Radalbuvir (also known as GS-9669 ) is a Hepatitis C virus NS 5 protein inhibitor for the treatment of hepatitis C virus (HCV) infection developed by Gilead Sciences. Radalbuvir is a highly optimized thumb site II nonnucleoside inhibitor, with a binding affinity of 1.35 nM for the genotype (GT) 1b protein. It is a selective inhibitor of HCV RNA replication, with a mean 50% effective concentration of ≤ 11 nM in genotype 1 and 5 replicon assays, but lacks useful activity against genotypes 2 to 4. In preclinical Radalbuvir exhibited at least additive activity in combination with agents encompassing four other direct modes of action (NS3 protease, NS5A, NS5B via an alternative allosteric binding site, and NS5B nucleotide) as well as with alpha interferon or ribavirin in replicon assays. It exhibited high metabolic stability in vitro human liver microsomal assays, which, in combination with its pharmacokinetic profiles in rat, dog, and two monkey species, is predictive of good human pharmacokinetics. In clinical trials, Radalbuvir shows highly effective inhibition of wild-type HCV.