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Background <p>DOX, an anthracycline antibiotic, is extensively utilized in the treatment of various solid tumors and hematological malignancies but is constrained by its cumulative cardiotoxicity. PDA has emerged as a promising drug delivery platform owing to its superior biocompatibility, pH-responsive drug release capability, and multifunctional surface properties.The FH peptide, which specifically targets Tenascin-C overexpressed in DOX-injured myocardium, offers a promising strategy to enhance cardiac-specific drug accumulation.</p> Methods <p>In vitro experiments were performed using primary neonatal mouse cardiomyocytes. Cardioprotective efficacy was evaluated in an acute DOX-induced myocardial injury mouse model, and antitumor activity was assessed in a 4T1 tumor-bearing mouse model.</p> Results <p>Our comprehensive analysis, including spectroscopic methods and physicochemical characterization, confirmed the successful integration of Dex and FH onto the PDA platform. Both in vitro and in vivo studies demonstrated that PDA-Dex/FH effectively treats DOX-induced cardiotoxicity, with FH incorporation enhancing cardiac targeting while preserving DOX’s antitumor efficacy.</p> Conclusions <p>we demonstrated that, under the experimental conditions of this study, PDA-Dex/FH not only markedly mitigates myocardial injury with enhanced cardiac accumulation but also retains the chemotherapeutic efficacy of doxorubicin, thereby.</p>

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Engineering a bi-functional nanoplatform containing FH peptide for preferential cardiac delivery to counteract doxorubicin-induced cardiotoxicity

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月18日

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  • Jun Li,
  • Zheng-long Zhong,
  • Jing Tang,
  • Yi Chen,
  • Chang-pei Xiang,
  • Jing Li,
  • Ju-long Tian,
  • Xiao-ming Luo,
  • Jian-jie Zou,
  • Yu-qing Tian

摘要

Background

DOX, an anthracycline antibiotic, is extensively utilized in the treatment of various solid tumors and hematological malignancies but is constrained by its cumulative cardiotoxicity. PDA has emerged as a promising drug delivery platform owing to its superior biocompatibility, pH-responsive drug release capability, and multifunctional surface properties.The FH peptide, which specifically targets Tenascin-C overexpressed in DOX-injured myocardium, offers a promising strategy to enhance cardiac-specific drug accumulation.

Methods

In vitro experiments were performed using primary neonatal mouse cardiomyocytes. Cardioprotective efficacy was evaluated in an acute DOX-induced myocardial injury mouse model, and antitumor activity was assessed in a 4T1 tumor-bearing mouse model.

Results

Our comprehensive analysis, including spectroscopic methods and physicochemical characterization, confirmed the successful integration of Dex and FH onto the PDA platform. Both in vitro and in vivo studies demonstrated that PDA-Dex/FH effectively treats DOX-induced cardiotoxicity, with FH incorporation enhancing cardiac targeting while preserving DOX’s antitumor efficacy.

Conclusions

we demonstrated that, under the experimental conditions of this study, PDA-Dex/FH not only markedly mitigates myocardial injury with enhanced cardiac accumulation but also retains the chemotherapeutic efficacy of doxorubicin, thereby.