Patients with gout can be categorized into two groups: (1) overproducers of uric acid or (2) underexcreters of uric acid. Hyperuricemia can thus result from the endogenous production of uric acid, a high rate of renal urate reabsorption, or a diet high in purines. XO inhibitors are effective in treating patients with both categories of gout as a result of their inhibition of uric acid synthesis by impairing the conversion of hypoxanthine to xanthine, which results in uric acid formation.
As a non-purine selective XO inhibitor, febuxostat inhibits both oxidized and reduced types of XO. It does not inhibit enzymes involved in purine or pyrimidine metabolism, as does allopurinol. Febuxostat is also structurally unrelated to allopurinol; its structure does not resemble a pyrimidine or a purine. The drug’s active ingredient is 2-(3-cyano-4[2-methylpropoxy] phenyl)-4-methylthiazole-5-carboxylic acid. The empirical formula is C16H16N2O3S, with a molecular weight of 316.38. As a result of its selectivity and structural differences, febuxostat tends to cause fewer adverse events when compared with allopurinol.