Mantle cell lymphoma (MCL) remains a clinically challenging B-cell malignancy because of its aggressive course, recurrent relapse, and eventual treatment resistance. Given the vulnerability of cancer cells to redox imbalance, we examined the antitumor potential of a biomimetic iron complex designed to enhance intracellular reactive oxygen species (ROS). The iron complex induced robust ROS accumulation and cytotoxicity across multiple MCL cell lines at single-digit micromolar concentrations. Mechanistically, ROS amplification suppressed major lymphoma survival pathways, including BCR/CD19–PI3K/AKT, NF-κB, and MEK/ERK signaling. In parallel, the iron complex increased lipid peroxidation and ferroptotic stress and induced oxidative DNA damage, DNA damage response signaling, and PARP cleavage. Rescue experiments further demonstrated that intracellular iron accumulation drives lipid peroxidation and subsequent oxidative DNA damage. Consistent with these findings, the iron complex significantly suppressed tumor growth in an MCL xenograft model. Collectively, our findings demonstrate that a biomimetic iron complex exploits the redox vulnerability of MCL by promoting lipid peroxidation and oxidative DNA damage-associated cell death, supporting redox-active metal-based therapeutics as a distinct therapeutic strategy for MCL.