A type II anti-CD20 glycoengineered monoclonal antibody used to deplete B cells and reduce anti-drug antibodies/modify the immune milieu.
Type II anti-CD20 glycoengineered humanized IgG1 that binds CD20 on B cells with enhanced FcγRIII affinity, driving potent ADCC/ADCP and direct, caspase‑independent cell death to deplete CD20+ B cells and modulate the immune milieu.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells and its Fc engages FcγRIIIa (CD16a) on NK cells/macrophages to trigger ADCC/ADCP, killing CD20+ B cells; CD16a+ effector cells are not the cytotoxic targets.
A type II anti-CD20 glycoengineered monoclonal antibody used to deplete B cells and reduce anti-drug antibodies/modify the immune milieu.
Type II anti-CD20 glycoengineered humanized IgG1 that binds CD20 on B cells with enhanced FcγRIII affinity, driving potent ADCC/ADCP and direct, caspase‑independent cell death to deplete CD20+ B cells and modulate the immune milieu.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its Fc engages FcγRIII receptors (including CD16b on neutrophils) to recruit effector functions (ADCC/ADCP), causing death of CD20+ B cells. The CD16b-expressing cells are effectors, not the cells killed.
Humanized IgG1 monoclonal antibody against EGFR (HER1/ErbB1); blocks ligand binding and downstream MAPK/ERK and PI3K/AKT signaling, inhibits proliferation, and can induce ADCC.
Humanized IgG1 monoclonal antibody targeting EGFR; binds the receptor’s extracellular domain to block ligand binding and receptor activation, inhibiting MAPK/ERK and PI3K/AKT signaling, suppressing tumor cell proliferation and survival, and engaging Fc-mediated ADCC.
YES
DIRECT
Nimotuzumab (IgG1) binds EGFR on target cells and its Fc engages Fcγ receptors on immune effectors (e.g., NK cells), triggering ADCC (± some CDC), leading to lysis of EGFR+ cells; EGFR blockade also suppresses survival signaling.
Anti-EGFR IgG1 monoclonal antibody that blocks EGFR signaling and induces antibody-dependent cellular cytotoxicity (ADCC) via CD16 on NK cells.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream signaling (e.g., MAPK/PI3K pathways), suppressing tumor cell proliferation; its Fc engages CD16 (FcγRIIIa) on NK cells to trigger antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages CD16 (FcγRIIIa) on NK cells to trigger ADCC, leading to lysis of EGFR+ cells (with possible CDC/apoptosis).
Genetically modified autologous T cells engineered to express an HLA-A2–restricted T-cell receptor specific for NY-ESO-1, enabling recognition and cytotoxic killing of NY-ESO-1–expressing tumor cells.
Autologous T lymphocytes genetically modified to express an HLA-A2-restricted T-cell receptor specific for NY-ESO-1. These TCR-T cells recognize NY-ESO-1 peptide presented by HLA-A2 on tumor cells and, upon TCR engagement, activate cytotoxic effector functions (perforin/granzyme and cytokine release) to kill NY-ESO-1-positive cancer cells.
YES
DIRECT
TCR-engineered autologous T cells recognize NY-ESO-1 peptide presented by HLA-A2 on tumor cells and directly kill them via perforin/granzyme-mediated cytotoxicity (and Fas-FasL apoptosis).