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ND-646

  Cat. No.:  DC9810   Featured
Chemical Structure
1434639-57-2
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More than 5000 active chemicals with high quality for research!
Field of application
ND-646(ND646) is a small-molecule allosteric inhibitor of acetyl-CoA carboxylase (ACC).
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
Cas No.: 1434639-57-2
Chemical Name: ND646,ND 646
Synonyms: ND646,ND 646
SMILES: C([C@H](OC1CCOCC1)CN1C(=O)N(C(C)(C)C(=O)N)C(=O)C2C(C)=C(C3=NC=CO3)SC1=2)1=C(OC)C=CC=C1
Formula: C17H10F5NO4S
M.Wt: 568.2
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: ND-646 is an orally bioavailable and steric inhibitor of acetyl-CoA carboxylase (ACC) with IC50s of 3.5 nM and 4.1 nM for recombinant hACC1 and hACC2, respectively.
In Vivo: To explore the impact of chronic ND-646 treatment on NSCLC tumor growth and to determine the efficacy of twice-daily dosing, athymic nude mice bearing established A549 subcutaneous tumors are treated orally with either vehicle twice daily (BID), 25 mg/kg ND-646 once daily (QD), 25 mg/kg ND-646 BID or 50 mg/kg ND-646 QD for 31 days. ND-646 at 25 mg/kg QD is ineffective at inhibiting tumor growth. However, ND-646 administered at 25 mg/kg BID or 50 mg/kg QD significantly inhibits subcutaneous A549 tumor growth. ND-646 is well tolerated throughout the treatment period, with no significant weight loss occurring after chronic ND-646 dosing, suggesting that the maximum tolerated dose (MTD) has not been reached. Mice are sacrificed at 1 hr post final dose and tissues are either prepared for immunohistochemistry (IHC) or immunoblot analysis. Tumors treated with all doses of ND-646 have lost detection of P-ACC at 1 hr, demonstrating effective tumor penetration and acute ACC inhibition by ND-646. Notably, only at the doses of ND-646 that lead to significant tumor growth inhibition (25 mg/kg BID and 50 mg/kg QD) is significant elevation of P-EIF2αS51 expression observed in tumor lysates[1].
In Vitro: ND-646 inhibits both ACC1 and ACC2 and therefore precludes the ability of ACC2 to compensate for ACC1 inhibition. ND-646 inhibits dimerization of recombinant human ACC2 BC domain (hACC2-BC) under native conditions; hACC2-BC migrates as a dimer in its absence and a monomer in its presence. In cell free systems, ND-646 inhibits enzymatic activity of recombinant human ACC1 (hACC1) with an IC50 of 3.5 nM and recombinant human ACC2 (hACC2) with an IC50 of 4.1 nM[1].
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
2018-0101
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