CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.
mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.
YES
DIRECT
CIK cells recognize ULBP2 via NKG2D and directly kill target cells through perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis.
CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.
mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.
YES
DIRECT
NKG2D on mRNA-CIK cells recognizes ULBP3 on target cells, triggering cytotoxicity via perforin/granzyme release and Fas/FasL-mediated apoptosis.
CIK cells transiently enhanced by mRNA modification to boost activity; retain MHC-unrestricted cytotoxicity via NKG2D with perforin/granzyme and Fas/FasL pathways; experimental arm.
mRNA-engineered cytokine-induced killer (CIK) cells that transiently boost activation and cytotoxic function while retaining MHC-unrestricted killing via NKG2D recognition of stress ligands (e.g., MICA/B, ULBPs), mediating tumor cell death through perforin/granzyme release and Fas/FasL pathways.
YES
DIRECT
NKG2D on mRNA-enhanced CIK cells binds ULBP4 on target cells, triggering perforin/granzyme-mediated lysis and Fas–FasL–induced apoptosis.
Anti-HER2 monoclonal antibody that inhibits HER2 signaling and mediates ADCC.
Humanized monoclonal antibody that binds HER2 (ERBB2) on tumor cells, blocks HER2 signaling and proliferation, and engages Fc receptors on immune cells to mediate antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing cells.
YES
DIRECT
Trastuzumab binds HER2 on tumor cells and its Fc engages Fcγ receptors on NK cells/macrophages to trigger antibody‑dependent cellular cytotoxicity (ADCC), leading to target cell lysis (with possible complement activation).
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.
YES
INDIRECT
CUSP06 binds CDH6 on tumor cells, is internalized, and releases exatecan, which inhibits DNA topoisomerase I, stabilizing the topo I–DNA complex and causing DNA breaks, replication arrest, and apoptosis (with potential bystander killing).