Febuxostat (ULORIC) is a novel, xanthine oxidase/dehydrogenase (XO/XDH) inhibitor being developed by Teijin, TAP Pharmaceuticals, and Ipsen for the treatment of gout. The currently available XO inhibitor, allopurinol, has been associated with serious instances of severe hypersensitivity, in some cases leading to fatalities. There is some suggestion that febuxostat is less prone to excacerbate systemic inflammatory events in animal studies. Febuxostat, a xanthine oxidase inhibitor, achieves its therapeutic effect by decreasing serum uric acid. Febuxostat is not expected to inhibit other enzymes involved in purine and pyrimidine synthesis and metabolism at therapeutic concentrations. Febuxostat is used for the treatment of hyperuricemia in patients with gout.

Allopurinol is a xanthine oxidase inhibitor used to decrease high blood uric acid levels. Allopurinol is specifically used to prevent gout, prevent specific types of kidney stones, and for the high uric acid levels that can occur with chemotherapy. Allopurinol acts on purine catabolism, without disrupting the biosynthesis of purines. It reduces the production of uric acid by inhibiting the biochemical reactions immediately preceding its formation. Allopurinol is a structural analog of the natural purine base, hypoxanthine. It is an inhibitor of xanthine oxidase, the enzyme responsible for the conversion of hypoxanthine to xanthine and of xanthine to uric acid, the end product of purine metabolism in man. Allopurinol is metabolized to the corresponding xanthine analog, oxypurinol (Allopurinol), which also is an inhibitor of xanthine oxidase. Allopurinol is taken by mouth or injected into a vein. Common side effects, when used by mouth, include itchiness and rash. Common side effects when used by injection include vomiting and kidney problems.

Probenecid is the prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy. Probenecid is used for treatment of the hyperuricemia associated with gout and gouty arthritis. Probenecid is a uricosuric and renal tubular blocking agent. It inhibits the tubular reabsorption of urate, thus increasing the urinary excretion of uric acid and decreasing serum urate levels. Effective uricosuria reduces the miscible urate pool, retards urate deposition, and promotes resorption of urate deposits. Probenecid inhibits the tubular secretion of penicillin and usually increases penicillin plasma levels by any route the antibiotic is given. A 2-fold to 4-fold elevation has been demonstrated for various penicillins. Probenecid decreases both hepatic and renal excretion of sulfobromophthalein (BSP). The tubular reabsorption of phosphorus is inhibited in hypoparathyroid but not in euparathyroid individuals. Probenecid does not influence plasma concentrations of salicylates, nor the excretion of streptomycin, chloramphenicol, chlortetracycline, oxytetracycline, or neomycin.

Seclazone was developed as a non-steroidal anti-inflammatory agent. This compound also possesses analgesic and antipyretic properties. Information about the current use of this compound is not available.

Verinurad (RDEA3170) is a selective uric acid reabsorption inhibitor in clinical development for the treatment of gout and asymptomatic hyperuricemia. Verinurad specifically inhibits URAT1 with a potency of 25 nM. High affinity inhibition of uric acid transport requires URAT1 residues Cys-32, Ser-35, Phe-365 and Ile-481. Unlike other available uricosuric agents, the requirement for Cys-32 is unique to verinurad. Verinurad doses as low as 2.5 mg produce significant sUA lowering in humans, and this greater reduction in sUA may lead to improved outcomes and medical benefits for patients with gout. Verinurad in monotherapy studies has been associated with increased urinary uric acid concentrations and low rates of serum creatinine (sCr) elevation. Verinurad combined with febuxostat decreased sUA dose-dependently while maintaining uric acid excretion similar to baseline. All dose combinations of verinurad and febuxostat were generally well tolerated.

IRTEMAZOLE is a uricosuric agent exhibiting a rapid uricosuric effect in normouricemic as well as in hyperuricemic persons.

Ciapilome is pyrimidinone derivative patented by German pharmaceutical company Byk Gulden Lomberg Chemical Factory GmbH as xanthine oxidase inhibitor for the treatment of gout, arrhythmia, and heart insufficiencies. Ciapilome causes a pronounced decrease in uric acid blood levels in rats on peroral administration.

Neocinchophen is an analgesic and uricosuric. Cinchophen and neocinchophen (introduced by Chemische Fabrik auf Aktien as Atophan and Novatophan) were being advertised as superior substitutes for salicylates in the treatment of rheumatic fever. Chemically, cinchophen is phenylcinchoninic acid, and neocinchophen is the ethyl ester of its methyl derivative.

Nicoxamat (nicotinohydroxamic acid) is a uricosuric drug that increased urinary excretion of urea and depressed urease activity in the stomach and the colon. Patients receiving nicoxamat showed significant improvement in blood ammonia levels as compared to patients receiving neomycin. In a double-blind clinical trial, 24 patients with the advanced chronic liver disease received 1.2 g of the drug daily. Nicoxamat induced some side effects, such as mild diarrhea, constipation, and anorexia.

Halofenate (MK-185) was invented as a hypolipidemic and hypouricemic agent. It was shown that halofenate lower serum triglycerides and uric acid in patients with a variety of hyperlipidemias. Treatment of dyslipidemic type 2 diabetic patients also showed triglyceride lowering and, surprisingly, significant reductions in plasma glucose and insulin. Halofenate is a selective PPAR-γ modulator (SPPARγM). SPPARγMs are believed to bind in distinct manners to the ligand-binding pocket of PPAR-γ, leading to altered receptor conformational stability and resulting in distinct patterns of gene expression. Thus, was suggested that halofenate hold promising therapeutic potential in the treatment of type 2 diabetes, without the side effects. However, information about the current use of this compound is not available.