Imatinib Mesylate - CAS 220127-57-1
Catalog number: 220127-57-1
Category: Inhibitor
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Imatinib (INN), marketed by Novartis as Gleevec (Canada, South Africa and the USA) or Glivec (Australia, Europe and Latin America), and sometimes referred to by its investigational name STI-571, is a tyrosine-kinase inhibitor used in the treatment of multiple cancers, most notably Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML).
CGP-57148B; CGP 57148B; CGP57148B; Gleevec, Imatinib
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1.C-Kit non-mutated metastatic melanoma showing positive response to Nilotinib.
Alkeraye S1, Dadban A, Lok C, Arnault JP, Chaby G. Dermatol Online J. 2016 Jan 15;22(1). pii: 13030/qt13s758x1.
Melanoma is an aggressive tumor with advanced disease characterized by widespread metastatic lesions and the tumor hastraditionally been resistant to most forms of treatment. Indeed, metastatic melanoma has a very poor prognosis with a median survival time of 8-9 months and an estimated 3-year survival rate of less than 15 % [1].Recent advances in our understanding of the genetic profile of melanoma cells and the molecular factors that drive malignant transformation have resulted in the identification of numerous new therapeutic targets.KIT is an established therapeutic target in cancers with activating mutations of KIT, such as gastrointestinal stromal tumors (GIST), and considerable efficacy has been achieved with various small molecule inhibitors of KIT including imatinib mesylate [2].Nilotinib is an inhibitor of ligand-induced PDGFRα and PDFGRβ kinase activity and autophosphorylation of constitutively activated KIT harboring exon 13 or exon 11 mutations (IC50 values of 0.
2.Distinct Dasatinib-Induced Mechanisms of Apoptotic Response and Exosome Release in Imatinib-Resistant Human Chronic Myeloid Leukemia Cells.
Liu J1, Zhang Y2, Liu A3, Wang J4, Li L5, Chen X6, Gao X7, Xue Y8, Zhang X9, Liu Y10. Int J Mol Sci. 2016 Apr 8;17(4). pii: E531. doi: 10.3390/ijms17040531.
Although dasatinib is effective in most imatinib mesylate (IMT)-resistant chronic myeloid leukemia (CML) patients, the underlying mechanism of its effectiveness in eliminating imatinib-resistant cells is only partially understood. This study investigated the effects of dasatinib on signaling mechanisms driving-resistance in imatinib-resistant CML cell line K562 (K562R(IMT)). Compared with K562 control cells, exsomal release, the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/ mammalian target of rapamycin (mTOR) signaling and autophagic activity were increased significantly in K562R(IMT) cells and mTOR-independent beclin-1/Vps34 signaling was shown to be involved in exosomal release in these cells. We found that Notch1 activation-mediated reduction of phosphatase and tensin homolog (PTEN) was responsible for the increased Akt/mTOR activities in K562R(IMT) cells and treatment with Notch1 γ-secretase inhibitor prevented activation of Akt/mTOR.
3.Safety of combination treatment with imatinib mesylate, carboplatin, and cetuximab in a patient with multiple cancers: a case report.
Pala L1, Bergamini C1, Imbimbo M1, Granata R1, Locati L1, Alfieri S1, Licitra L1, Bossi P1. Tumori. 2016 Mar 14:0. doi: 10.5301/tj.5000485. [Epub ahead of print]
PURPOSE: Therapies directed against multiple signaling pathways have been validated in the clinical setting as effective anticancer treatments. The combination of different agents is particularly helpful in patients with multiple cancer diagnoses, while data on cross-toxicity are frequently missing, as for imatinib and cetuximab plus platinum drugs.
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