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wakawaka36's avatar

How to cure Hepatitis C without interferon?

Asked by wakawaka36 (72points) July 24th, 2013

My mom has Hep C, and she is allergic to interferon. I am crying myself to death and I need a cure NOW.

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7 Answers

Rarebear's avatar

Looks like that link doesn’t work if you’re not a subscriber.

Here it is cut and pasted. You won’t understand most of it, but new therapies are coming down the line.

What About Interferon-free Regimens?

Interferon-free regimens are widely being tested in clinical trials with encouraging results. The following selected trials demonstrate how rapidly progress is being made. Beginning in 2010, studies demonstrated the potential for antiviral efficacy of an all-oral regimen using combinations of drugs with different targets.

Interferon-free regimen for the management of HCV-1 (INFORM-1) was a phase 1 proof of concept study from 2010 using combination DAA without interferon.[27] Danoprevir, an NS3/4A protease inhibitor, and RG7128 (later named mericitabine), a NS5B nucleoside polymerase inhibitor, were given for up to 13 days in multiple different dosing arms to assess the ability of an interferon-free regimen to suppress viral load. After the treatment period, all patients subsequently were given standard of care pegylated interferon and ribavirin for 48 weeks. Overall, the DAA combination therapy was well tolerated, and there were no treatment-related study withdrawals or dose reductions during the treatment period. Most common adverse event was headache. The DAA combination regimen showed very potent activity against HCV in all participants, including previous null responders giving encouragement that interferon-free all DAA regimens are possible. Of note, patients with cirrhosis were excluded.

SOUND-1 and SOUND-2 trials included an NS3/4A protease inhibitor (BI-201335) and an NNI NS5B polymerase inhibitor (BI-207127) and ribavirin to demonstrate proof of potent antiviral activity against HCV with rapid viral response rates of 73–100% dependent on dosing. Genotype 1b responded more favorably than 1a and the ribavirin-sparing arm in the later trial showed reasonable but substantially lower response rates. Final results were presented in abstract form at the American Association for the Study of Liver Diseases (AASLD) Liver Meeting 2012.[29] Patient results were randomized by genotype 1a versus 1b and by IL-28 genotype CC/CT/TT. Ribavirin arms with variable DAA dosing demonstrated a range in SVR12 (SVR after only 12 weeks off therapy), of 52–69% but only 39% in ribavirin-free arms. Genotype 1b responded better than 1a and IL-28 appeared to be an independent predictor of SVR. All IL-28 genotype of 1b and IL-28 CC 1a patients demonstrated SVR 12 rates as high as 84% with the all-oral regimen.

More recently, exciting results from the phase 2 ELECTRON trial were reported.[30] Sofosbuvir (formerly known as GS-7977) NS5B polymerase inhibitor in a once daily dose was combined with ribavirin for 12 weeks, pegylated interferon and ribavirin for 4, 8, or 12 weeks in naive patients with genotypes 2 or 3 or sofosbuvir monotherapy for 12 weeks in naive patients with genotypes 2 or 3. An additional group of 35 genotype 1 patients was enrolled, 25 naive patients and 10 prior nonresponders who were also treated with sofosbuvir and ribavirin for 12 weeks. After 24 weeks of therapy, all naive genotype 2 and 3 patients on combination therapy had an SVR at 24 weeks (100%). SVR was seen in only 60% of the genotype 2 and 3 patients on monotherapy. Among genotype 1, treatment-naive patients demonstrated 84% SVR and prior nonresponders fared less well with an SVR of only 10%. Sofosbuvir appears to be well tolerated and to have a high barrier to resistance. This study suggests a new DAA option may soon be available for naive patients with genotype 1, 2, and 3; however, ribavirin still plays a role in maintenance of an antiviral response.[30]

Another new phase 2 clinical trial was found to show even better responses in genotype 1 patients. ABT-450 (an NS3 protease inhibitor) combined with low-dose ritonavir, ABT-333 (a non-nucleoside NS5B polymerase inhibitor), and ribavirin were used in varying doses in treatment-naive and experienced patients excluding those with cirrhosis for 12 weeks. Treatment-naive patients demonstrated an SVR12 of 93–95% depending on dose and treatment experienced patients an SVR12 of 47%. Some viral breakthrough and resistance was noted during treatment in the prior nonresponder population and the study suggests this population will need a modified DAA regimen as extending duration would not have changed outcome. Overall, this 12-week combination therapy may be an effective future therapy for HCV genotype 1.[31]

Dutchess_III's avatar

English @Rarebear! Please!

Rarebear's avatar

@Dutchess_III If you wait, you can take pills.

Nullo's avatar

You could also print off @Rarebear‘s Great Wall of Text and give it to your mom’s doctor.

@Rarebear Think she could get in on future trials?

Rarebear's avatar

@Nullo No idea. We’re telling all of our patients who can wait (meaning that they don’t have significant fibrosis on biopsy) to wait. Formal FDA approval is a year or two away. The pharmaceutical companies have a lot of skin in this game as there is a ton of money to be made. So trials are proceeding apace.

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