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(E)-N-(4-((3-chloro-4-(pyridin-2-ylmethoxy)phenyl)amino)-7-ethoxyquinazolin-6-yl)-4-(dimethylamino)-2-fluorobut-2-enamide is a chemical with a specific purpose. Lookchem provides you with multiple data and supplier information of this chemical.

1420404-04-1

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  • (E)-N-(4-((3-chloro-4-(pyridin-2-ylmethoxy)phenyl)amino)-7-ethoxyquinazolin-6-yl)-4-(dimethylamino)-2-fluorobut-2-enamide

    Cas No: 1420404-04-1

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1420404-04-1 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 1420404-04-1 includes 10 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 7 digits, 1,4,2,0,4,0 and 4 respectively; the second part has 2 digits, 0 and 4 respectively.
Calculate Digit Verification of CAS Registry Number 1420404-04:
(9*1)+(8*4)+(7*2)+(6*0)+(5*4)+(4*0)+(3*4)+(2*0)+(1*4)=91
91 % 10 = 1
So 1420404-04-1 is a valid CAS Registry Number.

1420404-04-1Downstream Products

1420404-04-1Relevant articles and documents

A chemical tuned strategy to develop novel irreversible EGFR-TK inhibitors with improved safety and pharmacokinetic profiles

Xia, Guangxin,Chen, Wenteng,Zhang, Jing,Shao, Jiaan,Zhang, Yong,Huang, Wei,Zhang, Leduo,Qi, Weixing,Sun, Xing,Li, Bojun,Xiang, Zhixiong,Ma, Chen,Xu, Jia,Deng, Hailin,Li, Yufeng,Li, Ping,Miao, Hong,Han, Jiansheng,Liu, Yanjun,Shen, Jingkang,Yu, Yongping

, p. 9889 - 9900 (2014)

Gatekeeper T790 M mutation in EGFR is the most prevalent factor underlying acquired resistance. Acrylamide-bearing quinazoline derivatives are powerful irreversible inhibitors for overcoming resistance. Nevertheless, concerns about the risk of nonspecific covalent modification have motivated the development of novel cysteine-targeting inhibitors. In this paper, we demonstrate that fluoro-substituted olefins can be tuned to alter Michael addition reactivity. Incorporation of these olefins into the quinazoline templates produced potent EGFR inhibitors with improved safety and pharmacokinetic properties. A lead compound 5a was validated against EGFRWT, EGFRT790M as well as A431 and H1975 cancer cell lines. Additionally, compound 5a displayed a weaker inhibition against the EGFR-independent cancer cell line SW620 when compared with afatinib. Oral administration of 5a at a dose of 30 mg/kg induced tumor regression in a murine-EGFRL858R/T790M driven H1975 xenograft model. Also, 5a exhibited improved oral bioavailability and safety as well as favorable tissue distribution properties and enhanced brain uptake. These findings provide the basis of a promising strategy toward the treatment of NSCLC patients with drug resistance.

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