ArticleDiscover oncology2026
Bioinformatics and computational exploration of novel inhibitors targeting KRAS G12C mutant protein in lung adenocarcinoma.
Article in Discover oncology, 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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Abstract
backgroundThe KRAS p.G12C mutation is a major oncogenic driver in lung adenocarcinoma (LUAD), a prevalent subtype of non-small cell lung cancer (NSCLC). The development of sotorasib has provided a new targeted therapeutic option for patients with this mutation.
methodsKRAS G12C mutations and expression in LUAD were analyzed. A pharmacophore model-based screening of over 1.4 billion conformations was conducted. Molecular docking, drug-likeness, pharmacokinetics, and toxicity predictions were carried out to explore ligands. Binding stability and key residue interactions were evaluated using extra-precision docking, molecular dynamics, H-bond lifetimes, FEL, PCA, and MM-GBSA analyses.
resultsKRAS mutations were identified in 36% of LUAD samples, with G12C being the most frequent. KRAS p.G12C expression was significantly elevated in mutants (log
conclusionsThe compounds, including PubChem-137,082,465 and PubChem-154,677,904, exhibited favorable binding and favorable interaction profiles, comparable to sotorasib, positioning them as computationally prioritized candidates for KRAS p.G12C inhibition in LUAD.
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