A chimeric anti-CD20 monoclonal antibody that depletes CD20-positive B cells, reducing pathogenic autoantibody production and immune complex–mediated tissue damage.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby reducing pathogenic autoantibody production and immune complex–mediated tissue injury.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc receptor–mediated effector killing (ADCC/ADCP), with additional apoptosis upon crosslinking.
An autologous chimeric antigen receptor (CAR) T-cell therapy targeting Claudin 18.2 (CLDN18.2). Patient T cells are engineered to express a CAR that binds CLDN18.2 on tumor cells, triggering T-cell activation, cytokine release, and perforin/granzyme-mediated cytotoxicity to lyse CLDN18.2-positive cancer cells.
Autologous T cells engineered to express a CLDN18.2-specific chimeric antigen receptor (CAR). Binding to CLDN18.2 on tumor cells activates the T cells, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of CLDN18.2-positive cancer cells.
CLDN18.2-specific CAR T cells bind CLDN18.2 on target cells, activate, and kill them via perforin/granzyme-mediated cytolysis (apoptosis).
Chimeric IgG1 monoclonal antibody (Qarziba) targeting GD2 on neuroblastoma cells; mediates ADCC (via NK cells and macrophages), complement-dependent cytotoxicity, and antibody-dependent phagocytosis; may also promote apoptosis.
Chimeric IgG1 monoclonal antibody targeting GD2 on neuroblastoma cells; induces tumor cell killing via Fc‑mediated ADCC (engaging NK cells and macrophages/monocytes), complement‑dependent cytotoxicity, and antibody‑dependent phagocytosis, with potential induction of apoptosis.
Binds GD2 on tumor cells and recruits immune effectors via Fc (NK cells/macrophages) to mediate ADCC and antibody-dependent phagocytosis; also activates complement for CDC, leading to target-cell lysis.
An intravenous antibody–drug conjugate (RC48) consisting of an anti‑HER2 monoclonal antibody linked to the microtubule inhibitor MMAE; binds HER2, internalizes, and releases MMAE to disrupt microtubules, causing G2/M arrest, apoptosis, and bystander killing.
Disitamab vedotin is a humanized anti‑HER2 monoclonal antibody conjugated to the microtubule inhibitor monomethyl auristatin E (MMAE). It binds HER2 on tumor cells, is internalized, and releases MMAE intracellularly to inhibit tubulin polymerization, disrupting microtubules and causing G2/M arrest and apoptosis; the membrane‑permeable payload can also produce bystander killing.
ADC binds HER2, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis; membrane-permeable payload can also cause bystander killing.
Anti-EGFR antibody–drug conjugate delivering the microtubule-disrupting payload MMAE to EGFR-expressing tumor cells, causing mitotic arrest and apoptosis.
Anti-EGFR monoclonal antibody linked to MMAE; binds EGFR on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in EGFR-expressing cells.
ADC binds EGFR, is internalized, and releases MMAE, which inhibits tubulin polymerization leading to G2/M arrest and apoptosis of EGFR-expressing cells.