An antibody-drug conjugate targeting TROP-2 that delivers the cytotoxic payload SN-38 (a topoisomerase I inhibitor) to tumor cells, causing DNA damage and cell death, with potential bystander effect.
Humanized anti-TROP-2 monoclonal antibody linked via a cleavable linker to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells, the ADC is internalized and releases SN-38, which stabilizes topoisomerase I-DNA complexes, causing DNA breaks, inhibition of replication, and apoptosis; released payload can also exert a bystander effect.
ADC binds TROP-2, is internalized, linker is cleaved to release SN-38 (topoisomerase I inhibitor), causing DNA damage, replication arrest, and apoptosis; released payload can also cause a bystander effect.
Oral small-molecule HER2-selective tyrosine kinase inhibitor that blocks ERBB2 signaling (PI3K/AKT, MAPK) with CNS activity.
Oral HER2-selective tyrosine kinase inhibitor that binds the ERBB2 (HER2) intracellular kinase domain, blocks receptor phosphorylation and downstream PI3K/AKT and MAPK signaling, leading to inhibition of proliferation and death of HER2-overexpressing tumor cells; exhibits CNS penetration/activity.
Tucatinib directly inhibits the HER2 tyrosine kinase, blocking PI3K/AKT and MAPK signaling, leading to growth arrest and apoptosis of HER2-expressing tumor cells.
Humanized anti-HER2 monoclonal antibody that binds extracellular HER2, inhibits signaling, and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized monoclonal antibody against HER2 (ERBB2) that binds the extracellular domain, inhibits receptor dimerization/activation and downstream MAPK/PI3K signaling, and promotes immune-mediated tumor cell killing via antibody-dependent cellular cytotoxicity (ADCC) in HER2-overexpressing cancers.
Trastuzumab binds HER2 on target cells and recruits FcγR-expressing immune effectors (e.g., NK cells) to mediate antibody-dependent cellular cytotoxicity (ADCC), with possible complement-dependent cytotoxicity (CDC).
An anti-HER2 antibody-drug conjugate consisting of a recombinant anti-HER2 monoclonal antibody linked to a camptothecin-derived topoisomerase I inhibitor payload; upon binding HER2 and internalization, it releases the payload to inhibit Topo I, causing DNA damage and tumor cell death, and may also suppress HER2 signaling and engage Fc-mediated effector functions.
Anti-HER2 monoclonal antibody linked to a camptothecin-derived topoisomerase I inhibitor; binds HER2 and is internalized, then releases the payload to inhibit Topo I, causing DNA damage, cell-cycle arrest, and tumor cell death; may also suppress HER2 signaling and engage Fc-mediated effector functions.
The anti-HER2 ADC binds HER2 on target cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that causes DNA damage, cell-cycle arrest, and apoptosis; Fc-mediated effector functions may add cytotoxicity.
Anti-CD38 human IgG1κ monoclonal antibody given intravenously (16 mg/kg weekly for 4 doses) that binds CD38 on plasma cells/plasmablasts and depletes them via ADCC/ADCP, complement-dependent cytotoxicity, and apoptosis to reduce anti-platelet autoantibody production in ITP.
Human IgG1κ monoclonal antibody that binds CD38 on plasma cells and other CD38+ immune cells and depletes them via ADCC, ADCP, complement-dependent cytotoxicity, and apoptosis, thereby reducing pathogenic autoantibody production.
Anti-CD38 IgG1 binds CD38 on target cells and triggers Fc-mediated ADCC (NK cells), ADCP (macrophages), complement-dependent cytotoxicity (CDC), and can induce apoptosis upon cross-linking, leading to depletion of CD38+ cells.