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To Purchase # 9084S

9084S 5 mg $59.00.0


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PhosphoSitePlus® Resource

  • Additional protein information
  • Analytical tools


Western blot analysis of extracts from K-562 cells, untreated (-) or treated with imatinib (10 μM, 1 hr; +), using PathScan® Bcr/Abl Activity Assay: Phospho-c-Abl, Phospho-Stat5 and Phospho-CrkL Multiplex Western Detection Cocktail #5300 to detect inhibition of phospho-Bcr-Abl, phospho-Stat5, and phospho-CrkL.

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Chemical structure of imatinib.

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Product Usage Information

Imatinib is supplied as a lyophilized powder. For a 10 mM stock, reconstitute the 5 mg in 847.9 μl DMSO. Working concentrations and length of treatment can vary depending on the desired effect, but it is typically used at 1-10 μM for 1-2 hours. Soluble in DMSO at 100 mg/ml; poorly soluble in ethanol. Soluble in water at 200 mg/ml.

Storage: Store lyophilized or in solution at -20ºC, desiccated. Protect from light. In lyophilized form, the chemical is stable for 24 months. Once in solution, use within 3 months to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Product Description

Molecular Weight:

589.71 g/mol



Molecular Formula:

C29H31N7O + CH4SO3

Imatinib is a tyrosine kinase (TK) inhibitor that is a relatively specific ATP-binding site antagonist of Bcr-Abl, PDGF receptor, and c-Kit TKs (1-3). Results are encouraging in chronic myeloid leukemia (CML) clinical trials and imatinib has become a paradigm for targeted cancer therapeutics (4-6). Signal transduction through phospho-tyrosine pathways has been studied extensively, and tyrosine phosphorylation has been linked to multiple cell growth and differentiation pathways (7-9). Because the observed leukemic state of CML is dependent on the intact Bcr-Abl tyrosine kinase activity, extensive work has been done to identify substrates of Bcr-Abl and thus possible mechanisms leading to a myeloid expansion. Many groups have characterized prominent tyrosine-phosphorylated protein substrates in both CML blasts and Bcr-Abl-expressing cell lines, including SHIP, c-Cbl, Dok, Shc, and CrkL (10-15). In addition, key signal transduction pathways involving PI3 kinase, Ras, Myc, and Stat5 are also activated in a Bcr-Abl kinase-dependent manner (16).

1.  Buchdunger, E. et al. (1996) Cancer Res 56, 100-4.

2.  Heinrich, M.C. et al. (2000) Blood 96, 925-32.

3.  Blume-Jensen, P. and Hunter, T. (2001) Nature 411, 355-65.

4.  Druker, B.J. et al. (1996) Nat Med 2, 561-6.

5.  Mauro, M.J. and Druker, B.J. (2001) Curr Oncol Rep 3, 223-7.

6.  Druker, B.J. et al. (2001) N Engl J Med 344, 1031-7.

7.  Druker, B.J. et al. (2001) N Engl J Med 344, 1038-42.

8.  Ullrich, A. and Schlessinger, J. (1990) Cell 61, 203-12.

9.  Cantley, L.C. et al. (1991) Cell 64, 281-302.

10.  ten Hoeve, J. et al. (1994) Blood 84, 1731-6.

11.  Matsuguchi, T. et al. (1994) J Biol Chem 269, 5016-21.

12.  Carpino, N. et al. (1997) Cell 88, 197-204.

13.  Sattler, M. et al. (1997) Oncogene 15, 2379-84.

14.  Cristofano, A. D. et al. (1998) J. Biol. Chem. 273, 4827-4830.

15.  Wisniewski, D. et al. (1999) Blood 93, 2707-20.

16.  Kabarowski, J.H. and Witte, O.N. (2000) Stem Cells 18, 399-408.

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