Antibody–drug conjugate (ADC) also known as izalontamab brengitecan (iza-bren; BMS-986507); administered intravenously. The monoclonal antibody binds a tumor-associated surface antigen, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload to induce DNA damage and tumor cell death.
Bispecific anti-EGFR/anti-HER3 antibody–drug conjugate that binds EGFR/HER3 on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload, inducing DNA damage and tumor cell death.
YES
DIRECT
ADC binds HER3 on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload that inhibits topoisomerase I, causing DNA damage and tumor cell death.
Antibody–drug conjugate (ADC) also known as izalontamab brengitecan (iza-bren; BMS-986507); administered intravenously. The monoclonal antibody binds a tumor-associated surface antigen, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload to induce DNA damage and tumor cell death.
Bispecific anti-EGFR/anti-HER3 antibody–drug conjugate that binds EGFR/HER3 on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor payload, inducing DNA damage and tumor cell death.
NO
INDIRECT
The ADC binds EGFR/HER3 on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor that causes DNA damage and cell death; Topoisomerase I is the intracellular payload target, not the binding target determining selectivity.
MC1R-targeted peptide radiopharmaceutical delivering alpha-particle therapy via 212Pb decay (212Pb→212Bi/212Po) to induce short-range, high-LET DNA double-strand breaks in melanoma cells; administered IV approximately every 8 weeks as mono- or combination therapy.
MC1R-targeted peptide (VMT01) delivers the alpha-emitting radionuclide 212Pb (decaying via 212Bi/212Po) to MC1R-expressing tumor cells, producing short-range, high-LET alpha radiation that induces clustered DNA double-strand breaks and tumor cell death.
YES
DIRECT
The VMT01 peptide binds MC1R on tumor cells and delivers 212Pb; subsequent alpha-particle emissions (via 212Bi/212Po) deposit short-range, high-LET radiation that induces clustered DNA double-strand breaks, leading to tumor cell death.
An autologous BCMA-directed chimeric antigen receptor T-cell (CAR-T) therapy in which a patient's T cells are gene-modified to express a CAR targeting BCMA, leading to T-cell activation, cytokine release, expansion, and targeted cytotoxic killing of malignant plasma cells in multiple myeloma.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting BCMA on malignant plasma cells; antigen engagement activates the T cells, inducing cytokine release, clonal expansion, and targeted cytotoxic killing of multiple myeloma cells.
YES
DIRECT
BCMA-specific CAR T cells bind BCMA on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis and apoptosis (with contribution from Fas–FasL).
Fully human IgG1 anti-CD20 monoclonal antibody immunotherapy administered subcutaneously; depletes CD20+ B lymphocytes via CDC, ADCC, and apoptosis, reducing naive and memory B cells while sparing stem cells and plasma cells.
Fully human IgG1 anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and apoptosis, reducing naive and memory B cells while sparing hematopoietic stem cells and plasma cells.
YES
DIRECT
Ofatumumab binds CD20 on B cells, triggers complement-dependent cytotoxicity (CDC) and Fc-mediated ADCC/ADCP by NK cells/macrophages, and can induce apoptosis of the bound cells.