• ATNM-400 demonstrates pan-tumor activity across prostate, lung, and breast cancer models, supporting multi-indication development potential
  • In prostate cancer, ATNM-400 demonstrates efficacy across both high PSMA-expressing and, importantly, low PSMA-expressing prostate cancer models, unlike many PSMA-targeted radioligand therapies that work only in PSMA-high settings
  • In EGFR-mutant non-small cell lung cancer, ATNM-400 demonstrates greater tumor growth inhibition than osimertinib (a tyrosine kinase inhibitor) plus chemotherapy and outperforms the approved Trop-2 ADC Dato-DXd (DATROWAY®), the EGFR-cMET bispecific antibody amivantamab (RYBREVANT®) and the experimental EGFR-HER3 ADC izalontamab brengitecan, supporting potential use across first-, second-, and third-line treatment settings
  • In breast cancer, new head-to-head data shows ATNM-400 achieves efficacy comparable to the approved HER2-ADC trastuzumab deruxtecan (ENHERTU®) in trastuzumab-resistant models, with durable tumor control observed after treatment discontinuation - extending the Company's prior SABCS 2025 data and supporting potential for less frequent dosing of ATNM-400 compared to ADCs
  • ATNM-400 is well tolerated, with no in vivo toxicities observed at efficacious doses, providing a favorable therapeutic index that supports monotherapy and combination development

NEW YORK, April 22, 2026 /PRNewswire/ -- Actinium Pharmaceuticals, Inc. (NYSE:ATNM) (Actinium or the Company), a pioneer in the development of targeted radiotherapies, today announced preclinical results for ATNM-400 across prostate, lung, and breast cancer models presented at the American Association for Cancer Research (AACR) Annual Meeting in San Diego, CA. ATNM-400 is a novel, first-in-class targeted radiotherapy utilizing the Actinium-225 (Ac-225) radioisotope that targets a non-PSMA membrane antigen overexpressed in advanced and therapy-refractory solid tumors across multiple oncology indications.

ATNM-400 is a novel, first-in-class targeted radiotherapy whose differentiation stems from both its target and its isotope. The target is a non-PSMA membrane antigen associated with treatment resistance in advanced solid tumors that is overexpressed across prostate cancer, non-small cell lung cancer (NSCLC), and breast cancer, and is further upregulated following treatment with standard-of-care therapies — providing a strong mechanistic rationale for ATNM-400 in the treatment-resistant disease settings that represent the greatest unmet need, and for combination regimens designed to exploit this treatment-induced target upregulation. The isotope, Actinium-225 (Ac-225), is a potent alpha emitter that, compared to beta emitters such as Lu-177, delivers high-energy radiation capable of inducing irreversible double-stranded DNA breaks, with a shorter path length that may limit off-target effects and enhance therapeutic precision. Together, this target-and-isotope combination positions ATNM-400 to overcome conventional resistance pathways and deliver durable tumor control while potentially avoiding toxicities such as interstitial lung disease that limit the use of antibody-drug conjugates — expanding the population of patients who could benefit from treatment.