scFv(MSLN)-CD3zeta CAR-T Lentivirus

scFv(MSLN)-CD3ζ CAR-T Lentivirus is a gene-delivery reagent designed to generate T cells that recognize mesothelin (MSLN), a cell-surface glycoprotein expressed at elevated levels in several solid tumors. The encoded chimeric antigen receptor combines an extracellular anti-MSLN single-chain variable fragment (scFv) with membrane-anchoring elements and the intracellular signaling domain of CD3ζ. The scFv provides antibody-like recognition of surface MSLN without requiring peptide presentation by the major histocompatibility complex, while CD3ζ initiates T-cell activation after antigen engagement. Because the construct contains CD3ζ without an additional costimulatory domain, it represents a first-generation CAR design. Lentiviral delivery supports efficient gene transfer and stable receptor expression in transduced T cells, providing a consistent system for examining the fundamental activity of MSLN-directed CAR-T cells.

This product is intended for research on mesothelin-targeted cellular immunotherapy and antigen-specific T-cell function. Experimental CAR-T cells generated with the lentivirus can be evaluated for receptor expression, MSLN-dependent activation, target-cell killing, cytokine secretion, proliferation, and changes in cellular phenotype. Researchers may compare MSLN-high, MSLN-low, and MSLN-negative target cells to investigate antigen-density requirements, selectivity, and potential on-target effects in cells with different expression levels. The resulting cells are suitable for appropriately designed studies involving malignant mesothelioma, pancreatic cancer, ovarian cancer, and other MSLN-expressing solid-tumor models. As a first-generation construct, scFv(MSLN)-CD3ζ CAR-T Lentivirus also provides a useful reference for assessing how added costimulatory domains, modified binders, or alternative receptor architectures affect CAR-T-cell performance. Further applications include studies of soluble or shed mesothelin, repeated antigen exposure, tumor-cell resistance, immune escape, and suppression within the tumor microenvironment.