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Novel astaxanthin prodrug (CDX-085) attenuates thrombosis in a mouse model
Sanjoy K Khan1, Tadeusz Malinski, R Preston Mason
1School of Kinesiology, University of Michigan, Ann Arbor, MI, USA.
Insights
This study shows that astaxanthin (CDX-085) reduces thrombus formation and improves blood flow in mice. It increases nitric oxide and decreases peroxynitrite in cells, suggesting potential for treating cardiovascular disease.
Area of Science:
- Cardiovascular research
- Pharmacology
- Oxidative stress and inflammation
Background:
- Cardiovascular disease is a leading cause of death globally.
- Oxidative stress and chronic inflammation contribute to vascular dysfunction and thrombosis.
- Endothelial and platelet dysfunction are key factors in thrombogenesis.
Purpose of the Study:
- To investigate the effect of astaxanthin prodrug (CDX-085) on arterial thrombosis using a mouse model.
- To evaluate the impact of astaxanthin on human endothelial cells and rat platelets to elucidate mechanisms of action.
Main Methods:
- Oral administration of CDX-085 to mice, followed by assessment of astaxanthin levels in plasma and tissues.
- Evaluation of arterial blood flow and thrombus formation in a mouse model of vascular injury.
- In vitro studies on human umbilical vein endothelial cells (HUVECs) and rat platelets treated with astaxanthin to measure nitric oxide (NO) and peroxynitrite (ONOO-) levels.
Main Results:
- CDX-085 administration led to significant astaxanthin levels in mouse plasma, liver, heart, and platelets.
- Mice treated with CDX-085 showed increased basal arterial blood flow and delayed thrombus formation.
- Astaxanthin treatment increased nitric oxide (NO) and decreased peroxynitrite (ONOO-) in HUVECs and platelets.
Conclusions:
- Increased NO and decreased ONOO- levels in endothelial cells and platelets support astaxanthin's mechanism of action.
- Astaxanthin (CDX-085) shows potential for the treatment or prevention of thrombotic cardiovascular complications.
Background:
Cardiovascular disease remains the leading cause of morbidity and premature mortality in most industrialized countries as well as in developing nations. A pro-oxidative state appears to promote and/or exacerbate vascular disease complications. Furthermore, a state of low-grade chronic inflammation can promote increased oxidative stress and lead to endothelial cell and platelet dysfunction ultimately contributing to thrombogenesis.
Objectives:
In this study, the effect of a proprietary astaxanthin prodrug (CDX-085) on thrombus formation was investigated using a mouse model of arterial thrombosis. The influence of free astaxanthin, the active drug of CDX-085, on human endothelial cells and rat platelets was evaluated to investigate potential mechanisms of action.
Methods And Results:
Oral administration of CDX-085 (0.4% in chow, approximately 500 mg/kg/day) to 6-8 week old C57BL/6 male mice for 14 days resulted in significant levels of free astaxanthin in the plasma, liver, heart and platelets. When compared to control mice, the CDX-085 fed group exhibited significant increases in basal arterial blood flow and significant delays in occlusive thrombus formation following the onset of vascular endothelial injury. Primary human umbilical vein endothelial cells (HUVECs) and platelets isolated from Wistar-Kyoto rats treated with free astaxanthin demonstrated significantly increased levels of released nitric oxide (NO) and significantly decreased peroxynitrite (ONOO-) levels.
Conclusion:
Observations of increased NO and decreased ONOO- levels in endothelial cells and platelets support a potential mechanism of action for astaxanthin (CDX-085 active drug). These studies support the potential of CDX-085 and its metabolite astaxanthin in the treatment or prevention of thrombotic cardiovascular complications.
