Afucosylated humanized IgG1κ monoclonal antibody (brand name Fasenra) that binds IL‑5 receptor alpha (IL‑5Rα) on eosinophils and basophils, blocks IL‑5 signaling, and induces antibody‑dependent cell‑mediated cytotoxicity (ADCC), leading to near-complete eosinophil depletion and reduction of type‑2 eosinophilic inflammation in severe eosinophilic asthma.
Afucosylated humanized IgG1κ monoclonal antibody that binds IL‑5 receptor alpha (IL‑5Rα) on eosinophils and basophils, blocks IL‑5 signaling, and induces potent NK cell–mediated ADCC, leading to near-complete eosinophil depletion and reduction of type‑2 eosinophilic inflammation.
Benralizumab binds IL-5Ralpha on eosinophils/basophils and engages Fc gamma RIIIa on NK cells to trigger potent ADCC, directly killing IL-5Ralpha+ cells (with additional IL-5 signaling blockade).
An antibody-drug conjugate targeting mesothelin (MSLN). The monoclonal antibody binds MSLN on tumor cells, is internalized, and releases a cytotoxic payload intracellularly to induce tumor cell death, with potential bystander effect.
Monoclonal antibody targets mesothelin (MSLN) on tumor cells, is internalized, and releases an attached cytotoxic payload inside the cell to induce tumor cell death, with potential bystander killing of adjacent cells.
ADC binds mesothelin on target cells, is internalized, and releases a cytotoxic payload inside the cell, causing cell death (with potential bystander killing).
Antibody–drug conjugate targeting Nectin-4 on urothelial tumor cells; after binding and internalization it releases the microtubule toxin monomethyl auristatin E (MMAE), disrupting tubulin polymerization and causing G2/M arrest and apoptosis.
Enfortumab vedotin is an antibody–drug conjugate targeting Nectin‑4 on tumor cells. Upon binding and internalization, a cleavable linker releases the cytotoxic payload MMAE, which binds tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis in Nectin‑4–expressing cells.
ADC binds Nectin-4 on target cells, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis.
Rabbit polyclonal antilymphocyte globulin used for in vivo T-cell depletion to reduce graft-versus-host disease risk.
Rabbit polyclonal IgG against multiple human T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA) that depletes T lymphocytes via complement-dependent cytotoxicity, Fc-mediated ADCC/phagocytosis, and apoptosis, producing in vivo T‑cell immunosuppression to reduce GVHD risk.
rATG contains antibodies that bind T‑cell antigens including CD11a, opsonizing these cells and inducing complement-dependent lysis and Fc receptor–mediated ADCC/phagocytosis, leading to apoptosis and depletion.
An anti-EGFR antibody–drug conjugate (ADC) with a drug–antibody ratio of 8 that couples an EGFR-specific monoclonal antibody to a high-potency DNA topoisomerase I inhibitor. After binding EGFR and internalization, it releases the topo I inhibitor to cause DNA damage and apoptosis; the antibody component may also inhibit EGFR signaling.
EGFR-targeting IgG1 monoclonal antibody conjugated via a cleavable linker to a high-potency topoisomerase I inhibitor. After binding EGFR on tumor cells and internalization/cleavage, it releases the TOP1 inhibitor to block DNA topoisomerase I, causing DNA damage, replication arrest, and apoptosis; the antibody may also inhibit EGFR signaling and can mediate bystander killing.
An EGFR-targeting ADC binds EGFR on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload that causes DNA damage/replication arrest leading to apoptosis; may also cause bystander killing.