CLEC7A (Dectin-1) on myeloid cells (plus tumor antigen)

Class

Bispecific myeloid cell-engaging antibody (phagocytosis-inducing bispecific)

Pathway

Binds CLEC7A/Dectin-1, a phagocytic receptor on myeloid cells, together with a tumor antigen, inducing antigen-restricted myeloid cell activation and tumor cell depletion while limiting systemic cytokine release/neurotoxicity risk

CLEC7A, also called Dectin-1, is a receptor found on myeloid cells such as macrophages, dendritic cells, and neutrophils. It normally functions as part of the innate immune system, recognizing sugar patterns on pathogens like fungi and triggering the cells to engulf and destroy them, a process called phagocytosis. This mechanism uses a bispecific antibody, a molecule built to bind two different targets at once, to link CLEC7A on a myeloid cell with an antigen displayed on a tumor cell. By bridging the two, the antibody redirects the myeloid cell's natural engulfing and destructive machinery toward the tumor, rather than requiring T cells, which many tumors evade by suppressing antigen presentation or excluding T cells from the tumor site. This approach is being explored in cancers where T cell-based immunotherapies are less effective. A key design goal of such myeloid engagers is to activate immune cells specifically where both the receptor and tumor antigen are present, which is intended to reduce the widespread cytokine release and neurological side effects sometimes seen with T cell-engaging antibodies. The broader rationale is to harness an underused arm of the immune system, innate myeloid cells, as an additional route to tumor clearance.