Autologous anti-CD19 CAR T-cell therapy that redirects patient T cells to kill CD19-positive B-cell malignancies.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor with CD28 costimulation and CD3ζ signaling. After infusion, CAR engagement of CD19 on B cells activates T-cell effector functions (proliferation, cytokine release, cytotoxicity) leading to selective killing of CD19-positive malignant B cells.
Anti-CD19 CAR T cells bind CD19 and directly kill CD19+ cells via T‑cell cytotoxic mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis).
Autologous anti-CD19 CAR T-cell therapy used to target and eliminate CD19-positive malignant B cells.
Autologous T cells engineered via lentiviral transduction to express an anti-CD19 chimeric antigen receptor with 4-1BB costimulatory and CD3-zeta signaling domains; upon infusion, they recognize CD19 on B cells, activate, proliferate, and kill CD19-positive malignant B cells.
Anti-CD19 CAR T cells recognize CD19 on target cells, become activated, and kill CD19+ cells via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis.
Autologous anti-CD19 CAR T-cell therapy directed against CD19-positive B-cell malignancies.
Autologous CD4+/CD8+ T cells engineered with a lentiviral anti-CD19 CAR (scFv–4-1BB–CD3ζ) that recognize CD19 on B-cell malignancies and induce cytotoxic killing; 4-1BB costimulation enhances expansion and persistence; truncated EGFR enables in vivo tracking and potential elimination with cetuximab.
Anti-CD19 CAR T cells recognize CD19 on target cells and kill them via T‑cell effector mechanisms (perforin/granzyme-mediated cytolysis and apoptosis, e.g., Fas–FasL).
Intravenous bispecific monoclonal antibody that binds CD20 on B cells and CD3 on T cells to engage endogenous T cells to kill CD20-positive B cells.
Humanized bispecific monoclonal antibody that binds CD20 on B cells and CD3 on T cells, cross-linking T cells to CD20+ B cells to activate cytotoxic T-cell responses and induce targeted lysis of malignant B cells.
Mosunetuzumab bridges CD20 on B cells and CD3 on T cells, activating T cells to form immune synapses and kill CD20+ cells via perforin/granzyme-mediated cytotoxicity (and Fas–FasL).
Intravenous anti-CD79b antibody–drug conjugate that delivers the microtubule inhibitor MMAE to CD79b-positive B cells.
Anti-CD79b monoclonal antibody delivers the cytotoxic payload MMAE to CD79b-positive B cells. After binding and internalization, proteolytic cleavage releases MMAE, which inhibits tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis.
The anti-CD79B ADC binds CD79B, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of the target cell.