Mechanism of action<unk>  inhibits URAT1, a protein that is responsible for reabsorption of uric acid in the kidneys. This leads to increased uric acid excretion with the urine, and consequently lower blood levels. It also inhibits the protein OAT4, which is associated with hyperuricemia caused by diuretic drugs. Pharmacokinetics The main metabolic pathways in humans. Involved enzymes are 2C9 = CYP2C9 and mEH = microsomal epoxide hydrolase.<unk>  is quickly and practically completely absorbed from the gut. Highest blood plasma concentrations are reached after one to four hours. When in the bloodstream, the substance is almost completely (>98%) bound to plasma proteins, mainly albumin. It is metabolized mainly by the liver enzyme CYP2C9 to various oxidation products, predominantly to a hydroxylated substance called M3 and an epoxide, M3c. The latter is quickly hydrolyzed to the diol M4 by microsomal epoxide hydrolase (mEH). The enzymes CYP1A1, CYP2C19 and CYP3A only play minor roles in its metabolization. Glucuronidation by the enzymes UGT1A1 and UGT2B7 has also been detected.<unk>  is excreted via the urine (63%) and feces (32%), with a biological half-life of about five hours. Of the excreted dose, 30% are unchanged<unk> , and the rest are metabolites. Pharmacogenomics People who are CYP2C9 poor metabolizers are exposed to<unk>  concentrations that are about 1.8-fold higher than those with a normal function of this enzyme.
Lesinurad
Keldur
Krebiozen
Nicogel
Vagisil
Pegcetacoplan
Itruvone
Custirsen