CP-610431
CP-610431 is a reversible, ATP-uncompetitive, isozyme-nonselective acetyl-CoA carboxylase (ACC) inhibitor. CP-610431 inhibits ACC1 and ACC2 with IC50s of ~50 nM. CP-610431 can be used for the research of metabolic syndrome.
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研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- CAS 番号: 591778-83-5
- 分子式: C30H37N3O2
- 分子量:471.63
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
製品説明
体外実験
CP-610431 is the active R-enantiomer of CP-497485. CP-610431 is more potent than the racemate CP-497485 in inhibiting rat ACC1 (IC50=35.7 nM) and ACC2 (IC50=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 EC50s 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 IC50 values of 0.11 and 1.2 μM and inhibits TG secretion with an IC50 of 10 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:HepG2 cells
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Concentration:0.1, 1, 10 μM
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Incubation Time:24 hours
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Result:Dose-dependently inhibited HepG2 cell fatty acid synthesis with an IC50 of 1.6 μM, TG synthesis with an IC50 of 1.8 μM, TG secretion with an IC50 of 3.0 μM, and apoB secretion with an IC50 of 5.7 μM.
体内実験
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:CD1 mice[1]
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Dosage:30 and 100 mg/kg for fasting CD1 mice; 10, 30, and 100 mg/kg for non-fasting CD1 mice
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Administration:Intraperitoneal administration; 1 hour
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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.
化学情報
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CAS 番号 591778-83-5
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分子量 471.63
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分子式 C30H37N3O2
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SMILES
O=C([C@H]1CN(C2CCN(C(C3=C4C=CC=CC4=CC5=CC=CC=C35)=O)CC2)CCC1)N(CC)CC
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
純度とドキュメンテーション
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. [Content Brief]
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)