Flumatinib, a selective inhibitor of BCR-ABL/PDGFR/KIT, effectively overcomes drug resistance of certain KIT mutants
Article first published online: 4 JAN 2014
© 2013 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japan Cancer Association.
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Volume 105, Issue 1, pages 117–125, January 2014
How to Cite
Cancer Sci 105 (2014) 117–125
- Issue published online: 24 JAN 2014
- Article first published online: 4 JAN 2014
- Accepted manuscript online: 10 NOV 2013 10:17PM EST
- Manuscript Accepted: 5 NOV 2013
- Manuscript Revised: 22 OCT 2013
- Manuscript Received: 21 AUG 2013
- National Natural Science Foundation of China. Grant Numbers: Y201181042, 81273546
- National Science and Technology Major Project. Grant Numbers: 2013ZX09102008, 2013ZX09402102-001-004
Doc. S1. Supporting information regarding molecular docking.
Fig. S1. Effects of imatinib, flumatinib, and sunitinib on the phosphorylation of KIT, ERK1/2, and signal transducer and activator of transcription-3 (STAT3) in 32D-V559D + N822K and 32D-V559D + A829P cells.
Fig. S2. Effects of imatinib, flumatinib, and sunitinib on the body weight of mice after injection of 32D-V559D or 32D-V559D + Y823D cells.
Fig. S3. Effects of imatinib, flumatinib, and sunitinib on the phosphorylation of KIT, ERK1/2, and signal transducer and activator of transcription-3 (STAT3) in 32D-D816H and 32D-N822K cells.
Fig. S4. Plane diagrams showing the interactions between KIT kinase domain and imatinib/flumatinib.
Table S1. Imatinib, flumatinib, sunitinib, nilotinib, dasatinib, sorafenib, and cabozantinib IC50 values of 32D cell lines expressing transforming KIT mutants.
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