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Merck

SML1505

Sigma-Aldrich

AZD1480

≥98% (HPLC)

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

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About This Item

经验公式(希尔记法):
C14H14ClFN8
分子量:
348.77
分類程式碼代碼:
12352200
NACRES:
NA.77

品質等級

化驗

≥98% (HPLC)

形狀

powder

顏色

white to beige

溶解度

DMSO: 5 mg/mL, clear (warmed)

儲存溫度

−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 密鑰

PDOQBOJDRPLBQU-QMMMGPOBSA-N

應用

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.

象形圖

Exclamation mark

訊號詞

Warning

危險聲明

危險分類

Acute Tox. 4 Oral

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


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AURKA regulates JAK2?STAT3 activity in human gastric and esophageal cancers.
Ahmed K, et al.
Molecular Oncology, 8(8), 1419-1428 (2014)
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)
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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