Anti-GD2 antibody therapy has provided clinical benefits to neuroblastoma patients; however, its efficacy is likely impaired by the immunosuppressive tumour microenvironment. Using a multi-omics approach, we have previously defined a link between intratumoral copper levels and immune evasion. Here, we report that co-adjuvant copper chelation potentiates anti-GD2 antibody therapy, conferring durable tumour control in both transgenic and syngeneic neuroblastoma models. Multi-omics analyses revealed that copper chelation creates an immune-primed tumour microenvironment, enhancing the infiltration and activity of Fc-receptor-bearing cells, specifically neutrophils, which are emerging as key effectors of antibody therapy. Moreover, copper sequestration by neuroblastoma was shown to attenuate neutrophil function, a defect successfully reversed with copper chelation. Importantly, we repurpose the clinically approved copper chelation agent, Cuprior, as a non-toxic, efficacious immunomodulatory strategy. Collectively, our findings provide robust justification for clinical testing of Cuprior as a co-adjuvant agent to enhance anti-GD2 antibody therapy and improve outcomes for neuroblastoma patients.