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. 2019 Oct 10;9:14627. doi: 10.1038/s41598-019-51217-6

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Antiproliferative effect of an FGFR inhibitor and 3D structures of FGFR4. (A) Antiproliferative effect of ASP5878 on (a) G636C-FGFR4/BaF3 and (b) G636C-FGFR4/3T3 cells. Three independent experiments were performed in triplicate, and representative data are shown as the mean ± SD. Geometric mean IC₅₀ values and 95% confidence intervals (CIs) were determined from three independent experiments. (B) Mice engrafted with G636C-R4/3T3 cells were orally administered ASP5878 (3 mg/kg, once daily). Tumour volumes were measured, and data are shown as the mean ± SEM (n = 5). Tumour volumes on day 7 were compared between the ASP5878-treated and vehicle control groups (Student t test). (C) 3D models of FGFR4 wild-type and G636C with ASP5878. (a) Overview of 3D models of the kinase domain of FGFR4 (cyan, wild-type; pink, G636C). The heavy atoms of ASP5878, G636 or C636 are represented as sticks. (b) Close-up of the binding site of ASP5878.