Intravenous anti-HER2 IgG1 monoclonal antibody that inhibits HER2 signaling/dimerization and mediates ADCC in HER2-overexpressing tumors.
Humanized IgG1 monoclonal antibody targeting HER2 (ERBB2); binds the extracellular domain to block HER2 signaling and dimerization, inhibiting downstream PI3K/AKT and MAPK pathways, and recruits immune effector cells to induce antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
YES
DIRECT
Trastuzumab binds HER2 on tumor cells and engages Fcγ receptors on NK cells/macrophages to mediate antibody-dependent cellular cytotoxicity (ADCC), killing HER2-expressing cells; it may also inhibit signaling and modestly activate complement.
Obrixtamig; an intravenous bispecific T-cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells to activate T-cell–mediated cytotoxicity.
Obrixtamig (BI 764532) is a bispecific T-cell–engaging antibody that binds DLL3 on tumor cells and CD3 on T cells, creating an immune synapse that activates and redirects cytotoxic T cells to kill DLL3-expressing cancer cells.
YES
DIRECT
The bispecific T-cell engager binds DLL3 on target cells and CD3 on T cells, forming an immune synapse that activates T cells to kill DLL3-expressing cells via perforin/granzyme-mediated cytotoxicity.
Obrixtamig; an intravenous bispecific T-cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells to activate T-cell–mediated cytotoxicity.
Obrixtamig (BI 764532) is a bispecific T-cell–engaging antibody that binds DLL3 on tumor cells and CD3 on T cells, creating an immune synapse that activates and redirects cytotoxic T cells to kill DLL3-expressing cancer cells.
NO
INDIRECT
BI 764532 engages CD3ε on T cells to activate them and redirect cytotoxicity toward DLL3-expressing tumor cells (perforin/granzyme-mediated killing). CD3E+ T cells are not the targets of killing.
A glycoengineered type II anti-CD20 IgG1 monoclonal antibody used as pre-treatment to debulk B cells and mitigate cytokine release syndrome; induces direct cell death and antibody-dependent cellular cytotoxicity (ADCC) of CD20+ B cells.
Obinutuzumab is a glycoengineered, humanized type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells; its afucosylated Fc increases affinity for Fc gamma RIII receptors to enhance antibody-dependent cellular cytotoxicity and it induces direct cell death, resulting in depletion of CD20+ B cells (used to debulk B cells and mitigate cytokine release syndrome risk).
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages CD16a on NK cells to trigger ADCC, killing CD20+ B cells. CD16a-expressing cells act as effectors and are not killed.
An autologous dual-target CAR T-cell therapy engineered to express chimeric antigen receptors against BCMA and CD19; patient T cells are collected, modified ex vivo, and reinfused after lymphodepletion to eliminate BCMA+/CD19+ clonal plasma and B cells in relapsed/refractory systemic AL amyloidosis.
Autologous T cells are engineered ex vivo to express dual chimeric antigen receptors targeting BCMA and CD19. After lymphodepletion, the cells are reinfused to recognize and kill BCMA+ plasma cells and CD19+ B-lineage cells via CAR-mediated activation, degranulation (perforin/granzyme), and cytokine release, aiming to eliminate clonal cells that produce amyloidogenic light chains in systemic AL amyloidosis.
YES
DIRECT
BCMA-targeted CAR T cells recognize BCMA on tumor cells and kill them via CAR-mediated activation with degranulation (perforin/granzyme) and apoptosis pathways (e.g., Fas/FasL).