Actinium Highlights Transcriptional Reprogramming as a Key Mechanism Underpinning Mutation-Agnostic Activity of Actimab-A in AML at the 2026 American Association of Cancer Research Annual Meeting
Actimab-A combinations enhanced in vivo AML cell killing across multiple preclinical models, independent of mutation status, when combined with standard-of-care targeted and non-targeted therapies including revumenib (menin-KMT2A inhibitor), gilteritinib (FLT3 inhibitor), and azacitidine (hypomethylating agent) - three pillars of modern AML treatment - supporting its potential role as a universal combination backbone Transcriptional reprogramming identified as a central mechanism showing that Actimab-A combinations don't just add cytotoxicity, they reprogram AML cells from proliferation toward differentiation and apoptosis, providing the mechanistic basis for deeper, more durable MRD-negative responses and reinforcing Actimab-A's role as a universal combination backbone across AML Robust cytotoxicity observed in primary AML patient samples across key mutations (FLT3, KMT2A, NPM1, IDH1, IDH2, or TP53), reinforcing Actimab-A's potential as a mutation-agnostic backbone therapy, complementing the manageable safety profile of Actimab-A observed across prior clinical trials in over 150 AML patients NEW YORK, April 22, 2026 /PRNewswire/ -- Actinium Pharmaceuticals, Inc. (NYSE AMERICAN: ATNM) (Actinium or the Company), a pioneer in the development of targeted radiotherapies, today highlighted data presented at the American Association for Cancer Research (AACR) Annual Meeting supporting transcriptional reprogramming as a central mechanism driving the mutation-agnostic anti-leukemic activity of Actimab-A (lintuzumab-Ac225) in acute myeloid leukemia (AML). Preclinical translational data demonstrated that lintuzumab-Ac225 delivers potent cytotoxic activity across AML models harboring common mutations, including FLT3, NPM1, KMT2A, and TP53, as well as in primary patient samples.