An afucosylated human IgG1 monoclonal antibody that binds the BAFF receptor (BAFF-R/TNFRSF13C) on B cells, blocking BAFF/BLyS survival signaling and enhancing ADCC to deplete B cells; administered subcutaneously (e.g., 300 mg monthly).
Afucosylated human IgG1 monoclonal antibody targeting BAFF receptor (BAFF‑R/TNFRSF13C) on B cells; blocks BAFF/BLyS survival signaling and enhances FcγR-mediated ADCC, leading to depletion of BAFF‑R–expressing B cells and reduced autoantibody production.
Afucosylated IgG1 binds BAFF-R on B cells and engages Fcγ receptors on NK cells/macrophages to induce ADCC/ADCP, depleting BAFF-R+ cells; BAFF signaling blockade may also promote apoptosis.
Recombinant bispecific monoclonal antibody targeting CD38 and CD47; blocks the CD47–SIRPα checkpoint to enhance macrophage-mediated phagocytosis and engages CD38 on malignant plasma/B cells to mediate ADCC and CDC; administered intravenously weekly (0.01–6 mg/kg).
Bispecific monoclonal antibody targeting CD47 and CD38. By blocking the CD47-SIRPa checkpoint it promotes macrophage-mediated phagocytosis of tumor cells, and by binding CD38 on malignant plasma/B cells it engages Fc effector functions to induce ADCC and complement-dependent cytotoxicity, leading to depletion of CD38-positive tumor cells and relief of immunosuppression.
By binding CD38 on target cells, the antibody engages Fc effector functions to trigger NK cell–mediated ADCC, complement-dependent cytotoxicity (CDC), and antibody-dependent phagocytosis; CD47 blockade further enhances macrophage phagocytosis of CD38+ cells.
Allogeneic T cells engineered with an anti-CD7 chimeric antigen receptor to selectively eliminate CD7-expressing lymphocytes (T cells and some NK cells), providing deep lymphodepletion and immunosuppression prior to transplant in severe aplastic anemia.
Allogeneic donor T cells are genetically engineered to express an anti-CD7 chimeric antigen receptor. Upon binding CD7 on T cells (and some NK cells), the CAR redirects cytotoxic killing to deplete CD7-positive lymphocytes, inducing deep lymphodepletion and immunosuppression to remove autoreactive T cells and facilitate engraftment prior to allo-HSCT in severe aplastic anemia.
Anti-CD7 CAR-T cells bind CD7 on target lymphocytes, become activated, and kill via cytolytic degranulation (perforin/granzyme) and death-receptor pathways (e.g., Fas/FasL), inducing apoptosis of CD7+ cells.
Allogeneic unmodified invariant natural killer T (iNKT) cell therapy; iNKT cells recognize glycolipid antigens via CD1d, secrete Th1 cytokines, and activate NK cells, CD8 T cells, and macrophages to kill tumor and remodel the tumor microenvironment.
Allogeneic, unmodified invariant NKT cells that recognize CD1d-presented glycolipid antigens and stress ligands via invariant TCR and NKG2D, secrete Th1 cytokines (e.g., IFN-γ), activate NK cells, CD8 T cells, and macrophages, and directly lyse tumor cells to remodel the tumor microenvironment.
iNKT cells recognize the CD1d–glycolipid complex via their invariant TCR and directly kill the presenting cell by releasing cytotoxic granules (perforin/granzyme) and engaging death-receptor pathways.
Allogeneic unmodified invariant natural killer T (iNKT) cell therapy; iNKT cells recognize glycolipid antigens via CD1d, secrete Th1 cytokines, and activate NK cells, CD8 T cells, and macrophages to kill tumor and remodel the tumor microenvironment.
Allogeneic, unmodified invariant NKT cells that recognize CD1d-presented glycolipid antigens and stress ligands via invariant TCR and NKG2D, secrete Th1 cytokines (e.g., IFN-γ), activate NK cells, CD8 T cells, and macrophages, and directly lyse tumor cells to remodel the tumor microenvironment.
iNKT cells in AgenT-797 express NKG2D, which binds MICA on target cells and triggers direct cytotoxic degranulation (perforin/granzymes) leading to apoptosis; Th1 cytokines further enhance killing.