CiglitazoneCiglitazone
MedChemExpress (MCE)
HY-W011220
74772-77-3
ADD-3878
U-63287
98.89%
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Room temperature in continental US
may vary elsewhere.
Ciglitazone is a potent and selective PPARγ agonist (EC50=3 μM). Ciglitazone inhibits proliferation and differentiation of th17 cells. Ciglitazone is a hypoglycemic agent orally active in the obese-hyperglycemic animal models. Ciglitazone induces apoptosis accompanied by activation of p38 MAPK and nuclear translocation of apoptosis inducing factor (AIF) in opossum kidney (OK) renal epithelial cells.
Ciglitazone (0-20 μM
24 hours) induces apoptosis through PPAR-independent mechanism. Ciglitazone causes generation of ROS and an increase in intracellular Ca2+[4].
In C57BL/6J-ob/ob mice, Ciglitazone (100 mg/kg/day
2 days) elicits a drastic fall in blood glucose. Regranulation of islet beta-cells and increased pancreatic insulin content are observed in ob/ob mice treated for 41-44 days with 100 mg/kg/day Ciglitazone[3].
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[1]. Willson TM, et al. The structure-activity relationship between peroxisome proliferator-activated receptor gamma agonism and the antihyperglycemic activity of thiazolidinediones. J Med Chem. 1996
39(3):665-668. [Content Brief]
[2]. Kim DH, et al. Ciglitazone, a peroxisome proliferator-activated receptor gamma ligand, inhibits proliferation and differentiation of th17 cells. Biomol Ther (Seoul). 2015
23(1):71-76. [Content Brief]
[3]. Chang AY, et al. Ciglitazone, a new hypoglycemic agent. I. Studies in ob/ob and db/db mice, diabetic Chinese hamsters, and normal and streptozotocin-diabetic rats. Diabetes. 1983
32(9):830-838. [Content Brief]
[4]. Kwon CH, et al. Ciglitazone induces apoptosis via activation of p38 MAPK and AIF nuclear translocation mediated by reactive oxygen species and Ca(2+) in opossum kidney cells. Toxicology. 2009
257(1-2):1-9. [Content Brief]