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NIR-Triggered Organic Semiconductor Bulk Heterostructure Nanoparticles Enable Dual-Mechanism Photodynamic Anti-Tumor
Ying Huang1, Shida Ma1, Yongrui He1
1School of Pharmacy, Shandong Second Medical University, Weifang, Shandong, P. R. China.
Advanced Healthcare Materials
|June 17, 2026
Summary
This study developed novel nanoparticles that enhance reactive oxygen species (ROS) production for photodynamic therapy (PDT). These nanoparticles effectively target and eliminate cancer cells, offering a promising new strategy for tumor treatment.
Area of Science:
- Biomaterials Science
- Nanotechnology
- Photodynamic Therapy
Background:
- Low-bandgap non-fullerene acceptors (NFAs) show potential for photodynamic therapy (PDT) against hypoxic tumors by generating reactive oxygen species (ROS) via type-I process.
- However, the tumor microenvironment's hypoxia can promote tumor survival and metastasis by upregulating apoptosis-suppressing genes and immunosuppression.
- Existing PDT strategies require enhancement to overcome tumor resistance mechanisms.
Purpose of the Study:
- To design and synthesize novel bulk heterostructured nanoparticles (BHNs) for enhanced ROS production in PDT.
- To investigate the role of PFN-Br integration in promoting J-aggregation and spin-orbit coupling (SOC) for efficient intersystem crossing (ISC).
- To evaluate the antitumor efficacy of the developed BHNs by disrupting intracellular redox homeostasis and inducing apoptosis and pyroptosis.
Main Methods:
- Construction of bulk heterostructured nanoparticles (H2 (10:1)@NPs) by integrating PFN-Br with NFA (H1).
- Characterization of nanoparticle structure, J-aggregation, and spin-orbit coupling (SOC) enhancement via heavy-atom effect.
- Assessment of enhanced intersystem crossing (ISC) from singlet (S1) to triplet (T1) states.
- Evaluation of type-I and type-II ROS production.
- In vitro studies on intracellular redox homeostasis disruption and induction of apoptotic and pyroptotic cell death pathways.
Main Results:
- The integrated structure promoted J-aggregation and enhanced SOC, leading to efficient ISC.
- Increased T1 exciton augmented charge and energy transfer, significantly boosting type-I and type-II ROS production.
- PFN-Br acted as a ROS amplifier within the BHNs, disrupting cellular redox balance.
- The nanoparticles effectively activated both apoptotic and pyroptotic cell death pathways, demonstrating pronounced antitumor efficacy.
Conclusions:
- The developed PFN-Br integrated BHNs significantly enhance ROS generation for improved PDT efficacy.
- This strategy effectively overcomes tumor resistance mechanisms by disrupting redox homeostasis and inducing multiple cell death pathways.
- The study provides strategic insights for advancing high-performance photocatalytic tumor therapy towards clinical applications.
