02; Figure 1C), however without any significant differences in DPPIV activity (P=0.4). The 600 ng/mL sCD26 cut-off value yielded a 93% (12 of 13) SVR rate for the patients below 600 ng/mL compared with a 57% molarity calculator (13 of 23) SVR rate for of the patients above 600 ng/mL sCD26 (P=0.03). Interestingly, genotype 2 or 3 infected patients showed significantly lower baseline sCD26 concentrations compared with the genotype 1 patients (P=0.03; Figure 3) with a trend towards higher sCD26 concentrations for the three genotype 2/3 patients not achieving SVR (median 498 vs. 618 ng/mL sCD26 for SVR and non-SVR patients respectively; n=58, P=0.07). In addition, grouping the patients above or below the 600 ng/mL sCD26 cut-off resulted in 100% (37 of 37) SVR for the patients with <600 ng/mL sCD26 and 86% (18 of 21) SVR for the >600 ng/mL sCD26 patients (P=0.

02). Figure 3 Baseline sCD26 concentrations in genotype 1, 2 and 3 patients in the DITTO-HCV study. sCD26 Independently Predicts SVR In order to determine if sCD26 independently impacts treatment outcome for HCV genotype 1 infected patients, a stepwise binary logistic regression was performed using the baseline factors in Table 4. Lower sCD26 concentrations independently predicted SVR among HCV genotype 1 infected patients, with a 0.2% odds reduction for achieving SVR for each incremental ng/mL sCD26 concentration increase (P < 0.05; Table 5). The other independent baseline predictive markers of SVR were lower HCV RNA concentration (P=0.001), lower BMI (P=0.01), male gender (P=0.004), and favorable IL28Brs12980275 genetic variant (P=0.

03). Furthermore, using the 600 ng/mL sCD26 cut-off concentration resulted in 65% sensitivity, 61% specificity, a 65% positive predictive value (PPV), and a 61% negative predictive value (NPV) (Table 6). Table 5 Odds ratio (OR) and stepwise binary logistic regression analysis identifying pretreatment factors independently predictive of SVR in DITTO-HCV genotype 1 patients. Table 6 Predictive values for SVR among the DITTO-HCV genotype 1 patients included in the study. We have previously reported that IP-10 levels are weakly but significantly associated with IL28B genetic variants [13]. However, no such association was observed between the baseline sCD26 concentration and IL28B rs12970860 (P=0.4, Kruskal-Wallis test), rs12980275 (P=0.6), or rs809917 (P=0.

6) SNPs or IL28B genotype distribution (Table 4) for the Drug_discovery DITTO-HCV genotype 1 patients. In agreement with the observation that there was no association between the baseline sCD26 concentration and IL28B genotypes, having below the 600 ng/mL sCD26 cut-off value significantly improved the treatment response rate in the genotype 1 DITTO-HCV patients with one or two IL28B risk alleles (CT/TTrs12970860 P=0.04, AG/GGrs12980275 P=0.01, and rs809917 P=0.007; Table 7).