Description
Imatinib 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).
Storage
2 years at -20centigrade Powder
Targets
v-Abl, c-Kit, PDGFR
Molecular Formula
C29H31N7O
Solubility
DMSO 3 mg/mL Water
In vitro
Imatinib 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 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 would induce cytogenetic remissions in the majority of chronic myeloid leukemia patients. Imatinib has been approved as an effective treatment for chronic myeloid leukemia.
In vivo
Imatinib 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 is dose-dependent.
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