Dramatic Changes in Hepatitis C Treatment Expected to Continue

9/6/11

Earlier this year the FDA approved telaprevir (Incivek) from Vertex Pharmaceuticals and boceprevir (Victrelis) from Merck for the treatment of hepatitis C. Both agents are protease inhibitors and represent the first approvals of direct acting antivirals for hepatitis C. Direct acting antivirals are a broad class of agents that act to block the growth of viruses by directly disrupting essential viral functions. The benefit of these drugs for hepatitis C follows the dramatic success of this class over the last 15 years in HIV. Now the future advances of direct acting antiviral therapy for hepatitis C is expected to follow a central theme of their use in HIV: that combination of multiple antivirals in a single treatment regimen will provide greater benefit than use of any one antiviral drug alone.

The new protease inhibitors were approved for use only in combination with two previously approved agents, pegylated interferon and ribavirin. The addition of either protease inhibitor increased clinical cure rates, known formally as sustained viral response (SVR) rates, by 30 to 40 percentage points over control groups receiving the standard pegylated interferon and ribavirin alone. As dramatic as these improvements are, there is a good chance for even more dramatic improvements if all-oral regimens, assembled by combining multiple direct acting antivirals, are able to maintain high cure rates while eliminating injectable interferon and its associated flu-like side effects that patients have long sought to avoid.

Next in the development queue are three agents that entered Phase III development this year, including two additional protease inhibitors (TMC435 from Johnson & Johnson’s Tibotec unit and BI201335 from Boehringer Ingelheim) and a cyclophilin inhibitor that disrupts a host function required for viral replication (alisporivir from Novartis). All three Phase III programs are exploring a modality similar to the approved agents, i.e. addition of a single new agent to the standard pegylated interferon/ribavirin. The ongoing Phase III programs will hope to demonstrate one or more advantage over the recently approved agents, potentially including better tolerability, further increases in cure rates, shorter duration of therapy and/or an increased proportion of patients successfully treated with shortened therapy. While such improvements may well be achieved, they may become less important or even irrelevant if the rapidly expanding number of direct acting antiviral combination trials leads to identification of new regimens that surpass all regimens that are based on a single antiviral drug added to the old standard regimen.

Investigation of direct acting antiviral combination regimens has exploded in the last 12 months. This advance has become possible because of the diversity of antiviral mechanisms distinct from protease inhibitors that are now represented in the pipeline of hepatitis C drugs in Phase II development across the industry. Diverse mechanisms are important because they typically provide distinct resistance profiles, and antiviral combinations are being assembled using new compounds with non-overlapping resistance profiles to provide a greater barrier to the development of antiviral resistance. Additional factors that are considered important in assembling optimal combinations include the safety and tolerability profile of each agent, compatible pharmacokinetic profiles and a low potential for unfavorable drug-drug interactions. The more extensively characterized each individual antiviral drug is, the lower the risk of … Next Page »

Steve Worland is the president and CEO of San Diego-based Anadys Pharmaceuticals. Follow @

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  • http://WilsonRx.com Jim Wilson

    When will post transplant patient populations be included in clinical trials of HCV agents? Current new drugs interfere with Tacrilimus levels causing potentially toxic increased levels and potential kidney damage. This area represents a significant patient population yet companies seem to avoid.

  • Talat Mehmood

    I hope that all the efforts made to treat Hepatitis C will be succesful.we will pray to achive the goal.may God help u.mail me further developments.

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  • Jeffrey Fried

    And what about those of us for whom combination therapies with interferon is not an option? When will these companies provide a non-interferon based solution?

  • suzan krieger

    Hepatitis C genotype 2 –failed on riberviran and interferon due to hemoglobin reaction. will there be something for me?

  • Mike Murphy

    I’d like to echo the observations of Jim Wilson – when will a post-transplant regimen be available to this population? I’ve tried the interferon/ribavirin programs twice without achieving SRV. It’s like living with a time bomb.

  • Suzan

    When will the treatment for hepatitis c genotype 4 be availble for non responders and above 60 years old? Please email me the answer.
    Thanks

  • taz

    I so hope that they get meds for all geno types & all of us with hep c!! i am a non responder & will get to try the incivik for two weeks. if i respond weel, then i get to stay on it, if not i get off it.. it seems to hurt u in being resistant to any possible new drugs? is the way i understand it! weird.. i did the SOC twice for 3 months. didn’t work. wish i had not done it the second time.. God be with us & the scientists who are working hard to discover new meds..

  • onindo

    can i drink bear after taking the hepatites c treatment?

  • Edward

    Trials for genotype 4?

  • alfred

    How do herbal medicines ( such as Sho-Saiko-to, recently studied at Sloan Kettering ) compare. There results seem at least as good.

  • Gabriel

    I’ve been on Victrelis for 4 months and the virus is starting to climb again after going from 2.3 million to 1196 in 7 weeks.
    I gave blood to see if there are Protease Inhibitor mutations. If there are, we stop treatment. If not and the viral load is still climbing, the doctor is considering switching me over to Incivek. Anybody have any thoughts on this switching?

  • Susan Cosco

    I think that some of these trials should be allowing Protease Inhibitor -failure patients. If a company could proof that their drug could clear the virus in a patient who had failed treatment using Pegasys+Incivek (I was exposed to these 2 drugs in trial, but was randomized into the no Riba group), then, it would definitely show that their drug was a superior drug in this subset of patients. I happen to know of several protease inhib. (Hep C) patients, who failed this drug therapy.

  • Ben

    How does one acquire such break through treatment with out insurance?

  • wendy

    Please develop a non interferon treatment that can be tolerated well and effective for all genotypes!

  • Jeff

    I took pegylated interferon and ribavirin for 11 months in 2003-2004 but the virus was detected again 6 months after completing the treatments. In July 2011, I began the same treatment with the new Victrelis. On October 31, 2011, I was found on the floor foaming at the mouth and was rushed to the ER. I spent 9 days in ICU with Pneumonia and Pulmonary Edema. I was told it wasn’t due to the meds but when asked if it could have caused my immune system to allow it, I didn’t get a straight answer. Could it have contributed? I was told I had several seizures for a few days and doctors told me that initially they thought if I survived, I would have a good chance of having brain damage. I think I have a good doctor but I don’t feel he keeps me advised on my condition. I was taken off the treatments while I was in ICU and I don’t see my doctor again for 6 months (July 2012). I am so confused, I don’t know what to do or expect and have no family. May God help us all to make the correct decisions and get well with minimal side effects ASAP.

  • c.hemsley

    Im hcv genotype 1 ive had first lot of standard tx and was a non responder now been asked to participate in clinical trials. But after being on peginterferon/ribvarin and treatment was stopped after 12wks no virological response of 2 logs or more, also low platelets and white cell count would i still not encounter the same issues with the newer drugs or maybe not any advice would be great.The liver specialist said either the clinical trials would be at barts or cambridge hospital in the uk.Thanks Colin.

  • Bill Pomeroy

    I have end-stage liver disease caused by Hep C. Transplant is only option. Has this drug been tested on patients pre-transplant and/or post-transplant?

  • Sharon

    I am Genotype 1b and have had Hep C for approx 37 years.  I started the newly approved “triple treatment” (pegylated interferon, ribavirin and  telaprevir (Incivek)) Oct, 2011 and completed treatment April, 2012.  The bad news – the first 12 weeks on Incivek almost killed me it was so difficult.  The good news – I went viral load “undectable” at week 2 and have stayed that way throughout and after the treatment.  In Oct I will know for sure if I cleared the virus.  The downside was the treatment – the UP side is I feel better then I have in years.  I am so glad they continue to develop new treatments for this difficult disease.  I wish you all the best. 

    • Nola

      My husband is going to start the same treatment with the same Genotype.  The first interferon/ribavirin treatment did not work.  He said he knew it didn’t prior to the six months due to how his body felt.  May your body continue to feel great and in October you receive the results of “non detectable”. 

  • bruce

    have you herd of bht for treatment

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