Autologous dual-target CAR-T cell therapy in which a patient’s T cells are engineered to express chimeric antigen receptors recognizing CD19 and CD20 on B cells, triggering CD3ζ-based signaling with costimulation to induce cytokine release and cytotoxic killing; dual targeting aims to limit antigen escape in B‑cell malignancies.
Autologous T cells are genetically engineered to express dual CARs recognizing CD19 and CD20 on B cells. Antigen engagement triggers CD3ζ signaling with costimulation, activating and expanding the T cells to secrete cytokines and mediate cytotoxic killing of malignant B cells; dual targeting is intended to limit antigen escape.
YES
DIRECT
CAR-T cells engineered to recognize CD19 are activated via CD3ζ/costimulatory signaling and directly kill CD19+ cells through perforin–granzyme cytolysis and death-receptor pathways.
Autologous dual-target CAR-T cell therapy in which a patient’s T cells are engineered to express chimeric antigen receptors recognizing CD19 and CD20 on B cells, triggering CD3ζ-based signaling with costimulation to induce cytokine release and cytotoxic killing; dual targeting aims to limit antigen escape in B‑cell malignancies.
Autologous T cells are genetically engineered to express dual CARs recognizing CD19 and CD20 on B cells. Antigen engagement triggers CD3ζ signaling with costimulation, activating and expanding the T cells to secrete cytokines and mediate cytotoxic killing of malignant B cells; dual targeting is intended to limit antigen escape.
YES
DIRECT
CAR-T cells recognize CD20 via the CAR, triggering CD3zeta/costimulatory signaling and T-cell effector functions (perforin/granzyme release and Fas–FasL interactions) to kill the target cell.
Patient-derived T cells genetically engineered to express a chimeric antigen receptor targeting BCMA (TNFRSF17); administered intravenously at 2–4 × 10^6 BCMA CAR+ T cells/kg to eliminate residual multiple myeloma via CAR-mediated T-cell cytotoxicity and cytokine release.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting BCMA; upon binding BCMA on myeloma/plasma cells, the CAR activates the T cells to deliver targeted cytotoxicity and cytokine release, killing BCMA-positive malignant cells and clearing residual disease.
YES
DIRECT
BCMA-specific CAR-T cells bind BCMA on target cells, become activated, and directly kill them via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, with supportive cytokine release.
A humanized anti-HER2 IgG1 monoclonal antibody that inhibits HER2 signaling and dimerization and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti-HER2 IgG1 monoclonal antibody that binds the HER2 extracellular domain, inhibits receptor dimerization and downstream MAPK/PI3K-AKT signaling, and mediates antibody-dependent cellular cytotoxicity (ADCC) by engaging immune effector cells against HER2-overexpressing tumor cells.
YES
DIRECT
Trastuzumab binds HER2 on tumor cells and engages Fcγ receptor–bearing immune cells (e.g., NK cells) to induce antibody-dependent cellular cytotoxicity; it may also contribute via complement activation and HER2 signaling blockade leading to apoptosis.
Oral small-molecule BH3-mimetic BCL-2 inhibitor that induces intrinsic apoptosis in BCL-2–dependent myeloma (notably t(11;14)).
Selective BH3-mimetic BCL-2 inhibitor that binds the hydrophobic groove of BCL-2, neutralizing its anti-apoptotic function and freeing pro-apoptotic proteins to activate BAX/BAK, induce mitochondrial outer membrane permeabilization, and trigger caspase-dependent intrinsic apoptosis. Spares BCL-XL, reducing thrombocytopenia risk. Particularly effective in BCL-2–dependent tumors such as t(11;14) multiple myeloma.
YES
DIRECT
Venetoclax binds and inhibits BCL-2, releasing pro-apoptotic BH3 proteins to activate BAX/BAK, cause mitochondrial outer membrane permeabilization, caspase activation, and intrinsic apoptosis of BCL-2–dependent cells.