Inebilizumab is designed to bind to CD19, a cell surface molecule broadly expressed on B cells, initiating B cell depletion. This depletion stops autoreactive B cells from differentiating into antibody-secreting plasmablasts and plasma cells, which may decrease the production of pathogenic autoantibodies and therefore, the autoimmune response.
CD40/CD40L Co-stimulatory Pathway
VIB4920 is designed to bind to CD40L on activated T cells, blocking CD40L’s interaction with CD40-expressing B cells. Inhibiting CD40/CD40L interaction prevents B cells from differentiating into plasmablasts and plasma cells, potentially resulting in powerful immunomodulation for targeting T and B cell-driven autoimmune diseases.
Innate Cytokine Pathway
VIB7734 is designed to target and bind to ILT7—a cell surface molecule specific to plasmacytoid dendritic cells (pDCs)—causing apoptosis, or cell death. pDCs generate inflammatory cytokines, such as type I interferons, TNF-α and IL-6, in pathological states. As a result, the depletion of pDCs may decrease the production of inflammatory mediators involved in autoimmune diseases.