Anti-inflammatory agent 50 (compound a1), a derivative of Fusidic acid, exerts its effects through inhibition of inflammatory mediators including NO, IL-6, and TNF-α. It mitigates acute lung injury by modulating these mediators and suppressing the MAPK, NF-κB, and NLRP3 inflammasome signaling pathways [1].

In LPS-stimulated RAW264.7 cells, Anti-inflammatory agent 50 (compound a1) inhibits inflammatory mediators including nitric oxide (NO) with an IC50 of 3.26 μM, interleukin-6 (IL-6) with an IC50 of 1.85 μM, and tumor necrosis factor-alpha (TNF-α) with an IC50 of 3.88 μM. Additionally, Anti-inflammatory agent 50 significantly suppresses the expression of certain immunorelated cytotoxic factors, such as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) [1].

Anti-inflammatory agent 50 (compound a1) mitigates pulmonary inflammation and decreases levels of NO, IL-6, TNF-α, COX-2, and iNOS in mice with LPS-induced acute lung injury (ALI). It accomplishes this by attenuating the phosphorylation of p38 MAPK, c-JNK, and ERK, thereby inhibiting the MAPK signaling pathway. Additionally, Anti-inflammatory agent 50 inhibits the NF-κB signaling pathway by preventing the phosphorylation of IκBα [1].