The Liver Meeting 2015
Every year at The Liver Meeting, an international group of experts convene to discuss the latest advances in hepatology, and as has been the case for many years, there was intense focus on hepatitis C virus.
HCV Next had the opportunity to sit down with leading experts in the field after they attended The Liver Meeting and they each provided insight into the data presented and how it will impact care of patients with HCV. These included Co-Chief Medical Editor, Ira M. Jacobson, MD, chair of the department of medicine at Mount Sinai Beth Israel Medical Center in New York City; and editorial board member, Catherine T. Frenette, MD, medical director of the department of Organ Transplantation at Scripps Green Hospital in San Diego.
Catherine T. Frenette, MD
One of the most impactful studies for HCV treaters was the study that my group from Scripps presented at the Presidential Plenary about the reversal of advanced fibrosis and cirrhosis after sustained virologic response. Physicians often field that question from patients and it’s important for them to realize that cirrhosis is reversible.
The retrospective chart review and prospective collection of data after SVR utilized FibroScan, biopsy and/or clinical assessment of portal hypertension to determine fibrosis and cirrhosis score.
In the 6-month interval follow-up where FibroScan was used to assess patients, 69% of patients with F3 to F4 fibrosis improved, while 55% of those with cirrhosis improved. Overall, the combined cohort showed 60% improvement over a median follow-up time of 2.5 years.
This does not mean that you stop screening for hepatocellular carcinoma if fibrosis or cirrhosis improves, but it is important to know that patients do have reversal of fibrosis.
You must continue screening as rates of HCC remain elevated, as shown by Hashem El-Serag, MD, from Baylor College of Medicine.
In a retrospective cohort study looking at more than 10,000 patients with more than 30,000 person years of follow-up, El-Serag and colleagues found that 100 patients were diagnosed with HCC, for an incidence rate of 0.327% per year. In those patients who did not achieve SVR, the incidence rate of HCC was 1.32% per year. This resulted in a hazard ratio of 0.358 for SVR vs. no SVR. Older age, cirrhosis, diabetes and genotype 3 were all increased risk factors for HCC.
At the Postgraduate Course, there was a discussion of treatment of end-stage renal disease. This discussion revealed that, as initially reported at the International Liver Congress 2015, the elbasvir/grazoprevir (Merck) regimen at 12 weeks without ribavirin produced a 99% SVR, while the sofosbuvir-based regimens were linked to issues with worsening renal function and renal and urinary system adverse events. The newer regimen might end up being a safer option for our end-stage renal disease patients, upon its approval.
Week 4 RNA, Long-Term SVR
Vincent Leroy, MD, from France, and colleagues presented compelling data to show you cannot use week 4 HCV RNA as a prediction of SVR when looking at the sofosbuvir/daclatasvir (Sovaldi, Gilead Sciences; Daklinza, Bristol-Myers Squibb) regimen post-liver transplant.
We were accustomed to predicting treatment outcome or even changing our plan based on early viral kinetics in the era of interferon-based therapy, but with interferon-free therapy in general and with sofosbuvir/daclatasvir in particular, as presented at AASLD 2015, a predictive role or practical import of viral kinetics has been much more difficult to demonstrate. With sofosbuvir/daclatasvir at week 4, just 53% of patients met the lower limit of quantification of 15 IU/mL. This increased to 87% by week 8, 95% by week 12 and 100% by week 24.
There were some predictors of detectable HCV RNA at week 4 that were not surprising — more immune suppressed, more advanced fibrosis and a higher baseline viral load were more likely to have a positive week 4 RNA. But again, those did not have an impact on SVR rate.
Overall, the velpatasvir (GS-5816, Gilead Sciences) data was very encouraging, bringing the promise of equivalent high rates of SVR across genotypes.
The ASTRAL 1 study, presented by Jordan J. Feld, MD, showed the pangenotypic efficacy of sofosbuvir/velpatasvir for 12 weeks in all major genotypes except genotype 3. The overall SVR12 rate in the sofosbuvir/velpatasvir group was 99% (95% CI, 97.9%-99.6%); 99% for genotype 1; 100% for genotypes 2, 4 and 6; and 97% for genotype 5.
Sofosbuvir/velpatasvir showed promise in genotype 2, according to Mark Sulkowski, MD, of Johns Hopkins University, who presented the ASTRAL-2 data. This study demonstrated 99% SVR, as compared to 94% in a standard of care group treated with sofosbuvir and ribavirin. This regimen, slated for mid-2016 approval, will be a good option for our genotype 2 patients who can’t tolerate ribavirin because we haven’t had anything to offer to them.
The ASTRAL-3 study evaluated genotype 3 patients and showed an overall SVR12 rate of 95%, although somewhat lower for those with cirrhosis. Still, this regimen seems likely destined to be the regimen of choice for genotype 3 patients once it is approved. It can be argued that the SVR rates for daclatasvir plus sofosbuvir currently come close, but 16 to 24 weeks is needed for those with cirrhosis.
See the Take Home from Ira M. Jacobson, MD, for additional information on the ASTRAL studies.
The regimen I’m most excited about and that is garnering much interest in the field is sofosbuvir/velpatasvir/GS-9857, presented by Edward J. Gane, MD, from New Zealand, because GS-9857 (Gilead Sciences) has activity against several resistance-associated variants (RAVs) associated with first-generation protease inhibitors, with which we’re all struggling.
With this regimen, SVR12 rates were 100% for the treatment-naive patients with cirrhosis and genotype 1 treated for 8 weeks; 89% for the patients who previously failed other therapies; 83% for the naive patients treated for 6 weeks; and 100% for the experienced patients treated for 8 weeks.
The 6-week regimen showed a fair number of patients with SVR, but 4 weeks is just too short and that will likely hold true.
Ten patients in Gane’s study had dual NS5A/NS34 RAVs and nine out of the 10 achieved SVR with 8 weeks of triple therapy. Those patients who have failed and have these RAVs, but do not have cirrhosis, can probably hold out for approval of this or similar regimens. This is critical to the management of these patients.
The other triple therapy presentation delivered by Eric J. Lawitz, MD, reported a regimen of simeprevir (Olysio, Janssen), sofosbuvir and daclatasvir without ribavirin given to patients with cirrhosis produced 100% SVR in both Child’s A and Child’s B patients. Success occurred despite the fact that in 53% of the Child’s A cohort and 30% of the Child’s B group had baseline NS3 and NS5A RAVs.
By giving triple therapy for 12 weeks without ribavirin, they saw very good SVR rates in those difficult-to-treat patients.
The SURVEYOR-1 data presented by Fred Poordad, MD, of the Texas Liver Institute, also showed the activity of ABT-493 and ABT-530 (AbbVie), an advanced NS3/4A protease inhibitor and NS5A inhibitor, respectively, against common RAVs. This exciting refinement of a previous proof-of-concept showed that a two-drug regimen without a nucleotide polymerase inhibitor can work very effectively. These next generation drugs cover most or nearly all of the RAVs that emerge after exposure to first generation members of these two classes.
The robustness of this concept was demonstrated by the SVR rates of 97% to 100% with 12 weeks of therapy in non-cirrhotic, genotype 1 patients, including prior nonresponders across two arms that looked at two doses of ABT-530 (40 mg vs. 120 mg).
Researchers also looked at the same regimen with 8 weeks of therapy and remarkably showed 97% SVR12, testifying further to the potency of this regimen in eradicating the virus in almost everybody with only 8 weeks of exposure.
In genotype 3 patients, since this is a pangenotypic regimen, four different arms divided along ribavirin vs. no ribavirin and different doses, SVR rates ranged from 83% to 94% with three of the arms coming in at 93% to 94%. It was very encouraging for genotype 3. There was a trend for the treatment-naive patients to do better than the relatively few treatment-experienced patients.
In genotype 2, the study included three different arms, looking at two different doses of ABT-493 and one arm with ribavirin, two without. SVR rates ranged from 96% to 100%.
In his Late Breaker presentation, Poordad also showed 58% of patients treated with the new combination had NS3 or NS5A variants and all achieved SVR12; the only treatment failure occurred in a patient with dual RAVs.
Lastly, the hepatitis C Special Interest Group was very informative.
There was much discussion on “difficult-to-treat” patients, as many of these populations are going away. Overall, that’s a big take home from this meeting that continues a major theme emerging in the last couple of years. Those populations are slowly dwindling away, but those with decompensated cirrhosis or those with cirrhosis who are treatment experienced remain difficult-to-treat. In the Special Interest Group, it was emphasized that in Child’s B and C, ribavirin should be at 600 mg while simeprevir and the 3D regimen should not be used.
At the International Liver Congress 2015 and again recently, various regimens produced favorable results in those with decompensated cirrhosis: higher than 90% SVR, for example, in ALLY-1 in Child’s A and B, but not C; grazoprevir/elbasvir achieved 90% SVR in Child’s B with administration of 50 mg of grazoprevir, half the usual dose; and in the just-presented ASTRAL-4 sofosbuvir/velpatasvir with ribavirin produced an SVR rate of about 95% for decompensated cirrhosis. Jacobson breaks down the latest grazoprevir/elbasvir and ASTRAL-4 data in his Take Home.
You still have to realize these patients are going to have adverse events. They are going to decompensate. They have to be monitored closely.
David Wyles, MD, gave an excellent talk on RAVs during the HCV Special Interest Group.
The NS3 resistant RAVs appear to clear in 1 to 2 years, but we don’t know if, clinically, they still might matter, since the assays only get down to certain thresholds of RAV detectability. There does seem to be a decreased SVR if you’ve already failed a primary intervention, but we just might not be able to test them. As clinicians, we must remember that. NS5A RAVs appear at baseline in about 10% of patients and impair response in some regimens, but not all.
Basically, the SVRs go from 97% to 98% down to 92% to 93%, so it depends on the situation and what you’re using. Ribavirin, in general, seems to overcome the NS5A RAVs, so that is helpful.
Extending duration seems to also overcome RAVs. With grazoprevir/elbasvir, as shown, going from 12 weeks to 16 weeks with ribavirin negates the effect of RAVs. The discussion was whether we should consider testing baseline before we treat. There’s still not a good answer, but maybe this might be useful in treatment-experienced cirrhotics to predict whether ribavirin or extended duration is needed.
The NS5A RAVs present differently from NS3 RAVs in that the NS5As persist — 86% are there after 2 years.
This discussion helps the understanding of RAVs and how they can be managed.
Lawitz also presented a retreatment of the C-SWIFT patients with grazoprevir/elbasvir/sofosbuvir and ribavirin for 12 weeks, producing 100% SVR. This points to these patients who have failed therapies possibly requiring triple or quad therapy.
Ira M. Jacobson, MD
Real-World Database, 8-Week Regimens
As referenced in my editorial, the TRIO network, a pharmacy-derived database, looked at 8- and 12-week regimens of ledipasvir and sofosbuvir in treatment-naive patients without cirrhosis. There was a particular emphasis on trying to verify whether the shortened 8-week regimen of ledipasvir/sofosbuvir for people with low viral loads who met certain criteria — that is treatment-naive, genotype 1, no cirrhosis and viral load less than 6 million IU/mL — would not sacrifice efficacy by stopping 4 weeks short.
Some clinicians had expressed concern after approval of this regimen that the stipulation of acceptability of the 8 week regimen in the package insert could result in the inability of clinicians to obtain access to 12 weeks of covered therapy for these patients because of insurance carrier restrictions arising from the savings in resources. The concern among such clinicians emanated from the fact that the recommendation originated from a retrospective analysis from ION-3. There were no other phase 3 trials in which 8 weeks of this regimen was evaluated.
On the whole, this is a reassuring story in that TRIO showed the 8 week regimen for patients who meet the criteria in question was as effective as the 12 week regimen — 95% and 96% SVR, respectively. Notably, for the small number of patients in TRIO who were either purposefully or inadvertently treated for 8 weeks despite baseline viral levels of 6 million IU/mL (n = 8), all achieved SVR. This doesn’t mean we should stop short of 12 weeks for those patients because the numbers are much too small, but it gives us an added margin of comfort in telling our lower viral load patients that it’s acceptable to stop treatment after 8 weeks. And, perhaps we don’t have to engage in the battles with insurance companies that some of us have undertaken until now due to the lack of robustness in the original database.
The TRIO investigators further documented that patients who were treated outside of established guidelines, not surprisingly, had somewhat inferior SVR rates. It’s important for clinicians to be aware of recommendations embedded within the package inserts and/or expert society guidelines such as the AASLD/IDSA Guidance document available online. Clinicians need to understand what the right regimens are for specific patient populations and not make the mistake of thinking any of these are homogenous regimens that come in the same size and shape for all patients.
The TARGET database, also a very large database involving more than 55 centers, came to similar, equally resounding and reassuring conclusions. The analysis showed 97% SVR rates for ledipasvir/sofosbuvir for both 8 and 12 weeks in patients with genotype 1, no cirrhosis, treatment-naive and baseline viral loads less than 6 million IU/mL. Clinicians should note that two-thirds of our patients fall within those parameters.
In another study supporting the possibility of 8-week regimens, Peter Buggisch, MD, medical director of the Liver-Centre Hamburg, reported on a completed data set looking at 42 patients. All patients achieved SVR after 8 weeks of therapy as long as they met the viral load criteria outlined previously.
The only negative observation with regard to the parity of 8 weeks vs. 12 weeks came from a Veterans Affairs study. It was the largest database presented and showed about a 3% decrease in SVR if patients received 8 weeks of therapy, but some have questioned whether this controls for multiple other variables in that analysis.
On the whole, the emerging consensus is that the data from AASLD vindicate the recommendation that 8 weeks is sufficient.
PPI Use, Impact on SVR
Another important component of the TARGET database was the analysis of SVR rates in patients who were taking a proton pump inhibitor at baseline for acid-related problems. There was no other specific data offered as to dosing or whether the patients took PPIs throughout therapy, but the bottom line is that SVR rates for either 8 or 12 weeks were 5% less with PPIs vs. not — 93% vs. 98%, respectively.
We know that ledipasvir requires an acidic environment for maximum absorption and, without being able to break it down further, this data from TARGET give us a hint that the package insert should be adhered to with regard to the limitations on PPI intake. Some clinicians in attendance said they are more comfortable keeping patients off PPIs completely, while others are comfortable with the limit of 20 mg omeprazole daily or its equivalent.
Clinicians have expressed variable opinions about how many patients really are unable to avoid taking more than 20 mg of omeprazole daily during a 12-week period, but experienced gastroenterologists know there is a subset of reflux patients who indeed need higher doses of acid-suppressing medication. In those cases, there’s an evolving consensus that it may be best to use another regimen if you keep patients’ acid-related symptoms adequately managed with 20 mg omeprazole or its equivalent.
This meeting also gave us a picture of emerging regimens, including elbasvir/grazoprevir, which is slated for approval in the first quarter of 2016.
I presented the results of an integrated analysis showing SVR rates of 97% to 100% in 402 patients with cirrhosis drawn from six different trials, including treatment-naive (12 weeks without or with ribavirin) and treatment-experienced patients (12, 16 or 18 weeks without or with ribavirin), some with chronic kidney disease or HIV co-infection, as well as a smaller number of patients who had failed prior treatment with peginterferon, ribavirin and a protease inhibitor.
If one looked at the different regimens that have been used to treat these populations, we can glean a rule that grazoprevir/elbasvir for 12 weeks without ribavirin represents optimized treatment for treatment-naive patients with cirrhosis, producing an SVR rate of 97.8%. With ribavirin, SVR rate was 90%, clearly indicating that ribavirin offers no benefit in this group of patients.
Interferon-experienced patients treated with grazoprevir/elbasvir responded optimally to a 16-week regimen including ribavirin with an SVR rate of 100%, somewhat better than the results without ribavirin or with 12 weeks of therapy either with or without ribavirin. However, among the subset of prior relapsers previously treated with PEG-IFN and ribavirin, 100% attained SVR with 12 weeks of treatment without ribavirin. In contrast, in the prior interferon nonresponders treated for 12 weeks, 91.4% of those treated with ribavirin achieved SVR12 while 100% of those treated for 16 or 18 weeks with ribavirin achieved SVR12.
Previous data on grazoprevir/elbasvir suggested these same rules may apply to patients who have baseline RAVs, with SVR rates approaching 100% with extension of therapy to 16 weeks and the addition of ribavirin.
I also had the opportunity to present a robust analysis of RAVs from the grazoprevir/elbasvir development program in a Late Breaker poster. An extensive analysis correlation between the results of RAV testing by population sequencing and deep sequencing in terms of the yield of baseline variants and their clinical impact. Population sequencing requires that 20% of viral population consist of a given variant, while deep sequencing is designed to get down to detection levels of 1% of the viral population as consisting of a given variant.
Our study showed that if the deep sequencing results are set at that cutoff, one catches a lot of baseline variants with no impact on therapeutic outcomes. On the other hand, the yield and clinical impact of RAVs detected by deep sequencing correlated very well with population sequencing results when the results of deep sequencing are set with cutoffs of 10%, or optimally 20%, of the viral population. Thus, using population sequencing, which is commercially available, to identify high-level resistant variants to elbasvir, in particular, as opposed to NS5A inhibitors in general, is a powerful tool for identifying which patients appear to benefit from prolongation of therapy with grazoprevir/elbasvir to 16 weeks and the addition of ribavirin. Note that not all variants that are resistant to first generation NS5As are resistant to the same degree to elbasvir, if at all.
Using population sequencing to identify high-level resistant variants to elbasvir, in particular, as opposed to NS5A inhibitors in general, is a powerful tool for identifying which patients appear to benefit from prolongation of therapy and the addition of ribavirin. Note that not all variants that are resistant to first generation NS5As are resistant to the same degree to elbasvir, if at all.
As mentioned in the accompanying editorial, we further identified the variants at the 30, 31 and 93 positions as the ones that have the most substantive impact on outcome of therapy and which appear to require an adjustment in the therapeutic regimen.
We also heard excellent results from an elegant study by Gregory Dore, MD, from Australia, and colleagues on the use of grazoprevir/elbasvir given to patients on opiate antagonist therapy. The study included large numbers of patients and demonstrated better than 90% SVR, clearly challenging the continued assertion by some clinicians that people who use drugs actively should have treatment withheld.
Another new regimen presented was the combination of sofosbuvir and velpatasvir, a pangenotypic NS5A inhibitor, presented in the ASTRAL studies mentioned earlier by Frenette. This fixed-dose combination delivered for 12 weeks covers a broad spectrum of patients across all genotypes and spanning treatment-naive and -experienced patients as well as those with and without cirrhosis.
ASTRAL-1 looked at all genotypes except genotype 3. The results in 624 patients, including more than 300 with genotype 1, demonstrated a 97% to 100% SVR in genotypes, including the largest cohort of patients yet studied in a pivotal HCV trial with genotype 5, in which there was a 97% SVR with one patient failing, accounting for SVR in 34 of 35 patients.
Equally impressive were the data from ASTRAL-2 in which researchers showed genotype 2 patients had an SVR rate of 99% with 12 weeks of therapy, compared to 94% with the current standard of sofosbuvir and ribavirin alone.
The results even in genotype 2 alone are of profound importance because although the results of interferon therapy and the emerging regimen of sofosbuvir/ribavirin have been favorable for genotype 2, there has been a low but real incidence of treatment failures. It is not difficult to imagine that sofosbuvir/velpatasvir without ribavirin for 12 weeks can be expected to become the first-line treatment for genotype 2 patients and will replace sofosbuvir/ribavirin. It may also be useful for “rescuing” the patients who have failed sofosbuvir/ribavirin or interferon-based therapy in the past.
Due to that low rate of success with sofosbuvir/ribavirin in genotype 3, especially in cirrhotics, the AASLD/IDSA guidance document had already removed sofosbuvir/ribavirin from its first line option recommendations in October 2015 and replaced it with daclatasvir/sofosbuvir or PEG-IFN/ribavirin/sofosbuvir for genotype 3.
The genotype 3 patients evaluated in the ASTRAL-3 study showed an SVR rate of 95% with 12 weeks of treatment, no ribavirin, compared to 80% in the control group with sofosbuvir/ribavirin for 24 weeks. Treatment-naive patients without and with cirrhosis had SVR in 98% and 93%, respectively, while in treatment experienced patients the SVR rates were 91% and 89%, respectively.
Despite the persistent impact of cirrhosis on SVR with this regimen, the adverse impact of cirrhosis was markedly attenuated compared to its impact in ALLY-3, which evaluated daclatasvir/sofosbuvir without ribavirin for 12 weeks and demonstrated only 58% to 69% SVR in cirrhotics, whether treatment-experienced or treatment-naive.
The last study was ASTRAL-4 in decompensated cirrhotics. Here, we saw similar or better SVR rates than what we saw with ledipasvir/sofosbuvir and ribavirin in the SOLAR-1 and -2 studies, where the SVR rates were between 86% and 90% when that regimen was given for 12 or 24 weeks with ribavirin.
Patients who received sofosbuvir/velpatasvir for 12 weeks had an SVR of 83% (95% CI, 74%-90%) across all genotypes; patients who received sofosbuvir/velpatasvir plus ribavirin for 12 weeks had an SVR of 94% (95% CI, 87%-98%); and patients who received sofosbuvir/velpatasvir for 24 weeks had an SVR of 86% (95% CI, 77%-92%).
Arithmetically, the results were better with ribavirin for 12 weeks than without ribavirin for 24 weeks, perhaps surprisingly, but providing reassurance that you can safely truncate therapy to 12 weeks if you add ribavirin and that may even be superior.
This could be reasonably be expected to become the treatment of choice for decompensated cirrhotics. This is particularly true since recent developments with the ombitasvir/paritaprevir/ritonavir and dasabuvir regimen, in particular, and pharmacokinetic considerations with protease inhibitors, in general, suggest that a regimen free of protease inhibitors is probably safer in the long run with decompensated cirrhosis.
There was a presentation of a very short duration regimen treatment course of 4 weeks showing relatively low SVR rates with a four-DAA regimen with daclatasvir/asunaprevir/beclabuvir (BMS-650032/BMS791325, Bristol-Myers Squibb) plus sofosbuvir, suggesting — as did previous studies — that no matter how much artillery you level at the virus, there’s still a finite amount of time you need to eradicate all virus to prevent relapse.
On the other hand, triplet regimens including a nucleotide polymerase inhibitor were evaluated by two other manufacturers with promising results with 8 weeks of therapy that is being evaluated further in clinical trials in both general HCV populations and those that have failed a regimen of DAA, with durations in the latter population ranging up to 12 weeks.
On the horizon of the HCV treatment paradigm, the most intriguing study at the meeting evaluating novel agents other than viral protein inhibitors focused on RG-101 (Regulus Therapeutics), a miR-122 inhibitor. The virus uses this micro RNA to replicate and inhibition of it was previously shown to have long-lasting viral inhibition ranging up to a number of weeks.
This showed that, in a cohort of 28 patients given a single injection of the product at two different doses, six had undetectable virus for up to 28 weeks. This is a remarkable finding that makes us think there may still be a route to ultrashort treatment durations with treatments like this when combined with protein inhibitors. This will require extensive additional research.
- Backus LI, et al. Abstract 93. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Buggisch P, et al. Abstract 1205. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Charlton M, et al. Abstract LB-13. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Crissien AM, et al. Abstract 108. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Curry MP, et al. Abstract 1108. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Curry MP, et al. Abstract 1046. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Feld JJ, et al. Abstract LB-2. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Gane EJ, et al. Abstract 38. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Howe AY, et al. Abstract 40. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Lawitz E, et al. Abstract 39. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Jacobson IM, et al. Abstract 42. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Jacobson IM, et al. Abstract LB-22. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Kwo PY, et al. Abstract 248. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Maasoumy, B, et al. Abstract 1131. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Mangia A, et al. Abstract 249. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Poordad F, et al. Abstract 41. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Richardson P, et al. Abstract 86. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Sulkowski MS, et al. Abstract 205. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Sulkowski MS, et al. Abstract 702. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
- Van der Ree MH, et al. Abstract 208. Presented at: The Liver Meeting; Nov. 13-17, 2015; San Francisco.
Disclosure: Frenette reports financial relationships with Bayer, Gilead Sciences and Salix. Jacobson reports financial relationships with AbbVie, Achillion, Alnylam, Bristol-Myers Squibb, Enanta, Janssen Therapeutics, Merck and Tobira.