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Treatment success with incivek
I' m undergoing treatment for the 4th time-this time with incivek as wel as the pegasys and interferon. What is the success rate for someone like me? Last treatment had viral load of 0 by the 10th week and was 0 through week 48. Follow up Tati g 30 days after treatment ended viral load was >5million.
During your last treatment, maybe the virus mutated and went into hiding (i.e., it left your bloodstream and hide somewhere where the Pegasys & Ribavirin couldn't find it). When the virus realized you were no longer taking the Pegasys & Ribavirin it released itself into your bloodstream -- at over 5M units per measure. That's what I believe happened to me in 2009. I was undetectable for over 60 weeks and 2 weeks after i stopped treatment the virus resurfaced at a very high level.
As far as your current treatment goes, it's possible the Incivek killed the virus before it had a chance to mutate and go into hiding. I'm currently on triple therapy (treatment week #20 -- took Incivek for the first 12 weeks). Virus was undetectable at 2 weeks and has been undetectable ever since. My therapy will end at 24 weeks (April 9th). If the virus is in hiding, I'll know within a couple of weeks after stoping treatment. Hang in there!
As far as your current treatment goes, it's possible the Incivek killed the virus before it had a chance to mutate and go into hiding. I'm currently on triple therapy (treatment week #20 -- took Incivek for the first 12 weeks). Virus was undetectable at 2 weeks and has been undetectable ever since. My therapy will end at 24 weeks (April 9th). If the virus is in hiding, I'll know within a couple of weeks after stoping treatment. Hang in there!
Previously Treated Adults
Study C216 (REALIZE)
Study C216 was a randomized, double-blind, placebo-controlled, trial conducted in subjects who did not achieve SVR with prior treatment with Peg-IFNalfa- 2a/RBV or Peg-IFN-alfa-2b/RBV. The study enrolled prior relapsers (subjects with HCV-RNA undetectable at end of treatment with a pegylated interferon-based regimen, but HCV RNA detectable within 24 weeks of treatment follow-up) and prior non-responders (subjects who did not have undetectable HCV-RNA levels during or at the end of a prior course of at least 12 weeks of treatment). The nonresponder population included 2 subgroups: prior partial responders (greater than or equal to 2-log10 reduction in HCV-RNA at week 12, but not achieving HCV RNA undetectable at end of treatment with peginterferon alfa and ribavirin) and prior null responders (less than 2-log10 reduction in HCV-RNA at week 12 of prior treatment with peginterferon alfa and ribavirin).
Subjects were randomized in a 2:2:1 ratio to one of two INCIVEK combination treatment groups (with and without a Peg-IFN-alfa-2a/RBV lead-in) or a control group. The T12/PR48 group received INCIVEK and Peg-IFN-alfa-2a/RBV for 12 weeks (without a lead-in), followed by placebo and Peg-IFN-alfa-2a/RBV for 4 weeks, followed by Peg-IFN-alfa-2a/RBV for 32 weeks. The T12(DS)/PR48 group had a lead-in (delayed start of INCIVEK) with placebo and Peg-IFN-alfa-2a/RBV for 4 weeks, followed by INCIVEK and Peg-IFN-alfa-2a/RBV for 12 weeks, followed by Peg-IFN-alfa-2a/RBV for 32 weeks. The Pbo/PR48 group received placebo and Peg-IFN-alfa-2a/RBV for 16 weeks, followed by Peg-IFN-alfa-2a/RBV for 32 weeks.
The 662 enrolled subjects had a median age of 51 years (range: 21 to 70); 70% of the subjects were male; 26% had a body mass index greater than or equal to 30 kg/m2; 5% were Black; 11% were Hispanic or Latino; 89% had baseline HCV-RNA levels greater than 800,000 IU/mL; 22% had bridging fibrosis; 26% had cirrhosis; 54% had HCV genotype 1a, and 46% had HCV genotype 1b. Null and partial responders had higher baseline HCV-RNA levels and more advanced liver disease (cirrhosis) than relapsers; other characteristics were similar across these populations.
The lead-in and immediate start regimens produced comparable SVR and no SVR rates, so data from these two groups were pooled (Table 11).
Treatment Outcome All T12/PR48 % (n/N) Pbo/PR48 % (n/N)
SVR rate
Prior relapsers 86% (246/286) 22% (15/68)
Prior partial responders 59% (57/97) 15% (4/27)
Prior null responders 32% (47/147) 5% (2/37)
On-treatment virologic failure
Prior relapsers 1% (3/286) 10% (7/68)
Prior partial responders 15% (15/97) 26% (7/27)
Prior null responders 50% (74/147) 22% (8/37)
Relapse
Prior relapsers 3% (8/254) 63% (27/43)
Prior partial responders 20% (14/71) 0% (0/4)
Prior null responders 24% (15/62) 50% (2/4)
Lead-in and immediate start T12/PR regimens pooled
On-treatment virologic failure includes subjects who met a protocol-defined virologic stopping rule or who had detectable HCV-RNA at the time of their
last dose of INCIVEK and subjects who had viral breakthrough on peginterferon alfa/ribavirin.
Relapse rates are calculated with a denominator of subjects with undetectable HCV-RNA at the end of treatment.
Among prior relapsers, 76% (218/286) achieved an eRVR and of those 95% (208/218) achieved an SVR. In an earlier, dose-finding clinical trial, 78% (52/67) of prior relapsers achieved an eRVR and were treated with 24 weeks of peginterferon alfa and ribavirin (T12/PR24); of those 94% (49/52) achieved an SVR.
For all populations in the study (prior relapsers, prior partial responders, and prior null responders), SVR rates were higher for the T12/PR group than for the Pbo/PR48 group across subgroups by sex, age, ethnicity, body mass index, HCV genotype subtype, baseline HCV-RNA level, and extent of liver fibrosis. Twenty-three percent of INCIVEK-treated subjects had cirrhosis at baseline. SVR rates among cirrhotic subjects who received INCIVEK combination treatment compared to Pbo/PR48 were: 87% (48/55) compared to 13% (2/15) for prior relapsers, 34% (11/32) compared to 20% (1/5) for prior partial responders, and 14% (7/50) compared to 10% (1/10) for prior null responders.
Four percent (19/530) of treatment experienced subjects who received INCIVEK combination treatment were Black/African Americans; the SVR rate for these subjects was 63% (12/19) compared to 65% (328/503) for Caucasians.
Study C216 (REALIZE)
Study C216 was a randomized, double-blind, placebo-controlled, trial conducted in subjects who did not achieve SVR with prior treatment with Peg-IFNalfa- 2a/RBV or Peg-IFN-alfa-2b/RBV. The study enrolled prior relapsers (subjects with HCV-RNA undetectable at end of treatment with a pegylated interferon-based regimen, but HCV RNA detectable within 24 weeks of treatment follow-up) and prior non-responders (subjects who did not have undetectable HCV-RNA levels during or at the end of a prior course of at least 12 weeks of treatment). The nonresponder population included 2 subgroups: prior partial responders (greater than or equal to 2-log10 reduction in HCV-RNA at week 12, but not achieving HCV RNA undetectable at end of treatment with peginterferon alfa and ribavirin) and prior null responders (less than 2-log10 reduction in HCV-RNA at week 12 of prior treatment with peginterferon alfa and ribavirin).
Subjects were randomized in a 2:2:1 ratio to one of two INCIVEK combination treatment groups (with and without a Peg-IFN-alfa-2a/RBV lead-in) or a control group. The T12/PR48 group received INCIVEK and Peg-IFN-alfa-2a/RBV for 12 weeks (without a lead-in), followed by placebo and Peg-IFN-alfa-2a/RBV for 4 weeks, followed by Peg-IFN-alfa-2a/RBV for 32 weeks. The T12(DS)/PR48 group had a lead-in (delayed start of INCIVEK) with placebo and Peg-IFN-alfa-2a/RBV for 4 weeks, followed by INCIVEK and Peg-IFN-alfa-2a/RBV for 12 weeks, followed by Peg-IFN-alfa-2a/RBV for 32 weeks. The Pbo/PR48 group received placebo and Peg-IFN-alfa-2a/RBV for 16 weeks, followed by Peg-IFN-alfa-2a/RBV for 32 weeks.
The 662 enrolled subjects had a median age of 51 years (range: 21 to 70); 70% of the subjects were male; 26% had a body mass index greater than or equal to 30 kg/m2; 5% were Black; 11% were Hispanic or Latino; 89% had baseline HCV-RNA levels greater than 800,000 IU/mL; 22% had bridging fibrosis; 26% had cirrhosis; 54% had HCV genotype 1a, and 46% had HCV genotype 1b. Null and partial responders had higher baseline HCV-RNA levels and more advanced liver disease (cirrhosis) than relapsers; other characteristics were similar across these populations.
The lead-in and immediate start regimens produced comparable SVR and no SVR rates, so data from these two groups were pooled (Table 11).
Treatment Outcome All T12/PR48 % (n/N) Pbo/PR48 % (n/N)
SVR rate
Prior relapsers 86% (246/286) 22% (15/68)
Prior partial responders 59% (57/97) 15% (4/27)
Prior null responders 32% (47/147) 5% (2/37)
On-treatment virologic failure
Prior relapsers 1% (3/286) 10% (7/68)
Prior partial responders 15% (15/97) 26% (7/27)
Prior null responders 50% (74/147) 22% (8/37)
Relapse
Prior relapsers 3% (8/254) 63% (27/43)
Prior partial responders 20% (14/71) 0% (0/4)
Prior null responders 24% (15/62) 50% (2/4)
Lead-in and immediate start T12/PR regimens pooled
On-treatment virologic failure includes subjects who met a protocol-defined virologic stopping rule or who had detectable HCV-RNA at the time of their
last dose of INCIVEK and subjects who had viral breakthrough on peginterferon alfa/ribavirin.
Relapse rates are calculated with a denominator of subjects with undetectable HCV-RNA at the end of treatment.
Among prior relapsers, 76% (218/286) achieved an eRVR and of those 95% (208/218) achieved an SVR. In an earlier, dose-finding clinical trial, 78% (52/67) of prior relapsers achieved an eRVR and were treated with 24 weeks of peginterferon alfa and ribavirin (T12/PR24); of those 94% (49/52) achieved an SVR.
For all populations in the study (prior relapsers, prior partial responders, and prior null responders), SVR rates were higher for the T12/PR group than for the Pbo/PR48 group across subgroups by sex, age, ethnicity, body mass index, HCV genotype subtype, baseline HCV-RNA level, and extent of liver fibrosis. Twenty-three percent of INCIVEK-treated subjects had cirrhosis at baseline. SVR rates among cirrhotic subjects who received INCIVEK combination treatment compared to Pbo/PR48 were: 87% (48/55) compared to 13% (2/15) for prior relapsers, 34% (11/32) compared to 20% (1/5) for prior partial responders, and 14% (7/50) compared to 10% (1/10) for prior null responders.
Four percent (19/530) of treatment experienced subjects who received INCIVEK combination treatment were Black/African Americans; the SVR rate for these subjects was 63% (12/19) compared to 65% (328/503) for Caucasians.
Your success rate will also be on how fast you respond to this treatment, und at week 4 and 12 better the odds....... Good luck
Good luck with your treatment. This is a great place for information. There all lots of people that are well read on this topic.
We need more info on you condition.
Liver stage?
What were your other responses to treatment? VL and weeks of treatment.
Dates of treatments?
What other weeks was your VL tested after week 10?
Were you compliant during treatment. Ever miss doses. Ever dose reduce either drug?
Hector
Liver stage?
What were your other responses to treatment? VL and weeks of treatment.
Dates of treatments?
What other weeks was your VL tested after week 10?
Were you compliant during treatment. Ever miss doses. Ever dose reduce either drug?
Hector
SVR rate
Prior relapsers 86% (246/286)
http://pi.vrtx.com/files/uspi_telaprevir.pdf
Follow the link and see section 14.2 table 11
Prior relapsers 86% (246/286)
http://pi.vrtx.com/files/uspi_telaprevir.pdf
Follow the link and see section 14.2 table 11
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