Humanized IgG1 monoclonal antibody targeting HER2/ERBB2 that blocks receptor signaling and mediates ADCC.
Humanized IgG1 monoclonal antibody targeting HER2/ERBB2; binds HER2 on tumor cells to block receptor signaling and dimerization, inhibiting PI3K/AKT/MAPK pathways, and engages Fc gamma receptors to trigger antibody-dependent cellular cytotoxicity (ADCC).
Trastuzumab binds HER2 on tumor cells and engages Fc gamma receptors on NK cells/macrophages to trigger antibody-dependent cellular cytotoxicity (and phagocytosis); it can also activate complement (CDC).
An autologous BCMA-directed CAR T-cell gene therapy in which a patient's T cells are lentiviral-transduced to express a chimeric antigen receptor targeting BCMA (TNFRSF17) on malignant plasma cells, leading to CAR-mediated T-cell activation, expansion, cytokine release, and perforin/granzyme-dependent cytotoxic killing; CAR T cells may persist long term due to genomic integration.
Autologous T cells are lentivirally transduced to express a chimeric antigen receptor targeting BCMA (TNFRSF17) on malignant plasma cells. Antigen engagement triggers T‑cell activation, clonal expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BCMA-positive cells; integrated CAR transgene enables potential long-term persistence.
BCMA-directed CAR T cells bind BCMA on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis (and related death pathways).
Autologous T cells genetically modified to express dual CARs targeting CD19 and CD20 with an autocrine p40 cytokine module to enhance activation, expansion, and persistence; administered after lymphodepleting chemotherapy.
Autologous T cells engineered with dual chimeric antigen receptors targeting CD19 and CD20 recognize malignant B cells and, upon antigen engagement, activate and mediate cytolytic killing; an autocrine p40 cytokine module augments activation, expansion, and persistence, with lymphodepletion supporting engraftment.
CD19-directed CAR T cells recognize CD19 on target cells and, upon activation, kill them via perforin/granzyme cytolysis and Fas–FasL–mediated apoptosis.
Autologous T cells genetically modified to express dual CARs targeting CD19 and CD20 with an autocrine p40 cytokine module to enhance activation, expansion, and persistence; administered after lymphodepleting chemotherapy.
Autologous T cells engineered with dual chimeric antigen receptors targeting CD19 and CD20 recognize malignant B cells and, upon antigen engagement, activate and mediate cytolytic killing; an autocrine p40 cytokine module augments activation, expansion, and persistence, with lymphodepletion supporting engraftment.
CD19/CD20 CAR T cells recognize CD20 on target cells, activate, and induce cytolytic killing via perforin/granzyme-mediated apoptosis and death receptor pathways.
Autologous T cells genetically modified to express a CD19-directed CAR with an autocrine p40 cytokine module to enhance activation, expansion, and persistence; administered after lymphodepleting chemotherapy.
Autologous T cells engineered to express a CD19-directed chimeric antigen receptor that recognizes CD19 on malignant B cells and triggers T-cell activation and cytolytic killing. An autocrine p40 cytokine module augments activation, expansion, and persistence of the CAR T cells. Administered after lymphodepleting chemotherapy to enhance engraftment and activity.
CD19-directed CAR T cells bind CD19 on target cells, become activated, and kill via T-cell cytotoxic pathways (perforin/granzyme-mediated lysis and apoptosis).