Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity, ADCC, and apoptosis; used to reduce anti-PLA2R autoantibodies in membranous nephropathy.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on pre‑B and mature B cells and induces B‑cell depletion via complement‑dependent cytotoxicity, antibody‑dependent cellular cytotoxicity, and apoptosis, thereby reducing pathogenic autoantibody production (e.g., anti‑PLA2R).
Anti-CD20 mAb binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC/phagocytosis, and can trigger apoptosis, depleting CD20+ cells.
Anti-HER2 antibody–drug conjugate (RC48) that binds HER2, internalizes, and releases MMAE to disrupt microtubules, causing G2/M arrest and apoptosis; may also mediate ADCC/bystander effects.
Anti-HER2 antibody–drug conjugate: disitamab binds HER2 on tumor cells, is internalized, and via a cleavable linker releases MMAE, which binds tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis; may also induce ADCC and bystander killing.
HER2-targeted ADC binds HER2, is internalized, then releases MMAE that disrupts microtubules (tubulin inhibition), causing G2/M arrest and apoptosis; may also trigger ADCC/bystander killing.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy with 4-1BB/CD3ζ signaling domains that targets and kills CD19-positive B-cell malignancies.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor with 4-1BB costimulatory and CD3ζ signaling domains. Upon binding CD19 on B-cell malignancies, CAR signaling triggers T-cell activation, proliferation, and cytotoxic effector functions (perforin/granzyme release and cytokine secretion), resulting in targeted lysis of CD19-positive cells and antitumor activity.
Anti-CD19 CAR T cells bind CD19 and, upon CAR activation, kill target cells via perforin/granzyme-mediated cytotoxicity (and death-receptor pathways), leading to apoptosis and lysis of CD19-positive cells.
An anti-PSMA IgG monoclonal antibody conjugated with the tetraxetan chelator and radiolabeled with actinium-225; a targeted alpha therapy delivering high-LET alpha emissions to PSMA-expressing tumor cells, causing DNA double-strand breaks and tumor cell death.
Anti-PSMA IgG monoclonal antibody chelated with tetraxetan delivers actinium-225 to PSMA-expressing tumor cells. The Ac-225 emits high-LET alpha particles that induce localized DNA double-strand breaks, leading to targeted cytotoxicity and tumor cell death.
An anti-PSMA antibody delivers actinium-225 to PSMA-expressing cells; emitted alpha particles induce localized DNA double-strand breaks, causing lethal damage to the target cells.
Chimeric IgG1 monoclonal antibody against EGFR that blocks ligand binding and receptor activation, inhibiting downstream signaling (RAS/RAF/MEK/ERK and PI3K/AKT) and mediating antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocks ligand binding and receptor dimerization/activation, inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling; additionally mediates ADCC via Fcγ receptor–bearing effector cells.
Cetuximab binds EGFR on target cells and engages Fcγ receptor–bearing effector cells (e.g., NK cells) to induce ADCC, killing the EGFR+ cells.