4% (5/7) in partial responders with genotype 1b treated with response-guided therapy, namely, patients who achieved and did not achieve XL184 molecular weight eRVR were treated with T12PR24 and T12PR48, respectively.[15]

These results suggest that approximately 70% of partial responders may achieve SVR using response-guided therapy, but the SVR rate was extremely low in null responders treated with T12PR24. Although the study of Muir et al. was not a randomized controlled trial study, their results indicated that T12PR48 may improve the SVR rate in null responders to a greater extent than T12PR24.[15] The present study revealed the SVR rates of partial and null responders treated with T12PR24 were 70.0% and 22.6%, respectively. The lower SVR rate in null responders than partial responders is concordant with the results of the previous study on T12PR24.[15] To our knowledge, besides our previous reports,[22-24] only two studies performed in Japan have analyzed non-responders to PR classified as partial and null responders.[16, 25] Akuta et al. reported that the SVR rates in partial and null responders treated with T12PR24 in clinical trials were 50% (4/8) and 0% (0/7), respectively.[16] Meanwhile, Ogawa Protein Tyrosine Kinase inhibitor et al. recently reported that the SVR rates in partial and null responders for CHC patients with advanced fibrosis (METAVIR score F3–4) treated with T12PR24 in clinical practice were 50% (9/18) and 16.7% (2/12), respectively.[25]

Similarly, the SVR rate was Fenbendazole lower in null responders than partial responders in the present study, when treated with T12PR24. Genetic variations near the IL28B gene (rs8099917 and rs12979860) are strongly associated with treatment outcome of PR.[32-34] In addition, these genetic variations are also strong predictors of SVR with the T12PR24 regimen when including both treatment-naïve and treatment-experienced patients.[14, 20-25, 35] However, Pol et al. reported the IL28B genotype (rs12979860) has a limited and non-significant impact on SVR in treatment-experienced patients treated with T12PR48 regardless of relapsers, partial responders or null responders to previous PR.[19] In the present study, the SVR rate of partial

responders with the TT genotype treated with T12PR24 was very high at approximately 90%, whereas that in patients with the non-TT genotype was significantly lower. Similarly, among null responders, the SVR rate was significantly lower in those with the non-TT genotype than those with the TT genotype. Ogawa et al. reported a similar trend that among previous partial and null responders treated with T12PR24, the SVR rate was lower in patients with the non-TT genotype than those with the TT genotype.[25] In contrast, the SVR rate did not differ significantly between either partial or null responders with the IL28B TT or non-TT genotype treated with T12PR48 in our study, although there were too few patients to make a meaningful comparison.