dresbuxelimab

A humanized monoclonal antibody targeting the ectoenzyme 5'-ecto-nucleotidase (cluster of differentiation 73; CD73; 5'-NT; ecto-5'-nucleotidase; NT5E), with potential immunomodulating, anti-viral and antineoplastic activities. Upon administration,dresbuxelimab targets and binds to CD73 on tumor cells, thereby inhibiting the activity of CD73. This prevents CD73-mediated conversion of extracellular adenosine monophosphate (AMP) to adenosine and the adenosine-mediated suppression of lymphocyte activity and trafficking. This increases the activity of cytotoxic T lymphocytes (CTLs), activates macrophages and reduces the activity of both myeloid-derived suppressor cells (MDSCs) and regulatory T lymphocytes (Tregs). By abrogating the inhibitory effect on the immune system and enhancing the CTL-mediated immune response against cancer cells, tumor cell growth is decreased. In addition, dresbuxelimab may stimulate the production of anti-SARS-CoV-2 antibodies from B cells which may lead to the rapid clearance of the virus. Also, by inhibiting CD73, extracellular ATP levels are increased, which induces the production of interferon-beta, and may enhance the cellular resistance to viral infection and may trigger apoptosis of virus-infected cells. CD73, a plasma membrane protein belonging to the 5'-nucleotidase (NTase) family, is upregulated on a number of cancer cell types and catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the tumor microenvironment (TME).