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.
同義詞:
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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About This Item
經驗公式(希爾表示法):
C19H13Cl2F2NO2S
分子量::
428.28
分類程式碼代碼:
12352200
NACRES:
NA.77
暫時無法取得訂價和供貨情況
推薦產品
品質等級
化驗
≥95% (HPLC)
形狀
solid
製造商/商標名
Calbiochem®
儲存條件
OK to freeze
protect from light
顏色
off-white
溶解度
DMSO: 50 mg/mL
運輸包裝
wet ice
儲存溫度
2-8°C
一般說明
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).
包裝
Packaged under inert gas
警告
Toxicity: Standard Handling (A)
其他說明
Suwa, A., et al. 2010. Eur. J. Pharmacol.642, 177.
Suwa, A., et al. 2009. Br. J. Pharmacol.158, 879.
Suwa, A., et al. 2009. Br. J. Pharmacol.158, 879.
法律資訊
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
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)
輸入產品批次/批號來搜索 分析證明 (COA)。在產品’s標籤上找到批次和批號,寫有 ‘Lot’或‘Batch’.。
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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