摘要
Abstract 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.
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