- New KRAS-mutant data show ATNM-400 outperformed standard-of-care inhibitors sotorasib and adagrasib as a monotherapy. Treatment with these agents increased expression of the ATNM-400 target greater than 3.5x and enhanced their effect in combination
- Additional data in the EGFR-mutant setting demonstrated powerful synergy with osimertinib due to enhanced target expression in treated animals resulting in complete tumor regression in the combination arm
- The data with EGFR and KRAS mutations which account for approximately 40-50 percent of all NSCLC cases provide compelling evidence of the potential of ATNM-400 as a monotherapy or in combination with inhibitory agents against these mutations
- ATNM-400 is a radioconjgate comprising an antibody coupled to Actinium-225 which causes cell death via double stranded DNA breaks independent of cellular mechanisms and offers broad potential as a mutation agnostic agent in NSCLC where its target is expressed in over 90 percent of tumors with greater expression as resistance emerges
NEW YORK, June 3, 2026 /PRNewswire/ -- Actinium Pharmaceuticals, Inc. (NYSE:ATNM) (Actinium or the Company), a pioneer in the development of targeted radiotherapies, on June 2, 2026, presented new preclinical data on ATNM-400 in non-small cell lung cancer (NSCLC) at the Society of Nuclear Medicine and Molecular Imaging (SNMMI) 2026 Annual Meeting in Los Angeles, California.
The new KRAS-mutant data, together with a growing body of EGFR-mutant data, demonstrate ATNM-400's activity across the two major mutation driver classes in NSCLC and support a distinct strategic opportunity. ATNM-400 can be developed as a potential mutation-agnostic backbone for the broader NSCLC market, alone or in combination with standard-of-care therapies, rather than as another mutation-specific drug for a narrow subset.
NSCLC accounts for roughly 85% of the more than two million lung cancer cases diagnosed globally each year, a market more than twice the size of prostate cancer. It is also highly heterogeneous: no single mutation dominates, so treatments are fragmented across mutation-specific therapies such as EGFR, KRAS, BRAF, ALK and others, each marketed by different companies, each addressing only a molecular subset, and each ultimately limited by acquired resistance. ATNM-400, Actinium's first-in-class Actinium-225 (Ac-225) antibody radioconjugate, is designed to break out of that single-mutation paradigm. Rather than blocking a specific mutant protein, it delivers a high-linear-energy-transfer alpha-particle payload that induces dense, irreversible double-strand DNA breaks and tumor-cell death independent of a tumor's driver mutation or signaling pathway, the mechanistic basis of its mutation-agnostic activity.
ATNM-400's target antigen, from previously published immunohistochemistry studies, is present in approximately 98% of NSCLC tumors and highly expressed in approximately 70% of those tumors. It is conserved across EGFR-, KRAS-, and other driver-defined subgroups, and further increased in tumors that have become resistant to EGFR, KRAS, and immune-checkpoint therapies. In new KRAS-mutant studies presented at SNMMI, sotorasib (active ingredient in LUMAKRAS®/Amgen) and adagrasib (active ingredient in KRAZATI®/BMS) increased ATNM-400's target up to 3.5- and 3.8-fold, respectively, and adding ATNM-400 deepened tumor-cell killing beyond either inhibitor alone. These results demonstrate the same target-expression increasing, synergy-enabling biology shown previously with the EGFR inhibitor osimertinib, which produced tumor growth inhibition of 107% when combined with ATNM-400.
These combination benefits also broaden ATNM-400's commercial opportunity. The franchises it could enhance are substantial; the KRAS inhibitor class in NSCLC is projected to exceed $5 billion in peak sales, and the EGFR-mutant segment has peak sales estimates over $15 billion, led by osimertinib (active ingredient in TAGRISSO®/AZ), which generated $7.3 billion in 2025. This positions ATNM-400 to participate in these established markets by enhancing the standard of care, while also reaching the broader NSCLC population beyond any single mutation.