Humanized, glycoengineered type II anti-CD20 monoclonal antibody with enhanced FcγRIIIa binding, promoting stronger ADCC and direct cell death, leading to deeper and more sustained B-cell depletion.
Humanized, glycoengineered type II anti-CD20 IgG1 that binds CD20 on B cells and, through enhanced Fc-gamma receptor IIIa engagement, mediates strong antibody-dependent cellular cytotoxicity and phagocytosis and induces direct, caspase-independent cell death, leading to deep and sustained depletion of CD20+ B cells.
Obinutuzumab binds CD20 on B cells, triggering direct caspase‑independent cell death and engaging Fc-gamma RIIIa on effector cells to mediate ADCC and antibody-dependent phagocytosis.
DLL3×CD3 bispecific T-cell engager antibody immunotherapy (also known as obrixtamig) that binds DLL3 on tumor cells and CD3 on T cells to activate cytotoxic T-cell killing.
A DLL3xCD3 bispecific T-cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells, activating and redirecting cytotoxic T cells to form immune synapses and kill DLL3-expressing cancer cells.
The DLL3×CD3 bispecific antibody bridges CD3+ T cells to DLL3+ cells, forming immune synapses and triggering T‑cell cytotoxicity (perforin/granzyme-mediated lysis) of DLL3-expressing cells.
Autologous BCMA-directed CAR T-cell therapy in which a patient's T cells are engineered ex vivo to express a CAR recognizing BCMA on malignant plasma cells, triggering cytokine release and cytolytic killing in multiple myeloma.
Autologous T cells are genetically modified ex vivo to express a chimeric antigen receptor targeting BCMA on malignant plasma cells; CAR engagement triggers T-cell activation, cytokine release, proliferation, and perforin/granzyme-mediated cytolytic killing of BCMA-positive cells in multiple myeloma.
BCMA-specific CAR T cells recognize BCMA on target cells and, upon activation, kill them via perforin/granzyme-mediated cytolysis (apoptosis).
Autologous CD19-directed CAR T-cell therapy in which a patient's T cells are engineered ex vivo to express a CAR recognizing CD19 on malignant B cells, inducing T-cell effector functions and cytotoxicity in NHL/CLL.
Autologous T cells engineered ex vivo to express a CD19-specific chimeric antigen receptor; upon binding CD19 on malignant B cells, the CAR activates T-cell effector functions (cytokine release and perforin/granzyme-mediated cytotoxicity) to eliminate CD19+ cells.
CD19-directed CAR T cells bind CD19 on target cells, triggering T-cell activation and killing via perforin/granzyme-mediated cytolysis and Fas–FasL–mediated apoptosis.
Subcutaneous bispecific T‑cell–engaging antibody (CD3×CD20) that redirects cytotoxic T cells to kill CD20+ B cells.
Bispecific monoclonal antibody that simultaneously binds CD3 on T cells and CD20 on B cells, crosslinking T cells to CD20+ malignant B cells to trigger T‑cell activation and cytotoxic killing (immune synapse formation, perforin/granzyme release, cytokine production) of the target B cells.
CD3×CD20 bispecific antibody crosslinks T cells to CD20+ cells, forming an immune synapse and inducing T-cell cytotoxicity via perforin/granzyme (and death receptor) pathways, killing the CD20-expressing cells.