Replies to post #64992 on Biotech Values

[DewDiligence]

SGP / Boceprevir – The bottom line is that these results are comparable to the treatment-naïve results for Telaprevir seen in VRTX’s PROVE-1 and PROVE-2 trials.

Although the Boceprevir SVR data have not yet been reported for the 48-week arms, we already have enough data to see that adding Boceprevir to SoC increased SVR relative to SoC alone by about 20 percentage points in the short-duration arms (24-28 weeks). We know this because the SVR rate for the 48-week control arm cannot exceed the reported SVR12 rate of 38%, and it will in all likelihood drop a little further to, say, 35-36%; SVR in the 24-28-week Boceprevir arms was 55-56% (hence the delta of 20 percentage points).

The delta relative to SoC seen in VRTX’s PROVE-1 and PROVE-2 studies was also 20 percentage points (#msg-29019931).

p.s. When the prior results from the Boceprevir trial were reported in April, I argued in #msg-28863807 (while rebutting one the worst articles ever from Adam Feuerstein) that Boceprevir could end up showing show results comparable to Telaprevir, even as some of the loudest VRTX bulls tried to tell me I was out to lunch.




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[genisi]

Boceprevir in null responders:

Response-Guided Therapy (RGT) for Boceprevir (Boc) Combination Treatment? – Results from HCV SPRINT-1

Background: HCV SPRINT-1 investigated a 4-week lead-in of PegIntron (P;1.5 mcg/kg/QW) plus Ribavirin (R;800-1400 mg/day) prior to the addition of Boc (800 mg TID) for 24 or 44 weeks. Analysis of this data may lead to RGT paradigms.
Methods: Viral response was assessed by Roche TaqMan (LLD=15 IU/ml) at multiple time points including treatment weeks 4, 8, 12, 24 and 24 weeks post-treatment (sustained virologic response; SVR). Results: Patients were all G1 (1a>1b) with 15% African-Americans, 7% cirrhotics and 90% high viral load. W8 virology was available for all 103 patients in each arm. The majority of patients (64%) became negative by week 8 and SVR rates were similar for the long (94%) and short (82%) treatment arms (p=NS). In contrast, patients who first became negative between week 8 and 16, benefited from longer therapy (SVR 79% vs 21%; p=0.004), but represented only 18% of the population. A third group never achieved undetectable HCV-RNA by W16; this group primarily comprises null responders (11/18 in 48W arm) at week 4.
Conclusions: The majority of patients (64%) had undetectable HCV-RNA after 4 weeks of triple therapy following the lead-in and had a high rate of SVR (82%) following a shortened 28-week treatment duration. Only 18% of patients first achieving undetectable HCV-RNA after week 8 and before week 16 of therapy benefited from a longer treatment regimen of 48 weeks. These data suggest that only a minority of treatment-naïve G1 patients will require more than 28 weeks of therapy, and response-guided therapy based on week-8 viral response may be a powerful predictive tool to individualize therapy. The SPRINT-2 trial is designed to prospectively confirm this treatment paradigm.