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Merck
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Key Documents

SML1855

Sigma-Aldrich

AZD5438

≥97% (HPLC)

同義詞:

4-[2-Methyl-1-(1-methylethyl)-1H-imidazol-5-yl]-N-[4-(methylsulfonyl)phenyl]-2-pyrimidinamine, AZD 5438, AZD-5438

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About This Item

經驗公式（希爾表示法）:
C18H21N5O2S
CAS號碼:
602306-29-6
分子量：:
371.46
分類程式碼代碼:
12352200
NACRES:
NA.77

品質等級

100

化驗

≥97% (HPLC)

形狀

powder

顏色

yellow to orange

溶解度

DMSO: 20 mg/mL, clear

儲存溫度

2-8°C

InChI

1S/C18H21N5O2S/c1-12(2)23-13(3)20-11-17(23)16-9-10-19-18(22-16)21-14-5-7-15(8-6-14)26(4,24)25/h5-12H,1-4H3,(H,19,21,22)

InChI 密鑰

WJRRGYBTGDJBFX-UHFFFAOYSA-N

生化／生理作用

AZD5438 is an orally active, potent and reversible inhibitor against cyclin-dependent kinases (IC50 = 6 nM/Cyc E-CDK2, 14 nM/p25-CDK5, 16 nM/Cyc B1-CDK1, 20 nM/Cyc T-CDK9, 21 nM/Cyc D3-CDK6, 45 nM/Cyc A-CDK2, 449 nM/Cyc D1-CDK4, 821 nM/Cyc H-CDK7; [ATP] = Km) and glycogen synthase kinase GSK-3β≤ (IC50 = 17 nM) without significant inhibitory potency toward 30 other kinases (≤75% inhibition at 10 μM). AZD5438 effectively inhibits cellular CDK substrates phosphorylation and displays antiproliferation activity against a broad spectrum of human cancer cultures (IC50 from 0.2 μM/MCF to 1.7 μM/ARH-77) by inducing cell cycle arrest at G2-M, S, and G1. Oral administration (50 mg/kg/12 h or 75 mg/kg/day) is efficacious against human tumor xenograft growth in mice in vivo.

儲存類別代碼

11 - Combustible Solids

水污染物質分類（WGK）

WGK 3

閃點（°F）

Not applicable

閃點（°C）

Not applicable

分析證明 (COA)

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Camille D A Terfve et al.
Nature communications, 6, 8033-8033 (2015-09-12)
Mass spectrometry is widely used to probe the proteome and its modifications in an untargeted manner, with unrivalled coverage. Applied to phosphoproteomics, it has tremendous potential to interrogate phospho-signalling and its therapeutic implications. However, this task is complicated by issues
Nozomi Tomimatsu et al.
Nature communications, 5, 3561-3561 (2014-04-08)
Resection of DNA double-strand breaks (DSBs) is a pivotal step during which the choice between NHEJ and HR DNA repair pathways is made. Although CDKs are known to control initiation of resection, their role in regulating long-range resection remains elusive.
Kate F Byth et al.
Molecular cancer therapeutics, 8(7), 1856-1866 (2009-06-11)
Deregulation of the cell cycle has long been recognized as an essential driver of tumorigenesis, and agents that selectively target key cell cycle components continue to hold promise as potential therapeutics. We have developed AZD5438, a 4-(1-isopropyl-2-methylimidazol-5-yl)-2-(4-methylsulphonylanilino) pyrimidine, as a

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