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Войти в исследования Journal of medicinal chemistry · 2026
Fluorination-Tuned Ionizable Lipids Regulate Nano-PROTAC Trafficking for Enhanced Targeted Protein Degradation.
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Li 李军瑶 Junyao, Min 闵欢 Huan, Song 宋焱 Yan, Huo 霍荣 Rong, Du 杜琳 Lin, Li 李永正 Yongzheng, Du 杜亚静 Yajing, Ding 丁卫 Wei, Zhang 张银龙 Yinlong, Li 李一叶 Yiye, Nie 聂广军 Guangjun, Qi 祁迎秋 Yingqiu
Аннотация
Nanoscale proteolysis-targeting chimeras (nano-PROTACs) offer modular platforms for targeted protein degradcine-rich α-2-glycoprotein 1 (LRG1). i16αCF3-LipoTAC showed greater degradation potend endocytosis, and promoted endosomal escape. In 4T1 tumor models, i16αCF3-LipoTAC prolonged circulation, increased tumor accumulation and target depletion, and improved antitumor efficacy. These findings support fluorination tuning as a strategy to enhance nano-PROTAC trafficking and degradation efficiency.Nanoscale proteolysis-targeting chimeras (nano-PROTACs) offer modular platforms for targeted protein degradcine-rich α-2-glycoprotein 1 (LRG1). i16αCF3-LipoTAC showed greater degradation potend endocytosis, and promoted endosomal escape. In 4T1 tumor models, i16αCF3-LipoTAC prolonged circulation, increased tumor accumulation and target depletion, and improved antitumor efficacy. These findings support fluorination tuning as a strategy to enhance nano-PROTAC trafficking and degradation efficiency.Nanoscale proteolysis-targeting chimeras (nano-PROTACs) offer modular platforms for targeted protein degradcine-rich α-2-glycoprotein 1 (LRG1). i16αCF3-LipoTAC showed greater degradation potend endocytosis, and promoted endosomal escape. In 4T1 tumor models, i16αCF3-LipoTAC prolonged circulation, increased tumor accumulation and target depletion, and improved antitumor efficacy. These findings support fluorination tuning as a strategy to enhance nano-PROTAC trafficking and degradation efficiency.Nanoscale proteolysis-targeting chimeras (nano-PROTACs) offer modular platforms for targeted protein degradcine-rich α-2-glycoprotein 1 (LRG1). i16αCF3-LipoTAC showed greater degradation potend endocytosis, and promoted endosomal escape. In 4T1 tumor models, i16αCF3-LipoTAC prolonged circulation, increased tumor accumulation and target depletion, and improved antitumor efficacy. These findings support fluorination tuning as a strategy to enhance nano-PROTAC trafficking and degradation efficiency.