ArticleInnovation (Cambridge (Mass.))2026
Design and development of novel EGFR inhibitors spanning all subgroups of EGFR mutations in non-small cell lung cancer.
Article in Innovation (Cambridge (Mass.)), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
20 authors.
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Abstract
EGFR mutations are common in non-small cell lung cancer (NSCLC), with classical mutations (L858R and exon 19 deletions [Ex19del]) and T790M mutation responsive to three generations of EGFR inhibitors (TKIs). However, the other 30% EGFR mutations, which are classified into exon 20 insertions (Ex20ins) and PACC (P loop/αC-helix compressing) often confer resistance to current TKIs, thereby inducing limited clinical efficacy. In this article, a conserved subpocket behind the ATP-binding domain was detected with our precursor from in-house virtual screening and structural superposition against all subgroups of mutations. This subpocket was utilized combining with traditional ATP pocket in the design and optimization of pan-EGFR inhibitors. The representative compound
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