Anti-CD20 × anti-CD3 bispecific IgG T‑cell engager (REGN1979) that binds CD20 on B cells and CD3 on T cells to redirect cytotoxic T cells to kill malignant CD20+ B cells.
Bispecific anti‑CD20×CD3 monoclonal antibody that simultaneously binds CD20 on B cells and CD3 on T cells, physically bridging T cells to malignant CD20+ B cells to trigger T‑cell activation and cytotoxic killing (perforin/granzyme) of the target B cells.
Odronextamab bridges CD20 on target B cells with CD3 on T cells, activating T cells to kill CD20+ cells via perforin/granzyme-mediated cytolysis.
Chimeric anti‑CD20 monoclonal antibody that depletes B cells via ADCC, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ B cells via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and induction of apoptosis.
Anti‑CD20 antibody binds CD20 on B cells and induces killing via Fc-mediated ADCC by immune effector cells, complement-dependent cytotoxicity, and direct pro-apoptotic signaling.
Antibody–drug conjugate targeting TROP2; internalizes and releases a topoisomerase I inhibitor payload to induce DNA damage and apoptosis (possible bystander effect).
Anti-TROP2 antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload to induce DNA damage and apoptosis, with potential bystander effect.
Anti-TROP2 ADC binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload that causes DNA damage and apoptosis (with possible bystander effect).
An antibody–drug conjugate targeting HER2, consisting of trastuzumab linked to deruxtecan (a topoisomerase I inhibitor). It binds HER2 on tumor cells, is internalized, and releases a DNA-damaging payload with a bystander effect; it also inhibits HER2 signaling and can mediate ADCC.
Anti-HER2 monoclonal antibody (trastuzumab) linked to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor. After HER2 binding and internalization, lysosomal cleavage releases DXd to cause DNA damage (topoisomerase I inhibition) with a bystander effect in neighboring cells. The antibody component also inhibits HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
The anti-HER2 antibody binds HER2 and is internalized; lysosomal cleavage releases deruxtecan, a topoisomerase I inhibitor, causing DNA damage and death of HER2+ cells. The Fc domain can also trigger ADCC; the payload may exert a bystander effect on neighboring cells.
Autologous tumor-infiltrating lymphocytes (TILs) expanded/activated ex vivo and reinfused as cellular immunotherapy targeting patient-specific tumor antigens.
Autologous tumor-infiltrating lymphocytes are expanded and activated ex vivo and reinfused; they recognize patient-specific tumor antigens via endogenous TCRs and mediate cytotoxicity through perforin/granzyme release and proinflammatory cytokines (e.g., IFN-gamma), leading to targeted tumor cell killing.
Adoptively transferred TILs recognize the mutant neoantigen peptide–HLA complex via their endogenous TCR and kill target cells by perforin/granzyme-mediated cytolysis and Fas–FasL–induced apoptosis, aided by proinflammatory cytokines (e.g., IFN-γ).