- Imatinib Mesylate (STI571)
- Saracatinib (AZD0530)
- Bosutinib (SKI-606)
- Dasatinib (BMS-354825)
| GNF 2Bcr-Abl inhibitor |
Sample solution is provided at 25 µL, 10mM.
Nature.2017 Jan 19;541(7637):417-420.
Nature.2018 Nov;563(7731):407-411.Nature.2018 Jun 13.Nature.2018 Jun 27.Nature.2018 Mar 29;555(7698):673-677.Nature.2017 Sep 7;549(7670):96-100.Nature.2016 Apr 21;532(7599):398-401.
Science.2016 Aug 5;353(6299)594-8Nat Nanotechnol.2017 Dec;12(12):1190-1198.Nature Biotechnology.2017 Jun;35(6):569-576Nat Med.2018 Sep 17.Cell.2018 Dec 21. pii: S0092-8674(18)31561-7.Cell.Available online 25 October 2018.Cell.2018 Sep 27. pii: S0092-8674(18)31183-8.Cell.2018 Jun 28;174(1):172-186.e21.Cell.2018 Feb 22;172(5):1007-1021.e17.Cell.2017 Nov 30;171(6):1284-1300.e21.Cell.2017 Aug 17. pii: S0092-8674(17)30869-3.Cell.2017 Jul 13;170(2):312-323Nat Med.2018 Jan 29.Nat Med.2017 Nov;23(11):1342-1351.Cell.2017 Apr 6;169(2):286-300.Cell.2015 Aug 27;162(5):987-1002.Cell.2015 Feb 12;160(4):729-44.Nature Medicine.2017 Apr;23(4):493-500.Cancer Cell.2018 May 14;33(5):905-921.e5.Cancer Cell.2018 Apr 9;33(4):752-769.e8.Cancer Cell.2018 Mar 12;33(3):401-416.e8.Cancer Cell.2017 Aug 14;32(2):253-267.e5.Nat Methods.2018 Jul;15(7):523-526.Cell Stem Cell.2018 May 3;22(5):769-778.e4.Cell Stem Cell.2017 Nov 20. pii: S1934-5909(17)30375-2.Quality Control & MSDS
- View current batch:
- Purity = 99.58%
- COA (Certificate Of Analysis)
- HPLC
- NMR (Nuclear Magnetic Resonance)
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- Datasheet
Chemical structure
| Description | GNF-2 is a highly selective non-ATP competitive inhibitor of Bcr-Abl | |||||
| Targets | Bcr-Abl | |||||
| IC50 | 268 nM (SUP-B15 cell line) 273 nM (K562 cell line) | |||||
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| Cas No. | 778270-11-4 | SDF | Download SDF |
| Chemical Name | 3-[6-[4-(trifluoromethoxy)anilino]pyrimidin-4-yl]benzamide | ||
| Canonical SMILES | C1=CC(=CC(=C1)C(=O)N)C2=CC(=NC=N2)NC3=CC=C(C=C3)OC(F)(F)F | ||
| Formula | C18H13F3N4O2 | M.Wt | 374.32 |
| Solubility | ≥18.7mg/mL in DMSO | Storage | Store at -20°C |
| Physical Appearance | A 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. | ||
GNF-2 is a highly selective non-ATP competitive inhibitor of Bcr-Abl with an IC50 value of 100 to 300 nM in various cell lines.BCR-ABL gene is fused by the BCR and ABL1 genes [1]. BCR-ABL increased production of tyrosine kinase and played an essential role in the pathogenesis of chronic myelogenous leukemia (CML) [2]. Unlike imatinib® that competitively inhibited the ATP-binding site of BCR-ABL kinase activity [3], GNF-2 allosterically inhibited (through binding the myristate-binding site of ABL[4]) the proliferation of BCR-ABL positive cell and induces cell apoptosis. In Ba/F3.p210 Bcr-abl–expressing cells, 48 h treatment of GNF-2 was able to inhibit the proliferation of cells with an IC50 value of 138 nM [5]. In addition, GNF-2 has been found to inhibit E255V and Y253H mutant Ba/F3 cells cell growth, with an IC50 value of 268 and 194 nM, respectively [5]. GNF-2 also caused growth inhibition of K562 and SUP-B15 with an IC50 value of 273 nM and 268 nM, respectively[5].Injecting with BCR-ABL–expressing Ba/F3-p210 cells, 4 % lymphocytes reduction in eperipheral blood was induced [6]. References:[1].REDDY, K. S. & GROVE, B. 1998. A Philadelphia-Negative Chronic Myeloid Leukemia with a BCR/ABL Fusion Gene on Chromosome 9. Cancer Genetics and Cytogenetics, 107, 48-50.[2].RUMPOLD, H. & WEBERSINKE, G. 2011. Molecular pathogenesis of Philadelphia-positive chronic myeloid leukemia - is it all BCR-ABL? Curr Cancer Drug Targets, 11, 3-19.[3].SEGGEWISS, R., LORE, K., GREINER, E., MAGNUSSON, M. K., PRICE, D. A., DOUEK, D. C., DUNBAR, C. E. & WIESTNER, A. 2005. Imatinib inhibits T-cell receptor-mediated T-cell proliferation and activation in a dose-dependent manner. Blood, 105, 2473-2479.[4].FABBRO, D., MANLEY, P. W., JAHNKE, W., LIEBETANZ, J., SZYTTENHOLM, A., FENDRICH, G., STRAUSS, A., ZHANG, J., GRAY, N. S., ADRIAN, F., WARMUTH, M., PELLE, X., GROTZFELD, R., BERST, F., MARZINZIK, A., COWAN-JACOB, S. W., FURET, P. & MESTAN, J. 2010. Inhibitors of the Abl kinase directed at either the ATP- or myristate-binding site. Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics, 1804, 454-462.[5].ADRIAN, F. J., DING, Q., SIM, T., VELENTZA, A., SLOAN, C., LIU, Y., ZHANG, G., HUR, W., DING, S., MANLEY, P., MESTAN, J., FABBRO, D. & GRAY, N. S. 2006. Allosteric inhibitors of Bcr-abl-dependent cell proliferation. Nat Chem Biol, 2, 95-102.[6]. ADRIAN, F. J., DING, Q., SIM, T., VELENTZA, A., SLOAN, C., LIU, Y., ZHANG, G., HUR, W., DING, S., MANLEY, P., MESTAN, J., FABBRO, D. & GRAY, N. S. 2006. Allosteric inhibitors of Bcr-abl-dependent cell proliferation. Nat Chem Biol, 2, 95-102.
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