A CD3xCD20 bispecific T-cell–engager antibody that binds CD3 on T cells and CD20 on malignant B cells, activating cytotoxic T cells to kill CD20+ CLL/SLL cells via perforin/granzyme release and caspase-dependent apoptosis.
Bispecific CD3xCD20 antibody that bridges CD3 on T cells to CD20 on malignant B cells, activating cytotoxic T cells to kill CD20+ cells via perforin/granzyme release and caspase-dependent apoptosis.
NO
INDIRECT
Epcoritamab binds CD3 on T cells to recruit/activate them against CD20+ B cells; the activated T cells kill the CD20-expressing cells via perforin/granzyme-mediated apoptosis, not the CD3+ T cells.
Autologous gene-modified T cells engineered to express a dual-target chimeric antigen receptor against CD19 and BCMA, intended to deplete CD19+ B cells and BCMA+ plasmablasts/plasma cells to suppress pathogenic autoantibody production in refractory immune thrombocytopenia.
Autologous T cells gene-modified to express dual chimeric antigen receptors targeting CD19 and BCMA. Upon binding CD19+ B cells and BCMA+ plasmablasts/plasma cells, CAR signaling activates T‑cell cytotoxicity and cytokine release, depleting B‑lineage cells and suppressing pathogenic autoantibody production; dual targeting reduces antigen escape.
YES
DIRECT
BCMA-expressing cells are recognized by the BCMA CAR on the engineered T cells, triggering T‑cell activation and killing via perforin/granzyme release and death-receptor (Fas/FasL) apoptosis.
Glycoengineered chimeric IgG1 anti-CD20 monoclonal antibody (brand: BRIUMVI) that depletes CD20+ B cells via enhanced antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity, reducing antigen presentation, costimulation, and proinflammatory cytokine production driving MS relapses.
Glycoengineered chimeric IgG1 anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity, reducing antigen presentation, costimulation, and proinflammatory cytokine production.
YES
DIRECT
Binds CD20 on B cells and triggers Fc-mediated effector killing (ADCC by NK cells/macrophages) and complement-dependent cytotoxicity, causing lysis/apoptosis of CD20+ cells.
A HER2-targeted antibody-drug conjugate (brand name Enhertu) that binds HER2, is internalized, and releases a topoisomerase I inhibitor (DXd) to induce DNA damage and apoptosis; also inhibits HER2 signaling and can mediate ADCC with a bystander effect.
HER2-targeted antibody-drug conjugate: trastuzumab binds HER2 on tumor cells, is internalized, and releases the topoisomerase I inhibitor DXd to cause DNA damage, replication arrest, and apoptosis; also inhibits HER2 signaling and mediates ADCC with a bystander effect.
YES
DIRECT
The ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor inside target cells, causing DNA damage, replication arrest, and apoptosis; it can also trigger Fc-mediated ADCC and a bystander effect.
A HER2-targeted antibody-drug conjugate (brand name Enhertu) that binds HER2, is internalized, and releases a topoisomerase I inhibitor (DXd) to induce DNA damage and apoptosis; also inhibits HER2 signaling and can mediate ADCC with a bystander effect.
HER2-targeted antibody-drug conjugate: trastuzumab binds HER2 on tumor cells, is internalized, and releases the topoisomerase I inhibitor DXd to cause DNA damage, replication arrest, and apoptosis; also inhibits HER2 signaling and mediates ADCC with a bystander effect.
NO
INDIRECT
The ADC binds HER2 (not topoisomerase I), is internalized, and releases DXd, which inhibits topoisomerase I to cause DNA damage and apoptosis; killing is driven by HER2 targeting with possible bystander effect and ADCC, not by topoisomerase I expression itself.