Immunotherapies targeting public neoantigens (NeoAgs) provide a promising avenue for targeted cancer treatment with reduced off-target risks. A prime target stems from the R175H mutation in TP53, the most frequently mutated gene in cancer. Patients harboring TP53(R175H) and the HLA-A*02:01 allele present a targetable public NeoAg with broad clinical applicability across multiple cancer types, including colorectal, ovarian, and pancreatic cancers. Despite therapeutic potential, there are currently no FDA-approved therapies targeting the TP53(R175H) NeoAg. We isolated TCR7A, a high-affinity T-cell receptor (TCR) clone specific to the TP53(R175H)/HLA-A*02:01 complex, and evaluated its efficacy as a TCR-engineered T-cell (TCR-T) therapy. To enhance therapeutic potential, we engineered “armored” T cells to co-express TCR7A, the CD8 co-receptor to stabilize TCR-NeoAg interactions, and constitutive Interleukin-18 (IL-18) to counteract T-cell exhaustion. Armored T cells exhibited significantly stronger tumor-specific cytotoxicity, with sustained tumor killing through four successive rechallenges. Armoring also increased T-cell activation, significantly increasing secretion of interferon-gamma and tumor necrosis factor-alpha upon exposure to NeoAg-expressing cancer cell lines. Additionally, the engineered T cells maintained a high degree of specificity, as confirmed by amino acid mutagenesis scanning which showed no expanded off-target reactivity compared to the TCR7A-only control. These findings establish a potent and specific armored TCR-T platform for targeting a high-prevalence driver mutation, supporting the clinical translation of this "off-the-shelf" therapeutic.