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Here, we develop a copper\u2010doped nano\u2010aluminum adjuvant (CuNA) to overcome this resistance by targeting mitochondrial vulnerability. Upon internalization, CuNA releases Cu\n                    <jats:sup>2<\/jats:sup>\n                    <jats:sup>+<\/jats:sup>\n                    , leading to intracellular Cu\n                    <jats:sup>2+<\/jats:sup>\n                    overload, which disrupts mitochondrial function and induces ferroptosis in drug\u2010resistant AML cells, thereby markedly enhancing cytarabine sensitivity. Moreover, CuNA downregulates cholesterol biosynthesis and antioxidant defense pathways, including suppression of HMG\u2010CoA reductase and glutathione peroxidase 4, further amplifying ferroptosis in\u00a0combination with cytarabine. In drug\u2010resistant AML mouse models, CuNA coated with AML cell membranes demonstrates efficient tumor targeting, robust suppression of leukemia progression, and prolonged survival. This study highlights CuNA as a promising tool to overcome chemoresistance mediated by mitochondrial reprogramming in AML.\n                  <\/jats:p>","DOI":"10.1002\/adhm.202504039","type":"journal-article","created":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T08:56:21Z","timestamp":1773132981000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Biomimetic Copper\u2010Doped Nano\u2010Aluminum Adjuvant Potentiates Therapy in Chemoresistant Acute Myeloid Leukemia"],"prefix":"10.1002","volume":"15","author":[{"given":"Chao","family":"He","sequence":"first","affiliation":[{"name":"Institute of Chemical Biology Shenzhen Bay Laboratory  Shenzhen P. R. 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