hello copyman i am on rollover from prove 3 unblinded so far not bad 3 time relapser week 1 under 25 detected week 2 not detected waiting on week 3 and 4 results no rash as of yet in week 5 alot more itching then usual other then severe insomnia not bad
No, the nurse doesn't get it - and the nurse doesn't get it. You need to ask somebody higher up the food chain who understands the significance of your resistance data and is willing to go to Vertex and request it on your behalf.
thanks for that info. i'm in the 2nd part of the phase 3 study for naive patients. the 2nd part study is "open label" so everyone knows they are getting the real drug. the only thing blinded is the viral loads. May I ask what your starting VL was. Seems you are on your way to killing this dragon once and for all. best of luck
I hope they give you the viral mutation data. I can't see them giving that info up easily. The last thing they want stock investors seeing is data that supports viral mutation. I don't think they want that type of data public just yeat. Good luck
Vertex has been quite open about resistance to telaprevir and viral mutation. Here's a study they published.:
Evaluation of Viral Variants During a Phase 2 Study (PROVE2) of Telaprevir with Peginterferon alfa-2A and Ribavirin in Treatment-naïve HCV Genotype 1-Infected Patients
J. Pawlotsky5; T. Kieffer1; Y. Zhou1; E. Zhang1; M. Marcial1; R. Byrn1; T. Pfeiffer1; J. Miller1; A. Tigges1; D. Bartels1; A. Kwong1; P. Ferenci2; G. Dusheiko3; S. Zeuzem4
1. Infectious Diseases, Vertex Pharmaceuticals Incorporated, Cambridge, MA, USA.
2. Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
3. Centre for Hepatology, Royal Free Hospital, London, United Kingdom.
4. Department of Medicine I, J.W. Goethe University Hospital, Frankfurt, Germany.
5. Department of Virology, Henri Mondor Hospital, University of Paris XII, Créteil, France.
Background: The VX05-950-104EU study (PROVE2) is a Phase 2 study of an HCV protease inhibitor, telaprevir (VX-950, TVR) 750 mg q8h, in combination with Peg-IFN-alfa-2a (P) 180 µg/week and ribavirin (R) 1000-1200 mg/day in treatment naive subjects with genotype 1 hepatitis C. Subjects were randomized into 4 groups that received: 1) TVR/P/R for 12 weeks, 2) TVR/P for 12 weeks, 3) TVR/P/R for 12 weeks followed by 12 weeks of P/R, and 4) P/R for 48 weeks (control group). Viral breakthrough (increase of > 1-log above HCV RNA nadir or increase to > 100 IU/mL in previously undetectable patients) was observed in some subjects during the first 12 weeks of therapy. Viral sequencing was used to evaluate the contribution of TVR resistance to antiviral response.
Methods: Plasma samples for viral sequencing were taken at baseline and at each HCV RNA assessment. The NS3-4A RNA region was amplified by nested RT-PCR and sequenced in samples with HCV RNA > 1,000 IU/mL. Prospectively defined criteria for identifying potential resistance mutations were applied using a Poisson distribution.
Results: HCV RNA was undetectable (LOD 10 IU/mL) at Week 4 in 14% of subjects in the P/R group, 74% in the TVR/P/R groups (p<0.001), and 53% in the TVR/P group (p<0.001); and at Week 12 in 43% of subjects in the P/R group, 79% in the TVR/P/R groups (p<0.001), and 63% in the TVR/P group (p<0.015). During the first 12 weeks on treatment, 6 of 152 subjects (4%) in the TVR/P/R groups, 19 of 76 subjects in the TVR/P group (25%), and 1 of 77 subjects (1%) in the P/R group had viral breakthrough. The breakthroughs were associated with wild-type virus in the P/R group and previously identified TVR-resistant variants in the TVR groups (TVR/P/R: genotype 1a, n=4: mainly V36M and R155K; genotype 1b, n=2: mainly A156T; TVR/P: genotype 1a, n=12: mainly V36M and R155K; genotype 1b, n=7: mainly V36A, T54A, R155K, and A156S/T).
Conclusions: In this interim analysis, TVR/P/R produced a significantly greater antiviral response at Weeks 4 and 12 compared to TVR/P and P/R in treatment naïve subjects with genotype 1 HCV. In the TVR groups, viral breakthroughs were associated with the selection of known TVR-resistant variants. The breakthrough rate in the TVR/P group was higher than in the TVR/P/R groups, suggesting that suboptimal inhibition of viral replication provides a greater probability for selection of TVR-resistant variants. Some subjects with viral breakthrough on TVR had a subsequent decline in HCV RNA during treatment with P/R, indicating that emergence of TVR-resistance does not preclude response to P/R.
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