Anti-CD20 chimeric monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity (CDC), recruits FcγR+ effector cells for antibody-dependent cellular cytotoxicity/phagocytosis (ADCC/ADCP), and can trigger apoptosis of the target cells.
Autologous chimeric antigen receptor (CAR) T-cell therapy engineered from a patient’s T cells to express a CAR targeting LGR5, leading to antigen-dependent T-cell activation and cytotoxic killing of LGR5-positive tumor cells; administered as a single IV infusion after lymphodepleting chemotherapy with dose levels ranging from 2.5×10^7 to 1.5×10^9 cells.
Autologous T cells engineered to express a chimeric antigen receptor specific for LGR5; CAR engagement of LGR5 on tumor cells triggers antigen-dependent T-cell activation and cytotoxic killing of LGR5-positive cancer cells.
LGR5-specific CAR T cells bind LGR5 on target cells, become activated, and kill LGR5-positive cells via T-cell cytotoxic pathways (perforin/granzyme release and Fas/FasL-mediated apoptosis).
Humanized anti-HER2 IgG1 monoclonal antibody that binds HER2, inhibits HER2 signaling, and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody against HER2 that binds the extracellular domain, inhibits HER2 signaling and dimerization, promotes receptor internalization, and engages immune effector cells to mediate ADCC against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on target cells and recruits Fcγ receptor–bearing immune effectors (e.g., NK cells) to mediate ADCC, leading to target-cell lysis; it also inhibits HER2 signaling, promoting apoptosis.
An intravenous bispecific T‑cell–engager monoclonal antibody that binds BCMA on malignant plasma cells and CD3 on T cells to redirect T‑cell cytotoxicity against myeloma.
Bispecific monoclonal antibody that binds BCMA on malignant plasma cells and CD3 on T cells, bringing T cells into proximity to activate CD3/TCR signaling, form an immune synapse, and induce perforin/granzyme-mediated cytotoxic killing of BCMA-positive myeloma cells.
Bispecific T-cell engager bridges BCMA on target cells and CD3 on T cells, activating T cells to form an immune synapse and release perforin/granzymes to kill BCMA-positive cells.
Subcutaneous CD20xCD3 T-cell–engaging bispecific monoclonal antibody that bridges CD20 on malignant B cells and CD3 on T cells to redirect cytotoxic T cells and deplete B cells.
Humanized bispecific monoclonal antibody that binds CD20 on B cells and CD3 on T cells to crosslink them, activate cytotoxic T cells, and drive targeted killing and depletion of CD20-expressing malignant B cells.
Mosunetuzumab bridges CD20 on B cells to CD3 on T cells, activating T cells to release perforin/granzymes and induce apoptosis of CD20+ target cells.