This product is an unconjugated, non-therapeutic recombinant analog of the anti-CD73 antibody oleclumab, produced for research use only. It reproduces the antigen-binding specificity of the originator molecule against human CD73 (ecto-5'-nucleotidase, NT5E; UniProt P21589) in a human IgG1-lambda framework carrying Fc-region substitutions that reduce effector engagement, matching the reported low-effector design of the originator. It is not the clinical drug and is not intended for human or veterinary use. As a research reagent it is useful as a defined, sequence-consistent tool for benchmarking CD73-directed binders, as a positive control in binding and enzyme-inhibition assays, for epitope and cross-reactivity comparisons, for developing and validating anti-CD73 detection or capture assays, and as a reference in ADC-development and neutralization workflows. It supports both in-vitro cell-based studies and preclinical experimental design. The antibody is supplied unconjugated and can be offered as low-endotoxin, in-vivo-grade material (research grade typically <1 EU/mg; ultra-low <0.5 EU/mg) and in bulk milligram-to-gram quantities to support screening, formulation, and scale-dependent studies.
CD73, encoded by NT5E (UniProt P21589), is a GPI-anchored, homodimeric ecto-5'-nucleotidase expressed on many epithelial, endothelial, stromal, and immune cell populations. It catalyzes the dephosphorylation of extracellular AMP to adenosine and inorganic phosphate, acting as the terminal, rate-limiting step in the CD39/CD73 purinergic cascade that converts pro-inflammatory extracellular ATP into immunosuppressive adenosine. The adenosine generated signals through P1 receptors (notably A2A and A2B), dampening effector T-cell and NK-cell activity, promoting regulatory phenotypes, and contributing to an immunosuppressive tissue microenvironment. CD73 activity is frequently elevated in tumor and inflammatory settings, where extracellular adenosine accumulation supports immune evasion, angiogenesis, and tissue remodeling. Because of this role, CD73 is a widely studied node in tumor immunology and inflammation, and enzymatic inhibition or blockade of CD73 is a common experimental strategy for relieving adenosine-mediated immune suppression.