5'-nucleotidase ecto (CD73) (CD73)

5'-nucleotidase ecto (CD73) is a glycosylphosphatidylinositol (GPI)-anchored cell-surface enzyme that catalyzes the conversion of extracellular adenosine monophosphate (AMP) into adenosine (UniProt, 2024; NIH, 2023). This reaction represents the rate-limiting step in the extracellular purinergic signaling pathway, which regulates the balance between pro-inflammatory ATP and immunosuppressive adenosine (NIH, 2024). In the tumor microenvironment, CD73 is frequently overexpressed by both malignant and stromal cells, leading to an accumulation of adenosine that suppresses the activity of cytotoxic T cells and natural killer (NK) cells via A2A and A2B receptors (Frontiers, 2020; NIH, 2023). Consequently, CD73 has become a major target in immuno-oncology, with several monoclonal antibodies and small-molecule inhibitors designed to block its enzymatic active site and restore anti-tumor immunity (ACS, 2025; NIH, 2024). Beyond cancer, CD73 plays essential roles in maintaining vascular barrier function, regulating inflammation, and protecting tissues from ischemic injury (NIH, 2021; Frontiers, 2024). Therapeutic challenges include potential autoimmune side effects and the risk of arterial calcification associated with long-term CD73 deficiency (Frontiers, 2024).

Other names

Ecto-5'-nucleotidaseNT5E5'-NTeNeNTCluster of differentiation 73

Inhibition of the enzymatic activity of CD73 to prevent the conversion of extracellular adenosine monophosphate (AMP) into immunosuppressive adenosine, thereby reversing immune evasion in the tumor microenvironment.