An intravenous glyco-humanized polyclonal antibody (biologic immunotherapy) engineered with human-like glycosylation to reduce immunogenic carbohydrate residues and enhance Fc effector function; expected to mediate tumor cell killing via ADCC, ADCP, and CDC in advanced/metastatic solid tumors.
Glyco‑humanized polyclonal antibody that binds multiple tumor epitopes and is engineered with human-like Fc glycosylation to enhance Fc effector function and reduce immunogenic carbohydrates; kills tumor cells via Fc-dependent mechanisms including ADCC (via Fcγ receptor–bearing NK cells), ADCP (macrophages), and CDC (classical complement activation).
YES
DIRECT
Antibody binds tumor-associated antigens and kills via Fc-dependent effector functions: ADCC by NK cells (FcγR), ADCP by macrophages, and complement-dependent cytotoxicity (CDC).
Anti-CD20 monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity, with potential direct apoptotic effects, thereby reducing pathogenic B-cell activity.
YES
DIRECT
Rituximab binds CD20 on B cells and its Fc engages immune effectors to trigger antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity; CD20 crosslinking can also induce apoptosis.
An intravenous glyco-humanized polyclonal antibody (biologic immunotherapy) engineered with human-like glycosylation to reduce immunogenic carbohydrate residues and enhance Fc effector function; expected to mediate tumor cell killing via ADCC, ADCP, and CDC in advanced/metastatic solid tumors.
Glyco‑humanized polyclonal antibody that binds multiple tumor epitopes and is engineered with human-like Fc glycosylation to enhance Fc effector function and reduce immunogenic carbohydrates; kills tumor cells via Fc-dependent mechanisms including ADCC (via Fcγ receptor–bearing NK cells), ADCP (macrophages), and CDC (classical complement activation).
NO
INDIRECT
The antibody binds tumor antigens with its Fab and engages CD16A on NK cells via its Fc to trigger ADCC (and also ADCP/CDC), killing the antibody-opsonized tumor cells; CD16A+ cells are effectors, not targets of killing.
An intravenous glyco-humanized polyclonal antibody (biologic immunotherapy) engineered with human-like glycosylation to reduce immunogenic carbohydrate residues and enhance Fc effector function; expected to mediate tumor cell killing via ADCC, ADCP, and CDC in advanced/metastatic solid tumors.
Glyco‑humanized polyclonal antibody that binds multiple tumor epitopes and is engineered with human-like Fc glycosylation to enhance Fc effector function and reduce immunogenic carbohydrates; kills tumor cells via Fc-dependent mechanisms including ADCC (via Fcγ receptor–bearing NK cells), ADCP (macrophages), and CDC (classical complement activation).
NO
INDIRECT
CD16B (Fc gamma receptor IIIb) is an Fc receptor on neutrophils; it is engaged by the antibody’s Fc to activate effector functions. XON7 binds tumor antigens and then recruits CD16-bearing effector cells to mediate ADCC/ADCP and CDC against the antibody-coated tumor cells, not the CD16B+ cells.
An intravenous glyco-humanized polyclonal antibody (biologic immunotherapy) engineered with human-like glycosylation to reduce immunogenic carbohydrate residues and enhance Fc effector function; expected to mediate tumor cell killing via ADCC, ADCP, and CDC in advanced/metastatic solid tumors.
Glyco‑humanized polyclonal antibody that binds multiple tumor epitopes and is engineered with human-like Fc glycosylation to enhance Fc effector function and reduce immunogenic carbohydrates; kills tumor cells via Fc-dependent mechanisms including ADCC (via Fcγ receptor–bearing NK cells), ADCP (macrophages), and CDC (classical complement activation).
NO
INDIRECT
XON7 opsonizes tumor antigens and engages Fcγ receptors (including CD32A) on immune effectors to drive ADCC/ADCP and CDC against the antibody-coated tumor cells; CD32A+ cells act as effectors, not targets of killing.