Gout is caused by hyperuricemia.

Hyperuricemia, the chronic condition which affects approximately 55 million people worldwide, results in uric acid crystals settling in joints producing severe pain, swelling and redness. Patients can experience debilitating acute gout attacks suddenly.

A 2013 study published in Current Therapeutic Research found that the total annual cost of care for gout patients in the U.S, particularly for those with uncontrolled gout, is “likely in the tens of billions of dollars.”
The total worldwide market value for gout treatments was $2.4 billion in 2019.

In a 2017 study in the Journal of Rheumatology researchers found that the incidence of gout doubled over the past 20 years. “This increase,” they concluded, “together with the more frequent occurrence of co-morbid conditions and cardiovascular risk factors represents a significant public health challenge.

The prevalence of chronic gout, with no effective treatments, doubled in past 20 years and is increasing with a global market value for therapeutics of $2.4 billion a year.

Learn about the causes of gout in our interview with noted rheumatologist and Atom Bioscience advisor, Dr. N. Lawrence Edwards

Atom Bioscience's ABP-671 is an inhibitor of urate transporter 1 proteins, which are involved in reabsorption of uric acid by the kidneys.

ABP-671 is an inhibitor of urate transporter 1 (URAT1) proteins, which are involved in reabsorption of uric acid by the kidneys. As a first line monotherapy, administered once a day in an oral tablet, ABP-671 reduces uric acid reabsorption, increasing its excretion in urine to reduce serum uric acid (sUA) levels. In long-term treatment this will reduce the number and size of tophi which will prevent gout attacks. By maintaining normal levels of sUA, the drug can also reduce the potential for complications associated with hyperuricemia, such as diabetes and heart and kidney disease.

For the treatment of gout, there is a general agreement that targeting sUA levels of less than 6 and 5 mg/dL will inhibit the formation of new crystals and promote dissolution of existing crystals. Reduction of sUA levels to less than 5 mg/dL can further increase the velocity of tophi resolution, in both number and size.

ABP-671 has demonstrated the ability to reach both sUA targets in a recent Phase 2a clinical trial. Approximately 93% and 77% of participants receiving ABP-671 treatment experienced reduction in sUA level to less than 6 and 5 mg/dL, respectively. With these positive results, Atom Bioscience is advancing ABP-671 to global Phase 3 trials and commercialization.

Atom Bioscience’s advantage over competitors is the unique, patented molecular structure of ABP-671, which makes it more potent than existing uric acid lowering drugs. ABP-671 eliminates the problems associated with other compounds whose required higher doses cause severe and fatal toxic side effects.

Efficacy Comparison Between ABP-671 Phase 2a Study and Phase 3 of Marketed Drugs

Achievement of sUA ≤ 6.0 & ≤ 5.0 mg/dL