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.
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Synonym(s):
β-Catenin/Tcf Inhibitor II, PKF118-310, 1,6-Dimethylpyrimido[5,6-e][1,2,4]triazine-5,7-dione, Wnt Pathway Inhibitor X
Empirical Formula (Hill Notation):
C7H7N5O2
Recommended Products
Quality Level
Assay
≥95% (HPLC)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
protect from light
color
dark yellow
solubility
DMSO: 100 mg/mL
shipped in
ambient
storage temp.
2-8°C
General description
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.
Packaging
Packaged under inert gas
Warning
Toxicity: Standard Handling (A)
Reconstitution
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.
Other Notes
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.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Signal Word
Danger
Hazard Statements
Precautionary Statements
Hazard Classifications
Acute Tox. 2 Oral
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Yinfei Tan et al.
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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