A bispecific T-cell engager (BiTE) antibody construct that binds CD19 on B cells and CD3 on T cells to redirect cytotoxic T cells to eliminate CD19+ B cells, reducing pathogenic B cells/plasmablasts and autoantibody production.
Blinatumomab is a BiTE antibody that simultaneously binds CD19 on B cells and CD3 on T cells, bringing T cells into contact with CD19+ B cells to activate cytotoxic T-cell killing (perforin/granzyme), leading to rapid depletion of pathogenic B cells/plasmablasts and reduced autoantibody production.
NO
INDIRECT
Blinatumomab binds CD3 on T cells to activate them; CD3E+ T cells act as effectors and kill CD19+ B cells via perforin/granzyme, not the CD3E+ cells themselves.
IgG1 monoclonal antibody against HER2 domain II that blocks HER2 dimerization (especially HER2:HER3), suppressing downstream PI3K/AKT and MAPK signaling; also mediates ADCC.
Humanized IgG1 monoclonal antibody that binds HER2 extracellular domain II, blocking HER2 dimerization (especially HER2:HER3), thereby inhibiting downstream PI3K/AKT and MAPK signaling and reducing tumor cell proliferation; also mediates antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Binds HER2 on target cells and engages Fcγ receptor–bearing effector cells via its IgG1 Fc to trigger antibody‑dependent cellular cytotoxicity (ADCC), killing HER2+ cells; also inhibits HER2 signaling, which can promote apoptosis.
IgG1 monoclonal antibody that binds the HER2 extracellular domain IV, inhibits HER2 signaling and receptor shedding, and triggers antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting HER2 extracellular domain IV; blocks HER2 signaling and receptor shedding, suppressing downstream PI3K/AKT and MAPK pathways, and induces Fc-mediated ADCC against HER2-overexpressing tumor cells.
YES
DIRECT
Trastuzumab binds HER2 domain IV and engages Fcγ receptor–bearing immune effectors (e.g., NK cells) to trigger ADCC (and some complement activation), killing HER2+ cells; it also inhibits HER2 signaling.
IgG1 monoclonal antibody that binds the HER2 extracellular domain IV, inhibits HER2 signaling and receptor shedding, and triggers antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting HER2 extracellular domain IV; blocks HER2 signaling and receptor shedding, suppressing downstream PI3K/AKT and MAPK pathways, and induces Fc-mediated ADCC against HER2-overexpressing tumor cells.
NO
INDIRECT
Trastuzumab binds HER2 on tumor cells; its Fc engages CD16A (FcγRIIIa) on NK cells to trigger ADCC that kills HER2-expressing targets. CD16A+ cells act as effectors and are not killed.
An antibody–drug conjugate (IMMU-132; Trodelvy) consisting of a humanized anti–TROP-2 monoclonal antibody linked via a hydrolyzable linker to SN-38, the active metabolite of irinotecan (a topoisomerase I inhibitor). After binding TROP-2 on tumor cells, it is internalized and releases SN-38 to inhibit topoisomerase I, causing DNA damage/replication stress and apoptosis, with a bystander effect.
Humanized anti–TROP-2 monoclonal antibody linked via a hydrolyzable linker to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells, the ADC is internalized and releases SN-38, which stabilizes Topo I–DNA complexes, causing DNA breaks, replication stress, and apoptosis; membrane-permeable SN-38 enables a bystander effect.
YES
DIRECT
ADC binds TROP-2 on target cells, is internalized, and releases SN-38 (topoisomerase I inhibitor) that stabilizes Topo I–DNA complexes, causing DNA damage and apoptosis; membrane-permeable SN-38 can also produce a bystander effect.