An antibody-drug conjugate (also known as izalontamab brengitecan, BMS-986507, iza-bren) targeting TROP2 that delivers the camptothecin-derived topoisomerase I inhibitor payload brengitecan to induce DNA damage and apoptosis.
TROP2-targeting antibody-drug conjugate that binds TROP2 on tumor cells, is internalized, and releases the camptothecin-derived topoisomerase I inhibitor brengitecan to induce DNA damage and apoptosis.
NO
INDIRECT
The ADC binds TROP2 on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan to cause DNA damage and apoptosis. Topoisomerase I is the intracellular enzymatic payload target, not the antigen determining selective killing.
Chimeric IgG1 monoclonal antibody against EGFR that competitively blocks ligand binding and EGFR activation; used to curb feedback/reactivation of MAPK signaling.
Chimeric IgG1 monoclonal antibody against EGFR that competitively blocks ligand binding, preventing EGFR activation and dimerization and thereby inhibiting downstream RAS–RAF–MEK–ERK (MAPK) signaling and tumor cell proliferation; may also mediate Fc-dependent ADCC.
YES
DIRECT
Cetuximab binds EGFR on target cells and engages Fcγ receptors on immune effectors (e.g., NK cells) to mediate antibody‑dependent cellular cytotoxicity (and some complement-mediated lysis); signaling blockade is mainly cytostatic.
Personalized autologous dendritic cell cancer vaccine pulsed with six glioblastoma tumor-associated antigen peptides; given intradermally to present HLA-A2–restricted epitopes and prime antigen-specific cytotoxic T cells against GBM.
Autologous dendritic cells loaded with six glioblastoma-associated peptides (AIM2, MAGE-1, TRP-2, gp100, HER2, IL-13Rα2) present these antigens via MHC (HLA-A2–restricted) to T cells, priming antigen-specific cytotoxic T lymphocytes and helper responses that recognize and kill GBM cells expressing these TAAs, including stem-like tumor cells.
YES
INDIRECT
Autologous dendritic cells present AIM2-derived HLA-A2–restricted peptides to prime AIM2-specific CTLs, which then recognize peptide–MHC on tumor cells and kill them via perforin/granzyme (and Fas–FasL) pathways.
Personalized autologous dendritic cell cancer vaccine pulsed with six glioblastoma tumor-associated antigen peptides; given intradermally to present HLA-A2–restricted epitopes and prime antigen-specific cytotoxic T cells against GBM.
Autologous dendritic cells loaded with six glioblastoma-associated peptides (AIM2, MAGE-1, TRP-2, gp100, HER2, IL-13Rα2) present these antigens via MHC (HLA-A2–restricted) to T cells, priming antigen-specific cytotoxic T lymphocytes and helper responses that recognize and kill GBM cells expressing these TAAs, including stem-like tumor cells.
YES
INDIRECT
Dendritic cells present HLA-A2–restricted MAGE-1 peptides to T cells, inducing MAGE-1–specific CD8+ CTLs that recognize MAGE-1 peptide–HLA complexes on tumor cells and kill them via perforin/granzyme-mediated apoptosis.
Personalized autologous dendritic cell cancer vaccine pulsed with six glioblastoma tumor-associated antigen peptides; given intradermally to present HLA-A2–restricted epitopes and prime antigen-specific cytotoxic T cells against GBM.
Autologous dendritic cells loaded with six glioblastoma-associated peptides (AIM2, MAGE-1, TRP-2, gp100, HER2, IL-13Rα2) present these antigens via MHC (HLA-A2–restricted) to T cells, priming antigen-specific cytotoxic T lymphocytes and helper responses that recognize and kill GBM cells expressing these TAAs, including stem-like tumor cells.
YES
INDIRECT
The DC vaccine presents TRP-2 peptide (HLA-A2–restricted) to prime TRP-2–specific CD8+ T cells; these CTLs then recognize TRP-2 peptide–MHC I on tumor cells and kill them via perforin/granzyme-mediated cytolysis (and Fas–FasL).