| Indication | For the treatment of hyperuricemia associated with primary or secondary gout. Also indicated for the treatment of primary or secondary uric acid nephropathy, with or without the symptoms of gout, as well as chemotherapy-induced hyperuricemia and recurrent renal calculi. |
| Pharmacodynamics | Allopurinol, a structural analog of the natural purine base hypoxanthine, is used to prevent gout and renal calculi due to either uric acid or calcium oxalate and to treat uric acid nephropathy, hyperuricemia, and some solid tumors. |
| Mechanism of action | Allopurinol and its active metabolite, oxypurinol, inhibits the enzyme xanthine oxidase, blocking the conversion of the oxypurines hypoxanthine and xanthine to uric acid. Elevated concentrations of oxypurine and oxypurine inhibition of xanthine oxidase through negative feedback results in a decrease in the concentrations of uric acid in the serum and urine. Allopurinol also facilitates the incorporation of hypoxanthine and xanthine into DNA and RNA, leading to a feedback inhibition of de novo purin synthesis and a decrease in serum uric acid concentrations as a result of an increase in nucleotide concentration. |
| Absorption | Approximately 80-90% absorbed from the gastrointestinal tract. |
| Volume of distribution | Not Available |
| Protein binding | Allopurinol and oxypurinol are not bound to plasma proteins |
| Metabolism | Hepatic |
| Route of elimination | Approximately 20% of the ingested allopurinol is excreted in the feces. |
| Half life | 1-3 hours |
| Clearance | Not Available |
| Toxicity | LD50=214 mg/kg (in mice) |