EX229

1219739-36-2

C24H18ClN3O3

DMSO : 13 mg/mL (30.10 mM; Need ultrasonic and warming)

Epigenetics; PI3K/Akt/mTOR

EX229, a Benzimidazole derivative, is a potent and allosteric activator of AMP-activated protein kinase (AMPK), with K_ds of 0.06 uM, 0.06 uM and 0.51 uM for alpha1beta1gamma1, alpha2beta1gamma1 and alpha1beta2gamma1 in biolayer interferometry, respectively. IC50 & Target: Kd: 0.06 uM (alpha1beta1gamma1), 0.06 uM (alpha2beta1gamma1), 0.51 uM (alpha1beta2gamma1)^[1]. In Vitro: EX229 is a potent and allosteric activator of AMP-activated protein kinase (AMPK), with K_ds of 0.06 uM, 0.06 uM and 0.51 uM for alpha1beta1gamma1, alpha2beta1gamma1 and alpha1beta2gamma1, respectively.^[1]. Treatment of hepatocytes with EX229 (991) alone results in a slight increase in the phosphorylation of AMPK and RAPTOR only at 0.3 uM, whereas a robust increase in ACC phosphorylation is readily observed and saturated at a concentration of 0.03 uM EX229. AICAR or C13 alone robustly increases T172 phosphorylation of AMPKalpha, and when EX229 is coincubated, there is a modest additional dose-dependent increase in AMPKalpha phosphorylation. RAPTOR phosphorylation is modestly increased by AICAR or C13 alone, and it is dose dependently increased when coincubations are carried out with EX229. EX229 also dose dependently (0.01 and 0.1 uM) inhibits lipogenesis (34% and 63%, respectively), which is further reduced when it is coincubated with a low dose of AICAR (0.03 mM) or C13 (1 uM). Treatment with EX229 promotes dose-dependent increases in ACC and RAPTOR phosphorylation. Similar to the observations in hepatocytes^[2].