Bispecific T-cell engager (BiTE) antibody that links CD3 on T cells to CD19 on B cells to induce T cell–mediated cytotoxicity.
A bispecific T-cell engager (BiTE) antibody that binds CD3 on T cells and CD19 on B cells to form an immunologic synapse, redirecting and activating T cells to kill CD19+ B-lymphoblasts via perforin/granzyme-mediated cytotoxicity.
YES
DIRECT
Blinatumomab links CD3+ T cells to CD19+ cells, forming an immunologic synapse that triggers T‑cell cytotoxicity via perforin/granzyme-mediated apoptosis of the CD19-expressing cells.
Bispecific T-cell engager (BiTE) antibody that links CD3 on T cells to CD19 on B cells to induce T cell–mediated cytotoxicity.
A bispecific T-cell engager (BiTE) antibody that binds CD3 on T cells and CD19 on B cells to form an immunologic synapse, redirecting and activating T cells to kill CD19+ B-lymphoblasts via perforin/granzyme-mediated cytotoxicity.
NO
INDIRECT
Blinatumomab binds CD3ε to engage and activate T cells, which then kill CD19+ target cells via perforin/granzyme; CD3ε-expressing T cells are not themselves targeted for killing.
Chimeric IgG1 anti-EGFR monoclonal antibody that blocks EGFR ligand binding, inhibits EGFR signaling, promotes receptor internalization, and can induce ADCC.
Chimeric IgG1 monoclonal antibody against EGFR that blocks ligand binding and receptor dimerization, inhibits downstream EGFR→RAS/RAF/MEK/ERK signaling, promotes receptor internalization, and can mediate ADCC, leading to antiproliferative and antitumor effects.
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on NK cells/macrophages to induce ADCC (and sometimes CDC), leading to lysis of EGFR+ cells; EGFR blockade also causes antiproliferative effects.
Chimeric IgG1 anti-EGFR monoclonal antibody that blocks EGFR ligand binding, inhibits EGFR signaling, promotes receptor internalization, and can induce ADCC.
Chimeric IgG1 monoclonal antibody against EGFR that blocks ligand binding and receptor dimerization, inhibits downstream EGFR→RAS/RAF/MEK/ERK signaling, promotes receptor internalization, and can mediate ADCC, leading to antiproliferative and antitumor effects.
NO
INDIRECT
Cetuximab’s Fc engages CD16a on NK cells to mediate ADCC against EGFR-positive cells; CD16a-expressing cells serve as effectors and are not targeted or killed by the drug.
Anti-CD20 monoclonal antibody that depletes B cells via ADCC, complement activation, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via Fc-mediated ADCC, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 and induces killing via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (CDC), and apoptosis triggered by CD20 crosslinking.