Anti-CD20 monoclonal antibody that depletes CD20+ B cells, reducing ANCA production.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and apoptosis, thereby reducing ANCA production.
YES
DIRECT
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP, and can trigger apoptosis, leading to depletion of CD20+ cells.
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.
YES
DIRECT
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).
YES
DIRECT
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 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 binds FcRn via engineered Fc in endosomes to extend antibody half-life; this interaction does not recruit effector functions or complement. Any cytotoxicity is directed at HIV Env-expressing cells via ADCC/ADCP, not at FcRn-expressing cells.
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 binds HIV-1 Env on infected cells; its Fc engages CD16a on NK cells to trigger ADCC, killing Env-expressing cells. CD16a+ cells act as effectors, not targets.