Anti-CD38 IgG1 monoclonal antibody targeting CD38 on malignant plasma cells; mediates ADCC/CDC/ADCP, induces apoptosis, and inhibits CD38 ectoenzyme activity to reduce immunosuppressive adenosine.
Unconjugated anti-CD38 IgG1 monoclonal antibody that binds CD38 on malignant plasma cells and induces cell death via Fc-mediated ADCC, CDC, and ADCP; also directly triggers apoptosis and inhibits CD38 ectoenzyme activity, reducing immunosuppressive adenosine and depleting CD38+ tumor cells.
YES
DIRECT
Binds CD38 on target cells and induces killing via Fc-mediated ADCC, complement-dependent cytotoxicity, antibody-dependent phagocytosis, and can also directly trigger apoptosis.
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.
YES
DIRECT
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.
YES
DIRECT
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).
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.
NO
INDIRECT
BL-B01D1 does not target DNA topoisomerase I on cell surfaces; it binds EGFR/HER3, is internalized, and releases brengitecan, which inhibits topoisomerase I to cause DNA damage and apoptosis. Any killing of topoisomerase I–expressing cells occurs only secondarily (e.g., bystander diffusion) rather than by direct targeting of this antigen.
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.
YES
DIRECT
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.