Autologous anti-CD19 CAR T-cell therapy that targets CD19+ B cells to mediate cytotoxic killing, administered after lymphodepletion.
Autologous T cells engineered with an anti‑CD19 chimeric antigen receptor containing CD3ζ signaling and a 4‑1BB co‑stimulatory domain; after infusion they recognize CD19 on B‑cell malignancies, become activated, expand, and kill CD19+ cells via T‑cell cytotoxic mechanisms.
YES
DIRECT
Anti-CD19 CAR T cells recognize CD19 on target cells and induce killing via T-cell cytotoxic mechanisms, primarily perforin/granzyme-mediated lysis and apoptosis (and Fas–FasL signaling).
Anti-CD20 monoclonal antibody that depletes B cells via ADCC and complement-dependent cytotoxicity.
Rituximab is a chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and induction of apoptosis/phagocytosis.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers killing via Fc-mediated ADCC and phagocytosis by immune effector cells, complement-dependent cytotoxicity (CDC), and can induce apoptosis upon crosslinking.
Intravenous type II glycoengineered anti-CD20 monoclonal antibody that induces direct B-cell death and enhances ADCC/ADCP.
Glycoengineered type II humanized IgG1 anti-CD20 monoclonal antibody that binds CD20 on malignant B cells and mediates cytotoxicity via enhanced Fc-gamma RIII–dependent ADCC and ADCP, and by inducing direct, largely caspase-independent apoptosis, leading to B-cell depletion.
YES
DIRECT
Binds CD20 on B cells, inducing direct (largely caspase-independent) apoptosis and recruiting Fc receptor–bearing effector cells to mediate ADCC and ADCP, leading to CD20+ cell killing.
Allogeneic natural killer cells genetically engineered to express a chimeric antigen receptor targeting CD19; CAR engagement activates NK cytotoxic pathways to kill CD19-positive B-cell malignancies.
Allogeneic natural killer cells engineered to express an anti-CD19 chimeric antigen receptor bind CD19 on B cells, activating NK cytotoxic pathways (perforin/granzyme release and cytokine-mediated killing) to selectively lyse CD19-positive malignant cells; some designs include inhibitory signaling to reduce off-tumor effects.
YES
DIRECT
Anti-CD19 CAR NK cells bind CD19 on target cells and trigger NK effector functions, causing perforin/granzyme-mediated cytolysis (and death receptor pathways) of CD19+ cells.
Intravenous bispecific monoclonal antibody (T‑cell engager) that binds BCMA on plasma cells and CD3 on T cells, redirecting T‑cell cytotoxicity to deplete pathogenic plasma cells and reduce amyloidogenic light‑chain production in systemic AL amyloidosis. Also known as REGN5458; brand name Lynozyfic.
Bispecific monoclonal antibody that binds BCMA on plasma cells and CD3 on T cells, redirecting T‑cell cytotoxicity to deplete BCMA+ plasma cells and reduce amyloidogenic light‑chain production in AL amyloidosis.
YES
DIRECT
The bispecific antibody binds BCMA on target cells and CD3 on T cells, creating an immune synapse that redirects T-cell cytotoxicity (perforin/granzyme-mediated apoptosis) to kill BCMA+ cells.