Nature Communications · 2019 · 141 citations · 25 references
MedicineOncologyPharmacologyCancer PharmacologyChemotherapyMolecular OncologyCancer Cell SignalingLung Cancer PharmacotherapyOncogene MutationsOncogenic Signaling PathwaysAlk InhibitionKinase Domain MutationsMutationOncogenic Receptor Tyrosine Kinase MutationsRos1 InhibitorsRos1 OncogeneRos1-targeted TherapySecondary Mutations
ROS1 gene rearrangements occur in ~1–2 % of NSCLC and other cancers, and although crizotinib is initially effective, resistance frequently develops, notably through the ROS1‑G2032R mutation. The study aims to characterize DS‑6051b, a selective ROS1/NTRK inhibitor, in preclinical models of ROS1‑ or NTRK‑rearranged cancers. The authors evaluated DS‑6051b’s activity in vitro and in vivo using models harboring wild‑type or mutant ROS1 and NTRK rearrangements. DS‑6051b dramatically inhibited growth of both wild‑type and G2032R mutant ROS1‑rearranged cancers, as well as NTRK‑rearranged tumors, in vitro and in vivo, and proved effective against crizotinib‑resistant ROS1‑positive cancers harboring the G2032R mutation, which is resistant to crizotinib, lorlatinib, and entrectinib.
Abstract ROS1 gene rearrangement was observed in around 1–2 % of NSCLC patients and in several other cancers such as cholangiocarcinoma, glioblastoma, or colorectal cancer. Crizotinib, an ALK/ROS1/MET inhibitor, is highly effective against ROS1 -rearranged lung cancer and is used in clinic. However, crizotinib resistance is an emerging issue, and several resistance mechanisms, such as secondary kinase-domain mutations (e.g., ROS1-G2032R) have been identified in crizotinib-refractory patients. Here we characterize a new selective ROS1/NTRK inhibitor, DS-6051b, in preclinical models of ROS1- or NTRK-rearranged cancers. DS-6051b induces dramatic growth inhibition of both wild type and G2032R mutant ROS1–rearranged cancers or NTRK-rearranged cancers in vitro and in vivo . Here we report that DS-6051b is effective in treating ROS1- or NTRK-rearranged cancer in preclinical models, including crizotinib-resistant ROS1 positive cancer with secondary kinase domain mutations especially G2032R mutation which is highly resistant to crizotinib as well as lorlatinib and entrectinib, next generation ROS1 inhibitors.
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