Compugen Ltd. announced the online publication of preclinical data demonstrating the role of PVRIG as a novel immune checkpoint and the potential of COM701, Compugen's first-in-class inhibitory antibody targeting PVRIG, to serve as an effective cancer immunotherapy. The findings were published in two peer-reviewed papers in Cancer Immunology Research, an American Association for Cancer Research publication. Both papers were co-authored by Compugen's scientists in collaboration with scientists from Johns Hopkins University School of Medicine, headed by Drew Pardoll, M.D., Ph.D., Abeloff Professor of Oncology, Medicine, Pathology, and Molecular Biology and Genetics at Johns Hopkins University, School of Medicine, and Director of the Bloomberg~Kimmel Institute for Cancer Immunotherapy and Co-Director of the Cancer Immunology Program at the Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins, and Chairman of Compugen'sScientific Advisory Board. The paper entitled 'PVRIG and PVRL2 are induced in cancer and inhibit CD8+ T cell function' demonstrates increased expression of PVRIG and its ligand, PVRL2, in multiple tumor types, including in tumors that are PD-L1 negative and therefore less likely to respond to PD-1 pathway inhibition. In particular, PVRIG pathway expression appears to be dominant in ovarian, endometrial, and breast cancers. The study further demonstrates the parallel inhibitory roles of PVRIG and TIGIT in the DNAM signaling axis, and that dual targeting of the two results in synergistic activation of CD8+ effector T cells, suggesting an opportunity for effective clinical combinations of COM701 with anti-TIGIT antibodies. In addition, the findings also show the combination potential of COM701 with PD-1 inhibitors, which served as a key component in designing ongoing Phase 1 study combination of COM701 with Opdivo®. These results were further supported by mouse data published in the paper entitled 'Mouse PVRIG has CD8+ T-cell-specific co-inhibitory functions,' showing that mice lacking PVRIG have increased anti-tumor T cell activity, and that tumor growth in these mice is reduced relative to wild-type mice. This tumor growth reduction is further enhanced in combination with TIGIT blockade, demonstrating in vivo the parallel inhibitory roles of PVRIG and TIGIT in the DNAM signaling axis. Consistent with the finding in human systems, blocking both the PVRIG and the PD-1 pathways in mice also reduces tumor growth, providing an additional line of evidence for the therapeutic potential of the clinical combination of COM701 with Opdivo®.