ArticleDrug design, development and therapy2026
Deciphering Multitarget Mechanisms of Cardiac Glycosides in Acute Myeloid Leukemia Using a Network Pharmacology and Molecular Docking.
Article in Drug design, development and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: Acute myeloid leukemia (AML) remains the most aggressive form of leukemia, underscoring the urgent need for novel treatment strategies. Drug repurposing offers a promising approach to accelerate drug development process. Cardiac glycosides (CGs), traditionally used for heart conditions, have shown potential for AML therapy. As leukemic stem cells (LSCs) are key contributors to AML relapse and chemotherapy resistance, this study aims to elucidate the potential shared mechanisms of proscillaridin (PSN) and ouabain (OUA), two CGs with anti-LSC activity, focusing on their multitarget effects-an emerging strategy in cancer therapy. Methods: An integrative in silico framework combining network pharmacology, bioinformatics, and molecular docking was employed to elucidate the molecular mechanisms, identify clinically relevant targets, and evaluate the binding potential of PSN and OUA, with predictions were subsequently supported by in vitro validation. Results: Seventeen shared core targets of PSN-OUA in AML were identified by intersecting compound-predicted targets from SwissTargetPrediction with AML-relevant genes curated from clinical databases. Enrichment analyses using Gene Ontology, KEGG, and CancerGeneNet revealed strong associations of these core targets with key biological pathways involved in aggressive cancer phenotypes, including cell growth, apoptosis, and motility, which were subsequently validated to be affected by CGs in vitro. Protein-protein interaction mapping identified 10 hub targets-MTOR, PTGS2, ALB, ICAM1, SYK, PRKCA, MAPK14, MET, PRKCB, and MAP2K1-that are functionally interconnected and associated with clinical outcomes. Molecular docking and molecular dynamics simulations supported the high-affinity binding of PSN and OUA, particularly to MTOR and PTGS2. Consistently, both compounds suppressed MTOR- and PTGS2-associated downstream signaling in vitro. Conclusion: Our findings elucidate multiple mechanisms by which CGs may exert anti-LSC activity, which could be crucial for the design of novel therapeutic strategies for AML. The proposed in silico framework is broadly applicable and may accelerate drug repurposing in AML and other cancers.
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