Aa
Oh definitely yes! Sorry if I was unclear: knowing how you are classified (prior treatment response) determines how long you treat on triple therapy.
I was a prior partial and you were a null - that means both of us pretty much have to treat the whole 48 weeks with both PIs.
If you treat with Incivek (Telaprevir)
http://www.fda.gov/ForConsumers/ByAudience/ForPatientAdvocates/ucm256328.htm
If you treat with Victrelis (Boceprevir)
http://www.fda.gov/ForConsumers/ByAudience/ForPatientAdvocates/ucm255413.htm
Your last biopsy was within the past five years so that ought to be current enough. I guess next would thinking about your health overall and learning if you have any extrahepatic manifestations (conditions you may have developed over the years that turn out to be related to having HCV). Sometimes even people who are early in the disease (stage 1) may want to treat since when you treat the virus in essence you are treating an underlying or associated conditions). That is a huge topic on its own which someone might want to elaborate on in another post.
After that it would be determining if you are in a position to treat (can possibly take time off if need be, are in good health, have a decent support system, etc). There is more to it that that but those are some of the basics.
Lots of us have walked around with this disease for years without too many problems but fibrosis tends to progress more rapidly as we age so evaluating all of your treatment options is something that might be worth while either way.
There are less harsh, interferon-free, *all oral* HCV meds in trials that are highly efficacious with shorter treatment times so definitely learn a little about that. Some people opt to wait until those come out or try to get in a trial.
This may be premature since you are uncertain of your genotype but I just thought I would throw all this out there. Either way there is plenty of support here. I encourage you to hang around and read posts since a lot has changed since 1995
Best of luck♫
I was a prior partial and you were a null - that means both of us pretty much have to treat the whole 48 weeks with both PIs.
If you treat with Incivek (Telaprevir)
http://www.fda.gov/ForConsumers/ByAudience/ForPatientAdvocates/ucm256328.htm
If you treat with Victrelis (Boceprevir)
http://www.fda.gov/ForConsumers/ByAudience/ForPatientAdvocates/ucm255413.htm
Your last biopsy was within the past five years so that ought to be current enough. I guess next would thinking about your health overall and learning if you have any extrahepatic manifestations (conditions you may have developed over the years that turn out to be related to having HCV). Sometimes even people who are early in the disease (stage 1) may want to treat since when you treat the virus in essence you are treating an underlying or associated conditions). That is a huge topic on its own which someone might want to elaborate on in another post.
After that it would be determining if you are in a position to treat (can possibly take time off if need be, are in good health, have a decent support system, etc). There is more to it that that but those are some of the basics.
Lots of us have walked around with this disease for years without too many problems but fibrosis tends to progress more rapidly as we age so evaluating all of your treatment options is something that might be worth while either way.
There are less harsh, interferon-free, *all oral* HCV meds in trials that are highly efficacious with shorter treatment times so definitely learn a little about that. Some people opt to wait until those come out or try to get in a trial.
This may be premature since you are uncertain of your genotype but I just thought I would throw all this out there. Either way there is plenty of support here. I encourage you to hang around and read posts since a lot has changed since 1995
Best of luck♫
I was a Null responder (less than a 2 log10 drop by week 12) so would I still be a candidate for the treatment? My last 2009 biopsy showed stage 2 fibrosis.
OOps in my response I meant Telaprevir is the generic name for Incivek.
If you are a Genotype 1 there is another PI besides Incivek called Victrelis. They have different side effect profiles.
hrsepwrguy raises an issue to consider when treating. Your status is determined by your previous response to treatment so you must know ★★exactly★★ what happened and when:
What was your previous response to treatment...
Null responder (less than a 2 log10 drop by week 12)
or
Partial Responder ( ≥ 2 log drop in HCV RNA after 12 weeks therapy but never undetectable)
_______________________
Also it helps to know how far your fibrosis has progressed. If you are considering treating or weighing out your options you might want to have a physical, some recent labs and maybe even a biopsy (or some other means of assessing your stage of fibrosis)
If you are a Genotype 1 there is another PI besides Incivek called Victrelis. They have different side effect profiles.
hrsepwrguy raises an issue to consider when treating. Your status is determined by your previous response to treatment so you must know ★★exactly★★ what happened and when:
What was your previous response to treatment...
Null responder (less than a 2 log10 drop by week 12)
or
Partial Responder ( ≥ 2 log drop in HCV RNA after 12 weeks therapy but never undetectable)
_______________________
Also it helps to know how far your fibrosis has progressed. If you are considering treating or weighing out your options you might want to have a physical, some recent labs and maybe even a biopsy (or some other means of assessing your stage of fibrosis)
Incivek is a Direct Acting Antiviral Agent, which specifically targets the Hep C virus, unlike Interferon, which simply revs up our own immune systems, and Ribaviran, which boosts this process.
Incivek is a Protease Inhibitor, which means it inhibits the protein enzyme, which the hep c virus feeds on ,in order to live~
There is also another similar med, called Victrelis, which works the
same way, but with less side effect,s but one has to take it longer. These two meds tend to make a persons' chance of developing "hemolytic anemia" much greater. But the good news is: many more of us genotype 1's being cured, by adding this third med.
By the way, Incivek and Victrelis (aka Teleprivir and Boceprevir) are only effective against genotype 1~
Incivek is a Protease Inhibitor, which means it inhibits the protein enzyme, which the hep c virus feeds on ,in order to live~
There is also another similar med, called Victrelis, which works the
same way, but with less side effect,s but one has to take it longer. These two meds tend to make a persons' chance of developing "hemolytic anemia" much greater. But the good news is: many more of us genotype 1's being cured, by adding this third med.
By the way, Incivek and Victrelis (aka Teleprivir and Boceprevir) are only effective against genotype 1~
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
Forgot the the link to above info
http://pi.vrtx.com/files/uspi_telaprevir.pdf
Forgot the the link to above info
http://pi.vrtx.com/files/uspi_telaprevir.pdf
14.3 Previously Treated Adults Trial C216 (REALIZE)
Trial C216 was a randomized, double-blind, placebo-controlled trial conducted in subjects who did not achieve SVR with prior treatment with Peg- IFN-alfa-2a/RBV or Peg-IFN-alfa-2b/RBV. The trial 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 2 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 per 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 2 groups were pooled (Table 11).
Table 11: Response Rates: Trial C216
SVR rate
Prior relapsers 86% (246/286)
Prior partial responders 59% (57/97)
Prior null responders 32% (47/147)
Trial C216 was a randomized, double-blind, placebo-controlled trial conducted in subjects who did not achieve SVR with prior treatment with Peg- IFN-alfa-2a/RBV or Peg-IFN-alfa-2b/RBV. The trial 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 2 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 per 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 2 groups were pooled (Table 11).
Table 11: Response Rates: Trial C216
SVR rate
Prior relapsers 86% (246/286)
Prior partial responders 59% (57/97)
Prior null responders 32% (47/147)
Are you classified as a relapser (were undetectable for the virus at the end of treatment and it returned after stopping)
"So would Incivek have a chance after to fails with interferon therapy?"
Yes, incivek (telprevir) and victrelis (boceprevir, both new drugs released in 2011, have increased the average SVR (cure) rate to 70 to 80%, up from 40 to 50% in genotype 1 patients. Follow the link at the bottom of the page for more info
Boceprevir and telaprevir are the first two protease inhibitors available for the treatment of patients infected with hepatitis C virus (HCV) genotype 1. A sustained virological response (SVR) of 70–80% is observed when either of these protease inhibitors is utilized with pegylated interferon (PEG-IFN) and ribavirin (RBV) in treatment naïve patients. Both agents are also highly effective in patients who failed to achieve a SVR during previous treatment with PEG-IFN/RBV. A rapid virological response (RVR) is observed in 56–60% of treatment naïve patients. Patients who achieve a RVR can be treated with a shorter course of therapy (24–28 weeks) and still achieve a SVR rate of 90% or higher. Patients who do not achieve a RVR, those with cirrhosis and certain prior non-responders should be treated for 48 weeks. Although the SVR rates observed with boceprevir and telaprevir are quite similar both globally and within sub-populations, the treatment algorithms for the two agents are unique. The decision of which protease inhibitor to use should assess several factors including the treatment scheme, duration of therapy, adverse event profile, cost and the likelihood of achieving a RVR. The latter is highly dependent upon IFN sensitivity and the IL28B genotype.
AbbreviationsDAA
direct acting antivirals
eRVR
extended RVR
HCV
hepatitis C virus
IFN
interferon
PEG-IFN
pegylated interferon
RBV
ribavirin
RGT
response-guided therapy
RVR
rapid virological response
SOC
standard of care
SVR
sustained virological response
Boceprevir and telaprevir were the first two and are currently the only protease inhibitors to be approved by the US Food and Drug Administration (FDA) and the European Medicines Agency (EMA) for the treatment of patients infected with hepatitis C virus (HCV) genotype 1. For the past decade, only 40–45% of these patients achieved a SVR when treated with PEG-IFN/RBV [1-4]. The duration of therapy was for a fixed 48 weeks. In contrast, when either of these two protease inhibitors is added to PEG-IFN/RBV, the SVR rate in treatment naïve patients increases to 70–80% [5-7]. Boceprevir and telaprevir are also highly effective in patients who fail to achieve a SVR during previous treatment with PEG-IFN/RBV [8, 9]. The availability of these two protease inhibitors has therefore revolutionized the treatment of chronic HCV. For the first time, physicians can tell their patients that it is much more likely they will be ‘cured’ of HCV following treatment.
It has been recognized in recent years that the likelihood of achieving a SVR during treatment with PEG-IFN/RBV was directly related to when the patient became HCV RNA undetectable during therapy [10]. Patients with a RVR, who became HCV RNA undetectable within 4 weeks after initiating treatment, had SVR rates in the 85–90% range and several studies strongly suggested that these patients could receive only 24 weeks of PEG-IFN/RBV [11-14]. This observation forms the cornerstone of response guided therapy (RGT) [10, 15, 16]; a concept that was readily incorporated into the treatment schemes developed for boceprevir and telaprevir.
This manuscript will review data from the phase 3 clinical trials performed with boceprevir and telaprevir in the treatment naïve population [5-7] and in patients who previously failed to achieve a SVR with PEG-IFN/RBV [8, 9]. We conclude by discussing issues that may lead to the selection of a specific protease inhibitor. Throughout this discussion, the reader must keep in mind that the phase 2 and 3 clinical trials that led to the approval of boceprevir and telaprevir were each performed against a placebo control (with PEG-IFN/RBV) and that these two protease inhibitors have never been directly compared. It is therefore impossible to conclude that either protease inhibitor is universally superior for the treatment of patients with chronic HCV genotype 1.
http://onlinelibrary.wiley.com/doi/10.1111/j.1478-3231.2011.02718.x/full
Yes, incivek (telprevir) and victrelis (boceprevir, both new drugs released in 2011, have increased the average SVR (cure) rate to 70 to 80%, up from 40 to 50% in genotype 1 patients. Follow the link at the bottom of the page for more info
Boceprevir and telaprevir are the first two protease inhibitors available for the treatment of patients infected with hepatitis C virus (HCV) genotype 1. A sustained virological response (SVR) of 70–80% is observed when either of these protease inhibitors is utilized with pegylated interferon (PEG-IFN) and ribavirin (RBV) in treatment naïve patients. Both agents are also highly effective in patients who failed to achieve a SVR during previous treatment with PEG-IFN/RBV. A rapid virological response (RVR) is observed in 56–60% of treatment naïve patients. Patients who achieve a RVR can be treated with a shorter course of therapy (24–28 weeks) and still achieve a SVR rate of 90% or higher. Patients who do not achieve a RVR, those with cirrhosis and certain prior non-responders should be treated for 48 weeks. Although the SVR rates observed with boceprevir and telaprevir are quite similar both globally and within sub-populations, the treatment algorithms for the two agents are unique. The decision of which protease inhibitor to use should assess several factors including the treatment scheme, duration of therapy, adverse event profile, cost and the likelihood of achieving a RVR. The latter is highly dependent upon IFN sensitivity and the IL28B genotype.
AbbreviationsDAA
direct acting antivirals
eRVR
extended RVR
HCV
hepatitis C virus
IFN
interferon
PEG-IFN
pegylated interferon
RBV
ribavirin
RGT
response-guided therapy
RVR
rapid virological response
SOC
standard of care
SVR
sustained virological response
Boceprevir and telaprevir were the first two and are currently the only protease inhibitors to be approved by the US Food and Drug Administration (FDA) and the European Medicines Agency (EMA) for the treatment of patients infected with hepatitis C virus (HCV) genotype 1. For the past decade, only 40–45% of these patients achieved a SVR when treated with PEG-IFN/RBV [1-4]. The duration of therapy was for a fixed 48 weeks. In contrast, when either of these two protease inhibitors is added to PEG-IFN/RBV, the SVR rate in treatment naïve patients increases to 70–80% [5-7]. Boceprevir and telaprevir are also highly effective in patients who fail to achieve a SVR during previous treatment with PEG-IFN/RBV [8, 9]. The availability of these two protease inhibitors has therefore revolutionized the treatment of chronic HCV. For the first time, physicians can tell their patients that it is much more likely they will be ‘cured’ of HCV following treatment.
It has been recognized in recent years that the likelihood of achieving a SVR during treatment with PEG-IFN/RBV was directly related to when the patient became HCV RNA undetectable during therapy [10]. Patients with a RVR, who became HCV RNA undetectable within 4 weeks after initiating treatment, had SVR rates in the 85–90% range and several studies strongly suggested that these patients could receive only 24 weeks of PEG-IFN/RBV [11-14]. This observation forms the cornerstone of response guided therapy (RGT) [10, 15, 16]; a concept that was readily incorporated into the treatment schemes developed for boceprevir and telaprevir.
This manuscript will review data from the phase 3 clinical trials performed with boceprevir and telaprevir in the treatment naïve population [5-7] and in patients who previously failed to achieve a SVR with PEG-IFN/RBV [8, 9]. We conclude by discussing issues that may lead to the selection of a specific protease inhibitor. Throughout this discussion, the reader must keep in mind that the phase 2 and 3 clinical trials that led to the approval of boceprevir and telaprevir were each performed against a placebo control (with PEG-IFN/RBV) and that these two protease inhibitors have never been directly compared. It is therefore impossible to conclude that either protease inhibitor is universally superior for the treatment of patients with chronic HCV genotype 1.
http://onlinelibrary.wiley.com/doi/10.1111/j.1478-3231.2011.02718.x/full
Thanks for the info, I have had interferon treatment by itself in 1995 which did nothing to curtail my hep c. In 2005 I had the Pegasus interferon with ribavirin pills which also didn't work. I don't remember my genotype but I remember my doctor telling its the type that doesn't respond well to treatment. If there is another treatment I would like to try it. So would Incivek have a chance after to fails with interferon therapy?
Here is the WIKI
http://en.wikipedia.org/wiki/Telaprevir
The brand name is Telaprevir which is an antiviral drug known as protease inhibitor used in tandem with Interferon and Ribavarin to treat Chronic Hepatitis C primarily for people who have Genotypes 1a & 1b.
Back in the day it used to be just Interferon and Ribavirin but the success rate was abysmal so a third drug was finally added. The success rate is much higher now.
http://en.wikipedia.org/wiki/Telaprevir
http://en.wikipedia.org/wiki/Telaprevir
The brand name is Telaprevir which is an antiviral drug known as protease inhibitor used in tandem with Interferon and Ribavarin to treat Chronic Hepatitis C primarily for people who have Genotypes 1a & 1b.
Back in the day it used to be just Interferon and Ribavirin but the success rate was abysmal so a third drug was finally added. The success rate is much higher now.
http://en.wikipedia.org/wiki/Telaprevir
11 DESCRIPTION
INCIVEK (telaprevir) is an inhibitor of the HCV NS3/4A protease. The IUPAC name for telaprevir is (1S,3aR,6aS)-2-[(2S)-2-({(2S)-2-cyclohexyl-2-[(pyrazin-2-ylcarbonyl)amino]acetyl}amino)-3,3-dimethylbutanoyl]-N-[(3S)-1- (cyclopropylamino)-1,2-dioxohexan-3-yl]-3,3a,4,5,6,6a-hexahydro-1H-cyclopenta[c]pyrrole-1-carboxamide. Its molecular formula is C36H53N7O6 and its molecular weight is 679.85.
Telaprevir drug substance is a white to off-white powder with a solubility in water of 0.0047 mg/mL. Telaprevir interconverts to an R-diastereomer, VRT-127394, which is the major metabolite in plasma and is approximately 30-fold less potent than telaprevir. INCIVEK is available as a purple, capsule-shaped, film-coated tablet for oral administration containing 375 mg of telaprevir. Each tablet contains the inactive ingredients colloidal silicon dioxide, croscarmellose sodium, D&C Red No. 40, dibasic calcium phosphate (anhydrous), FD&C Blue No. 2, hypromellose acetate succinate, microcrystalline cellulose, polyethylene glycol, polyvinyl alcohol, sodium lauryl sulfate, sodium stearyl fumarate, talc, and titanium dioxide.
CLINICAL PHARMACOLOGY 12.1
Mechanism of Action Telaprevir is a direct-acting antiviral (DAA) agent against the hepatitis C virus [see Microbiology (12.4)].
12.4 Microbiology
Mechanism of Action Telaprevir is an inhibitor of the HCV NS3/4A serine protease, necessary for the proteolytic cleavage of the HCV encoded polyprotein into mature forms of the NS4A, NS4B, NS5A and NS5B proteins and essential for viral replication. In a biochemical assay, telaprevir inhibited the proteolytic activity of the recombinant HCV NS3 protease domain with an IC50 value of 10 nM.
http://pi.vrtx.com/files/uspi_telaprevir.pdf
INCIVEK (telaprevir) is an inhibitor of the HCV NS3/4A protease. The IUPAC name for telaprevir is (1S,3aR,6aS)-2-[(2S)-2-({(2S)-2-cyclohexyl-2-[(pyrazin-2-ylcarbonyl)amino]acetyl}amino)-3,3-dimethylbutanoyl]-N-[(3S)-1- (cyclopropylamino)-1,2-dioxohexan-3-yl]-3,3a,4,5,6,6a-hexahydro-1H-cyclopenta[c]pyrrole-1-carboxamide. Its molecular formula is C36H53N7O6 and its molecular weight is 679.85.
Telaprevir drug substance is a white to off-white powder with a solubility in water of 0.0047 mg/mL. Telaprevir interconverts to an R-diastereomer, VRT-127394, which is the major metabolite in plasma and is approximately 30-fold less potent than telaprevir. INCIVEK is available as a purple, capsule-shaped, film-coated tablet for oral administration containing 375 mg of telaprevir. Each tablet contains the inactive ingredients colloidal silicon dioxide, croscarmellose sodium, D&C Red No. 40, dibasic calcium phosphate (anhydrous), FD&C Blue No. 2, hypromellose acetate succinate, microcrystalline cellulose, polyethylene glycol, polyvinyl alcohol, sodium lauryl sulfate, sodium stearyl fumarate, talc, and titanium dioxide.
CLINICAL PHARMACOLOGY 12.1
Mechanism of Action Telaprevir is a direct-acting antiviral (DAA) agent against the hepatitis C virus [see Microbiology (12.4)].
12.4 Microbiology
Mechanism of Action Telaprevir is an inhibitor of the HCV NS3/4A serine protease, necessary for the proteolytic cleavage of the HCV encoded polyprotein into mature forms of the NS4A, NS4B, NS5A and NS5B proteins and essential for viral replication. In a biochemical assay, telaprevir inhibited the proteolytic activity of the recombinant HCV NS3 protease domain with an IC50 value of 10 nM.
http://pi.vrtx.com/files/uspi_telaprevir.pdf
What is INCIVEK?
INCIVEK® (telaprevir) is a prescription medicine used with the medicines peginterferon alfa and ribavirin to treat chronic (lasting a long time) hepatitis C genotype 1 infection in adults with stable liver problems, who have not been treated before or who have failed previous treatment.
http://www.incivek.com/
INCIVEK® (telaprevir) is a prescription medicine used with the medicines peginterferon alfa and ribavirin to treat chronic (lasting a long time) hepatitis C genotype 1 infection in adults with stable liver problems, who have not been treated before or who have failed previous treatment.
http://www.incivek.com/
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