Anti-HER2 IgG1 monoclonal antibody that inhibits HER2 signaling/dimerization and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting HER2 (ERBB2); binds the extracellular domain to inhibit HER2 dimerization/signaling and promote receptor downregulation, while engaging Fcγ receptors to mediate antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on tumor cells and its Fc engages Fc gamma receptors on immune effectors (e.g., NK cells, macrophages) to mediate antibody-dependent cellular cytotoxicity and phagocytosis, killing HER2+ cells; it also inhibits HER2 signaling.
Autologous, genetically engineered anti-CD19/CD20 chimeric antigen receptor (CAR) T-cell therapy; single IV infusion designed to deplete CD19+/CD20+ B cells to treat refractory autoimmune diseases.
Autologous T cells are genetically engineered to express a dual-target chimeric antigen receptor recognizing CD19 and CD20 on B cells. Upon antigen engagement, the CAR T cells become activated and mediate cytotoxic killing of CD19+/CD20+ B-lineage cells, leading to B-cell depletion and suppression of autoantibody-driven immune responses.
CD19-binding CAR T cells engage CD19 on B cells and induce cytolysis via immune-synapse–mediated perforin/granzyme release (and Fas–FasL apoptosis).
Autologous, genetically engineered anti-CD19/CD20 chimeric antigen receptor (CAR) T-cell therapy; single IV infusion designed to deplete CD19+/CD20+ B cells to treat refractory autoimmune diseases.
Autologous T cells are genetically engineered to express a dual-target chimeric antigen receptor recognizing CD19 and CD20 on B cells. Upon antigen engagement, the CAR T cells become activated and mediate cytotoxic killing of CD19+/CD20+ B-lineage cells, leading to B-cell depletion and suppression of autoantibody-driven immune responses.
Dual-target CAR T cells bind CD20 on B cells, become activated, and kill the bound cells via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis), depleting CD20+ cells.
Chimeric anti-CD20 monoclonal antibody given as 1000 mg IV infusion; depletes CD20+ B lymphocytes via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, reducing autoantibody production and pro-inflammatory signaling.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, reducing autoantibody production, antigen presentation, and pro-inflammatory signaling.
Binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC; can also induce apoptosis of target cells.
Human IgG1 anti–PD-L1 monoclonal antibody checkpoint inhibitor that blocks PD-L1 from binding PD-1/CD80 to restore cytotoxic T-cell activity and can engage NK cell ADCC.
Human IgG1 monoclonal antibody against PD-L1 that blocks PD-L1 interaction with PD-1/CD80, releasing checkpoint-mediated inhibition to restore cytotoxic T-cell activity; its Fc can engage NK cells to mediate ADCC against PD-L1-expressing tumor cells.
IgG1 Fc recruits NK cells via Fc gamma receptors to mediate ADCC against PD-L1–expressing cells; checkpoint blockade also restores CTL killing (indirect).