A half-life–extended bispecific T‑cell engager (BiTE) antibody construct that binds DLL3 on tumor cells and CD3 on T cells to redirect cytotoxic T cells, inducing tumor cell lysis and cytokine release; administered subcutaneously.
A half-life–extended bispecific T-cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells, redirecting and activating cytotoxic T lymphocytes to form an immune synapse and induce perforin/granzyme-mediated lysis and cytokine release against DLL3-expressing tumor cells.
YES
DIRECT
Tarlatamab bridges CD3+ T cells to DLL3-expressing cells, forming an immune synapse and activating CTLs to kill target cells via perforin/granzyme-mediated cytolysis and apoptosis.
A half-life–extended bispecific T‑cell engager (BiTE) antibody construct that binds DLL3 on tumor cells and CD3 on T cells to redirect cytotoxic T cells, inducing tumor cell lysis and cytokine release; administered subcutaneously.
A half-life–extended bispecific T-cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells, redirecting and activating cytotoxic T lymphocytes to form an immune synapse and induce perforin/granzyme-mediated lysis and cytokine release against DLL3-expressing tumor cells.
NO
INDIRECT
Tarlatamab binds CD3 on T cells to recruit and activate them against DLL3-expressing tumor cells; the T cells then kill DLL3+ targets via perforin/granzyme after immune synapse formation, not the CD3+ cells.
Patient-derived T cells engineered ex vivo to express a chimeric antigen receptor targeting CD19, then infused intravenously to ablate CD19+ B-lineage cells (naive/memory B cells and plasmablasts), producing B-cell depletion/aplasia and an immune reset.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor recognize CD19 on B-lineage cells and, upon engagement, become activated and kill these cells via cytotoxic mechanisms, producing profound depletion/aplasia of CD19+ B cells and reducing autoreactive B cells and autoantibody production (immune reset).
YES
DIRECT
Anti-CD19 CAR-T cells bind CD19 on target B-lineage cells and kill them via contact-dependent cytotoxicity (perforin/granzyme-mediated apoptosis and death-receptor pathways), leading to B-cell depletion.
Polyclonal antibody preparation that depletes T lymphocytes for induction immunosuppression.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional T-cell apoptosis and functional inhibition, producing potent immunosuppression.
YES
DIRECT
Polyclonal IgG in ATG binds CD45 on leukocytes and triggers complement-dependent lysis and Fc-mediated ADCC, with additional induction of apoptosis.
Recombinant humanized anti-CD20 monoclonal antibody administered subcutaneously; depletes CD20+ B cells via ADCC, CDC, and apoptosis to reduce autoantibody production. Evaluated in adults with primary membranous nephropathy (Phase I; 350–1000 mg on Days 1 and 15).
Humanized anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ B lymphocytes via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, thereby reducing pathogenic autoantibody production.
YES
DIRECT
The anti-CD20 antibody binds CD20 on B cells and induces killing via Fc-mediated ADCC (recruiting NK cells/macrophages), complement-dependent cytotoxicity, and direct apoptosis signaling, depleting CD20+ cells.