Tokom optimizacije inicijalnih inhibitora HSD17B13 primećena je značajna glukuronidacija fenolnog dela in vitro i in vivo.[8] UGT fenotipizacija je otkrila da je UGT1A9 glavni doprinosilac glukuronidaciji. Pored toga, sprovedene su studije tkivne raspodele kao i izlučivanja putem žuči.
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