Human IgG1 broadly neutralizing monoclonal antibody against HIV-1 Env with LS Fc mutations to increase FcRn binding and extend half-life. It targets the gp120 CD4-binding site to neutralize diverse HIV-1 strains, block gp120 engagement with CD4/co-receptors to prevent viral entry, and via Fc effector functions (ADCC/ADCP) may promote clearance of Env-expressing infected cells.
Human IgG1 broadly neutralizing monoclonal antibody targeting the HIV-1 Env gp120 CD4-binding site to block gp120 engagement with CD4/co-receptors and prevent viral entry; Fc region mediates ADCC/ADCP against Env-expressing cells; LS Fc mutations enhance FcRn binding to extend serum half-life.
Antibody binds gp120 on Env-expressing infected cells and engages Fcγ receptors to trigger immune effector killing (ADCC by NK cells, ADCP by phagocytes; potential complement-mediated lysis).
Type II anti‑CD20 monoclonal antibody given prior to glofitamab to debulk B cells and mitigate CRS; induces direct B‑cell death and Fc‑mediated ADCC/ADCP.
Type II anti-CD20 humanized IgG1 monoclonal antibody that binds CD20 on B cells; glycoengineering increases Fc-gamma RIIIa affinity to enhance antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), and it also induces direct, caspase-independent B-cell death, depleting CD20+ B cells (used pre-glofitamab to debulk and mitigate CRS).
Binds CD20 on B cells and recruits immune effectors via Fc to mediate ADCC (NK cells) and ADCP (macrophages); as a type II anti-CD20 it also induces direct, caspase-independent B-cell death (with minimal CDC).
Human IgG1 broadly neutralizing monoclonal antibody against HIV-1 Env with LS Fc mutations to increase FcRn binding and extend half-life. It targets the gp120 V3-glycan supersite to neutralize diverse HIV-1 strains, block gp120 engagement with CD4/co-receptors to prevent viral entry, and via Fc effector functions (ADCC/ADCP) may promote clearance of Env-expressing infected cells.
10-1074-LS is a human IgG1 broadly neutralizing monoclonal antibody that binds the HIV-1 Env gp120 V3-glycan supersite, neutralizing diverse virions and blocking gp120 engagement with CD4 and co-receptors to prevent viral entry. LS Fc mutations enhance FcRn binding and extend serum half-life. Through Fc effector functions (e.g., ADCC/ADCP), it may also promote clearance of Env-expressing infected cells.
IgG1 binding to Env on infected cells engages FcγR-bearing effector cells to mediate ADCC/ADCP (and potentially complement activation), leading to killing of Env-expressing cells.
An antibody-drug conjugate comprising a fully human anti–Nectin-4 monoclonal antibody linked to exatecan; it binds Nectin-4 on tumor cells, is internalized, and releases exatecan to inhibit topoisomerase I, causing replication-associated DNA damage and tumor cell death.
Fully human anti-Nectin-4 monoclonal antibody linked to exatecan; binds Nectin-4 on tumor cells, is internalized, and releases exatecan to inhibit topoisomerase I, trapping Topo I-DNA complexes and causing replication-associated DNA damage and tumor cell death.
The ADC binds Nectin-4 on target cells, is internalized, and releases exatecan; the payload inhibits topoisomerase I, trapping Topo I–DNA complexes and causing replication-associated DNA damage leading to cell death.
Afucosylated humanized IgG1 monoclonal antibody targeting the IL-5 receptor alpha (IL-5Rα) on eosinophils and basophils, inducing antibody-dependent cell-mediated cytotoxicity (ADCC) and resulting in near-complete eosinophil depletion.
Afucosylated humanized IgG1 monoclonal antibody targeting IL-5 receptor alpha on eosinophils and basophils; enhanced FcγRIIIa engagement drives potent ADCC, leading to near-complete depletion of eosinophils (and basophils) and functional blockade of IL-5 signaling, thereby reducing eosinophilic inflammation.
Benralizumab binds IL-5Rα on eosinophils/basophils and engages CD16a on NK cells, driving potent ADCC that lyses/apoptoses and depletes the target cells.