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BPU17 binds to PHB1 and causes mild defects in mitochondrial function by defects in the PHB1-PHB2 interaction. This impairment inhibits the SRF/CArG-box-dependent transcription, resulting in the suppression of epithelial-mesenchymal transition (EMT) of retinal pigment epithelial cells (RPEs). BPU17 exhibits antifibrotic activity in vivo. BPU17 is promising for research of anti-neovascular age-related macular degeneration (nAMD) agent[1]. | [References]
[1] Hayashi K, et al. The benzoylphenylurea derivative BPU17 acts as an inhibitor of prohibitin and exhibits antifibrotic activity. Exp Cell Res. 2024 Sep 1;442(1):114221. DOI:10.1016/j.yexcr.2024.114221 |
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