To confirm that the improved tumor-targeting selectivity observed with the affinity-modulated DuetMab variants was directly influenced by the affinity of the EGFR arm and not due to differences in the intrinsic sensitivity of parental NCI-H358 and NCI-H358.HER2.ko tumors to anti-EGFR treatment, we generated monospecific formats of the DuetMab variants by pairing the Fab domains of the EGFR affinity-reduced variants with a Fab of an isotype control (‘NMGC’). This evidence concerns the gene EGFR and neoplasm.