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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
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.
NO
INDIRECT
Linvoseltamab engages CD3ε on T cells to activate them and bridge to BCMA+ myeloma cells; the activated T cells kill BCMA-expressing tumor cells via perforin/granzyme. CD3ε-expressing T cells are not killed.
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.
YES
DIRECT
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.