Anti-CD38 IgG1 monoclonal antibody that mediates ADCC, ADCP, complement-dependent cytotoxicity, induces apoptosis via crosslinking, and depletes CD38+ immunosuppressive cells.
Anti-CD38 IgG1 monoclonal antibody that binds CD38 on malignant plasma cells, inducing cell death via ADCC, ADCP, and complement-dependent cytotoxicity; can trigger apoptosis upon crosslinking and depletes CD38+ immunosuppressive cells (e.g., Tregs, B cells, MDSCs), enhancing antitumor immunity.
YES
DIRECT
Anti-CD38 IgG1 antibody binds CD38 on target cells and triggers killing via Fc-mediated ADCC (NK cells), ADCP (macrophages), complement-dependent cytotoxicity (CDC), and can induce apoptosis upon crosslinking.
Autologous monocyte-derived dendritic cell (DC) vaccine pulsed with Epstein–Barr virus (EBV) antigens. Administered subcutaneously (5×10^6 cells/dose every 2 weeks for 3–5 doses) to present EBV peptides on MHC I/II and prime EBV-specific CD8+ and CD4+ T-cell responses in EBV+ nasopharyngeal carcinoma.
Autologous monocyte-derived dendritic cells are pulsed with EBV antigens (BLCL lysate) ex vivo and reinfused subcutaneously, where they present EBV peptides on MHC I/II to prime and expand EBV-specific CD8+ cytotoxic and CD4+ helper T cells, driving CTL-mediated lysis of EBV-positive tumor cells (e.g., nasopharyngeal carcinoma).
YES
INDIRECT
Dendritic-cell vaccination primes EBV-specific CD8+ T cells, which recognize EBV peptides presented on MHC I of EBV+ tumor cells and kill them via perforin/granzyme-mediated cytolysis (CTL-mediated lysis).
Bispecific IgG4 monoclonal antibody that binds BCMA on myeloma cells and CD3 on T cells to redirect T-cell cytotoxicity against BCMA-expressing plasma cells; administered with step-up dosing.
Bispecific humanized IgG4 monoclonal antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to form an immune synapse and activate T-cell cytotoxicity (perforin/granzyme release and cytokines), resulting in targeted lysis of BCMA-expressing myeloma cells.
YES
DIRECT
Teclistamab bridges CD3 on T cells to BCMA on target cells, forming an immune synapse that triggers T-cell cytotoxicity (perforin/granzyme release and cytokines) to lyse BCMA-expressing cells.
Bispecific IgG4 monoclonal antibody that binds BCMA on myeloma cells and CD3 on T cells to redirect T-cell cytotoxicity against BCMA-expressing plasma cells; administered with step-up dosing.
Bispecific humanized IgG4 monoclonal antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to form an immune synapse and activate T-cell cytotoxicity (perforin/granzyme release and cytokines), resulting in targeted lysis of BCMA-expressing myeloma cells.
NO
INDIRECT
Teclistamab binds CD3 on T cells to activate and bridge them to BCMA+ myeloma cells; the T cells then kill the BCMA-expressing tumor cells via perforin/granzyme, not the CD3+ cells.
Anti-HER2 antibody–drug conjugate (ADC) that binds HER2 (ERBB2), is internalized, and releases a cytotoxic payload to kill tumor cells; intended for HER2-high and HER2-low cohorts.
HER2-directed ADC (trastuzumab rezetecan). The antibody binds HER2 (ERBB2) on tumor cells and is internalized; a cleavable linker releases a camptothecin-derived topoisomerase I inhibitor that stabilizes TOP1–DNA complexes, causing DNA breaks, replication arrest, apoptosis, and tumor cell death in HER2-expressing tumors (including HER2-low).
YES
DIRECT
The ADC binds HER2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that stabilizes TOP1–DNA complexes, causing DNA damage, replication arrest, and apoptosis.