Preclinical evidence for Eyevistar®
A two-part programme: mechanistic testing in human retinal pigment epithelial cells, and a 42-day high-fat-diet animal model of AMD-like retinal change.
Scope of the research programme
Eyevistar®, standardized to 20% lutein and 4% zeaxanthin, was evaluated as a complete formulation rather than as isolated carotenoids. The in-vitro work used ARPE-19 human retinal pigment epithelial cells to examine cytotoxicity, proliferation, UV-A-induced damage and the accumulation of A2E and lipofuscin.
The in-vivo work used a high-fat-diet-induced model of AMD-like retinal stress, with oral Eyevistar® administered at 2.5, 5 and 10 mg/kg for 42 days. Endpoints included carotenoid bioavailability in plasma and macular tissue, antioxidant enzyme status, retinal stress biomarkers and retinal histology.
62.31%
Increase in ARPE-19 proliferation at 500 µg/mL
100.64%
Cell viability after UV-A at 500 µg/mL
11.02%
A2E accumulation vs 35.24% in UV control
4.3×
Plasma lutein vs high-fat-diet control
Safety and proliferation in ARPE-19 cells
Eyevistar® was prepared at 10 mg/mL in cell-culture medium and tested across a concentration range up to 1,000 µg/mL. No meaningful cytotoxicity was observed at the tested concentrations.
Retinal cell proliferative activity increased in a concentration-dependent manner, indicating that Eyevistar® supports the viability of the retinal pigment epithelium rather than merely being tolerated by it.
| Eyevistar® concentration | Increase in proliferation |
|---|---|
| 125 µg/mL | 33.59% |
| 250 µg/mL | 46.15% |
| 500 µg/mL | 62.31% |
Protection against UV-A-induced retinal cell damage
UV-A exposure reduced ARPE-19 cell viability to 50.98%. Pretreatment with Eyevistar® restored viability in a concentration-dependent manner, demonstrating a cytoprotective effect against light-associated oxidative injury.
| Condition | Cell viability |
|---|---|
| Untreated control | 100% |
| UV-A exposed | 50.98% |
| UV-A + Eyevistar® 250 µg/mL | 81.19% |
| UV-A + Eyevistar® 500 µg/mL | 100.64% |
Reduced A2E and lipofuscin accumulation
A2E is a major fluorescent component of lipofuscin, the age-associated material that accumulates within retinal pigment epithelial cells and acts as a photosensitizer under light exposure.
UV irradiation raised A2E accumulation in ARPE-19 cells from 1.79% to 35.24%. Eyevistar® reduced accumulation to 23.23% at 250 µg/mL and 11.02% at 500 µg/mL, and LC-MS/MS quantification confirmed lower A2E concentrations in treated cells.
Transmission electron microscopy supported these results. UV-exposed cells showed numerous electron-dense lipofuscin granules, while Eyevistar®-treated cells showed visibly reduced granule accumulation.
| Condition | A2E accumulation |
|---|---|
| Untreated control | 1.79% |
| UV-exposed | 35.24% |
| UV + Eyevistar® 250 µg/mL | 23.23% |
| UV + Eyevistar® 500 µg/mL | 11.02% |
Carotenoid restoration in plasma and macular tissue
High-fat diet feeding substantially depleted lutein and zeaxanthin. Oral Eyevistar® restored both carotenoids dose-dependently, with the clearest effects at 10 mg/kg — quantified by LC-MS/MS with a limit of detection of 2 ng/mL and a limit of quantification of 5 ng/mL.
| Measure | High-fat-diet control | Eyevistar® 10 mg/kg |
|---|---|---|
| Plasma lutein | 64.5 ng/mL | 276.5 ng/mL |
| Plasma zeaxanthin | Undetectable | 20.2 ng/mL |
| Macular lutein | 15.5 ng/mL | 68.1 ng/mL |
| Macular zeaxanthin | Undetectable | 2.2 ng/mL |
Antioxidant defense and retinal stress markers
Eyevistar® restored total antioxidant capacity and the activities of superoxide dismutase, catalase and glutathione peroxidase. Retinal stress biomarkers moved consistently in the protective direction, with the strongest response at 10 mg/kg.
| Biomarker | High-fat-diet control | Eyevistar® 10 mg/kg |
|---|---|---|
| VEGF | 588.6 ng/L | 202.7 ng/L |
| HSP60 | 20.4 ng/mL | 12.7 ng/mL |
| ARMS2 | 13.6 ng/mL | 5.8 ng/mL |
| Lipofuscin | 6.4 ng/mL | 4.0 ng/mL |
Histological evaluation showed preserved retinal architecture and reduced retinal thickening in treated animals compared with the untreated high-fat-diet group.
What the evidence supports
- Macular carotenoid delivery confirmed in plasma and retinal tissue
- Cytoprotection of retinal pigment epithelial cells under UV-A stress
- Reduced A2E and lipofuscin, confirmed biochemically and structurally
- Restoration of endogenous antioxidant enzyme activity
- Lower VEGF, HSP60 and ARMS2 stress signalling
- Preserved retinal architecture in a diet-induced stress model
Request the full preclinical dossier
Study summaries, analytical data and technical support are available for qualified partners.