Anti-CD20 chimeric monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (C1q activation/MAC lysis), and can trigger apoptosis signaling.
CD20×CD3 bispecific monoclonal antibody (T‑cell engager) that binds CD20 on B cells and CD3 on T cells, activating T‑cell cytotoxicity to eliminate CD20+ cells.
Mosunetuzumab is a humanized CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, cross-linking them to activate TCR signaling and immune synapse formation, redirecting T-cell cytotoxicity (perforin/granzyme) to kill and deplete CD20+ malignant B cells.
YES
DIRECT
Bispecific T-cell engager crosslinks CD20 on target cells with CD3 on T cells, forming an immune synapse and inducing perforin/granzyme-mediated cytotoxicity against CD20+ cells.
CD20×CD3 bispecific monoclonal antibody (T‑cell engager) that binds CD20 on B cells and CD3 on T cells, activating T‑cell cytotoxicity to eliminate CD20+ cells.
Mosunetuzumab is a humanized CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, cross-linking them to activate TCR signaling and immune synapse formation, redirecting T-cell cytotoxicity (perforin/granzyme) to kill and deplete CD20+ malignant B cells.
NO
INDIRECT
Mosunetuzumab engages CD3 on T cells to redirect their cytotoxicity toward CD20+ B cells; T cells (CD3ε+) are not the killed cells.
Chimeric anti‑CD20 IgG1 monoclonal antibody that depletes B cells via ADCC, CDC, ADCP, and apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and depletes them via Fc-mediated ADCC (NK cells), CDC (complement activation), ADCP (macrophages), and can also induce apoptosis.
Antibody–drug conjugate of farletuzumab linked to eribulin; targets FRα on tumor cells to deliver eribulin intracellularly, disrupting microtubules and inducing apoptosis.
FRα-targeted ADC: farletuzumab binds folate receptor‑α on tumor cells and is internalized; a cathepsin B–cleavable linker releases eribulin intracellularly, which binds the vinca domain of tubulin to inhibit microtubule polymerization, causing G2/M mitotic arrest and apoptosis (with potential bystander effect).
YES
DIRECT
Farletuzumab binds FRα on tumor cells, the ADC is internalized, cathepsin B cleaves the linker to release eribulin, which inhibits microtubule polymerization (vinca domain), causing G2/M arrest and apoptosis (with potential bystander effect).