Trop-2–directed antibody–drug conjugate that delivers SN-38 (a topoisomerase I inhibitor) to tumor cells, causing DNA damage and cell death with a potential bystander effect.
TROP-2–targeted antibody–drug conjugate (humanized anti–TROP-2 mAb linked to SN-38). After binding TROP-2 and internalization, the linker is cleaved to release SN-38, a topoisomerase I inhibitor that stabilizes topo I–DNA complexes, causing DNA damage and apoptosis; extracellular payload can produce a bystander effect.
ADC binds TROP-2, is internalized, and releases SN-38; the topoisomerase I inhibitor induces DNA damage leading to apoptosis (with possible bystander killing from extracellular SN-38).
Intravenous anti‑CD20 monoclonal antibody that depletes CD20+ B cells via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and direct apoptosis.
Anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and triggers Fc-mediated ADCC (NK cells/macrophages), activates complement for CDC/lysis, and can induce apoptosis via CD20 crosslinking.
Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
Rabbit anti-thymocyte IgG binds CD4 on T cells and induces complement-dependent lysis, Fc-mediated ADCC by effector cells, and apoptosis, depleting CD4+ T cells.
Anti-EGFR IgG1 monoclonal antibody that inhibits EGFR signaling to prevent RAS-pathway reactivation and tumor growth.
Chimeric IgG1 monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocking ligand binding and dimerization to inhibit downstream RAS–RAF–MEK–ERK and PI3K–AKT signaling, suppressing tumor cell proliferation and survival; Fc region may mediate ADCC.
Cetuximab binds EGFR on target cells and engages Fc receptors on immune effectors to induce ADCC (and possibly CDC), killing EGFR+ cells; it also blocks EGFR signaling (antiproliferative).
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B lymphocytes via complement-dependent cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and apoptosis; administered weekly until deep B-cell depletion is achieved.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ cells via complement-dependent cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and induction of apoptosis.
Binding to CD20 leads to complement-dependent cytotoxicity and Fc-mediated ADCC by immune effector cells, and can directly induce apoptosis of CD20+ B cells.