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AZD7762 HCl
本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。
AZD7762 HCl图片
CAS NO:1246094-78-9
规格:≥98%
包装与价格：
包装价格(元)
10mg电议
25mg电议
50mg电议
100mg电议
250mg电议
500mg电议

产品介绍
AZD7762 HCl (AZD-7762) is a novel, potent, selective, ATP-competitive, and synthetic small molecule checkpoint kinase (Chk) inhibitor with anticancer activity. It has an IC50 of 5 nM for Chk1. AZD-7762 has potential chemosensitizing activity by binding to and inhibits Chks, which may prevent cell cycle arrest and subsequent nucleotide excision repair in DNA-damaged tumor cells, resulting in tumor cell apoptosis. This agent may enhance the cytotoxicity of DNA-damaging agents. Chks are protein kinases that regulate either G1/S or G2/M transitions in the cell cycle. In the presence of DNA damage or incomplete DNA replication, Chks become activated and initiate cell cycle arrest to allow DNA repair or the completion of DNA replication.
理化性质和储存条件


Name: AZD7762 HCl

CAS#: 1246094-78-9 (HCl salt);

Chemical Formula: C17H20ClFN4O2S

Exact Mass: 398.098
Molecular Weight: 398.88
Storage-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Technical InformationSynonym: AZD-7762 Hydrochloride; AZD-7762 HCl; AZD7762; AZD 7762; AZD-7762.
Chemical Name: (S)-5-(3-Fluorophenyl)-N-(piperidin-3-yl)-3-ureidothiophene-2-carboxamide Hydrochloride
InChi Key: WFZBLOIXZRZEDG-YDALLXLXSA-N
InChi Code: InChI=1S/C17H19FN4O2S.ClH/c18-11-4-1-3-10(7-11)14-8-13(22-17(19)24)15(25-14)16(23)21-12-5-2-6-20-9-12;/h1,3-4,7-8,12,20H,2,5-6,9H2,(H,21,23)(H3,19,22,24);1H/t12-;/m0./s1
SMILES Code: O=C(C1=C(NC(N)=O)C=C(C2=CC=CC(F)=C2)S1)N[C@@H]3CNCCC3.[H]Cl
实验参考方法

AZD7762 HCl (AZD-7762) is a novel, potent, selective, ATP-competitive, and synthetic small molecule checkpoint kinase (Chk) inhibitor with anticancer activity. It has an IC50 of 5 nM for Chk1. AZD-7762 has potential chemosensitizing activity by binding to and inhibits Chks, which may prevent cell cycle arrest and subsequent nucleotide excision repair in DNA-damaged tumor cells, resulting in tumor cell apoptosis. This agent may enhance the cytotoxicity of DNA-damaging agents. Chks are protein kinases that regulate either G1/S or G2/M transitions in the cell cycle. In the presence of DNA damage or incomplete DNA replication, Chks become activated and initiate cell cycle arrest to allow DNA repair or the completion of DNA replication.

References: Oncotarget. 2016 Aug 2;7(31):49800-49818.; Mol Cancer Ther. 2008 Sep;7(9):2955-66.