COH-SR4

73439-19-7

350.03

DMSO : 125 mg/mL (ultrasonic)

Epigenetics; PI3K/Akt/mTOR

COH-SR4 is an AMPK activator. COH-SR4 shows potent anti-proliferative activities against leukemia, melanoma, breast and lung cancers. COH-SR4 inhibits adipocyte differentiation via AMPK activation, and can be used for the research of obesity and related metabolic disorders^[1]. IC50 & Target: AMPK^[1] In Vitro: COH-SR4 (1-5 uM; 24 hours) results in a dose-dependent increase in the phosphorylation of AMPK and its substrate ACC in 3T3-L1 preadipocytes, as well as in cancer cells such as HL-60, HeLa, MCF-7^[1].
COH-SR4 (3-5 uM; 7 days) significantly inhibits 3T3-L1 adipocyte differentiation in a dose-dependent manner^[1].
COH-SR4 (1-5 uM; 24 hours) promotes cell G1 cycle arrest^[1].
COH-SR4 significantly reduces intracellular lipid accumulation and downregulated the expression of key adipogenesis-related transcription factors and lipogenic proteins^[1].
In Vivo: COH-SR4 (5 mg/kg; i.g.; 3x/week; for 6 weeks) reduces body weight and fat mass in high fat diet (HFD) obese mice without affecting food intake^[2].
COH-SR4 improves glycemic control and dyslipidemia in HFD obese mice^[2].
COH-SR4 decreases adipose tissue hypertrophy and affects circulating adipokine levels in HFD obese mice^[2].
COH-SR4 prevents hepatic lipid accumulation and fatty liver in HFD obese mice^[2].
COH-SR4 regulates expression of genes involved in lipid and glucose metabolism^[2].
COH-SR4 inhibits hepatic lipogenic and gluconeogenic pathways^[2].
COH-SR4 indirectly activates AMPK independent of calcium signaling and LKB1 in vitro^[2].