AG 494Potent EGFR-kinase inhibitor |
Sample solution is provided at 25 µL, 10mM.
Quality Control & MSDS
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- Purity = 98.00%
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- MSDS (Material Safety Data Sheet)
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Chemical structure
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Cas No. | 133550-35-3 | SDF | Download SDF |
Chemical Name | (E)-2-cyano-3-(3,4-dihydroxyphenyl)-N-phenylacrylamide | ||
Canonical SMILES | OC1=CC(/C=C(C#N)/C(NC2=CC=CC=C2)=O)=CC=C1O | ||
Formula | C16H12N2O3 | M.Wt | 280.28 |
Solubility | Soluble in DMSO | Storage | Store at -20°C |
Physical Appearance | A crystalline solid | Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size:ship with RT , or blue ice upon request |
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. |
AG 494 is a potent and selective inhibitor of EGFR with IC50 value of 0.7 μM.
The epidermal growth factor receptor (EGFR) is the cell-surface receptor for epidermal growth factor and plays an important role in tumor invasion and cancer cell proliferation.
AG 494 is a potent and selective EGFR inhibitor. AG 494 inhibited autophosphorylation of EGFR and HER-2 with IC50 values of 1.1 and 39 μM, respectively. In DHER-14 cells, AG 494 inhibited Cdk2 activation and EGF-dependent DNA synthesis [1]. AG494 arrested cells at late G1 and S phase and inhibited the activation of Cdk2 by phosphorylating tyrosine 15 on Cdk2 [2]. Epidermal growth factor (EGF) increased (bone morphogenetic protein) BMP9-induced osteogenic markers of mesenchymal stem cells (MSCs), which was inhibited by AG-494 in a time- and dose-dependent way [3]. In human prostate (DU145) and lung (A549) cancer cell lines, AG494 reversibly and significantly inhibited autocrine growth in a dose-dependent way. Also, AG494 induced cell apoptosis in both cell lines and arrested cell growth in the G1 phase [4].
References:[1]. Osherov N, Levitzki A. Tyrphostin AG 494 blocks Cdk2 activation. FEBS Lett, 1997, 410(2-3): 187-190.[2]. Kleinberger-Doron N, Shelah N, Capone R, et al. Inhibition of Cdk2 activation by selected tyrphostins causes cell cycle arrest at late G1 and S phase. Exp Cell Res, 1998, 241(2): 340-351.[3]. Liu X, Qin J, Luo Q, et al. Cross-talk between EGF and BMP9 signalling pathways regulates the osteogenic differentiation of mesenchymal stem cells. J Cell Mol Med, 2013, 17(9): 1160-1172.[4]. Bojko A1, Reichert K, Adamczyk A, et al. The effect of tyrphostins AG494 and AG1478 on the autocrine growth regulation of A549 and DU145 cells. Folia Histochem Cytobiol, 2012, 50(2): 186-195.