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. 2023 Sep 21;4(9):1345–1361. doi: 10.1038/s43018-023-00630-y

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© The Author(s) 2023, corrected publication 2023

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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Extended Data Fig. 8 — Mice bearing (a) ECLC5 xenograft (n = 5), (b) LUAD-0057AS1 PDX (n = 8), (c) LUAD-0087AS2 PDX (n = 5) or (d) LUAD-0077AS1 (n = 5) were treated with RET multi-kinase or selective inhibitors. Mice bearing allograft tumors derived from Ba/F3 cells expressing KIF5B::RET^WT (e, n = 6) or KIF5B::RET^G810R (f and g, n = 5) fusions were administrated vepafestinib (TAS0953/HM06), selpercatinib or pralsetinib. Mice bearing Ba/F3-KIF5B::RET^WT allograft tumors were treated with vehicle, selpercatinib or pralsetinib (h and i, n = 5). Drugs or vehicle were administered orally at the indicated doses, once daily (QD) or twice daily (BID). Data is presented as mean ± SEM in each group. Tumor-bearing animals were weighed twice weekly *P = 0.0046, compared to the weight on day 0. ^#P = 0.0015, compared to weight on day 0. Data were compared by ANOVA with Dunnet’s multiple comparison tests. All tests were two sided.

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