Background: In the tumor microenvironment (TME), the endonucleotidase CD73 catalyzes the final
step in ATP hydrolysis, generating adenosine (ADO) from adenosine monophosphate (AMP).
Extracellular ADO suppresses immune function through activation of A2aR and A2bR receptors expressed on a variety of immune cells. Inhibition of CD73 eliminates
a major, non-redundant, pathway of ADO production in the TME, thereby limiting immune
suppression. Here we describe the ability of AB680, a small molecule CD73 inhibitor,
to potentiate the activity of immune checkpoint inhibitors (ICI) in immune function
assays.
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P04.03
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© 2018 Published by Elsevier Inc.
