Autologous BCMA-directed chimeric antigen receptor (CAR) T-cell therapy; engineered T cells bind BCMA on myeloma cells and trigger T-cell cytotoxicity and cytokine release to eliminate malignant plasma cells.
Autologous T cells engineered to express a BCMA-targeting chimeric antigen receptor (with 4-1BB costimulation) bind BCMA (TNFRSF17) on malignant plasma cells, triggering T-cell activation, cytokine release, and cytotoxic killing of BCMA-expressing myeloma cells.
BCMA-directed CAR T cells bind BCMA on target cells, triggering T-cell activation and immune-synapse–mediated killing via perforin/granzyme release (and Fas–FasL), leading to apoptosis of BCMA-expressing cells.
Investigational intravenous bispecific antibody (anti-PSMA × CD28) T-cell co-stimulatory engager that binds PSMA on tumor cells and CD28 on T cells to deliver conditional CD28 agonist co-stimulation, enhancing T-cell activation and tumor cell killing in PSMA-positive lesions.
A bispecific antibody that binds PSMA on tumor cells and CD28 on T cells to provide conditional CD28 co-stimulation at PSMA-positive sites, enhancing T-cell activation, proliferation, cytokine release, and cytotoxic killing of PSMA-expressing tumor cells.
Bispecific anti-PSMA×CD28 antibody provides localized CD28 co-stimulation on T cells at PSMA+ cells, activating/expanding T cells that then kill PSMA-expressing cells via cytotoxic T-cell mechanisms (perforin/granzyme, Fas–FasL).
Intravenous chimeric anti-CD20 IgG1 monoclonal antibody that targets CD20 on B cells, inducing B-cell depletion via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and direct apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and mediates B‑cell depletion via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and direct induction of apoptosis.
Anti-CD20 antibody binds CD20 on B cells, inducing complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC)/phagocytosis via Fcγ receptors, and direct apoptosis.
Autologous GPC3-targeted chimeric antigen receptor T-cell (CAR-T) therapy for advanced/recurrent hepatocellular carcinoma; patient T cells are collected via leukapheresis, engineered ex vivo to express a GPC3-specific CAR, and reinfused to mediate antigen-directed cytotoxicity.
Autologous T cells engineered with a GPC3-specific chimeric antigen receptor recognize glypican-3 on tumor cells, triggering T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity against GPC3-positive cells. The cells are armored with a dominant-negative TGF-beta receptor II to block TGF-beta signaling in the tumor microenvironment, increasing resistance to immunosuppression and enhancing antitumor activity.
GPC3-specific CAR-T cells bind glypican-3 on target cells, triggering T-cell activation and perforin/granzyme-mediated apoptosis/lysis.
A glycoengineered type II anti-CD20 monoclonal antibody (brand name Gazyva) given IV that depletes CD20+ B cells through enhanced direct cell death and Fc-mediated ADCC, with relatively reduced complement activation, to modulate humoral autoimmunity and increase platelet counts in pediatric ITP.
Glycoengineered type II anti-CD20 humanized IgG1 that binds CD20 on B cells and depletes them via enhanced Fc-gamma RIII–mediated ADCC and direct, caspase-independent type II cell death, with relatively reduced complement-dependent cytotoxicity; used to suppress pathogenic CD20+ B cells (e.g., in ITP).
Binds CD20 on B cells and depletes them via enhanced Fc gamma RIIIa–mediated ADCC (NK cells/monocytes) and induction of type II, caspase-independent direct cell death; complement lysis is relatively reduced.