Cas No.: | 199113-98-9 |
Chemical Name: | DRF-2593;NN-2344;DRF2593;NN2344;DRF 2593;NN 2344 |
Synonyms: | DRF-2593;NN-2344;DRF2593;NN2344;DRF 2593;NN 2344 |
SMILES: | O=C(N1)SC(CC2=CC=C(OCC(N3C)=NC4=C(C=CC=C4)C3=O)C=C2)C1=O |
Formula: | C20H17N3O4S |
M.Wt: | 395.4317 |
Description: | Balaglitazone is a selective partial PPARγ agonist with an EC50 of 1.351 μM for human PPARγ. |
In Vivo: | Balaglitazone (3 mg/kg, p.o.) shows antihyperglycaemic activity in fully diabetic and insulin resistant db/db mice, and is more potent than the full PPARγ agonist rosiglitazone[1]. Balaglitazone (10 mg/kg, p.o.) suppresses overall glucose, decreases insulin levels, and increases bodyweight in male diet-induced obese rats, and such effects are equal to that of 30 mg/kg pioglitazone[3]. |
In Vitro: | Balaglitazone is a selective partial PPARγ agonist with an EC50 of 1.351 μM[1]. Balaglitazone (5-100 μM) has equal cytotoxicity towards K562 and K562/DOX cells. Balaglitazone decreases doxorubicin cytotoxicity in K562 and K562/DOX cells, with IC50s of 0.117 μM and 0.53 μM, respectively. Balaglitazone reverses multidrug resistance (MDR) in K562/DOX cells. Balaglitazone (25 µM) increases Rh123 accumulation in K562/DOX cells, but does not increases MFI in K562 cells. Balaglitazone downregulates P-gp expression in K562/DOX cells, and such effects are via upregulation of PTEN in K562/DOX cells, and be abolished by PTEN inhibition[2]. |