CP-640186 hydrochlorideCP-640186 hydrochloride
MedChemExpress (MCE)
HY-15259A
591778-70-0
99.90%
4°C, sealed storage, away from moisture *In solvent : -80°C, 2 years
-20°C, 1 year (sealed storage, away from moisture)
Room temperature in continental US
may vary elsewhere.
CP-640186 hydrochloride is an orally active and cell-permeable Acetyl-CoA carboxylase (ACC) inhibitor with IC50s of 53 nM and 61 nM for rat liver ACC1 and rat skeletal muscle ACC2 respectively. Acetyl-CoA carboxylase (ACC) is a key enzyme of fatty acid metabolism that enables the synthesis of malonyl-CoA. CP-640186 hydrochloride can also stimulate muscle fatty acid oxidation.
CP-640186 (20 μM
48 h) treatment can inhibit H460 cell growth[3]. CP-640186 (0.1 nM-100 μM
2 h) treatment increases fatty acid metabolism in a concentration-dependent manner in C2C12 cells and muscle strips[1]. CP-640186 (0.62-1.8 μM
2 h) treatment inhibits fatty acid synthesis and TG synthesis in HepG2 cells[1].
CP-640186 (oral gavage
4.6-21 mg/kg
once) demonstrates acute efficacy[1]. CP-640186 (intravenous injection and oral gavage
Intravenous dose, 5 mg/kg
oral dose, 10 mg/kg
once) shows lowe drug exposure in the rat than the ob/ob mouse at equal doses[1]. CP-640186 (oral gavage
100 mg/kg
once) treatment shows a complete shift from carbohydrate utilization to fatty acid utilization as a source of energy at high exposure level[1].
IC50: 53 nM (rat liver ACC1) and 61 nM (rat skeletal muscle ACC2)[1] In Vitro CP-640186 (20 μM
48 h) treatment can inhibit H460 cell growth[3]. CP-640186 (0.1 nM-100 μM
2 h) treatment increases fatty acid metabolism in a concentration-dependent manner in C2C12 cells and muscle strips[1]. CP-640186 (0.62-1.8 μM
2 h) treatment inhibits fatty acid synthesis and TG synthesis in HepG2 cells[1]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> CP-640186 hydrochloride Related Antibodies Cell Proliferation Assay[3] Cell Line: Human fibroblasts and H460 cells
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[1]. Harwood HJ Jr, et al. Isozyme-nonselective N-substituted bipiperidylcarboxamide acetyl-CoA carboxylase inhibitors reduce tissue malonyl-CoA concentrations, inhibit fatty acid synthesis, and increase fatty acid oxidation in cultured cells and in experimental animals. J Biol Chem. 2003 Sep 26
278(39):37099-111. [Content Brief]
[2]. Yamashita T, et al. Design, synthesis, and structure-activity relationships of spirolactones bearing 2-ureidobenzothiophene as acetyl-CoA carboxylases inhibitors. Bioorg Med Chem Lett. 2011 Nov 1
21(21):6314-8. [Content Brief]
[3]. Daniel Hess, et al. Inhibition of stearoylCoA desaturase activity blocks cell cycle progression and induces programmed cell death in lung cancer cells. PLoS One. 2010 Jun 30
5(6):e11394. [Content Brief]