Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
Polyclonal rabbit IgG in Thymoglobulin binds CD25 on T cells, triggering complement-dependent cytotoxicity and Fc-mediated ADCC, and can induce apoptosis, depleting CD25+ cells.
Anti-CD47 monoclonal antibody (IgG4) that blocks the CD47–SIRPα 'don't‑eat‑me' signal to promote macrophage phagocytosis (ADCP) of tumor cells.
Humanized IgG4 anti-CD47 monoclonal antibody that blocks the CD47-SIRPalpha checkpoint, removing the 'don't-eat-me' signal to enable macrophage antibody-dependent cellular phagocytosis (ADCP) of tumor cells and stimulate downstream antitumor immune responses.
Anti-CD47 antibody blocks the CD47–SIRPα checkpoint and opsonizes CD47+ cells, enabling macrophage Fcγ receptor-mediated antibody-dependent cellular phagocytosis; secondary T-cell responses may also contribute.
Anti‑EGFR monoclonal antibody (IgG1) that inhibits EGFR signaling and mediates NK‑cell antibody‑dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream signaling (RAS/RAF/MEK/ERK and PI3K/AKT) and tumor proliferation. The IgG1 Fc also engages Fc gamma receptors on NK cells to mediate ADCC.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on effector cells (e.g., NK cells), inducing antibody-dependent cellular cytotoxicity (perforin/granzyme lysis; may also contribute via ADCP/CDC).
Universal (allogeneic) chimeric antigen receptor T cells engineered to target BCMA (TNFRSF17) to ablate BCMA-expressing plasmablasts and long‑lived plasma cells, aiming to reduce autoantibody production in lupus nephritis.
Allogeneic T cells engineered with a chimeric antigen receptor targeting BCMA (TNFRSF17) recognize and kill BCMA-expressing plasmablasts and long-lived plasma cells via CAR-mediated cytotoxicity, depleting antibody-secreting cells and reducing pathogenic autoantibody production in lupus nephritis.
BCMA-targeted CAR T cells recognize BCMA on plasmablasts/plasma cells and directly kill them via T-cell cytotoxicity (perforin/granzyme release and death-receptor–mediated apoptosis).
Universal (allogeneic) chimeric antigen receptor T cells targeting CD19 to deplete naïve, memory, and activated B cells, aiming to suppress humoral immunity in lupus nephritis.
Allogeneic gene-modified T cells expressing a CD19-directed chimeric antigen receptor bind CD19 on B-lineage cells and trigger cytotoxic killing (perforin/granzyme), depleting naive, memory, and activated B cells to suppress humoral immunity and reduce autoantibody production in lupus nephritis.
CD19 CAR-T cells bind CD19 on B cells and directly induce cytolysis via perforin/granzyme release (and death-receptor signaling), killing CD19+ cells.