Balaglitazone is a selective partial agonist of PPARγ with an effective concentration 50 (EC50) of 1.351 μM[1]. Within the concentration range of 5-100 μM, Balaglitazone exhibits uniform cytotoxicity against both K562 and K562/DOX cells. It moderates the toxicity of doxorubicin in these cells, showing IC50 values of 0.117 μM for K562 and 0.53 μM for K562/DOX cells. It is also effective in counteracting multidrug resistance (MDR) in K562/DOX cells. At a concentration of 25 µM, Balaglitazone enhances Rh123 accumulation in K562/DOX cells without affecting MFI in K562 cells. It suppresses P-gp expression in K562/DOX cells through the upregulation of PTEN, a process that can be reversed by PTEN inhibition[2].
体内研究
Administered orally at a dose of 3 mg/kg, Balaglitazone demonstrates antihyperglycemic properties in db/db mice, exhibiting greater potency than rosiglitazone, a full PPARγ agonist[1].
At a dose of 10 mg/kg orally, Balaglitazone reduces blood glucose levels, lowers insulin levels, and leads to an increase in body weight in male diet-induced obese rats, mirroring the effects observed with 30 mg/kg of pioglitazone[3].
体外研究
Balaglitazone is a selective partial agonist of PPARγ with an effective concentration 50 (EC50) of 1.351 μM[1].
Within the concentration range of 5-100 μM, Balaglitazone exhibits uniform cytotoxicity against both K562 and K562/DOX cells. It moderates the toxicity of doxorubicin in these cells, showing IC50 values of 0.117 μM for K562 and 0.53 μM for K562/DOX cells. It is also effective in counteracting multidrug resistance (MDR) in K562/DOX cells. At a concentration of 25 µM, Balaglitazone enhances Rh123 accumulation in K562/DOX cells without affecting MFI in K562 cells. It suppresses P-gp expression in K562/DOX cells through the upregulation of PTEN, a process that can be reversed by PTEN inhibition[2].
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