Autologous chimeric antigen receptor T-cell therapy engineered to target BCMA on malignant plasma cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes BCMA on malignant plasma cells, triggering MHC-independent T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of the target cells.
BCMA-specific CAR T cells bind BCMA on target cells, become activated, and directly kill via perforin/granzyme-mediated cytolysis (and death-receptor pathways).
Anti–IL-5Rα monoclonal antibody that induces antibody-dependent cell-mediated cytotoxicity to deplete eosinophils and basophils.
Afucosylated humanized monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα). Binds IL-5Rα on eosinophils and basophils and triggers enhanced antibody-dependent cell-mediated cytotoxicity (ADCC), leading to depletion/apoptosis of these cells and suppression of eosinophilic inflammation.
Benralizumab binds IL-5Rα on eosinophils/basophils and engages FcγRIIIa on NK cells (enhanced by afucosylation), triggering antibody-dependent cell-mediated cytotoxicity and apoptosis, depleting the target-expressing cells.
CD20×CD3 bispecific IgG that engages T cells via CD3 to redirect cytotoxicity against CD20-positive B cells.
Bispecific IgG that binds CD20 on B cells and CD3 on T cells, crosslinking them to form an immunologic synapse and redirect T‑cell cytotoxicity to lyse CD20‑positive malignant B cells.
Glofitamab bridges CD20 on target B cells and CD3 on T cells, forming an immunologic synapse that activates T cells to kill CD20+ cells via perforin/granzyme-mediated cytotoxicity.
Chimeric anti-CD20 monoclonal IgG1 antibody that depletes B cells via ADCC, complement activation, and apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive malignant and normal B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Anti-CD20 antibody binds CD20 on B cells and induces killing via ADCC (FcγR+ NK/macrophages), complement-dependent cytotoxicity (MAC), and direct apoptotic signaling.
Glycoengineered type II anti-CD20 monoclonal antibody with enhanced ADCC and induction of direct cell death.
Glycoengineered humanized IgG1 type II anti‑CD20 monoclonal antibody that binds CD20 on B cells; afucosylated Fc increases affinity for FcγRIIIa to enhance antibody‑dependent cellular cytotoxicity (and phagocytosis), and it induces potent direct, caspase‑independent cell death with relatively limited complement activation, leading to B‑cell depletion.
Anti-CD20 IgG1 binds CD20 on B cells and engages Fc gamma RIIIa (CD16a) on NK cells/macrophages to mediate ADCC/ADCP; as a type II antibody it also induces caspase-independent direct cell death (with limited CDC).