I was a Geno 3a, unresponsive to 24 weeks of SOC. In 2008/2009 I took part in a Roche/Pharmasset Phase 1 drug trial for a new polymerase inhibitor (R7128) with excellent results - I was UND at 4 weeks of triple therapy with SOC and R7128, I achieved SVR in October 2009. This drug is still in trials but has been fast tracked by the FDA as it is effective across ALL genotypes and currently the only drug of it's kind that is effective for Geno 3, which in some people can be as difficult to treat as Geno 1.
At this point in time they are trialling new drugs as an add-on to SOC however I do know they are working on non-interferon treatments which at this stage would combine the Poly Inhibitor with Ribavirin.
My doctor, a world renown liver specialist, told me that non-interferon treatments would be available in approx 2 to 3 years for Geno 1 and about 5 years after that for Geno 3.
Most research goes into Geno 1 as that is the most prevalent Genotype in the US. However, it is becoming increasingly clear that Geno 3 can also be very difficult to treat if the patient does not respond quickly to SOC.
I hope this is helpful to you.
OH, I think there are some issues with Telaprevir and GT-3; here’s something from EASL last year; not sure about Boceprevir, though. I do believe they both target NS-3 protease though…
http://www.natap.org/2009/EASL/EASL_13.htm
“EASL April 23-26 2009
Copenhagen, Denmark
Reported by Jules Levin
In phase IIb studies in treatment-naives, mostly caucasians, telaprevir in combination with peg/RBV improved SVR rates in half the time of treatment compared with standard of care:
--PROVE1: 61% vs 41% (p=0.02)
--PROVE2: 69% vs 46% (p=.004)
In this study genotype 2 treatment naive patients achieved a mean 4 log reduction in viral load after 6 days on monotherapy with telaprevir. The triple combination of telaprevir + peg/RBV achieved a mean 5.3 log reduction in viral load at day 16. But genootype 3 patients only achieved a -.80 reduction in viral load so therapy for genotype 3 won't be pursued.
ACTIVITY OF TELAPREVIR ALONE OR IN COMBINATION WITH PEGINTERFERON ALFA-2A AND RIBAVIRIN IN TREATMENT-NAIVE GENOTYPE 2 AND 3 HEPATITIS-C PATIENTS: INTERIM RESULTS OF STUDY C209
G.R. Foster1, C. Hezode2, J.-P. Bronowicki3, G. Carosi4, O. Weiland5, L. Verlinden6, R. van Heeswijk6, T. Vangeneugden6, G. Picchio7, M. Beumont-Mauviel6 1Barts and The London School of Medicine, Institute of Cellular and Molecular Science, London, UK, 2Hôpital Henri-Mondor, AP-HP, Université Paris XII, Créteil, 3Centre Hospitalier Universitaire de Nancy, Vandoeuvre-lès-Nancy, France, 4Clinic of Infectious and Tropical Diseases, University of Brescia, Brescia, Italy, 5Karolinska University Hospital Huddinge, Stockholm, Sweden, 6Tibotec BVBA, Mechelen, Belgium, 7Tibotec Inc., Yardley, PA, USA
Background: Telaprevir (TVR) produces rapid and consistent reductions of HCV-RNA plasma levels in G1 patients. Study C209 is an ongoing, partially blinded, randomized, Phase-2a study of TVR, administered alone or with peginterferon-alfa-2a (Peg-IFN) and ribavirin (RBV), investigating early viral kinetics of HCV-RNA decay in treatment-naIve subjects with genotype 2/3 (G2/3) infection. We report the results of the primary analysis conducted after 15 days of treatment.
Methods: 49 subjects were randomized to receive 15 days of either TVR 750mg q8h alone (armA;G2/3;n=10/8), TVR 750mg q8h with Peg-IFN 180µg/week and RBV 800mg/day (armB;G2/3;n=5/9), or Peg-IFN 180µg/week and RBV 800mg/day plus placebo (armC;G2/3;n=8/9) . Viral load was measured using Taqman assay (LOD1-log increase in HCV-RNA above nadir or >100 IU/mL HCV-RNA after previously undetectable HCV-RNA. An ITT analysis was performed when all treated subjects had completed 15 days of dosing or discontinued earlier.
Results: Mean baseline log10 HCV-RNA was 6.45 and 6.44 IU/mL among G2- and G3-infected subjects, respectively. The mean (SE) log10 changes in HCV-RNA at days 3/15 in G2-infected subjects were -3.0(0.37)/-3.1(0.64), -3.9(0.23)/-5.3(0.27), and -2.2(0.56)/-4.0(0.70) and in G3-infected subjects -0.8(0.33)/-0.5(0.11), -2.9(0.24)/-4.7(0.32), and -2.6(0.40)/-4.5(0.36) for arms A, B, and C, respectively. The mean (SE) log10 maximum HCV RNA change in G2/G3-infected subjects was -4.0(0.49)/-0.8(0.33), -5.5(0.24)/-4.7(0.32) and -4.0(0.70)/-4.5(0.36) for arms A, B and C, respectively. In G3-infected subjects, responses varied across subtypes. The proportion of G2/G3-infected subjects with undetectable HCV-RNA at day15 was 0%/0%, 40%/22% and 25%/11% for arms A, B and C, respectively. Among G2/G3 subjects receiving TVR monotherapy, 6 and 5 patients, respectively, developed a vBT by day15; no vBTs were observed in arms B or C. Overall incidence of AEs was similar across arms and the most common AEs in TVR arms were rash-related events, nausea, and influenza-like illness, in line with previous reports. One patient in arm B discontinued therapy due to rash. No SAEs were reported in this trial.
Conclusions: TVR demonstrated substantial antiviral activity against HCV G2, while its activity against G3 was limited. These findings support additional investigation of TVR for the treatment of G2 HCV infection.”
Bill
I don't get it. What do you mean that it doesn't work for genotype 3? Is this based on the studies which focused on genotype1?
And from what I understand its still the cocktail mix, of interferon +.
I'm curious about where you got your information.
Hi I've posted a few times on here about new drugs, although the majority of people on here don't seem very interested. But here we go again 2 in particular seem promising 1. Chronvac C, which is a theraputic vaccine, or a vaccine given to people already infected, the idea being it produces anti bodies that fight and kill the virus. A small test was started last year 8 patients I think? The usual low dose medium and high. All were geno 1 and had really low viral loads the best result was 99.7% reduction in viral load. The final results were released a couple off weeks ago. The company triptep (Swedish) have applied to the Swedish medicines board to give a final booster shot shortly. Google it you'll find all the info. It has yet to be tested on any other geno but some of the press releases state that it may also work on other genos. The second drug is called bavituximab. Company name perigrine. It's a monoccol anti body not sure that's the correct spelling. Anyway it works by attaching itself to cells infected by certain cancers and viruses. The infected cells kind of flip inside out exposing a fat normally on the inside of the cell. Bavituximab attaches to any cells it finds with the fat on the outside and flags them fir destruction by your immune system. It idea being you kill the cell you kill the virus lurking within. I think again only geno 1s in these trials but I also think that the cells flips no matter the what the geno. The results were very impressive and the language used by the company in their last press release Jan 2010 or dec 2009 not sure which, was very strong. All about how interferon is very hard to take with it's sides and how they would like to explore the possibility of maybe replacing interferon with bavituximab. So there is hope and maybe combined with direct inhibiting anti virals that are in the pipeline and again maybe with a theraputic vaccine this might do the trick. If you go back anlittle on the forum you should find two links I posted about these treatments, they are the latest press releases. I posted them on tuesday of last week I think. Hope this was of some help? Although I do tend to ramble a bit. P.S. Just interested? Are you against taking interferon?
Unfortunately all the new drugs that are expected to be released in the near future must be given with interferon and ribavirin. I don't know if boceprevir is having the same issues with genotype 3's or not. I haven't personally heard anything about it.
not using SOC do you mean? none in a word
with SOC boceprevier works with G 2, and 3 i thought ,,could be wrong