ArticleJournal of thoracic disease2026
Repurposing the MEK inhibitor binimetinib as a dual anti-inflammatory and antifibrotic agent in pulmonary fibrosis.
Article in Journal of thoracic disease, 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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10 authors.
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Abstract
Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease of unknown etiology with poor prognosis. The currently approved antifibrotic drugs only decelerate functional decline and fail to reverse established fibrosis or extend survival. Binimetinib, a highly selective and noncompetitive MEK1/2 inhibitor, has been approved for clinical use in malignancies such as melanoma and non-small cell lung cancer. This study aims to evaluate the therapeutic effects of binimetinib on IPF and to explore its underlying mechanism. Methods: In this study, the antifibrotic effects and underlying mechanisms of binimetinib were evaluated both Results: Conclusions: In summary, binimetinib exerted potent anti-inflammatory and antifibrotic effects by suppressing the activation of both fibroblasts and pulmonary macrophages, ultimately mitigating bleomycin-induced pulmonary fibrosis in mice.
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