Conclusions In summary, the results of this study demonstrate that different Kit mutations respond differently to motesanib or imatinib. This likely reflects differences in the molecules’ mode of action. The data also show that motesanib is active against Kit mutations associated with resistance, suggesting that it may have clinical utility in the treatment of
patients with primary and secondary imatinib-resistant GIST. Acknowledgements The authors wish to acknowledge Douglas Whittington and Joseph Kim (Amgen Inc., Cambridge, MA) for generating the model of motesanib bound to Kit. Additionally, the authors would like to thank Ali Hassan, PhD (Complete Healthcare Communications, Inc.), whose work was funded by Amgen Inc., and Beate Quednau, PhD (Amgen Inc.), for their assistance in the preparation of this manuscript. References 1. Heinrich selleck kinase inhibitor MC, Corless CL, Demetri GD, Blanke CD, von Mehren M, Joensuu H, McGreevey LS,
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