Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement- and Fc-mediated cytotoxicity and apoptosis, reducing B-cell receptor signaling, autoantibody production, and ectopic germinal center activity.
Chimeric anti-CD20 monoclonal IgG1 that binds CD20 on pre-B and mature B cells and depletes them via complement-dependent cytotoxicity, Fc-mediated ADCC, and apoptosis, reducing B-cell receptor signaling and autoantibody production.
Rituximab binds CD20 on B cells, triggering complement-dependent cytotoxicity and Fc-mediated ADCC by effector cells, and can directly induce apoptosis of CD20+ cells.
Engineered allogeneic cord blood–derived natural killer cells expressing an HLA-A*02:01–restricted T-cell receptor specific for PRAME to enable antigen-specific recognition and cytotoxic killing of PRAME-positive myeloid blasts.
Allogeneic cord blood-derived NK cells engineered to express an HLA-A*02:01-restricted T-cell receptor specific for PRAME. The TCR recognizes PRAME peptide-HLA-A*02:01 complexes on tumor cells, leading to antigen-specific NK activation and cytotoxic lysis (perforin/granzyme) of PRAME-positive myeloid blasts.
TCR-engineered NK cells recognize PRAME peptide–HLA-A*02:01 complexes on target cells and directly kill them via perforin/granzyme-mediated cytolysis.
Autologous T cells engineered to express a tri-specific chimeric antigen receptor targeting CD19, CD20, and CD22; CAR engagement triggers CD3ζ signaling, T-cell activation, cytokine release, and cytotoxic killing to eliminate malignant B cells and reduce antigen escape.
Autologous T cells engineered with a tri-specific CAR targeting CD19, CD20, and CD22; antigen binding triggers CD3zeta and costimulatory signaling to activate the T cell, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of malignant B cells, with multi-antigen targeting designed to reduce antigen escape.
CAR T cells recognize CD19 on target cells; CAR signaling activates T-cell cytotoxicity, causing perforin/granzyme-mediated apoptosis (and death-receptor killing) of CD19+ cells.
Autologous T cells engineered to express a tri-specific chimeric antigen receptor targeting CD19, CD20, and CD22; CAR engagement triggers CD3ζ signaling, T-cell activation, cytokine release, and cytotoxic killing to eliminate malignant B cells and reduce antigen escape.
Autologous T cells engineered with a tri-specific CAR targeting CD19, CD20, and CD22; antigen binding triggers CD3zeta and costimulatory signaling to activate the T cell, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of malignant B cells, with multi-antigen targeting designed to reduce antigen escape.
CAR T cells bind CD20 via the CAR, triggering CD3ζ/co-stimulatory signaling and T‑cell cytotoxicity (perforin/granzyme-mediated killing) of CD20+ cells.
Autologous T cells engineered to express a tri-specific chimeric antigen receptor targeting CD19, CD20, and CD22; CAR engagement triggers CD3ζ signaling, T-cell activation, cytokine release, and cytotoxic killing to eliminate malignant B cells and reduce antigen escape.
Autologous T cells engineered with a tri-specific CAR targeting CD19, CD20, and CD22; antigen binding triggers CD3zeta and costimulatory signaling to activate the T cell, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of malignant B cells, with multi-antigen targeting designed to reduce antigen escape.
CAR T cells bind CD22 on target cells, activating CD3zeta/costimulatory signaling and inducing cytotoxic degranulation (perforin/granzyme-mediated apoptosis; also death-receptor pathways) to kill the cells.