Ferroptosis, characterised by iron-dependent lipid peroxidation, represents a promising therapeutic goal for most cancers remedy. Methods that disrupt intracellular antioxidant methods to induce ferroptosis in most cancers cells have been extensively explored. Herein, we developed a pH-responsive phototheranostic agent (designed as FSB 4 Ca NPs) by encapsulating conjugated boron dipyrromethene tetramers (B4) inside ferric ion-sulfasalazine metallo-network polymercoated calcium carbonate hole nanoparticles. Sulfasalazine, a identified ferroptosis inducer that inhibits System X c –mediated cysteine inflow, synergizes with ferric ion-driven glutathione (GSH) depletion to collectively amplify intracellular lipid peroxidation. Along with serving as a second near-infrared (NIR-II) fluorophore for monitoring the in vivo distribution of FSB 4 Ca NPs, B4 mediates a photothermal impact that considerably enhances lipid peroxidation induction by boosting the Fenton catalytic exercise of ferrous ions. Mixed with localized 915-nm laser irradiation, intravenously administrated FSB 4 Ca NPs achieved substantial tumor suppression in mouse fashions, with an entire remission fee of 80%. This examine establishes a facile technique for creating long-circulating NIR-II phototheranostic brokers with self-amplified lipid peroxidation induction capability, enabling photothermally augmented ferroptosis for most cancers remedy.
