Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and induces complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and kills via complement-dependent cytotoxicity and Fc-mediated ADCC (engaging NK cells/macrophages), with additional direct apoptosis upon CD20 crosslinking.
Polyclonal antibody preparation that depletes T lymphocytes for induction immunosuppression.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional T-cell apoptosis and functional inhibition, producing potent immunosuppression.
ATG antibodies bind CD11a on T cells and induce complement-dependent lysis and Fc-mediated ADCC, with additional apoptosis, directly depleting CD11a+ cells.
Chimeric IgG monoclonal antibody against EGFR that blocks ligand binding and downstream MAPK/PI3K signaling.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization/activation, thereby inhibiting downstream MAPK and PI3K signaling and tumor cell proliferation.
Cetuximab binds EGFR on target cells and engages Fcγ receptors on immune effectors to mediate ADCC (and some CDC), leading to lysis; it also blocks EGFR signaling (cytostatic).
An autologous, fully human, dual-target CAR-T cell therapy engineered to recognize BCMA (TNFRSF17) and GPRC5D on malignant plasma cells; administered as a single infusion at approximately 1–6 × 10^5 CAR-T cells/kg. Binding to targets triggers CAR signaling, activating T-cell cytotoxicity and cytokine release to lyse tumor cells.
Autologous dual-target CAR-T cells engineered to recognize BCMA and GPRC5D on malignant plasma cells. Antigen binding activates CAR signaling, leading to T-cell activation, proliferation, cytokine release, and cytotoxic killing of tumor cells, aiming to overcome antigen escape via dual targeting.
BCMA recognition by the dual-target CAR on T cells triggers T‑cell activation and cytolytic killing of BCMA+ cells via perforin/granzyme release (and Fas/FasL), with supportive cytokine-mediated effects.
An autologous, fully human, dual-target CAR-T cell therapy engineered to recognize BCMA (TNFRSF17) and GPRC5D on malignant plasma cells; administered as a single infusion at approximately 1–6 × 10^5 CAR-T cells/kg. Binding to targets triggers CAR signaling, activating T-cell cytotoxicity and cytokine release to lyse tumor cells.
Autologous dual-target CAR-T cells engineered to recognize BCMA and GPRC5D on malignant plasma cells. Antigen binding activates CAR signaling, leading to T-cell activation, proliferation, cytokine release, and cytotoxic killing of tumor cells, aiming to overcome antigen escape via dual targeting.
CAR-T cells recognize GPRC5D on target cells and, upon engagement, kill them via T-cell cytotoxic pathways (perforin/granzyme and Fas–FasL), causing apoptotic/lytic death.