Therapeutic Strategies Targeting Anti-CD47 Therapies in Glioblastoma Multiforme: Lead or Dead End?

Glioblastoma multiforme (GBM) remains the most aggressive primary brain tumour in adults, characterised by marked cellular heterogeneity, stem-like subpopulations, and profound resistance to standard therapies. The failure of conventional approaches underscores the need for novel immunotherapeutic strategies that can effectively overcome tumour immune evasion. Multiple therapeutic strategies have been explored to disrupt CD47 signalling in GBM, including monoclonal antibodies, soluble SIRPα fusion proteins, recombinant or peptide fragments derived from TSP-1, dual CD47/CD36 inhibitors, and antisense oligonucleotides. Overall, anti-CD47 therapy represents a promising but incomplete strategy in GBM treatment. Its success will likely depend on multimodal approaches integrating surgical, cytotoxic and immune-modulatory interventions that also target glioma stem-like populations. Rational combinations that address both immune suppression and tumour heterogeneity could transform CD47 inhibition from a transient lead into a viable therapeutic path for this intractable malignancy.