ArticleFrontiers in pharmacology2026
Repurposing ivacaftor to attenuate LPS-induced acute lung injury: evidence from a non-cystic fibrosis model.
Article in Frontiers in pharmacology, 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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7 authors.
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Abstract
In this study, we explicitly evaluate the anti-inflammatory effects of ivacaftor as a route-of-delivery comparison (intraperitoneal vs. intratracheal) in a reproducible LPS-induced lung inflammation model. We evaluated the effects of ivacaftor [40 mg/kg, administered either intraperitoneally (IP) or intratracheally (IT)] on lipopolysaccharide (LPS, 8 μg)-induced lung inflammation in 8-10-week-old female C57BL/6 mice. Mice were euthanised at 24 or 72 h post-treatment, and serum, bronchoalveolar lavage fluid (BALF), and lung tissue were collected for analysis. Inflammation was assessed by measuring immune cell infiltration, fluorescence-activated cell sorting (FACS)-based leucocyte profiling, and histological changes. Ivacaftor concentrations in the samples were quantified using multiple reaction monitoring liquid chromatography-mass spectrometry (MRM-LCMS). At 24 h, both IT and IP ivacaftor significantly reduced the total BALF cell counts (∼40% reduction) and neutrophil infiltration compared to the LPS-only controls (
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