非布索坦作用及功效

The main ingredient is febuxostat, which is an agent that inhibits the oxidative decomposition of certain types of purines. Febuxostat is very effective in treating gout. It controls the level of uric acid in gout patients by inhibiting the metabolism of purine into uric acid. Febuxostat was developed in Japan in 2004, and was approved for marketing by European EMEA in 2008, the US FDA in 2009, and the State Food and Drug Administration of China in 2013. Today we will learn about the effects and efficacy of febuxostat.

A phase III clinical trial compared the efficacy of this product (80 and 120 mg/d) with that of allopurinol (300 mg/d). A 1-year study of 760 patients showed that compared with the allopurinol group, more patients in the this product group achieved the main trial efficacy indicator - the sUA concentration was measured below 60 mg/L in the last 3 months (all subjects were gout patients, and the sUA concentration before the test were all above 80 mg/L); after 52 weeks of treatment, this product failed to significantly reduce the area of tophi (tophi is unique to gout) aggregates of urate crystals), but in the high-dose group in the early stages of the trial, this effect was more obvious; in each treatment group, patients with sUA concentrations reaching the target (<60 mg/L) were less likely to have gout attacks, and their tophi area was more significantly reduced; adverse reactions and their incidence rates were similar in each treatment group, including abnormal liver function, diarrhea, headache, joint-related signs and symptoms, and musculoskeletal/connective tissue symptoms.

The starting dose of febuxostat is 40 mg/d. After taking this dose for 2 weeks, monitor the blood uric acid level. If the blood uric acid does not reach the standard, increase the dose to 80 mg/d. The usual dose is 40~120 mg/d. The efficacy of febuxostat 40 mg/d is equivalent to that of allopurinol 300 mg/d. Gout patients with mild to moderate renal insufficiency and mild hepatic insufficiency do not need to change the dosage of medication, but they also need to regularly monitor changes in liver and kidney indicators.

Febuxostat and allopurinol are both xanthine oxidase inhibitors, but their molecular structures are completely different from allopurinol and purine. They can bind to xanthine oxidase through a non-competitive mechanism, inhibit xanthine enzyme activity, and inhibit the production of uric acid. Moreover, febuxostat not only inhibits the reduced form, but also inhibits the oxidized xanthine oxidase, so it can exert a powerful inhibitory effect on xanthine oxidase at a smaller dose. In addition, febuxostat does not interfere with the synthesis of purine and pyrimidine, so it has fewer adverse reactions than allopurinol.

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