O-]1)=O)CC2=CC=C(OCCN3C(C)=CC=C3C4=CC=C(SC)C=C4)C=C2)[O-]C5=O)[C@H]5CC6=CC=C(OCCN7C(C)=CC=C7C8=CC=C(SC)C=C8)C=C6

1639792-20-3

PPARalpha: ic50 0.65pM (EC50, HepG2 cell)
PPARgamma: ic50 3nM (EC50, HepG2 cell)

In db/db mice, Saroglitazar (0.01-3mg/kg per day, orally) treatment with 12-day causes dose-dependent reductions in serum triglycerides (TG), free fatty acids (FFA), and glucose. The ED50 for these effects is found to be 0.05, 0.19, and 0.19mg/kg, respectively with highly significant (91%) reduction in serum insulin and AUC-glucose following oral glucose administration (59%) at 1mg/kg dose. In Wistar rats and marmosets A 90-day repeated dose comparative study confirms efficacy (TG lowering) potential of Saroglitazar and has indicated low risk of PPAR-associated side effects in humans. Based on efficacy and safety profile, Saroglitazar appears to have good potential as novel therapeutic agent for treatment of dyslipidemia and diabetes.