CD20×CD3 bispecific T-cell–engaging antibody that activates T cells to target and eliminate CD20-positive B cells.
Bispecific humanized antibody that binds CD20 on B cells and CD3 on T cells, cross-linking them to activate and redirect T cells to kill CD20-positive B cells via immune synapse formation and cytotoxic effector functions.
Mosunetuzumab binds CD20 on target cells and CD3 on T cells, bringing them together to form an immune synapse and activate T cells to kill CD20+ cells via perforin/granzyme-mediated cytotoxicity.
Anti-HER2 antibody–drug conjugate delivering the topoisomerase I inhibitor DXd.
Humanized anti-HER2 monoclonal antibody linked to the topoisomerase I inhibitor DXd. Binds HER2 on tumor cells, is internalized, and releases DXd to inhibit Top1–DNA complexes, causing DNA damage, replication blockade, cell-cycle arrest, and apoptosis; also mediates ADCC and exerts a bystander killing effect due to a membrane-permeable payload.
ADC binds HER2, is internalized, and releases the topoisomerase I inhibitor DXd, causing DNA damage and apoptosis; it also triggers ADCC and can induce bystander killing via a membrane-permeable payload.
Fresh donor-derived, second-generation CD19-directed CAR T cells (lentiviral-transduced) that express a CAR with CD3ζ and a costimulatory domain to recognize CD19 on B cells, leading to T-cell activation, proliferation, cytotoxic killing of CD19+ cells, and expected B-cell aplasia.
Allogeneic, lentiviral-transduced T cells engineered with a second-generation anti-CD19 CAR (CD3z plus a costimulatory domain) recognize CD19 on B cells, leading to T-cell activation, proliferation, and cytotoxic killing of CD19+ cells, with expected on-target B-cell aplasia.
Anti-CD19 CAR T cells recognize CD19 via the CAR and directly kill CD19+ cells through T-cell effector mechanisms (perforin/granzyme and Fas–FasL), leading to on-target B-cell aplasia.
Anti-CD20 monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Anti-CD20 chimeric monoclonal IgG1 that binds CD20 on pre-B and mature B cells and depletes them via Fc-mediated antibody-dependent cellular cytotoxicity and phagocytosis, complement-dependent cytotoxicity, and direct induction of apoptosis.
Anti-CD20 antibody binds CD20 on B cells and triggers Fc-mediated ADCC and phagocytosis, complement-dependent cytotoxicity, and can induce apoptosis of the target cells.
Autologous, gene-edited CD19-directed CAR T-cell therapy with a CD28 costimulatory domain and a 1XX ITAM-modulated CD3ζ chain; the CAR is inserted into the TRAC locus to knock out the endogenous TCR, standardize CAR expression, and reduce tonic signaling/GvHD risk; designed to eliminate CD19+ malignant B cells and enhance persistence while limiting exhaustion.
Autologous T cells are gene-edited to insert a CD19-targeted CAR with CD28 costimulation and a 1XX-modified CD3zeta activation domain into the TRAC locus, knocking out the endogenous TCR. Upon infusion, the cells bind CD19 on B cells, trigger CAR-mediated activation and cytotoxicity, and eliminate malignant B cells. TRAC integration reduces tonic signaling and GvHD risk and standardizes CAR expression, while the 1XX ITAM design tempers signaling to limit exhaustion and improve persistence.
Anti-CD19 CAR T cells bind CD19 on target cells and induce T cell–mediated killing via perforin/granzyme release and death receptor–mediated apoptosis.