About Gout    

            Gout is caused by hyperuricemia and is the most common cause of acute painful arthritis. Hyperuricemia is defined as serum uric acid (sUA) concentration >7.0 mg/dL for man and > 6.0 mg/dL for woman. Uric acid is the end product of purine metabolism in humans and has poor pH-dependent solubility. Its production is catalyzed by xanthine oxidase in the liver, and over 70% of the daily output of uric acid is excreted through the kidneys. A urate-anion transporter 1 (URAT1) plays a significant role in regulating serum urate through reabsorption of urate from the lumen to the cytosol in kidney tubules. The primary cause of gout and hyperuricemia is the inefficient excretion of uric acid by the kidneys.

           Uric acid has a poor pH-dependent solubility in aqueous solutions, which leads to the deposition of needle-like crystals in joints and soft tissues throughout the body. When this becomes symptomatic in a patient, gout is diagnosed. The symptoms of gout include an acute, extremely painful attack of arthritis accompanied by erythema, elevated temperature, swelling, and edema of the skin.  Additionally, gout commonly presents other serious health problems (comorbidities) including cardiovascular disease, obesity, diabetes and kidney impaired renal function. It was reported that hyperuricemia is associated with the progression of chronic kidney disease (CKD). Therefore, the management of sUA is clinically important to avoid complications related to hyperuricemia.

Gout Market
        In a statement from AstraZeneca, an estimated 16.3 million patients in the US, France, Germany, Italy, Spain, the UK, and Japan have gout. In a 2007-2008 report in the US, an estimated 8.3 million patients experienced gout. About 25% - 30% of adult Japanese men have been diagnosed by hyperuricemia. In China, gout patients have rapidly increased in the last 15 years. It was reported that the prevalence of hyperuricemia in China has reached 110 million, and among them, the number of gout patients exceeds 35 million. 

Severe Problems of Gout Medications

        Gout management involves both short-term and long-term medications. Short-term treatment only relieves pain and reduces inflammation during an acute attack.

       The goal for Long-term treatment of gout is to lower serum uric acid levels. These medications include uricosuric agents (URAT1 inhibitors) and xanthine oxidase inhibitors. Either uricosuric agents or xanthine oxidase inhibitors do not currently meet the requirement of gout medications. The world needs a good gout drug with an excellent efficacy lowering uric acid and great safety.

URAT1 Inhibitors for Gout treatment (Uricosuric Drug)
       Gout has over 50 million patients worldwide. Current medications do not meet the requirements of gout treatment because of their side effects.
        ABP-671 developed by Atom Bioscie
nce has completed the phase 1 clinical trials in the US. ABP-671 may become a potent and safe drug for the treatment of gout and hyperuricemia worldwide.

        Favorable Profiles of ABP-671

·         Clinically Significant Reduction of Serum Urate from Phase 1

·         Great Potency both in Vitro and in Vivo

·         Good Safety Profiles in Monkeys and Rats

·         Good PK

·         Potential Safe and Potent Gout Drug for Worldwide Market

Xanthine Oxidase Inhibitor for Gout treatment (decreasing production of uric acid)
        ABP-168 are the novel XO Inhibitor to decrease the production of uric acid. PCT patents (PCT/CN2013/087736)of these compounds are authorized by China, Europe, the US and Japan and other areas in the world.