In non-human tests, astaxanthin reduces TNF-α equivalent to a corticosteroid – considered to be the most potent of the anti-inflammatory compounds – as well as other important mediators of inflammation including hsCRP, prostaglandin E2 (“PGE-2”), interleukin 6 (“IL-6”), nuclear factor kappa B (“NF-κB”), and nitric oxide (“NO”).

We believe that no evidence of the immunosuppressive effects of steroids or TNF-α inhibitors has been seen in multiple animal or human studies using astaxanthin. In fact, in animals, astaxanthin administration is statistically significantly associated with fewer infections.

We estimate that there are more than 150 million people in developed nations that suffer from osteoarthritis who have the financial ability to pay for astaxanthin treatment. Assuming $1 per day for treatment, the potential market could exceed $50 billion annually.

Recent expenditures for treatment of arthritis are also substantial. The Centers for Disease Control and Prevention (the “CDC”) report that the amount of direct medical expenditures in the United States for arthritis and other rheumatic conditions in 2003 was $80.8 billion. According to Drugs.com, aggregate U.S. sales of the top three injected TNF-α inhibitors totaled more than $12 billion in 2012. New oral anti-inflammatory drugs may also be approved, further increasing the amount expended for drug treatment.

We expect that these drugs will be based on steroid, NSAID, or enzyme/receptor technologies and could pose significant side effects when administered chronically. In contrast, astaxanthin, at very low doses, reduces TNF-α in humans.