Main
cancer, death, tumor, Cancer
CANCER, TUMOR, CANCER
Cancer immunotherapy targeting inhibitory molecules such as the programmed cell death receptor 1 (PD-1) or ligand 1 (L1) axis or cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) (collectively referred to as immune checkpoint molecules) has improved outcomes across many cancer typesCombination CPI targeting PD-1 and CTLA-4 appears to increase clinical benefit in some tumor typesLymphocyte activation gene-3 (LAG-3; CD223), a member of the immunoglobulin superfamily, is expressed on exhausted or dysfunctional T cellsLike PD-1, LAG-3 prevents anti-tumor T cell activity and contributes to T cell exhaustionBispecific molecules represent a novel approach to target multiple immune checkpoints simultaneouslyBuilding on a hypothesis that alleviation of compensatory resistance in the TME associated with the induction of PD-1, PD-L1 and LAG-3 may improve anti-tumor response, we describe here tebotelimab anti-tumor activity and biomarkers associated with tebotelimab activity across multiple clinical settings. We further outline the rationale for the combination of tebotelimab with margetuximab, a therapeutic anti-HER2 mAb engineered for increased Fc-mediated effector function