ATNM-400 Elicits Durable Anti-tumor Responses in KRAS- and ALK-Driven NSCLC Models in a Mutation-Agnostic Manner (EANM 2026) - Sep 29, 2026 - Abstract #EPS-149; Pres time: Oct 19, 2026; 04:45 PM - 06:15 PM; Location: Hall G2; "Previously, we demonstrated that the ATNM-400 target is overexpressed in EGFR-mutant NSCLC models and exhibits strong efficacy as monotherapy and in combination with osimertinib...In vivo biodistribution and efficacy (monotherapy and combination) were evaluated in xenograft models, including tumors sensitive and resistant to KRAS G12C inhibitors (sotorasib, adagrasib) and ALK inhibitors (crizotinib, ceritinib, alectinib)... ATNM-400 exhibits potent antitumor activity and favorable tolerability across NSCLC models, independent of oncogenic mutation status. Broad baseline and therapy-induced target expression, combined with specific binding and high-linear energy transfer of 225Ac, enhances its efficacy in KRAS-and ALK-driven NSCLC tumors. These findings support ATNM-400 as a mutation-agnostic targeted alpha therapy and justify further translational and clinical development in advanced NSCLC."
Lung Cancer • Non Small Cell Lung Cancer • Oncology • Solid Tumor • ALK • EGFR • EML4 • KRAS
|
|
A. Kamal; S. Mukherjee; J. Li; K. Peregrina; D. Lewis; L. Lumkong; V. Chavez; K. Subramanian; A. S. Chin; M. Roy; J. Kim; S. Kazerounian
|