Uric acid (UA) (UA)

Uric acid is the final oxidation product of purine metabolism in humans, generated by the action of xanthine oxidase on xanthine and hypoxanthine [1][2]. Due to the evolutionary loss of the uricase enzyme, humans maintain higher systemic levels of urate compared to other mammals, where it functions as a significant extracellular antioxidant [2][3]. However, when serum concentrations exceed physiological solubility limits (hyperuricemia), urate can precipitate as monosodium urate crystals in joints and soft tissues, leading to the inflammatory condition known as gout [1][4]. Therapeutic intervention typically targets the proteins involved in urate homeostasis rather than the molecule itself; this includes inhibiting production via xanthine oxidase inhibitors (e.g., allopurinol) or increasing renal clearance by inhibiting reabsorption transporters like URAT1 (e.g., probenecid) [4][5]. Additionally, recombinant uricase enzymes (e.g., pegloticase) can be used to catalyze the conversion of urate into the more soluble metabolite allantoin for rapid reduction in severe cases [5][6]. Monitoring serum uric acid levels is essential for managing gout, preventing urate-related nephrolithiasis, and mitigating risks associated with tumor lysis syndrome [2][6].

Other names

7,9-dihydro-1H-purine-2,6,8(3H)-trioneLithic acid2,6,8-TrioxypurineMonosodium urateUA

Drugs lower urate levels by inhibiting xanthine oxidase (production), blocking renal transporters like URAT1 (excretion), or enzymatically converting urate to allantoin (degradation).