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1334922-19-8

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1334922-19-8 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 1334922-19-8 includes 10 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 7 digits, 1,3,3,4,9,2 and 2 respectively; the second part has 2 digits, 1 and 9 respectively.
Calculate Digit Verification of CAS Registry Number 1334922-19:
(9*1)+(8*3)+(7*3)+(6*4)+(5*9)+(4*2)+(3*2)+(2*1)+(1*9)=148
148 % 10 = 8
So 1334922-19-8 is a valid CAS Registry Number.

1334922-19-8Relevant articles and documents

Discovery of 4-aryl-N-arylcarbonyl-2-aminothiazoles as Hec1/Nek2 inhibitors. Part I: Optimization of in vitro potencies and pharmacokinetic properties

Lee, Ying-Shuan E.,Chuang, Shih-Hsien,Huang, Lynn Y. L.,Lai, Chun-Liang,Lin, Yu-Hsiang,Yang, Ju-Ying,Liu, Chia-Wei,Yang, Sheng-Chuan,Lin, Her-Sheng,Chang, Chia-Chi,Lai, Jun-Yu,Jian, Pei-Shiou,Lam, King,Chang, Jia-Ming,Lau, Johnson Y. N.,Huang, Jiann-Jyh

, p. 4098 - 4110 (2014/06/09)

A series of 4-aryl-N-arylcarbonyl-2-aminothiazoles of scaffold 4 was designed and synthesized as Hec1/Nek2 inhibitors. Structural optimization of 4 led to compound 32 bearing C-4′ 4-methoxyphenoxy and 4-(o-fluoropyridyl) carbonyl groups that showed low nanomolar in vitro antiproliferative activity (IC50: 16.3-42.7 nM), high intravenous AUC (64.9 μM·h, 2.0 mg/kg) in SD rats, and significant in vivo antitumor activity (T/C = 32%, 20 mg/kg, IV) in mice bearing human MDA-MB-231 xenografts. Cell responses resulting from Hec1/Nek2 inhibition were observed in cells treated with 32, including a reduced level of Hec1 coimmunoprecipitated with Nek2, degradation of Nek2, mitotic abnormalities, and apoptosis. Compound 32 showed selectivity toward cancer cells over normal phenotype cells and was inactive in a [ 3H]astemizole competitive binding assay for hERG liability screening. Therefore, 32 is as a good lead toward the discovery of a preclinical candidate targeting Hec1/Nek2 interaction.

Modulators Of HEC1 Activity And Methods Therefor

-

, (2011/10/10)

Compounds, compositions, and methods for modulation of Hec1/Nek2 interaction are provided. Especially preferred compounds disrupt Nek2/Hec1 binding and are therefore useful as chemotherapeutic agent for neoplastic diseases.

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