Ecto-5′-nucleotidase (CD73)

Ecto-5′-nucleotidase (CD73) is a glycosylphosphatidylinositol (GPI)-anchored membrane-bound enzyme that catalyzes the hydrolysis of extracellular adenosine 5′-monophosphate (AMP) to adenosine and phosphate[5][1]. It is ubiquitously expressed, present on the surface of many cell types, and plays a key role in regulating extracellular adenosine levels, influencing immune modulation, inflammation, tissue barrier maintenance, and vascular function[5][9][8]. CD73 activity is crucial for the immunosuppressive function of regulatory T cells, limiting excessive inflammation and contributing to immune homeostasis[5]. Therapeutically, CD73 is an emerging target in oncology because extracellular adenosine generated by CD73 suppresses antitumor immunity; thus, its inhibition is being studied for cancer immunotherapy[2][9]. CD73 is also involved in cardiovascular and neuroprotective roles, and loss-of-function mutations cause a rare genetic disorder leading to vascular calcification[9]. Inhibition of CD73 or modulation of its activity must be balanced against its normal protective effects in tissue and barrier function and risk of vascular injury[8][9].

Other names

CD735′-nucleotidase5′-NTNT5E (gene symbol)Cluster of differentiation 73

Inhibition of enzymatic activity (prevents conversion of AMP to adenosine, reducing extracellular adenosine-mediated immunosuppression) or Increased extracellular adenosine (by enhancing CD73 activity or providing soluble nucleotidase)