219331
β-Catenin/Tcf Inhibitor II, PKF118-310
The β-Catenin/Tcf Inhibitor II, PKF118-310 controls the biological activity of β-Catenin/Tcf. This small molecule/inhibitor is primarily used for Cancer applications.
别名:
β-Catenin/Tcf Inhibitor II, PKF118-310, 1,6-Dimethylpyrimido[5,6-e][1,2,4]triazine-5,7-dione, Wnt Pathway Inhibitor X
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About This Item
推荐产品
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
dark yellow
溶解度
DMSO: 100 mg/mL
運輸包裝
ambient
儲存溫度
2-8°C
一般說明
A synthetic cell-permeable actinobacteria pyrimidotriazine-dione that selectively disrupts β-catenin-Tcf4 interaction (IC50 = 0.8 µM in cell-free binding assays) and inhibits β-catenin-regulated cellular transcription activity (IC50 = 0.3 µM in HCT116-based reporter assays). PKF118-310 is demonstrated to reverse β-catenin, but not siamois, mRNA-induced ventral body axis formation in Xenopus embryos, while direct tumor site injection (1 mg/kg/0.5 wk) in HepG2 xenograph mice is shown to increase the number of apoptotic cells and decrease the expression of β-catenin target genes (cyclin D1, c-Myc, survivin) in the tumor mass, resulting in an effective tumor growth retardation (by ~60% after a 4-wk treatment period) in vivo.
包裝
Packaged under inert gas
警告
Toxicity: Standard Handling (A)
重構
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.
其他說明
Wei, W., et al. 2010. Int. J. Cancer126, 2426.
Lepourcelet, M., et al. 2004. Cancer Cell5, 91.
Lepourcelet, M., et al. 2004. Cancer Cell5, 91.
法律資訊
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
訊號詞
Danger
危險聲明
危險分類
Acute Tox. 2 Oral
儲存類別代碼
6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials
水污染物質分類(WGK)
WGK 3
閃點(°F)
Not applicable
閃點(°C)
Not applicable
Scientific reports, 10(1), 15837-15837 (2020-09-29)
The Dlx5 homeobox gene was first implicated as an oncogene in a T-ALL mouse model expressing myristoylated (Myr) Akt2. Furthermore, overexpression of Dlx5 was sufficient to drive T-ALL in mice by directly activating Akt and Notch signaling. These findings implied
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