Shiqin Jian, Jiasha Wu, Fusheng Xu, Yan Zuo, Huaxing Shen, Rui Ji, Luyi Wang, Na Li, Yanting Sun, Yongsheng Yu, Yejiao Shi, Honggang Hu, Feng Xu, Dan Huang, Xiaochun Hu
Limited aqueous dispersibility and potential off-target toxicity hinder the development and clinical translation of proteolysis-targeting chimeras (PROTACs). Herein, a bioactive self-delivering "Split Nano-Assembly of Photosensitizers and Targeting Chimeras" (SNAP-TAC) theranostic platform is developed to address these challenges and enable tumor-selective synergistic photo-immunotherapy. To ensure synchronized in vivo delivery, an intact BRD4 degrader is chemically split into a hydrophobic targeting precursor and an amphiphilic photosensitizer-conjugated peptide, which spontaneously co-assemble into discrete nanoparticles. Within the tumor microenvironment (TME), elevated cathepsin B and glutathione trigger dual-responsive peptide cleavage and disulfide reduction. This unloads the bulky photosensitizer and exposes the reactive 1,2-aminothiol motifs, driving the in situ bioorthogonal synthesis of the active PROTAC via metal-free CBT-Cys click condensation. Consequently, active degraders are preferentially generated in tumor-associated environments. Additionally, the intrinsic fluorescence of the photosensitizer enables real-time fluorescence tracking in vivo to guide localized therapy. Therapeutically, upon localized irradiation, the released photosensitizer induces immunogenic cell death, which synergizes with BRD4 depletion-mediated PD-L1 downregulation and immune-pathway modulation to activate anti-tumor immunity. In vivo evaluations demonstrate that this synergy effectively remodels the suppressive "cold" TME into a cytolytic "hot" phenotype. Ultimately, this chemical biology approach effectively addresses the intrinsic selectivity and delivery limitations of conventional PROTACs.