Gene-modified autologous T cells expanded with IL-7/IL-15 and engineered to express a CD19-specific scFv with 4-1BB/CD3ζ signaling; redirects T cells to kill CD19+ malignant B cells, with 4-1BB enhancing expansion and persistence.
Autologous T cells engineered to express a CD19-specific CAR (scFv linked to 4-1BB and CD3zeta). Binding to CD19 on malignant B cells triggers T-cell activation and cytotoxic killing; 4-1BB costimulation enhances expansion and persistence. Cells are expanded ex vivo with IL-7/IL-15.
CD19-specific CAR T cells bind CD19 on target cells, activating CD3zeta/4-1BB signaling and inducing T-cell cytolysis via perforin/granzyme release and death-receptor pathways, leading to apoptosis/lysis.
Autologous T lymphocytes engineered to express a chimeric antigen receptor targeting the disialoganglioside GD2 on neuroblastoma cells; upon infusion, CAR engagement activates T-cell cytotoxicity and cytokine-mediated antitumor effects.
Autologous T cells engineered to express a chimeric antigen receptor targeting GD2 on tumor cells; CAR engagement triggers T-cell activation, proliferation, cytokine release, and cytotoxic killing (perforin/granzyme) of GD2-expressing neuroblastoma cells.
GD2-CAR engagement activates the infused T cells to form an immunologic synapse and kill GD2+ cells via perforin/granzyme-mediated cytolysis (with possible Fas–FasL and cytokine-mediated apoptosis).
Anti-CD38 monoclonal antibody that induces ADCC, CDC, ADCP, and direct apoptosis of CD38-positive plasma cells while depleting CD38-positive immunosuppressive cells.
Human IgG1-kappa anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells to trigger direct apoptosis and immune effector-mediated killing (ADCC, CDC, ADCP), while depleting CD38-positive immunosuppressive cells (Tregs, Bregs, MDSCs) to enhance antitumor immunity.
Anti-CD38 IgG1 binds CD38 on target cells and kills them via Fc-mediated ADCC (NK cells), complement-dependent cytotoxicity, antibody-dependent cellular phagocytosis, and can trigger direct apoptosis upon cross-linking.
Anti-Claudin18.2 antibody–drug conjugate that targets CLDN18.2-expressing tumor cells and delivers a cytotoxic payload; intravenous administration.
Monoclonal antibody targeting Claudin18.2 delivers the microtubule inhibitor MMAE via a cleavable linker; after binding to CLDN18.2 on tumor cells and internalization, MMAE is released intracellularly to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in CLDN18.2-expressing cells.
The ADC binds CLDN18.2 on tumor cells, is internalized, and releases MMAE intracellularly, disrupting microtubules to cause G2/M arrest and apoptosis of CLDN18.2-expressing cells.
Chimeric anti-CD20 monoclonal antibody that depletes CD20-positive B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and induces depletion via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
CD20+ cells are eliminated via antibody-dependent cellular cytotoxicity (FcγR-mediated NK/macrophage killing), complement-dependent cytotoxicity (C1q-mediated lysis), and apoptosis triggered by CD20 crosslinking.