Inhibition of FGFR signaling and tumor growth in SNU-16 xenograft model by administration of E7090. Inhibition of FGFR signaling and tumor growth in SNU-16.

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Inhibition of FGFR signaling and tumor growth in SNU-16 xenograft model by administration of E7090. Inhibition of FGFR signaling and tumor growth in SNU-16 xenograft model by administration of E7090. Nude mice bearing SNU-16 xenografts were treated orally once daily for 14 days with either vehicle or E7090 succinate at the indicated doses. A, tumor volume. Data are shown as means ± SD (n = 6). ***, P < 0.001; ****, P < 0.0001 compared with vehicle-treated mice (Dunnett test). B, body weight measurements during the treatment. Data are shown as means ± SD (n = 6). C, pharmacodynamic analysis of E7090 in mice bearing SNU-16 tumors. E7090 was orally administered at the indicated doses, and blood and tumors were collected at the indicated time points. The percentage of FGFR2 phosphorylation compared with vehicle is plotted. Data are shown as means ± SD (E7090: n = 3; vehicle: n = 5). Western blotting data for each sample against FGFR2 or phospho-FGFR (Y653/654) are also shown in Supplementary Fig. S3. D, plasma FGF23 level 24 hours after administration of E7090 or vehicle (control). FGF23 concentrations were determined by ELISA from plasma. Data are shown as means ± SD. *, P < 0.05 compared with vehicle-treated mice (Dunnett test). E, pharmacokinetic analysis of E7090 in mice bearing SNU-16 tumors. E7090 was orally administered at the indicated doses, and blood and tumors were collected at the indicated time points. E7090 concentration in plasma is plotted. Saori Watanabe Miyano et al. Mol Cancer Ther 2016;15:2630-2639 ©2016 by American Association for Cancer Research