ArticleFrontiers in pharmacology2025
Degradation of IRAK4 for the treatment of lipopolysaccharide-induced acute lung injury in mice.
Article in Frontiers in pharmacology, 2025. 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
Excessive pulmonary inflammation in acute lung injury (ALI) results in high patient mortality. Interleukin-1 receptor-associated kinase 4 (IRAK4) is a potential therapeutic target for inflammatory diseases. However, due to the dual functionality of IRAK4 as both an active kinase and a scaffolding protein, inhibiting its kinase activity yield moderate anti-inflammatory results. The present study explored the efficacy of KT-474, a prototypical IRAK4 degrader, which effectively diminished cellular IRAK4 levels, achieving half-maximal degradation at a concentration of 4.0 nM in RAW 264.7 cells. KT-474 effectively inhibited the activation of downstream nuclear factor (NF)-κB signaling, exhibiting stronger pharmacological impacts compared to conventional kinase inhibitors. Additionally, a lipopolysaccharide-induced acute inflammatory mouse model was established, and KT-474 displayed significant therapeutic benefits
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