Description
Imatinib Mesylate inhibits c-kit, PDGFR and c-ABL by perfectly binding to adenosine triphosphate (ATP)-binding sites of the c-kit protooncogene product, platelet-derived growth factor receptor (PDGFR), and abelson kinase (c-ABL).
Alias
Glivec, CGP-57148B, STI-571
Storage
2 years at -20centigrade Powder
Synonyms
Glivec, CGP-57148B, STI-571
Targets
v-Abl, c-Kit, PDGFR
Molecular Formula
C29H31N7O.CH4SO3
Chemical Name
N-(4-methyl-3-(4-(pyridin-3-yl)pyrimidin-2-ylamino)phenyl)-4-((4-methylpiperazin-1-yl)methyl)benzamide methanesulfonic acid
Solubility
DMSO 118 mg/mL Water 118 mg/mL Ethanol
In vitro
Imatinib Mesylate inhibits c-kit, PDGFR and c-ABL by perfectly binding to adenosine triphosphate (ATP)-binding sites of the c-kit protooncogene product, platelet-derived growth factor receptor (PDGFR), and abelson kinase (c-ABL). In vitro, imatinib Mesylate inhibition of PDGFRs and c-kit phosphorylation was concentration dependent, with an IC50 value of 0.1 to 0.5 uM. By inhibiting bcr-abl kinase activity, Imatinib Mesylate would induce cytogenetic remissions in the majority of chronic myeloid leukemia patients. Imatinib Mesylate has been approved as an effective treatment for chronic myeloid leukemia.
In vivo
Imatinib Mesylate treatment (48 hours) of Leydig tumor cells cultured can reduce the growth rate of MA10 and LC540 cells by 50% to 60% with an IC50 of 5 umol/L. And in the 48 hours, the antiproliferative and apoptotic effect of imatinib Mesylate is dose-dependent.
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