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.
NO
INDIRECT
3BNC117-LS does not bind CD32a as an antigen; its Fc engages CD32a on effector myeloid cells to mediate ADCP/ADCC against HIV Env–expressing cells. CD32a+ cells serve as effectors, not targets, and are not killed by the drug.
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.
YES
DIRECT
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.
YES
DIRECT
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.
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.
NO
INDIRECT
BAT8007 targets Nectin-4 on the cell surface, is internalized, and releases exatecan, which inhibits topoisomerase I to cause replication-associated DNA damage and cell death. Cells are not killed because they express topoisomerase I per se; killing requires Nectin-4–mediated delivery.
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.
YES
DIRECT
Benralizumab binds IL-5Rα on eosinophils/basophils and engages CD16a on NK cells, driving potent ADCC that lyses/apoptoses and depletes the target cells.