Glycoengineered humanized type II anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via enhanced antibody-dependent cellular cytotoxicity/phagocytosis and direct non-complement cell death, aiming to reduce autoantibody production and immune complex formation; administered 1 g IV on day 1 and day 15, repeated at month 6.
Glycoengineered humanized type II anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via enhanced antibody-dependent cellular cytotoxicity/phagocytosis and direct non-complement-mediated cell death, reducing autoantibody production and immune complex formation.
Obinutuzumab binds CD20 on B cells and triggers killing via enhanced Fc-mediated ADCC/ADCP by NK cells/macrophages and induces direct, non–complement-mediated cell death (type II antibody).
An autologous, gene-modified T-cell therapy in which a patient’s peripheral blood T cells are engineered to express a CD19-specific chimeric antigen receptor (anti-CD19 scFv). CAR engagement enables MHC-independent recognition and activation of T-cell effector functions (cytotoxic killing and cytokine release), leading to depletion of CD19+ leukemic and normal B cells in CD19+ B-ALL.
Autologous T cells engineered to express a CD19-specific chimeric antigen receptor bind CD19 on B cells and trigger MHC-independent T-cell activation, cytotoxic killing, and cytokine release, resulting in depletion of CD19+ leukemic and normal B cells.
CD19 CAR-T cells bind CD19 on target B cells, triggering MHC-independent T-cell activation and cytolysis via perforin/granzyme (and Fas/FasL) pathways, leading to depletion of CD19+ cells.
An anti-c-Met antibody–drug conjugate (ADC) that binds MET (c-Met) on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload causing DNA damage and cell death; disrupts MET-driven signaling.
Monoclonal antibody targets MET (c-Met) on tumor cells; after binding and internalization, releases a topoisomerase I inhibitor payload that induces DNA damage and cell death while disrupting MET-driven signaling.
ADC binds MET on target cells, is internalized, and releases a topoisomerase I inhibitor payload that causes DNA damage leading to apoptosis/cell death.
Autologous CD19-directed CAR T-cell therapy (gene-modified cellular immunotherapy). Engineered T cells express a CAR with CD3ζ signaling and costimulatory domains to target CD19 on B cells, leading to T-cell activation/expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing; expected on-target B-cell aplasia.
Autologous T cells are genetically engineered to express a CD19-directed chimeric antigen receptor (with CD3zeta signaling and costimulatory domains). Upon binding CD19 on B cells, the CAR activates T-cell signaling, leading to T-cell activation and expansion, cytokine release, and perforin/granzyme-mediated killing of malignant B cells, with expected on-target B-cell aplasia.
CD19-directed CAR T cells bind CD19+ cells, activate, and kill them via perforin/granzyme-mediated cytolysis (and related T-cell effector mechanisms).
An IV BCMA×CD3 bispecific T‑cell–engaging monoclonal antibody that redirects CD3+ T cells to kill BCMA-expressing plasma cells, aiming to deplete IgE-producing plasma cells and lower food-specific IgE.
BCMA×CD3 bispecific T‑cell–engaging monoclonal antibody that binds BCMA on plasma cells and CD3 on T cells, bringing them into proximity to activate cytotoxic T cells and kill BCMA‑expressing antibody‑secreting plasma cells, thereby depleting IgE‑producing plasma cells and lowering food‑specific IgE.
The BCMA×CD3 bispecific antibody binds BCMA on target cells and CD3 on T cells, bringing them together and activating T cells to kill BCMA-expressing cells via perforin/granzyme-mediated cytotoxicity.