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Phosphatidylserine-Based Liposomes Encapsulating DMX-5804 Protect Against Doxorubicin-Induced Cardiotoxicity
Jessica Tetterton-Kellner1, Brian C Jensen2,3, Juliane Nguyen1,2
1Division of Pharmacoengineering and Molecular Pharmaceutics, Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Biorxiv : the Preprint Server for Biology
|February 23, 2026
Summary
A novel liposomal formulation, NanoDMX, containing DMX5804, effectively prevents doxorubicin-induced heart damage in mice. This breakthrough offers a potential strategy to mitigate cardiotoxicity in cancer patients undergoing chemotherapy.
Area of Science:
- Cardiology
- Oncology
- Pharmacology
Background:
- Anthracyclines, like doxorubicin, are potent chemotherapeutics but cause significant cardiotoxicity, leading to heart failure in cancer patients.
- This cardiotoxicity is a major cause of non-cancerous mortality in cancer survivors.
- Doxorubicin-induced cardiac contractile dysfunction can be irreversible.
Purpose of the Study:
- To develop and evaluate NanoDMX, a liposomal formulation of DMX5804, for preventing anthracycline-induced cardiotoxicity.
- To investigate the protective mechanisms of DMX-5804 against doxorubicin-induced cardiac damage.
Main Methods:
- Development of NanoDMX, a liposomal formulation of DMX5804 (a MAP4K4 inhibitor) with phosphatidylserine.
- Administration of NanoDMX to mice to assess prevention of doxorubicin-induced left ventricular dysfunction.
- In vitro studies to elucidate the protective mechanisms of DMX-5804 on cardiomyocytes.
Main Results:
- NanoDMX administration prevented doxorubicin-induced left ventricular dysfunction in a mouse model.
- DMX-5804 demonstrated protective effects on cardiomyocytes in vitro.
- The protective mechanisms involved pathways beyond JNK suppression.
Conclusions:
- NanoDMX, a novel liposomal system, successfully prevents doxorubicin-induced cardiac damage.
- DMX-5804 offers cardioprotection through multifaceted mechanisms.
- This formulation represents a promising strategy for mitigating chemotherapy-related heart failure.
