Phenocoll is an antineuralgic, analgesic and antipyretic drug. It is a derivative of phenacetin and thus has the same mechanism of action (COX-2 inhibition). Hydrochloride and salicylate salts of phenocoll were used to control inflammation in such diseases as gout, influenza, malaria, rheumatism and pleuritis. The drug is no longer available for marketing.

Topiroxostat was approved by Pharmaceuticals Medical Devices Agency of Japan (PMDA) on June 28, 2013. It was co-developed and marketed as Uriadec®/Topiloric® by Sanwa Kagaku Kenkyusho & Fuji Yakuhin. Topiroxostat is a xanthine oxidase inhibitor. Xanthine oxidase (XO) is a type of enzyme that generates reductive oxygen species, which catalyze the oxidation of hypoxanthine to xanthine and can further catalyze the oxidation of xanthine to uric acid. Topiroxostat could reduce the production of uric acid in the body through the inhibition of xanthine oxidase. It is usually used for the treatment of gout and hyperuricemia.

Oxametacin (1-p-chlorobenzoyl-2-methyl-5-methoxy-3-indolylacethydroxamic acid) is a non-steroidal anti-inflammatory compound that exerts analgesic, antipyretic and anti-inflammatory properties. This drug has been claimed to be effective in the treatment of acute attacks of gout. In the antiproliferative test, oxametacin exhibited leukemic cell lines selectivity against the solid tumor cell lines. Oxametacin also exhibited inhibitory activity toward histone deacetylases and thus could be used as a lead compound in the further development of histone deacetylase inhibitors for anticancer therapy.

Levotofisopam is the S-enantiomer of racemic tofisopam Monotherapy with levotofisopam led to clinically meaningful reduction of Serum Uric Acid (SUA) in patients with hyperuricemia and gout. Treatment was generally well tolerated with 23% of the patients experiencing gout flare. Increased fractional excretion of uric acid suggests that levotofisopam reduces SUA primarily through uricosuric activity. These results support further studies to investigate the potential role of levotofisopam for in the treatment of hyperuricemia in gout. Levotofisopam prescribed outside the United States for such stress-related disorders as anxiety, functional gastrointestinal disorders, and symptoms of menopause. Thought to affect autonomic tone via interaction with subcortical 2,3-benzodiazepine receptors, levotofisopam has shown promise in animal models of stress-related gastrointestinal dysfunction and menopause. We conducted a trial of levotofisopam in healthy human volunteers.Also was showed, that levotofisopam significantly reduced both objective and subjective measures of hot flash frequency in postmenopausal women within 7 days of treatment.

Benziodarone is a coronary dilatator drug. Benziodarone in therapeutic dosage has no effect on blood coagulation and does not alter the prothrombin level. Bleeding complications occurred, when benziodarone is given to patients receiving anticoagulant therapy with warfarin sodium. Jaundice might occurred from 8 to 16 weeks after the beginning of the treatment with Benziodarone. Combination of Flecainide with Benziodarone should be avoided or used only with strict monitoring. Benzbromarone is an other benzofuran derivative acting as anuricosuric agent by reducing the proximal tubular reabsorption of uric acid. The hypouricaemic action of benziodarone (Amplivex-Labaz) is prompt. The maximum drop of uricaemia after Amplivex administration (2 tablets/day) occurs during the first three days. The uric acid level declines by as much as 80% of the baseline value. For long-term treatment 1 tablet per day is sufficient, in some instances even 1 tablet twice a week. The tolerance of the preparation is satisfactory.

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.

Colchicine is an alkaloid obtained from the plant colchicum autumnale (also known as "meadow saffron"). Colchicine is an alternative medication for those unable to tolerate NSAIDs in gout. Mechanism of action of colchicine is inhibition of microtubule polymerization by binding to tubulin. Availability of tubulin is essential to mitosis, so colchicine effectively unctions as a "mitotic poison" or spindle poison.

Colchicine is an alkaloid obtained from the plant colchicum autumnale (also known as "meadow saffron"). Colchicine is an alternative medication for those unable to tolerate NSAIDs in gout. Mechanism of action of colchicine is inhibition of microtubule polymerization by binding to tubulin. Availability of tubulin is essential to mitosis, so colchicine effectively unctions as a "mitotic poison" or spindle poison.

Arhalofenate is a uricosuric drug which lowers serum urate by blocking its reabsorption by the proximal tubules of the kidney. Arhalofenate activity is mediated by inhibition of URAT1, OAT4 and OAT10. Additionally, arhalofenate has been suggested to exert potent anti-inflammatory activity. Arhalofenate has completed Phase 2 and is ready to advance to Phase 3 as a novel potential treatment for gout. The drug was also tested in patients with type 2 diabetes mellitus (phase III study), where it demonstrated its ability to lower glucose level, acting as a selective, partial PPAR-gamma agonist. However, the development of arhalofenate as an anti-diabetic drug was terminated.