SML1505
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
产品名称
AZD1480, ≥98% (HPLC)
SMILES string
Fc1cnc(nc1)[C@@H](Nc2nc(c(cn2)Cl)Nc3[nH]nc(c3)C)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
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 5 mg/mL, clear (warmed)
storage temp.
−20°C
Quality Level
Application
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.
Biochem/physiol Actions
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.
AZD1480 is an orally active, potent and selective inhibitor of Janus kinases JAK1 and JAK 2.
signalword
Warning
hcodes
Hazard Classifications
Acute Tox. 4 Oral
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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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