scFv(MSLN)-41BB-CD3zeta CAR-T Lentivirus

scFv(MSLN)-41BB-CD3ζ CAR-T Lentivirus is a gene-delivery reagent designed to generate T cells that recognize mesothelin (MSLN), a cell-surface glycoprotein found at elevated levels in several solid tumors. The encoded second-generation chimeric antigen receptor combines an extracellular anti-MSLN single-chain variable fragment (scFv) with membrane-anchoring elements, the intracellular costimulatory domain of 4-1BB (CD137), and the CD3ζ activation domain. The scFv enables antibody-like recognition of surface MSLN without requiring major histocompatibility complex presentation. After antigen binding, CD3ζ initiates the primary activation signal, while 4-1BB provides costimulation associated with T-cell survival, sustained activity, and persistence. Lentiviral delivery supports efficient gene transfer and stable CAR expression in transduced T cells, providing a consistent platform for producing MSLN-responsive effector cells for laboratory investigation.

This product is intended for research on mesothelin-targeted cellular immunotherapy and the functional behavior of second-generation CAR-T cells. Transduced T cells can be evaluated for receptor expression, MSLN-dependent activation, target-cell killing, cytokine secretion, proliferation, survival, memory phenotype, and response durability. Comparisons among MSLN-high, MSLN-low, and MSLN-negative target cells can help define antigen-density requirements, selectivity, and possible on-target effects across 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. The construct can also serve as a reference when comparing 4-1BB signaling with first-generation CD3ζ-only CARs or receptors containing alternative costimulatory domains. Additional applications include examining soluble or shed mesothelin, repeated antigen exposure, T-cell exhaustion, tumor-cell resistance, immune escape, and suppression within the tumor microenvironment.