Anti-CD20 chimeric monoclonal antibody that depletes malignant B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes CD20-positive B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity/phagocytosis, and direct induction of apoptosis.
Rituximab binds CD20 on B cells and induces killing via complement-dependent cytotoxicity (membrane attack complex) and Fc-mediated ADCC/ADCP by NK cells and macrophages; it can also directly trigger apoptosis upon CD20 crosslinking.
An intravenously administered, third-generation self-inactivating lentiviral gene therapy vector that transduces autologous T cells in vivo to express an anti-BCMA chimeric antigen receptor, resulting in in vivo–generated CAR-T cells that target BCMA (TNFRSF17) on myeloma cells.
An intravenously delivered, self-inactivating third-generation lentiviral vector that transduces patients' autologous T cells in vivo to express an anti-BCMA chimeric antigen receptor; the resultant in vivo–generated CAR-T cells recognize BCMA (TNFRSF17) on myeloma cells and induce T-cell activation and cytotoxic killing.
The lentiviral vector generates anti-BCMA CAR-T cells in vivo; these CAR-T cells bind BCMA on target cells and kill them via T-cell cytotoxic mechanisms (perforin/granzyme-mediated apoptosis, etc.).
Patient-derived T cells that are transduced in vivo by ESO-T01 to express an anti-BCMA CAR; these CAR-T cells recognize BCMA (TNFRSF17) on multiple myeloma cells and mediate T-cell activation and cytotoxicity.
Patient T cells are transduced in vivo by a lentiviral vector (ESO-T01) to express an anti-BCMA chimeric antigen receptor. The resulting autologous CAR-T cells recognize BCMA (TNFRSF17) on multiple myeloma cells, leading to T‑cell activation, cytokine release, proliferation, and targeted cytotoxic killing of BCMA-expressing tumor cells.
CAR-T cells bind BCMA on target cells, activating cytotoxic T-cell responses that kill targets via perforin/granzyme-mediated apoptosis (and Fas/FasL).
Autologous T cells engineered to express a chimeric antigen receptor targeting BCMA (TNFRSF17) on plasma cells, activating T-cell cytotoxicity to eliminate malignant plasma cells in multiple myeloma.
Autologous T cells are engineered to express a chimeric antigen receptor that binds BCMA (TNFRSF17) on malignant plasma cells; CAR engagement activates T-cell signaling and cytotoxic effector functions (perforin/granzyme release, cytokines) to eliminate multiple myeloma cells.
CAR T cells bind BCMA on target cells, forming an immune synapse and inducing perforin/granzyme-mediated apoptosis (and Fas/FasL-mediated killing).
Autologous T cells engineered to express a chimeric antigen receptor targeting GPRC5D, a GPCR highly expressed on plasma cells, to drive antigen-specific T-cell cytotoxicity against malignant plasma cells.
Autologous T cells engineered with a chimeric antigen receptor that recognizes GPRC5D on plasma cells; antigen binding triggers CAR signaling (CD3ζ with costimulatory domains) to activate T-cell cytotoxicity, cytokine release, and clonal expansion, leading to targeted lysis of GPRC5D-expressing malignant plasma cells.
CAR-T cells bind GPRC5D, triggering CAR signaling (CD3ζ + costimulation) and T-cell effector functions that lyse target cells via perforin/granzyme release and Fas–FasL apoptosis.