Anti-CD38 immunocytokine/fusion protein (TAK-573) that targets CD38 and delivers attenuated interferon-α to CD38+ cells, activating type I IFN signaling (IFNAR1/2 → JAK–STAT) to drive antiproliferative/apoptotic effects and immune stimulation.
Anti-CD38 IgG4–interferon-alpha immunocytokine that targets CD38+ cells and delivers attenuated IFN-alpha to engage IFNAR1/2, activating JAK–STAT type I interferon signaling to drive antiproliferative/apoptotic effects and immune stimulation against CD38-expressing tumor cells.
Binds CD38 on target cells and delivers IFN-alpha to engage IFNAR1/2 on the same cell, activating JAK-STAT type I interferon signaling that drives antiproliferative and apoptotic effects (IgG4 minimizes Fc-mediated killing).
Antigen-specific T cells expanded ex vivo and reinfused to recognize tumor peptides on MHC class I via the TCR, mediating cytotoxicity through perforin/granzyme release and IFN-gamma-mediated effects.
Autologous antigen-specific CTLs expanded ex vivo are reinfused to recognize tumor peptides presented on MHC class I via their endogenous TCR, inducing tumor-cell killing via perforin/granzyme release and death-receptor pathways (FasL/TRAIL), along with IFN-γ secretion to enhance antitumor immune responses.
Adoptively transferred CTLs recognize the tumor peptide–HLA-B complex via their TCR and kill targets by perforin/granzyme-mediated apoptosis and death-receptor signaling (FasL/TRAIL).
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.
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.
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.
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.
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).
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.