Flumatinib, a selective inhibitor of BCR-ABL/PDGFR/KIT, effectively overcomes drug resistance of certain KIT mutants
Version of Record online: 4 JAN 2014
© 2013 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japan Cancer Association.
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
Volume 105, Issue 1, pages 117–125, January 2014
How to Cite
Cancer Sci 105 (2014) 117–125
- Issue online: 24 JAN 2014
- Version of Record 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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