Astaxanthin is a potent and safe anti-inflammatory that can improve the health in humans and animals. Astaxanthin is proven to reduce inflammation at its source, without the harmful side effects of common anti-inflammatories and pain relievers.
Cardax’s pharmaceutical development program for astaxanthin will target conditions where inflammation is strongly implicated, including:
- Osteoarthritis: Astaxanthin is well positioned to meet the needs of patients suffering from osteoarthritis. Astaxanthin reduces inflammation equivalent a steroid (in non-human tests), but is far safer than steroids, NSAIDs, or TNF-α inhibitors. Learn more >>
- Metabolic Syndrome: Astaxanthin could decrease the risk of cardiovascular disease and diabetes. In humans, astaxanthin has been shown to significantly lower bad cholesterol (LDL-C) and triglycerides while simultaneously raising good cholesterol (HDL-C). Similarly, in animal models of disease, astaxanthin significantly decreased blood pressure and fasting glucose levels. Learn more >>
- Other Conditions: Astaxanthin has the potential to treat a variety of conditions driven by inflammation. Learn more >>
Proof of Concept
Astaxanthin has demonstrated efficacy in models of inflammatory-mediated disease, including reduction of TNF-α levels equivalent to a steroid, reduction of liver enzymes and liver histological damage, reduction of cholesterol levels, reduction of elevated triglycerides, decrease of atheroma formation, reduction of oxidized-LDL levels, reduction in blood clot formation with no increase in bleeding, and decrease in myocardial tissue damage following experimentally-induced myocardial infarction.
1,800+ peer reviewed papers featuring astaxanthin have been published in established scientific journals. Learn more >>
Mechanism of Action
Following oral administration of astaxanthin and intestinal uptake, astaxanthin is delivered initially to the liver via chylomicrons and subsequently distributed to tissues throughout the body via plasma lipoprotein particles including very low-density lipoprotein (“vLDL”), HDL, and LDL.
Once in the cell, astaxanthin accumulates within various organelles including nuclear, endoplasmic reticulum, and mitochondrial membranes. Localization within mitochondria is highly controlled by the cell and allows astaxanthin to uniquely regulate oxidative and nitrosative stress in a privileged location critical to normal metabolic function and often at the heart of metabolic dysfunction and aging. Due to its chemical structure, astaxanthin completely spans the lipid component of cell membranes, facilitating its biphasic (aqueous and lipid) anti-oxidant functions.
In support of the unique property of astaxanthin, one study examined X-ray diffraction profiles of five structurally related anti-oxidants embedded in a lipid matrix and demonstrated that each oriented differently with only astaxanthin traversing the lipid, potentially explaining, in part, why other well-known anti-oxidants, including beta-carotene, vitamin C, and vitamin E, have not achieved greater clinical success.
In addition to mitochondrial influence, astaxanthin’s remarkable aqueous and lipid anti-oxidant functions have the capacity to influence intracellular inflammatory and metabolic pathway signaling because many important intracellular pathways are directly modulated by inflammatory and oxidative stress mediators.
In support of strong anti-oxidant function within the body, astaxanthin administration has demonstrated statistically significant anti-oxidant capacity in humans as measured by decreased isoprostanes, decreased malondialdehyde (“MDA”) levels, increased total anti-oxidant capacity (“TAC”), and increased superoxide dismutase (“SOD”), as well as decreased lipid peroxidation. Likewise, numerous animal studies have supported the extensive and powerful anti-oxidant capacity of astaxanthin in vivo. Many studies support the strong influence of astaxanthin on mitochondrial functionality, as well as inflammatory and metabolic intracellular signaling in animals and in cell-based models.
Astaxanthin vs. Steroids and NSAIDs
Most anti-inflammatory drugs target highly specific biological enzymes or receptors such as cyclooxygenase 2 (“COX-2”), TNF-α, and C-C chemokine receptor type 2 (“CCR2”). While these natural targets play a significant role in inflammation, they are also critical components of other important biological pathways. With chronic use of most anti-inflammatories, these pathways may not function normally, resulting in adverse side effects including immune system suppression, liver damage, cardiovascular disease risk, and gastrointestinal bleeding.
In contrast, astaxanthin safely reduces inflammation at its source, in that it:
- Localizes in the plasma, mitochondrial, and nuclear membranes;
- Scavenges or quenches the unwanted initiators and effectors of inflammation—reactive oxygen (“ROS”) and nitrogen species (“RNS”); and
- Demonstrates no evidence of the immunosuppressive effects of steroids or TNF-α inhibitors or off-target effects (e.g., receptor or pathway).