OSE Immunotherapeutics SA announced the publication of data in the peer-reviewed journal Science Advances on a first-in-classpreclinical program with CLEC-1, its novel myeloid immune checkpoint target for cancer immunotherapy. Overall, CLEC-1 genetic deletion leads to a profound reinvigoration of the tumor immune microenvironment by enhancing infiltrates of dendritic cell (antigen presenting cells), increasing memory and activated T lymphocyte infiltrates, decreasing infiltrates of exhaustion marker PD1-expressing T lymphocytes and limiting the recruitment of immunosuppressive cells such as myeloid derived suppressor cells (MDSCs). - Importantly, CLEC-1 blockade using monoclonal antibody treatment demonstrates robust anti-tumor activity, also by reinvigorating the tumor immune microenvironment in several preclinical oncology models, thereby faithfully recapitulating the effect of CLEC-1 genetic deletion in the context of human CLEC-1-expressing mice.

Proprietary anti-CLEC-1 mAbs increase survival in monotherapy in orthotopic model of hepatocellular carcinoma while combination with chemotherapy increases preclinical tumor eradication in colon carcinoma model.