CD73 also known as ecto-5'-nucleotidase, or Ecto5'NTase, is a membrane-bound/free protein that can hydrolyze AMP to adenosine. Adenosine inhibits the tumor immune response through interaction with the adenosine receptors, or P1 receptors, on the cell surface. CD73 is often highly expressed and indicative of a poor prognosis in various tumor tissues, including gastric cancer, renal cell carcinoma, prostate cancer, triple negative breast cancer, and non-small cell adenocarcinoma.

JAB-BX102 specifically binds to CD73 and blocks its extracellular-5'-nucleotidase activity. This decreases the production of adenosine and consequently relieves the inhibitory effects of adenosine on the proliferation and tumor killing activity of CD8+ T cells. This modulation effectively enhances the anti-tumor immune response in the tumor microenvironment. Tumor immunotherapy represented by PD-(L)1 antibodies, has been widely used in clinical practice, but with its wide application, it also exposes defects such as limited response rate. Adenosine pathway activation is one of the important reasons for the low response rate of PD-(L)1 treatment. Therefore, the combination of CD73 monoclonal antibody and PD-(L)1 monoclonal antibody is expected to further improve the therapeutic effects of immune therapy.

CD73 is over-expressed in many malignant tumors, including melanoma, triple negative breast cancer, non-small cell lung cancer, renal cell carcinoma, bladder cancer, prostate cancer, gastric cancer, colorectal cancer, ovarian cancer, and malignant glioma. Preliminary clinical results of other CD73 inhibitors suggest that it has potential clinical efficacy in non-small cell lung cancer, triple negative breast cancer, renal cell carcinoma, and other solid tumors.