PeptideDB

CP-610431

CAS: 591778-83-5 F: C30H37N3O2 W: 471.63

CP-610431 is a reversible, ATP-uncompetitive, isozyme-nonselective acetyl-CoA carboxylase (ACC) inhibitor. CP-610431 inh
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This product is for research use only, not for human use. We do not sell to patients.

Bioactivity 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[1].
Invitro 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]. Cell Viability Assay[1] Cell Line:
In Vivo CP-610431 inhibits fatty acid synthesis in CD1 mice and ob/ob mice within 1 h after dose with ED50s of 22 and 4 mg/kg, respectively[1]. Animal Model:
Name CP-610431
CAS 591778-83-5
Formula C30H37N3O2
Molar Mass 471.63
Transport Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Reference [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 exper