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• W4362493313 abstract "<div>Abstract<p>First- and second-generation EGFR tyrosine kinase inhibitors (TKI) are effective clinical therapies for patients with non–small cell lung cancer (NSCLC) harboring EGFR-activating mutations. However, almost all patients develop resistance to these drugs. The EGFR T790M mutation of EGFR is the most predominant mechanism for resistance. In addition, activation of AXL signaling is one of the suggested alternative bypassing pathways for resistance to EGFR-TKIs. Here, we report that naquotinib, a pyrazine carboxamide–based EGFR-TKI, inhibited EGFR with activating mutations, as well as T790M resistance mutation while sparing wild-type (WT) EGFR. In <i>in vivo</i> murine xenograft models using cell lines and a patient-derived xenograft model, naquotinib induced tumor regression of NSCLC with EGFR-activating mutations with or without T790M resistance mutation, whereas it did not significantly inhibit WT EGFR signaling in skin. Furthermore, naquotinib suppressed tumor recurrence during the treatment period of 90 days. In addition, unlike erlotinib and osimertinib, naquotinib inhibited the phosphorylation of AXL and showed antitumor activity against PC-9 cells overexpressing AXL <i>in vitro</i> and <i>in vivo</i>. Our findings suggest that naquotinib has therapeutic potential in patients with NSCLC with EGFR-activating mutations, T790M resistance mutation, and AXL overexpression.</p></div>" @default.
• W4362493313 created "2023-04-05" @default.
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• W4362493313 date "2023-04-03" @default.
• W4362493313 modified "2023-10-01" @default.
• W4362493313 title "Data from Mutant-Selective Irreversible EGFR Inhibitor, Naquotinib, Inhibits Tumor Growth in NSCLC Models with EGFR-Activating Mutations, T790M Mutation, and AXL Overexpression" @default.
• W4362493313 doi "https://doi.org/10.1158/1535-7163.c.6538642.v1" @default.
• W4362493313 hasPublicationYear "2023" @default.
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