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Imatinib (Gleevec) Chemical Structure
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Biological Activity
Imatinib (Gleevec) is a number of tyrosine kinase enzymes specific inhibitor. It act by specifically inhibiting a certain enzyme that is characteristic of a particular cancer cell, rather than non-specifically inhibiting and killing all rapidly dividing cells, and served as a model for other targeted therapy modalities through tyrosine kinase inhibition. In chronic myelogenous leukemia, the Philadelphia chromosome leads to a fusion protein of abl with bcr (breakpoint cluster region), termed bcr-abl. As this is now a constitutively active tyrosine kinase, it is used to decrease bcr-abl activity. It is being used as an experimental agent to suppress platelet-derived growth factor (PDGF) by inhibiting its receptor (PDGF-Rβ). [1][2]
Chemical Information
| Molecular Weight (WM): | 493.6 |
|---|---|
| Formula: | C29H31N7O |
| CAS No.: | 152459-95-5 |
| Synonyms: |
STI571, Glivec
|
| Dissolve in (25°C): | DMSO ≥5mg/mL |
| Water <1mg/mL | |
| Ethanol ≥3mg/mL | |
| Storage: | 2 years-20°CPowder |
| 1 week-4°Cin DMSO | |
| 1 month-80°in DMSO |
Quality Control & MSDS
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Selleck's high quality products have been used in several published research findings, including the following:
Molecular Characterization of c-Abl/c-Src Kinase Inhibitors Targeted against Murine Tumour Progenitor Cells that Express Stem Cell Markers
Glucosylceramide synthase inhibitor PDMP sensitizes chronic myeloid leukemia T315I mutant to Bcr-Abl inhibitor and cooperatively induces glycogen synthase kinase-3-regulated apoptosis
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A. Viability curve for the c-Kit mutant MelMS melanoma cell line treated with increasing concentrations of imatinib for 72h (relative to DMSO-treated controls; mean ± sd; n=3) B. MelMS melanoma cells were treated with 50nM imatinib for 24h. The effects on c-Kit, ERK and AKT activation were determined by immunoblotting.
A. Viability curve for the c-Kit mutant MelMS melanoma cell line treated with increasing concentrations of imatinib for 72h (relative to DMSO-treated controls; mean ± sd; n=3) B. MelMS melanoma cells were treated with 50nM imatinib for 24h. The effects on c-Kit, ERK and AKT activation were determined by immunoblotting.
Data independently produced by Dr Helen Rizos from the university of Sydney Imatinib (Gleevec) purchased from Selleck
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Ba/F3-p210T315I cells were treated with indicated concentrations of imatinib with or without PDMP for 24 h. Apoptosis was determined as in A. Data are shown as percentage of sub-G1 for apoptosis in triplicate cultures. *P 0.05.
Ba/F3-p210T315I cells were treated with indicated concentrations of imatinib with or without PDMP for 24 h. Apoptosis was determined as in A. Data are shown as percentage of sub-G1 for apoptosis in triplicate cultures. *P 0.05.
Data from [FASEB J 2011.June;25:Ahead of print] Imatinib (Gleevec) purchased from Selleck
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Cell Viability assay results. A2C12, BetaD5, GammaA3, GammaD12, A549, CaCo2, HepG2 cell lines were treated with imatinib mesylate for 24h and 96h. - Cell Viability assay results. A2C12, BetaD5, GammaA3, GammaD12, A549, CaCo2, HepG2 cell lines were treated with imatinib mesylate for 24h and 96h.
Data independently produced by Dr Thomas Kruwel of Fraunhofer Imatinib (Gleevec) purchased from Selleck
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A. Viability curve for the c-Kit mutant MelMS melanoma cell line treated with increasing concentrations of imatinib for 72h (relative to DMSO-treated controls; mean ± sd; n=3) B. MelMS melanoma cells were treated with 50nM imatinib for 24h. The effects on c-Kit, ERK and AKT activation were determined by immunoblotting. |
Data independently produced by Dr Helen Rizos from the university of Sydney
Ba/F3-p210T315I cells were treated with indicated concentrations of imatinib with or without PDMP for 24 h. Apoptosis was determined as in A. Data are shown as percentage of sub-G1 for apoptosis in triplicate cultures. *P 0.05. |
Data from [FASEB J 2011.June;25:Ahead of print]
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