An antibody–drug conjugate (also known as iza-bren; izalontamab brengitecan; BMS-986507) that binds a tumor-associated antigen on TNBC cells and, upon internalization, releases the camptothecin-class topoisomerase I inhibitor brengitecan to induce DNA damage and apoptosis, with potential bystander effect.
Dual-targeted anti-EGFR/anti-HER3 antibody–drug conjugate that binds EGFR and HER3 on tumor cells. Upon internalization, it releases the camptothecin-class topoisomerase I inhibitor brengitecan, causing topoisomerase I inhibition, DNA damage, and apoptosis, with a potential bystander effect due to payload diffusion.
The ADC binds EGFR on the tumor cell, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and apoptosis (with potential bystander killing via payload diffusion).
An antibody–drug conjugate (also known as iza-bren; izalontamab brengitecan; BMS-986507) that binds a tumor-associated antigen on TNBC cells and, upon internalization, releases the camptothecin-class topoisomerase I inhibitor brengitecan to induce DNA damage and apoptosis, with potential bystander effect.
Dual-targeted anti-EGFR/anti-HER3 antibody–drug conjugate that binds EGFR and HER3 on tumor cells. Upon internalization, it releases the camptothecin-class topoisomerase I inhibitor brengitecan, causing topoisomerase I inhibition, DNA damage, and apoptosis, with a potential bystander effect due to payload diffusion.
The ADC binds HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and apoptosis (with potential bystander killing from payload diffusion).
Human IgG1 anti-CD38 monoclonal antibody immunotherapy that depletes plasma cells and NK cells via ADCC, CDC, ADCP, and apoptosis, and inhibits CD38 ectoenzyme activity; evaluated as monotherapy for chronic active antibody-mediated rejection after kidney transplant (16 mg/kg every 2 weeks ×12).
Human IgG1 monoclonal antibody targeting CD38 that depletes CD38+ cells (e.g., plasma cells, NK cells, immunosuppressive subsets) via ADCC, CDC, ADCP, and apoptosis, and inhibits CD38 ectoenzyme activity, thereby reducing pathogenic antibody production and modulating immune responses.
Anti-CD38 IgG1 binds CD38 on target cells and mediates Fc-dependent killing (ADCC by NK cells, ADCP by macrophages) and complement-dependent cytotoxicity (CDC); can also induce apoptosis.
Autologous, gene-modified anti-CD19 chimeric antigen receptor T-cell (CAR T) therapy given as a single infusion; engineered patient T cells target CD19 to deplete B cells/plasmablasts and reduce autoantibody-mediated pathology in idiopathic inflammatory myopathies.
Autologous T cells are engineered to express an anti-CD19 chimeric antigen receptor; after infusion, these CAR T cells recognize and kill CD19-positive B cells and plasmablasts, depleting autoreactive B-cell populations, lowering autoantibody production, and attenuating B cell–driven inflammation.
Anti-CD19 CAR T cells bind CD19 on target B-lineage cells, become activated, and kill them via T-cell effector functions (perforin/granzyme-mediated cytolysis and Fas–FasL–induced apoptosis).
Humanized IgG1 anti-EGFR monoclonal antibody that blocks EGFR ligand binding and dimerization, inhibiting RAS–MAPK and PI3K–AKT signaling, reducing proliferation and radioresistance, and enabling ADCC.
Humanized IgG1 anti-EGFR monoclonal antibody that blocks EGFR ligand binding and dimerization, inhibiting RAS–MAPK and PI3K–AKT signaling to reduce proliferation and survival; Fc-mediated ADCC may contribute and it can enhance radiosensitivity.
Fc-mediated ADCC by immune effector cells (e.g., NK cells) against EGFR-expressing cells; signaling blockade is mainly cytostatic, with radiosensitization enhancing kill with radiation.