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

The scFv(EGFR)-41BB-CD3zeta CAR-T lentiviral system is a second-generation chimeric antigen receptor vector designed to confer potent and specific recognition of epidermal growth factor receptor (EGFR) on tumor cells to human T cells, while supporting durable functionality and controllable activation. Its modular structure typically includes an anti-EGFR single-chain variable fragment for antigen binding, a hinge and transmembrane region for receptor stability, a 4-1BB (CD137) intracellular co-stimulatory domain for enhanced metabolic fitness and persistence, and a CD3 zeta signaling module to trigger T cell activation and cytotoxic programs. The use of a lentiviral vector backbone enables stable genomic integration and long-term CAR expression in primary T cells, ensuring consistent receptor density and functional performance across the cell population. Compared to transient transfection methods, lentiviral transduction supports sustained in vivo activity and memory cell formation, characteristics particularly important in solid tumor treatment, which often requires prolonged immune responses.

This EGFR-targeted second-generation CAR is widely used in preclinical oncology research to explore and advance T cell therapies against EGFR-positive malignancies, including but not limited to glioblastoma, head and neck squamous cell carcinoma, colorectal cancer, non-small cell lung cancer, and certain triple-negative breast cancers. It supports in vitro antigen-specific cytotoxicity assays, cytokine secretion profiling, and T cell phenotyping, allowing researchers to quantify potency, activation thresholds, antigen density dependence, and the kinetics of effector-to-memory cell conversion. In vivo, it is commonly used in xenograft and syngeneic models to study tumor control, pharmacodynamic biomarkers, CAR-T cell persistence, migration to solid tumor sites, and interactions with the immunosuppressive microenvironment. The 4-1BB-CD3zeta signaling pathway allows for detailed exploration of co-stimulatory biology, including comparisons with other domains, and facilitates the evaluation of combination therapy strategies (e.g., checkpoint blockade, metabolic reprogramming, or cytokine modulation) to enhance infiltration, persistence, and resistance to exhaustion.