NIR-Triggered Organic Semiconductor Bulk Heterostructure Nanoparticles Enable Dual-Mechanism Photodynamic Anti-tumor Therapy.
basic_science · Level V
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- Record sourced from PubMed, PMID 42306940.
- Also identified by DOI 10.1002/adhm.71356.
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Abstract
Low-bandgap non-fullerene acceptors (NFAs) predominantly generate a variety of reactive oxygen species (ROS) via the type-I photodynamic process, a feature that renders them particularly advantageous for the treatment of hypoxic solid tumors. However, the hypoxic microenvironment typically arises during type-I PDT can upregulate apoptosis-suppressing genes and promote immunosuppression, thereby facilitating tumor cell survival, invasion, and metastasis. To address these limitations, we integrated the charge-transport material PFN-Br with an NFA (H1) to construct bulk heterostructured nanoparticles (H2 (10:1)@NPs). This structural design not only promoted J-aggregation of H2-NPs, but also enhanced their spin-orbit coupling (SOC) through the external heavy-atom effect, thereby facilitating efficient intersystem crossing (ISC) from the singlet excited state (S<sub>1</sub>) to the triplet state (T<sub>1</sub>). The resulting increase in the T<sub>1</sub> exciton augmented both charge and energy transfer, leading to a marked enhancement in type-I and type-II ROS production. Consequently, PFN-Br as ROS amplifier within the bulk heterostructure, disrupting intracellular redox homeostasis and activating both apoptotic and pyroptotic cell death pathways to achieve pronounced antitumor efficacy. This study offers new strategic insights for advancing high-performance photocatalytic tumor therapy toward clinical application.