Zeaxanthin (98%)

• CAS: 144-68-3
• Catalog Number: ALC-FP-144683
• Category: Featured Products
• Description: By MS & NMRConsistent with the structure
• Appearance: Orange red solid
• Drying Loss: < 3.0%
• Sample Lot No.: A24X05091

Case Study

Zeaxanthin for Enhancing CD8+ T Cell-Mediated Anti-Tumor Immunity

Zhang FQ, et al. Cell Reports Medicine, 2025, 6(9), 102324.

Zeaxanthin (ZEA), a dietary carotenoid, was investigated for its immunomodulatory effects on CD8+ T cells. Using a co-culture-based screening platform with a blood nutrient compound library, ZEA was identified to enhance cytotoxic activity against tumor cells. In vitro, CD8+ T cells were treated with ZEA, and T cell receptor (TCR) stimulation was assessed via multi-omics analysis, revealing enhanced intracellular TCR signaling. In vivo, oral supplementation of ZEA, but not lutein, augmented anti-tumor immunity in mouse models and improved the efficacy of anti-PD1 immunotherapy. Additionally, human TCR-engineered CD8+ T cells exposed to ZEA exhibited increased cytotoxicity, demonstrating translational potential of ZEA as a dietary adjunct in immunotherapy.

Zeaxanthin for Mitigating Lipid Peroxidation-Induced Neuronal Damage

Morita S, et al. Biochemistry and Biophysics Reports, 2024, 40, 01835.

This case study evaluates the experimental application of zeaxanthin in a neuronal oxidative-stress model designed to mimic lipid peroxidation-driven neurodegeneration. Differentiated SH-SY5Y neuronal cells were exposed to a dual-inducer system-rotenone to impair mitochondrial respiratory function and RSL3 to inhibit GPX4-thereby elevating mitochondrial ROS and driving accumulation of peroxidized lipids. This combination reliably produced measurable neuronal injury, serving as a controlled in vitro platform to probe antioxidant interventions. Zeaxanthin was administered continuously for one week, during which it significantly suppressed mitochondrial oxidative stress and reduced lipid ROS formation. The carotenoid's ability to attenuate structural and functional neuronal damage highlights its utility as an experimental antioxidant reagent for probing lipid peroxidation-associated neurotoxicity.

Zeaxanthin in a Lipid Peroxidation-Driven Neuronal Damage Model

Wen X, et al. Experimental Eye Research, 2025, 259, 110557.

This case study evaluates zeaxanthin in an oxidative-stress neuronal model designed to mimic lipid peroxidation-associated neurodegeneration. Differentiated SH-SY5Y cells were exposed to a dual-inducer system-rotenone to disrupt mitochondrial complex I and RSL3 to inhibit GPX4-thereby elevating mitochondrial ROS and driving accumulation of peroxidized lipids. This combination produced consistent neuronal injury and provided a controlled platform to assess antioxidant interventions. Zeaxanthin was administered for one week and significantly suppressed mitochondrial oxidative stress while reducing lipid ROS formation. The carotenoid effectively attenuated structural and functional neuronal damage, indicating strong inhibitory activity against lipid peroxidation pathways. These findings support zeaxanthin as a useful experimental antioxidant reagent for probing mechanisms of oxidative lipid injury and neurotoxicity.