Date: 2011-11-08
Type of information:
phase: 2b
Announcement: results
Company: Boehringer Ingelheim (Germany)
Product: BI 201335
Action mechanism: BI 201335 is an oral protease inhibitor for the treatment of chronic hepatitis C virus (HCV).
Disease: chronic hepatitis C
Therapeutic area: Infectious diseases
Country:
Trial details:
Latest
news: Boehringer Ingelheim has announced results from two Phase IIb studies evaluating the combination of its next generation protease inhibitor, BI 201335, with pegylated interferon (PegIFN) and ribavirin (RBV) in treatment-naïve genotype 1 (GT1) hepatitis C (HCV) patients. These data were presented in oral sessions at the American Association for the Study of Liver Diseases (AASLD) 2011 Liver Meeting in San Francisco, USA. Data from the SILEN-C3 study showed the potential for BI 201335 to shorten patients’ treatment duration to 12 weeks and improve the likelihood of viral cure (sustained viral response; SVR) compared to the former traditional standard of care – 48 weeks of treatment with PegIFN/RBV alone. Furthermore, the SILEN-C1 study demonstrated the ability for BI 201335 to improve SVR in traditionally difficult to treat populations. The results from SILEN-C3 indicate that among patients achieving an extended rapid viral response (eRVR), 12 weeks of treatment with BI 201335 was sufficient to achieve SVR. Patients with undetectable HCV RNA in the blood prior to week 12 had similar SVR rates, whether they were treated for 12 or 24 weeks with BI 201335 (82% and 81%, respectively). 1 In addition to the SILEN-C3 study, the overall analysis of the SILEN-C1 study shows that 83.1% of patients treated with BI201335 240 mg QD achieved SVR, compared with 56.3% of patients on PegIFN/RBV alone (p<0.0001). The majority of patients with difficult to treat HCV subtypes, such as patients with the viral GT1a or the IL-28B non-CC gene variant (polymorphism), achieved SVR/ Specifically, among patients with GT1a HCV (n=32), a virus type that is more likely to resist treatment than GT1b, 82% achieved SVR, while for GT1b HCV patients (n=38), 84% achieved SVR In addition, SVR was 71% for patients with the non-CC polymorphism of the IL-28B gene (n=29). While patients with the CC polymorphism (n=11) achieved 100% SVR and those where IL-28B genotyping was missing (n=31) achieved 86% SVR.
