Among the next generation of cancer immune therapeutics, the CD73/CD39 axis constitutes one of the most promising pathways targeting the tumor microenvironment to potentially complement other immuno-oncology approaches.

CD73 and CD39 are two enzymes degrading adenosine triphosphate (ATP) into adenosine. CD73 is active on the last step of the degradation pathway and thereby plays a major role in promoting immunosuppression. Ecto-5′-nucleotidase (CD73) is considered as a key molecule, because the degradation of AMP into adenosine has a strong impact on the tumor microenvironment by generation of an immunosuppressed and pro-angiogenic niche that promotes progression of cancer.

Blockade of CD73 function has been shown to strongly reduce AMP catabolism and efficiently reverse adenosine-mediated T cell suppression in vitro. In preclinical studies targeting CD73 has resulted in favorable antitumor effects, encouraging studies on combined treatment with first generation checkpoint blockers targeting CTLA-4 and PD-1.

We develop and validate anti-CD73 monoclonal antibodies for immunohistochemistry of routine fixed FFPE tissue to allow careful analysis of CD73 expression within the histological and morphological context of a certain tumor. We believe that a monoclonal antibody against CD73 has a high value to understand the diagnostic potential of this novel biomarker as a prerequisite to better guide personalized cancer therapy.