Netoglitazone

Netoglitazone (MCC-555) is an orally active PPARγ ligand with an EC₅₀ of 8 μM. Netoglitazone mediates cell type-specific functional regulation, and modulates the transcriptional activity of PPARγ as a full agonist, partial agonist or antagonist. Netoglitazone induces adipogenesis, inhibits osteoblastogenesis, alters the weight of extramedullary fat depots and enhances insulin sensitivity. Netoglitazone reduces blood glucose levels. Netoglitazone can be used in research related to type 2 diabetes and non-insulin-dependent diabetes mellitus^[1][2][3][4]. In Vitro:Netoglitazone (0.01-10 μM) induces the differentiation of U-33/γ2 cells into adipocytes in a concentration-dependent manner in vitro^[1].
Netoglitazone (0.01-10 μM; 6 days) inhibits alkaline phosphatase activity in U-33/γ2 cells. A concentration higher than 1 μM is required for complete inhibition, and its potency after 6 days of treatment is at least 250-fold lower than that of rosiglitazone^[1].
Netoglitazone (0.01-10 μM; 6 days) inhibits osteoblast mineralization in U-33/γ2 cells^[1].
Netoglitazone (2 h) binds to PPARγ with an EC₅₀ of 8 μM^[3]. In Vivo:Netoglitazone (5-10 μg/g body weight/day; oral administration; once daily; for 4 consecutive days) exerts hypoglycemic effects comparable to those of rosiglitazone at 20 μg/g body weight/day in obese diabetic A^vy mice, reducing fasting blood glucose by approximately 15-20%^[1].
Netoglitazone maleate (10 μg/g body weight/day; oral administration; daily dosing for 7 weeks) alters fat depot weight and promotes bone marrow adipogenesis in non-diabetic male C57BL/6 mice, without affecting their trabecular bone microstructure or osteoblast gene expression, while causing a slight reduction in whole-body bone mineral content (BMC)^[1].
Netoglitazone (1-30 mg/kg/day; p.o.; daily; for 4 consecutive days) potently reduces plasma glucose levels in obese diabetic KK-A_y mice, with an ED₂₅ of 2.7 mg/kg/day, and regulates the expression of PPARγ-responsive genes in adipose tissue^[3].