DS-6930 is an potent and selective PPAR γ Agonists with EC50 of 41 nM. DS-6930 can effectively reduce plasma glucose (PG) level, and has less PPARγ-related adverse effects compared with Rosiglitazone. DS-6930 has research value in diabetes.

DS-6930 exhibits high potency in vitro with an intermediate PPARγ agonist activity (EC 50 =41 nM, E max =68%), and possesses high PPARα or PPARδ selectivity (13% PPARα activation at 10 μM and no PPARδ activation at 10 μM) [1]. DS-6930 (10-100 μM) exhibits lower cell toxicity at 100 μM [1].

DS-6930 (0.1-3 mg/kg; p.o. for 3 weeks) decreases plasma glucose (PG) levels in a dose-dependent manner in rats [1]. DS-6930 (100-1000 mg/kg; p.o.for 4 weeks) does not affect any liver enzyme activities and has no remarkable change in relative heart weigh in F344 rats [1]. DS-6930 exhibits C max =0.0792 μg/mL, T max =1.8 h, and AUC 0-24h =0.861 h μg/mL following oral (0.3 mg/kg) administration on day 22 in rats [1]. DS-6930 exhibits C max =2.25 μg/mL, T max =5.0 h, T 1/2 =13.5 h, and AUC last =23.5 h μg/mL following oral (3 mg/kg) administration in cynomolgus monkeys [1]. DS-6930 exhibits excellent bioavailability (F=89%), total body clearance (CL=2.06 mL/min/kg), and distribution volume at steady state (Vss=0.36 L/kg) following intravenous (1 mg/kg) administration in cynomolgus monkeys [1]. Animal Model: Male ZDF rats [1] Dosage: 0.1, 0.3, 1, 3 mg/kg Administration: P.o. daily for 3 weeks Result: 47% PG reduction at dose of 0.3 mg/kg vs vehicle control. Animal Model: Male ZDF rats [1] Dosage: 0.3 mg/kg (Pharmacokinetic Analysis) Administration: P.o. daily for 22 days Result: C max =0.0792 μg/mL; T max =1.8 h; AUC 0-24h =0.861 h μg/mL.