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. 2023 Apr 10;41(2):254–266. doi: 10.1007/s10637-023-01350-x

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© The Author(s) 2023, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

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Fig. 1 — Iruplinalkib inhibited kinase activity and the downstream signaling pathways of ALK and ROS1 in vitro. (a) Chemical formula of iruplinalkib. (b) Iruplinalkib and brigatinib inhibited the kinase activity of ALK^WT, ALK^L1196M, ALK^C1156Y, and EGFR^L858R/T790M. (c) The kinase selectivity of iruplinalkib and brigatinib to the fusion protein. Proliferation of Karpas299 (NPM-ALK), Ba/F3, Ba/F3 (EML4-ALK^WT), Ba/F3 (EML4-ALK^L1196M), Ba/F3 (EML4-ALK^C1156Y), NCI-H1975 (EGFR^L858R/T790M), HCC-78 (SLC34A2-ROS1), NIH-3T3 (CD74-ROS1), and Ba/F3 (SLC34A2-ROS1) cells. (d) The inhibitory effects of iruplinalkib on the phosphorylation of ALK, PI3K/AKT, RAS/MAPK and JAK/STAT3 pathways in NCI-H3122 cells, respectively. (e) Iruplinalkib inhibited phosphorylation of ROS1, PI3K/AKT and RAS/MAPK pathways in NIH-3T3 cells stably expressing CD74-ROS1, respectively. (f) Iruplinalkib inhibited phosphorylation of ROS1, RAS/MAPK and SHP-1 pathways in Ba/F3 cells stably expressing SLC34A2-ROS1, respectively