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CP-610431

产品编号 T40675 CAS 591778-83-5

CP-610431 is a reversible, ATP-uncompetitive inhibitor of acetyl-CoA carboxylase (ACC), exhibiting isozyme nonselectivity. It inhibits both ACC1 and ACC2 with IC50 values of approximately 50 nM. CP-610431 offers potential application in metabolic syndrome research.

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CP-610431, CAS 591778-83-5

规格	价格/CNY		货期	数量
25 mg	￥ 10,600		6-8周

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生物活性

化学信息

存储 & 溶解度

参考文献

产品描述	CP-610431 is a reversible, ATP-uncompetitive inhibitor of acetyl-CoA carboxylase (ACC), exhibiting isozyme nonselectivity. It inhibits both ACC1 and ACC2 with IC50 values of approximately 50 nM. CP-610431 offers potential application in metabolic syndrome research.
体外活性	CP-610431 is the active R-enantiomer of CP-497485. CP-610431 is more potent than the racemate CP-497485 in inhibiting rat ACC1 (IC 50 =35.7 nM) and ACC2 (IC 50 =55 nM), whereas the?S-enantiomer, CP-610432, does not substantially inhibit either ACC isoform at concentrations of up to 3 μM. CP-610431 is more potent than CP-497485 in inhibiting HepG2 cell fatty acid and triglyceride (TG) synthesis and in inhibiting TG and apoB secretion[1]. CP-610431 inhibits fatty acid synthesis, triglyceride synthesis, TG secretion, and apolipoprotein B secretion in HepG2 cells (ACC1) with EC 50 s of 1.6, 1.8, 3.0, and 5.7 μM, without affecting either cholesterol synthesis or apolipoprotein CIII secretion[1]. CP-610431 inhibits both liver and skeletal muscle ACC activity from all three species with essentially equal potency (rat, 36?versus?55 nM; mouse, 50?versus?63 nM; cynomolgus macaque, 70?versus?26 nM)[1]. CP-610431 inhibits mouse primary hepatocyte fatty acid and TG synthesis with IC 50 values of 0.11 and 1.2 μM?and inhibits TG secretion with an IC 50 of 10 μM[1]. Cell Viability Assay[1]Cell Line: HepG2 cells Concentration: 0.1, 1, 10 μM Incubation Time: 24 hours Result: Dose-dependently inhibited HepG2 cell fatty acid synthesis with an IC 50 of 1.6 μM, TG synthesis with an IC 50 of 1.8 μM, TG secretion with an IC 50 of 3.0 μM, and apoB secretion with an IC 50 of 5.7 μM.
体内活性	CP-610431 inhibits fatty acid synthesis in CD1 mice and ob/ob mice within 1 h after dose with ED 50 s of 22 and 4 mg/kg,?respectively[1]. Animal Model: CD1 mice[1]Dosage: 30 and 100 mg/kg for fasting CD1 mice; 10, 30, and 100 mg/kg for non-fasting CD1 mice Administration: Intraperitoneal administration; 1 hour Result: Inhibited hepatic fatty acid synthesis in fasting CD1 mice by 64±12%, and 77±4% at doses of 30 and 100 mg/kg, respectively. Inhibited hepatic fatty acid synthesis in non-fasting CD1 mice by 18%, 51%, and 75% at doses of 10, 30 and 100 mg/kg, respectively.

分子量	471.645
分子式	C30H37N3O2
CAS No.	591778-83-5

存储

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

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参考文献

1. H James Harwood 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.

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请在以下方框中输入您的动物实验信息后点击计算，可以得到母液配置方法和体内配方的制备方法：比如您的给药剂量是10 mg/kg，每只动物体重20 g，给药体积100 μL，一共给药动物10 只，您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。

母液配置方法：2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 50 μL DMSO 主液，加入 300 μL PEG300，混匀澄清，再加 50 μL Tween 80，混匀澄清，再加 600 μL ddH2O, 混匀澄清。

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