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Merck
CN

565840

SHIP2 Inhibitor, AS1938909

The SHIP2 Inhibitor, AS1938909 controls the biological activity of SHIP2. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

别名:

SHIP2 Inhibitor, AS1938909, 3-(2,4-Dichlorobenzyl)oxy]-N-(2,6-difluorobenzyl)thiophene-2-carboxamide, SH2 domain-containing inositol 5ʹ-phosphatase 2 (SHIP2) Inhibitor, AS1938909

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关于此项目

经验公式(希尔记法):
C19H13Cl2F2NO2S
分子量:
428.28
NACRES:
NA.77
UNSPSC Code:
12352200
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assay

≥95% (HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze, protect from light

color

off-white

solubility

DMSO: 50 mg/mL

shipped in

wet ice

Quality Level

General description

A cell-permeable thiophenecarboxamide compound that is shown to increase glucose metabolism and activate intracellular insulin signaling. Acts as a potent, competitive and reversible inhibitor of SHIP2 activity (Ki = 0.44 µM for hSHIP2) with moderate to excellent selectivity over SHIP1 and other related phosphatases (IC50 = 0.18, 0.57, 21, >50, >50 and >50 µM for mSHIP2, hSHIP2, hSHIP1, hPTEN, h-synaptojanin and h-myotubularin, respectively). Elevates insulin-induced pAkt-Ser473 levels and enhances glucose transporter GLUT1 mRNA expression in L6 myotubes. SHIP1 Inhibitor, 3AC is also available (Cat. No. 565835 ).

Packaging

Packaged under inert gas

Other Notes

Suwa, A., et al. 2010. Eur. J. Pharmacol.642, 177.
Suwa, A., et al. 2009. Br. J. Pharmacol.158, 879.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Toxicity: Standard Handling (A)

存储类别

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Petr Fojtík et al.
Frontiers in cell and developmental biology, 8, 607444-607444 (2021-02-09)
Mild hypoxia (5% O2) as well as FGFR1-induced activation of phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B (PI3K/AKT) and MAPK signaling pathways markedly support pluripotency in human pluripotent stem cells (hPSCs). This study demonstrates that the pluripotency-promoting PI3K/AKT signaling pathway is surprisingly attenuated

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