Merck
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文件

SML1505

Sigma-Aldrich

AZD1480

≥98% (HPLC)

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别名:
(S)-5-Chloro-N2-(1-(5-fluoropyrimidin-2-yl)ethyl)-N4-(5-methyl-1H-pyrazol-3-yl)pyrimidine-2,4-diamine, 5-Chloro-N2-[(1S)-1-(5-fluoro-2-pyrimidinyl)ethyl]-N4-(5-methyl-1H-pyrazol-3-yl)-2,4-pyrimidinediamine, AZD-1480
经验公式（希尔记法）:
C14H14ClFN8
CAS号:
935666-88-9
分子量:
348.77
NACRES:
NA.77

质量水平

100

检测方案

≥98% (HPLC)

形式

powder

颜色

white to beige

溶解性

DMSO: 5 mg/mL, clear (warmed)

储存温度

−20°C

InChI

1S/C14H14ClFN8/c1-7-3-11(24-23-7)21-13-10(15)6-19-14(22-13)20-8(2)12-17-4-9(16)5-18-12/h3-6,8H,1-2H3,(H3,19,20,21,22,23,24)/t8-/m0/s1

InChI key

PDOQBOJDRPLBQU-QMMMGPOBSA-N

相关类别

应用

AZD1480 has been used as an inhibitor of janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) in an in vitro cell model of upper gastrointestinal adenocarcinoma. It has also been used in combination with bortezomib to study tumor-associated macrophage-mediated survival of myeloma cells.

生化/生理作用

AZD1480 is an orally active, potent and selective inhibitor of Janus kinases JAK1 and JAK 2 with selectivity for JAK2 as evidenced by IC50 values of 1.3 nM for JAK1 and <0.4 nM for JAK2 in enzyme assays. AZD1480 inhibits endogenous as well as IL-6 induced STAT3 activation. AZD1480 reduces myeloid cell-mediated angiogenesis and metastasis. AZD1489 is an effective anticancer agent in bot adult and pediatric human tumors.

象形图

Exclamation mark
GHS07

警示用语：

Warning

危险声明

H302

危险分类

Acute Tox. 4 Oral

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

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Tumour-associated macrophage-mediated survival of myeloma cells through STAT3 activation.
De Beule N, et al.
The Journal of Pathology, 241(4), 534-546 (2017)
AURKA regulates JAK2?STAT3 activity in human gastric and esophageal cancers.
Ahmed K, et al.
Molecular Oncology, 8(8), 1419-1428 (2014)
Ilaria Marrocco et al.
Cells, 8(9) (2019-09-11)
Prostate cancer (PCa) is a multifactorial disease characterized by the aberrant activity of different regulatory pathways. STAT3 protein mediates some of these pathways and its activation is implicated in the modulation of several metabolic enzymes. A bioinformatic analysis indicated a
Namratha Sheshadri et al.
Cell death & disease, 12(11), 1038-1038 (2021-11-03)
Cancer cells experience endoplasmic reticulum (ER) stress due to activated oncogenes and conditions of nutrient deprivation and hypoxia. The ensuing unfolded protein response (UPR) is executed by ATF6, IRE1 and PERK pathways. Adaptation to mild ER stress promotes tumor cell

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