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.
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.²
SAP-001 has shown in clinical studies to be safe and effective in patients with symptomatic hyperuricemia and gout.
