Tuesday, March 8, 2011

Hepatitis C;Telaprevir, Boceprevir Boost SVR in Hep C

We are on the verge of triple-drug regimens that will improve response rates for genotype 1 hepatitis C to where rates for genotype 2/3 have been,while shortening the duration of therapy to 24 weeks for many patients,which can lower both cost and side effects.

However, therapy will be more complex and will require closer monitoring to manage side effects and monitorfor and prevent resistance.

DR. ROBERT S. BROWN JR. is the Frank Cardile Professor ofMedicine and Surgery and Chiefof the Center for Liver Diseaseand Transplantation at ColumbiaUniversity College of Physicians and Surgeons, New York.

Telaprevir, Boceprevir Boost SVR in Hep C

March GI and Hepatology News ;Download PDF _

BY DIANA MAHONEY

Elsevier Global Medical News BOSTON –


BOSTON – The forthcoming availability of the protease inhibitors telaprevir and boceprevir for the treatment of chronic hepatitis C is likely to vastly improve virologic response rates and cut treatment times, but experts warn that such advancements need to be balanced against the huge potential for misuse of the agents and the need to manage side effects and monitor for antiviral resistance.

When used in combination with standard therapy consisting of pegylated interferon plus ribavirin, each of these investigational drugs improved sustained virologic response (SVR) rates and reduced treatment duration, compared with standard therapy alone, in four pivotal, phase III trials reported at the annual meeting of the American Association for the Study of Liver Diseases.

Previous Nonresponders Benefit From Boceprevir

Response-guided, fixed-duration therapy with boceprevir was safe and effective in a cohort of HCV genotype 1 patients who were enrolled in the RESPOND-2 study and who failed standard therapy, said lead investigator Dr. Bruce R. Bacon of St. Louis University. The 403 patients included those in whom prior standard therapy resulted in either a partial response (HCV RNA less than 2 logs at 12 weeks but still positive) or a relapse, he said.

All patients underwent a 4- week lead-in phase of standard therapy followed by random assignment to continue standard therapy alone or in conjunction with 800 mg of boceprevir taken three times daily.

The treatment duration was 36 weeks for patients in the boceprevir arm with undetectable HCV RNA at study weeks 8 and 12, whereas those patients in whom HCV RNA was detectable at study week 8, but undetectable at week 12, stopped boceprevir at week 36 but continued standard therapy for an additional 12 weeks (total of 48 weeks). Controls were treated for 48 weeks.

The SVR rates at 24 weeks after treatment conclusion were significantly higher in the boceprevir groups, compared with the control group. In the responseguided and fixed-duration boceprevir groups, the SVR rates were 59% and 66%, respectively, compared with 21% in the control patients, Dr. Bacon said.

In the two boceprevir study arms, “previous historical relapsers and partial responders fared better than the patients receiving standard of care,” he noted.

Although the rates of anemia were significantly higher in the boceprevir arms, “the rate of treatment discontinuation related to side effects was similar across all three arms,” Dr. Bacon reported, possibly because the use of erythropoietin was allowed to treat anemia, he said.

The findings of this study answer an important question about response-guided therapy “by confirming that many patients can be treated successfully with a treatment duration that is reduced by 3 months relative to the current standard of care treatment,” Dr. Bacon said.

Boceprevir with a standard therapy lead-in strategy was also evaluated in the SPRINT-2 study involving HCV genotype 1 treatment-naive patients, according to Dr. Fred Poordad of Cedars-Sinai Medical Center in Los Angeles. The trial included 1,097 patients who underwent a similar 4-week standard therapy lead-in as defined above, followed by the addition of placebo for 44 more weeks or by the addition of boceprevir, either for 24 more weeks for patients with undetectable HCV RNA at week 8 or for 24 more weeks plus 20 additional weeks of standard therapy for patients with detectable HCV RNA at week 8, but not at week 24, Dr. Poordad explained. Patients with detectable HCV RNA at week 24 were discontinued for futility, he said.

“In both the response-guided and fixed-treatment arms, boceprevir increased viral cure rates significantly, by approximately 70%,” Dr. Poordad stated. The SVR rate was 63% in the 28-week response-guided group, 66% in the 48-week fixed-duration group, and 38% in the 48-week control group, he said.

In a cohort analysis of treatment response for the study’s 159 black patients, the relative improvement in SVR rates remained significant in the boceprevir arms, although the differences were not as robust, Dr. Poordad said. In this subgroup, the respective SVR rates in the response- guided therapy, fixed-duration therapy, and control groups were 42%, 53%, and 23%.

The rationale for using a lead-in strategy “is to help physicians identify patient responsiveness to interferon before adding boceprevir,” Dr. Poordad said. This can provide an early indication of the likelihood of treatment success. The advantage of subsequent response-guided therapy, he noted, is that it enables physicians to be flexible in managing their patients’ therapy “by adapting treatment duration to individual patient response.”

Telaprevir Boosts Viral Cure Rates

In the ADVANCE trial, a three-arm, double-blind, placebo-controlled study, investigators compared two telaprevir-based regimens with standard therapy in 1,088 treatment-naive patients with chronic genotype 1 hepatitis C virus (HCV) infection, according to lead investigator Dr. Ira M. Jacobson, AGAF, of New York Weill Cornell Medical Center in New York City.

Patients in treatment arms 1 and 2 received 750 mg of telaprevir plus standard therapy for 8 and 12 weeks, respectively, whereas patients in the control group received standard therapy alone, which consisted of 180 mcg/week of pegylated interferon alfa-2a and 1,000-1,200 mg/day of ribavirin.

Patients who had extended, rapid virologic response (RVR) – defined as undetectable HCV RNA viral load at treatment weeks 4 and 12 – were treated with standard therapy for an additional 16 and 12 weeks in the 8- and 12-week telaprevir arms, respectively, for a total of 24 weeks, Dr. Jacobson explained. Patients in whom HCV RNA was detectable at either week 4 or 12 received an additional 40 and 36 weeks of therapy, respectively, for a total of 48 weeks. The control group underwent standard therapy for 48 weeks.

Compared with 44% of patients in the control group who achieved SVR 24 weeks after the last treatment, significantly more patients in both telaprevir arms – 69% of the 8-week group and 75% of the 12-week group – met that end point, Dr. Jacobson reported. The extended RVR rates in the 8- and 12-week groups were 57% and 58%, respectively, compared with 8% in the control arm.

Significantly improved SVRs were also observed in difficult-to-treat subgroups. “Among black patients, the [SVR] rates were 58% and 62% in the 8- and 12-week treatment arms, and 25% in the control arm, and in cirrhotic patients the respective rates were 53%, 62%, and 33%,” he said. Rates of treatment discontinuation due to adverse events, such as rash and anemia, were 8% and 7% in the 8-and 12-week telaprevir groups and 4% in the control group, “which is an improvement, compared with the previously reported profile,” he said.

The phase III, open-label ILLUMINATE trial was designed to determine whether extending the telaprevir and standard therapy regimen from 24 to 48 weeks would be beneficial in treatment-naive, genotype 1 HCV patients who achieved extended RVR. In all, 540 patients were initially treated with the 12-week telaprevir regimen described above. Of the 352 patients who achieved RVR, 322 remained on treatment and were randomized to either a 24-week or 48-week treatment arm.

“The [SVR] rates associated with the 24-week and the 48-week arms were statistically similar, at 92% and 87.5%, respectively,” reported Dr. Kenneth E. Sherman of the University of Cincinnati. Analyses of the data based on race and extent of liver damage showed that 88% of black patients who had extended RVR achieved SVR in both the 24- and 48- week treatment arms, and 82% and 88% of patients with advanced fibrosis/cirrhosis achieved SVR in the 24-week and 48-week arms, respectively, he said.

There were more adverse event–related treatment discontinuations in the longertreatment group (12.5% vs. 0.6%), suggesting a benefit to the shorter duration, Dr. Sherman said. The high viral cure rate observed in the study – the overall SVR rate was 72% in an intent-to-treat analysis – “[supports] the role of response-guided therapy with telaprevir-based regimens” in treatment-naive patients,” he said.

All the sources disclosed relationships with numerous pharmaceutical companies. Among them, Dr. Jacobson and Dr. Sherman disclosed relationships with Vertex Pharmaceuticals, which manufactures telaprevir. Dr. Jacobson also has a relationship with Tibotec, which also is involved with the development of telaprevir. Dr. Poordad and Dr. Bacon also disclosed relationships with Merck, which manufactures boceprevir.

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