Anti-CD20 monoclonal antibody that depletes B cells as part of desensitization/antibody-mediated rejection therapy.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, thereby reducing CD20+ B-cell populations and downstream antibody production.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers Fc-mediated ADCC by NK/macrophages, complement-dependent cytotoxicity (CDC), and can induce apoptosis of CD20+ cells.
Subcutaneous, fully human anti-CD20 monoclonal antibody (Kesimpta) that binds a distinct CD20 epitope on B lymphocytes and induces complement-dependent cytotoxicity and antibody-dependent cell-mediated cytotoxicity, depleting CD20+ B cells and reducing antigen presentation and proinflammatory cytokines that drive MS activity.
Fully human anti-CD20 IgG1 monoclonal antibody that binds a distinct CD20 epitope on B lymphocytes and induces complement-dependent cytotoxicity and antibody-dependent cell-mediated cytotoxicity, depleting CD20+ B cells and reducing antigen presentation and proinflammatory cytokines that drive MS activity.
YES
DIRECT
Ofatumumab binds CD20 on B cells and triggers complement-dependent cytotoxicity (CDC) and Fc-mediated ADCC by effector cells, leading to lysis and depletion of CD20+ cells.
Izalontamab brengitecan (BMS-986507) is a bispecific antibody–drug conjugate targeting EGFR and HER3; after binding and internalization, a cleavable linker releases a topoisomerase I–inhibitor payload that induces DNA single-strand breaks and apoptosis, with potential bystander killing.
Bispecific ADC targeting EGFR and HER3; binding triggers internalization and cleavable-linker release of a topoisomerase I inhibitor payload, causing DNA single-strand breaks and apoptosis, with potential bystander killing of neighboring tumor cells.
YES
DIRECT
As a bispecific ADC, BL-B01D1 binds EGFR (and/or HER3) on tumor cells, is internalized, and releases a topoisomerase I–inhibitor via a cleavable linker, causing DNA single-strand breaks and apoptosis; can also produce bystander killing.
Izalontamab brengitecan (BMS-986507) is a bispecific antibody–drug conjugate targeting EGFR and HER3; after binding and internalization, a cleavable linker releases a topoisomerase I–inhibitor payload that induces DNA single-strand breaks and apoptosis, with potential bystander killing.
Bispecific ADC targeting EGFR and HER3; binding triggers internalization and cleavable-linker release of a topoisomerase I inhibitor payload, causing DNA single-strand breaks and apoptosis, with potential bystander killing of neighboring tumor cells.
YES
DIRECT
The bispecific ADC binds HER3 (and/or EGFR) on target cells, is internalized, and releases a cleavable topoisomerase I inhibitor payload that causes DNA single-strand breaks and apoptosis; bystander killing of neighboring cells may occur.
Izalontamab brengitecan (BMS-986507) is a bispecific antibody–drug conjugate targeting EGFR and HER3; after binding and internalization, a cleavable linker releases a topoisomerase I–inhibitor payload that induces DNA single-strand breaks and apoptosis, with potential bystander killing.
Bispecific ADC targeting EGFR and HER3; binding triggers internalization and cleavable-linker release of a topoisomerase I inhibitor payload, causing DNA single-strand breaks and apoptosis, with potential bystander killing of neighboring tumor cells.
NO
INDIRECT
BL-B01D1 binds EGFR/HER3 on tumor cells, is internalized, and releases a topoisomerase I–inhibitor payload that causes DNA damage and apoptosis; killing is driven by EGFR/HER3 binding, not by DNA topoisomerase I expression itself.