Combining uPAR targeting with albumin chemistry also exploits albumin’s natural transcytosis and tumor accumulation pathways, including gp60/CAV1, SPARC interactions in stroma, and FcRn-dependent recycling, which together increase tumor exposure and can extend systemic half-life, while albumin modifications such as redox-responsive or ligand-conjugated derivatives enable triggered intracellular release and CD44 co-targeting when appropriate [58]. Here, SPARC is linked to neoplasm.