Controlled Synthesis of the FeB Nanometallic Glasses with Stronger Electron Donating Capability to Activate Molecular Oxygen for the Enhanced Ferroptosis Therapy.

Adv Healthc Mater

School of Chemistry and Chemical Engineering, Center of Free Electron Laser & High Magnetic Field, Key Laboratory of Structure and Functional Regulation of Hybrid Materials Ministry of Education, Key Laboratory of Functional Inorganic Materials Chemistry of Anhui Province, Key Laboratory of Chemistr

Published: January 2025


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Article Abstract

Considering the strong electron-donating ability and the superior biocompatibility, the integration of zero-valent iron nanostructure Fe (electron-reservoir) and zero-valent boron nanostructure B offers great promise for fabricating novel ferroptosis nanoagents. Nevertheless, the controlled and facile synthesis of alloyed Fe and B nanostructure-FeB nanometallic glasses (NMGs) has remained a long-standing challenge. Herein, a complexion-reduction strategy is proposed for the controlled synthesis of FeB NMGs with greater electron donating capacity to activate the molecular oxygen for improved ferroptosis therapy. In-depth mechanism reveales that the complexion-reduction strategy effectively prevent the long-range diffusion of Fe, resulting in the amorphous alloyed Fe and B nanostructure-FeB nanoparticles (FeB NPs). The FeB NPs display stronger electron donating capability and electron transfer rate 9.4 times higher than that of the Fe NPs, which effectively activate the molecular oxygen to produce ∙O , HO and ∙OH. The in vitro cellular experiments confirm the FeB-ss-SiO₂ NPs (encapsulation with SiO outlayer containing -S-S- bonds) demonstrates the enhanced ferroptosis. The tumor-bearing mice models shows that FeB-ss-SiO₂ NPs exhibited superior biocompatibility and tumor inhibition effect (inhibition rate of 73%), which improve the overall survival rate for 30 days post-treatment. This study will provide an innovative way to design therapeutic nanoagents for cancer treatments.

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http://dx.doi.org/10.1002/adhm.202403582DOI Listing

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