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In the murine model of lipopolysaccharide (LPS)induced ALI, severely impaired FAO in alveolar EpiCs participated in the inflammatory response and lung injury, which might be attributed to the decreased expression of key mediators involved in FAO, such as CPT1A, and could partly be counteracted by treatment with a PPAR agonist, fenofibrate ( CPT1A aggravated EC apoptosis and lung injury, while treatment with L-carnitine attenuated the pathological changes (Yao et al., 2019)

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The alkyl interaction with ARG A:67 provided minimal hydrophobic stabilization but did not significantly improve the overall inhibitory potential

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