A humanized monoclonal antibody targeting HER2 (ERBB2), inhibiting signaling and mediating antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti-HER2 (ERBB2) IgG1 monoclonal antibody that binds the HER2 extracellular domain, blocks receptor signaling and dimerization, promotes receptor internalization, and mediates antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on target cells and engages Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate antibody-dependent cellular cytotoxicity; may also induce complement-dependent cytotoxicity, in addition to growth-signal blockade.
Engineered autologous T cells expressing a BCMA-directed chimeric antigen receptor to mediate cytotoxicity against malignant plasma cells.
Autologous T cells genetically engineered to express a BCMA-directed chimeric antigen receptor; engagement of BCMA (TNFRSF17) on malignant plasma cells triggers CAR signaling (CD3ζ with co-stimulatory domains), activating T-cell proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of myeloma cells.
CAR-T cells recognize BCMA on target cells and, upon engagement, activate and kill via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Bispecific CD20×CD3 IgG that redirects and activates T cells via CD3 to kill CD20-positive B cells through cytotoxic synapse formation and cytokine-mediated cytotoxicity.
Humanized bispecific IgG that binds CD3 on T cells and CD20 on B cells, cross-linking T cells to CD20+ tumor cells to activate cytotoxic T-cell responses (immune synapse formation, cytokine release, perforin/granzyme-mediated lysis) and eliminate malignant B cells.
Bispecific CD20×CD3 antibody bridges T cells to CD20+ cells, forming an immune synapse that activates T-cell cytotoxicity (perforin/granzyme release and cytokine-mediated killing) to lyse the CD20-expressing cells.
Type I anti-CD20 monoclonal antibody that depletes B cells via ADCC/ADCP, complement-dependent cytotoxicity, and direct apoptosis.
Type I anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via Fc-mediated ADCC/ADCP, complement-dependent cytotoxicity (CDC), and induction of direct apoptosis.
Binds CD20 on B cells and induces killing via Fc-mediated ADCC/ADCP, complement-dependent cytotoxicity (CDC), and can trigger direct apoptosis.
Glycoengineered type II anti-CD20 monoclonal antibody that depletes B cells through enhanced ADCC/ADCP and direct cell death, with reduced complement activation.
Glycoengineered humanized IgG1 type II anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced Fc gamma RIIIa–mediated ADCC and ADCP, along with direct caspase-independent cell death, with relatively reduced complement-dependent cytotoxicity.
Binds CD20 on B cells, recruiting effector cells for ADCC (via Fc-gamma RIIIa) and ADCP, and also induces direct caspase-independent cell death; complement cytotoxicity is limited.