Humanized IgG1 monoclonal antibody against HER2/ErbB2 that binds the extracellular domain to block receptor dimerization and activation, downregulating PI3K/AKT/MAPK signaling and promoting receptor internalization; additionally mediates antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing cells.
Trastuzumab binds HER2 on target cells and engages Fcγ receptors on NK cells/macrophages to trigger antibody-dependent cellular cytotoxicity (perforin/granzyme-mediated lysis); complement activation may also contribute.
T cells from a newly matched donor engineered to express an anti-CD5 chimeric antigen receptor to bind CD5 on malignant T cells and trigger CAR-mediated cytotoxic killing, with anticipated on-target depletion of normal CD5+ T cells.
Allogeneic donor T cells engineered to express an anti-CD5 chimeric antigen receptor bind CD5 on malignant T cells, triggering CAR-mediated activation (CD3ζ/costimulatory signaling), proliferation, and perforin/granzyme-dependent cytotoxic killing; on-target depletion of normal CD5+ T cells is anticipated.
Anti-CD5 CAR T cells bind CD5, triggering CAR (CD3ζ/costimulatory) activation and directly killing CD5+ cells via perforin/granzyme-mediated cytolysis (and related death receptor pathways).
CUSP06 is a cadherin-6 (CDH6)–directed antibody–drug conjugate (ADC). Its monoclonal antibody binds CDH6 on tumor cells, is internalized, and releases an intracellular cytotoxic payload (type not specified) to induce DNA damage and apoptosis in CDH6-positive tumors, including platinum-refractory/resistant ovarian cancer and other advanced solid tumors.
CUSP06 is an anti‑CDH6 antibody–drug conjugate that binds CDH6 on tumor cells, is internalized, and releases the exatecan payload via a protease‑cleavable linker. Exatecan inhibits topoisomerase I, stabilizing the topo I–DNA cleavable complex, causing DNA breaks, replication arrest, and apoptosis, with potential bystander killing of neighboring tumor cells.
An anti-CDH6 ADC binds CDH6 on tumor cells, is internalized, and releases exatecan via a protease-cleavable linker; exatecan inhibits topoisomerase I, causing DNA breaks, replication arrest, and apoptosis (with potential bystander effect).
Anti-CD20 chimeric monoclonal antibody that depletes B cells, lowering ANCA autoantibody production and antigen presentation.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, reducing ANCA autoantibody production and antigen presentation.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC/phagocytosis by NK cells/macrophages; it can also trigger apoptosis of CD20+ cells.
Investigational antitumor agent for injection; specific target/mechanism not disclosed in the registry; dose exploration ongoing.
IgG1 monoclonal antibody targeting nectin-4 delivers a cleavable topoisomerase I inhibitor payload; after binding and internalization in nectin-4–expressing tumor cells, linker cleavage releases the payload to inhibit topoisomerase I, blocking DNA replication and inducing cell cycle arrest and apoptosis.
ADC binds nectin-4 on tumor cells, is internalized, and releases a cleavable topoisomerase I inhibitor that blocks DNA replication and induces apoptosis.