Bispecific T‑cell–engaging antibody (BCMA×CD3) that redirects cytotoxic T cells to kill BCMA-positive malignant plasma cells.
Humanized bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to activate cytotoxic T lymphocytes and mediate targeted lysis of BCMA-positive cells via immune synapse formation and perforin/granzyme release.
Bispecific T-cell engager binds BCMA on target cells and CD3 on T cells, forming an immune synapse that triggers T-cell degranulation (perforin/granzyme) and kills BCMA-positive cells.
Bispecific T‑cell–engaging antibody (GPRC5D×CD3) that redirects T cells to GPRC5D-positive myeloma cells.
Humanized bispecific antibody that binds CD3 on T cells and GPRC5D on myeloma cells, cross-linking T cells to GPRC5D+ targets to form an immune synapse and trigger T-cell activation and cytotoxic killing (perforin/granzyme) of tumor cells while sparing most normal tissues.
Talquetamab bridges CD3 on T cells to GPRC5D on target cells, forming an immune synapse that activates T cells to kill GPRC5D+ cells via perforin/granzyme-mediated cytolysis.
Subcutaneous anti‑CD38 IgG1 monoclonal antibody that depletes CD38-positive plasma cells and immunosuppressive cells via ADCC/CDC/ADCP and augments T‑cell activity.
Subcutaneous daratumumab is an anti‑CD38 IgG1 monoclonal antibody that binds CD38 on plasma cells and other CD38+ immunosuppressive cells, inducing cell depletion via Fc‑mediated effector functions (ADCC, CDC, ADCP) and indirectly enhancing T‑cell activity.
Anti‑CD38 IgG1 binds CD38 on target cells and triggers Fc‑mediated effector functions—ADCC (NK cells), CDC (complement), and ADCP (phagocytes)—leading to depletion of CD38+ cells.
Afucosylated human IgG1 monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα) on eosinophils and basophils; blocks IL-5 signaling and induces potent ADCC via NK cells, leading to near-complete eosinophil depletion and reduced eosinophilic airway inflammation in severe eosinophilic asthma.
Afucosylated human IgG1 monoclonal antibody that binds IL-5 receptor alpha (IL-5Rα) on eosinophils and basophils, blocking IL‑5 signaling and engaging NK cells via enhanced FcγRIIIa binding to drive potent ADCC, resulting in near-complete eosinophil depletion and reduced eosinophilic inflammation.
Benralizumab binds IL-5Rα on eosinophils/basophils and engages NK cells via its afucosylated Fc (high-affinity FcγRIIIa), triggering antibody-dependent cellular cytotoxicity that depletes IL-5Rα+ cells.
Intravenous, type II glycoengineered anti‑CD20 monoclonal antibody that induces direct B‑cell death and enhances antibody‑dependent cellular cytotoxicity (ADCC).
Type II glycoengineered humanized IgG1 anti-CD20 mAb that binds CD20 on B cells and depletes them primarily via enhanced FcγRIIIa-mediated ADCC/ADCP and by inducing direct, caspase-independent cell death (with limited CDC).
Obinutuzumab binds CD20 on B cells and kills them via enhanced ADCC/ADCP through Fc-gamma RIIIa engagement on NK cells/macrophages, and by inducing direct, caspase-independent cell death (with limited CDC).