EGFR and glioblastoma: Cetuximab binds to EGFR with high affinity, competes for ligand binding, and down-regulates cell-surface receptor expression.63,64 Nimotuzumab binds to EGFR without intrinsic stimulating activity and with lower affinity than cetuximab, thus binding more specifically to EGFR-overexpressing cells.65 Cetuximab showed inhibitory activity for inhibiting EGFR-amplified GBM cells in vitro and in vivo66–68 but not in an early phase II clinical trial with recurrent GBM patients (NCT00463073).