While PVRIG and TIGIT were totally new targets and pathways upon discovery. With COM503 we are targeting a known pathway in a completely unique way with a potential first-in-class therapeutic candidate.

We identified a potential dominant immunosuppressive mechanism which is used by macrophages in tumors to escape the immune system. This is the “interleukin-18 binding protein and interleukin-18 complex”. The inflammasome-induced pro-inflammatory cytokine, interleukin-18, is present at high levels in the tumor microenvironment, where it is expected to naturally activate anti-tumor effector cells, such as T and NK cells. But IL-18 is one of the rare cytokines that is naturally blocked by an endogenous high affinity inhibitor, called IL-18 binding protein.

COM503, potential first-in-class therapeutic candidate, targets IL-18 binding protein to release endogenous, naturally occurring interleukin-18 to activate T and NK cells, in the tumor microenvironment.

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