Gout is the most common form of inflammatory arthritis, and the second most prevalent metabolic disease, caused by excess serum uric acid (sUA), with over 10 million patients diagnosed in the US alone.
Abnormal purine metabolism causes hyperuricemia.1 The initial clinical manifestation is asymptomatic hyperuricemia. However, as hyperuricemia persists, uric acid crystals are deposited in the body resulting in a chronic “storage disease” that is associated with subacute inflammation leading to end-organ damage, as well as manifesting with acute inflammatory responses, that typically cause acute joint inflammation (acute gout attacks), turning asymptomatic hyperuricemia into gout. Clinically, gout is classified into grades 1-5 according to different degrees of uric acid crystallinity.
The key to treatment of gout is to adjust purine metabolism to restore blood uric acid levels in the body to a normal range (3-6 mg/dL), but first, it is necessary to completely dissolve the crystal tophi that have been formed in the body, and this requires blood uric acid levels below 5 mg/dL.2 The shorter it takes to dissolve the crystal tophi, the more beneficial for patients in reducing the pain of gout attacks, as well as deplete the excess body stores of uric acid. Therefore, it is necessary to reduce blood uric acid levels to below 3 mg/dL to enable dissolution of tophi in the shortest amount of time, and to adjust the blood uric acid level to the 3-5 mg/dL range after the crystals are completely dissolved.
No drug currently approved can consistently reduce blood uric acid levels below 5 mg/dL, so they cannot completely eliminate gout by dissolving crystals, nor can they prevent patients with hyperuricemia from developing gout.
Less than a third of US patients diagnosed with gout receive treatment, primarily with xanthine-oxidase inhibitors. Of these treated patients, only half can tolerate, or effectively respond to treatment, by achieving reductions in their sUA levels to ≤ 6 mg/dL.3
It is estimated that 12-35% of patients with poorly controlled, refractive (or untreated) hyperuricemia and gout develop tophi.4 No oral product is currently available to patients to safely and completely eliminate tophi in a timely fashion.
SAP-001 has shown in clinical studies to be safe and effective in patients with symptomatic hyperuricemia and gout. SAP-001 is a convenient oral monotherapy that can bring blood uric acid below 3 mg/dL, and by reducing the dose, maintain uric acid levels between 3-5 mg/dL for a long period of time, dissolving tophi and preventing crystals from forming again.
