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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. COH-SR4 can be used for the research of obesity and related metabolic disorders[1].

COH-SR4 (1-5 μM; 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 μM; 7 days) significantly inhibits 3T3-L1 adipocyte differentiation in a dose-dependent manner[1].COH-SR4 (1-5 μM; 24 hours) promotes cell G1 cycle arrest[1].COH-SR4 significantly reduces intracellular lipid accumulation and downregulates the expression of key adipogenesis-related transcription factors and lipogenic proteins[1].

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].

[1]. James L Figarola, et al. Small?molecule COH-SR4 inhibits adipocyte differentiation via AMPK activation. Int J Mol Med. 2013 May;31(5):1166-76.

[2]. James Lester Figarola, et al. COH-SR4 Reduces Body Weight, Improves Glycemic Control and Prevents Hepatic Steatosis in High Fat Diet-Induced Obese Mice. PLoS One. 2013; 8(12): e83801.

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