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Achillion Pharmaceuticals (NASDAQ:ACHN)

Q2 2012 Earnings Call

August 08, 2012 10:00 am ET

Executives

Glenn Schulman - Director of Investor Relations

Michael D. Kishbauch - Chief Executive Officer, President and Director

Mary Kay Fenton - Chief Financial Officer, Principal Accounting Officer, Senior Vice President and Secretary

Milind S. Deshpande - Chief Scientific Officer and President of Research & Development

Joseph Truitt - Chief Commercial Officer and Senior Vice President of Business Development

Analysts

Thomas J. Russo - Robert W. Baird & Co. Incorporated, Research Division

Rachel L. McMinn - BofA Merrill Lynch, Research Division

Edward A. Tenthoff - Piper Jaffray Companies, Research Division

Brian Corey Abrahams - Wells Fargo Securities, LLC, Research Division

Y. Katherine Xu - William Blair & Company L.L.C., Research Division

Brian Skorney - Brean Murray, Carret & Co., LLC, Research Division

Matthew Harrison - UBS Investment Bank, Research Division

Philip Nadeau - Cowen and Company, LLC, Research Division

Nathan Cali - Noble Financial Group, Inc., Research Division

Heather Behanna - JMP Securities LLC, Research Division

Howard Liang - Leerink Swann LLC, Research Division

Koon Ching

Akiva Felt - Wedbush Securities Inc., Research Division

Jason Kolbert - Maxim Group LLC, Research Division

Operator

Good day, ladies and gentlemen, and welcome to the Achillion Semiannual Program Update Teleconference. [Operator Instructions] As a reminder, today's conference call is being recorded.

I'd now like to turn the conference over to your host, Mr. Glenn Schulman, Director of Investor Relations. Please go ahead.

Glenn Schulman

Thanks, Ally, and good morning, everyone. Thanks for joining us today as we provide an update on Achillion's second quarter 2012 financial results and provide an update on our pipeline of HCV compound.

Hopefully everyone received a copy of last evening's press release detailing the updated clinical trial results for sovaprevir or as we referred to it before by the generic name -- before its generic name, it's branded ACH-1625, as well as the press release we had out this morning detailing our second quarter and 6-month financial results. If you've not received this news releases or would like to be added to our distribution list, please feel free to call or email me in the office at (203) 752-5510 after the call. This news release is also available from our website at www.achillion.com.

This morning, we'll have a brief presentation from senior management team, followed by a Q&A session. Joining me on the call this morning from Achillion are Mike Kishbauch, our President and Chief Executive Officer; Milind Deshpande, President of Research of Development and Chief Scientific Officer; Gautam Shah, Executive Vice President and Chief Compliance Officer; Mary Kay Fenton, Senior Vice President and Chief Financial Officer; and Joe Truitt, Senior Vice President of Business Development and Chief Commercial Officer.

Before we begin, I'd like to caution that comments made during this conference call by management will contain forward-looking statements that involve risks and uncertainties regarding the operations and future results of Achillion. I encourage you to review the company's past and future filings with the Securities and Exchange Commission, including without limitation the company's Form 10-K, 10-Q, which identifies specific factors which may cause actual results or events to material differently from those described in the forward-looking statements. Furthermore, the content of this conference call contains time-sensitive information that is accurate only as of the date of the live broadcast today, August 8, 2012, and Achillion undertakes no obligation to revise or update any statements to reflect events or circumstances after the date of this conference call.

With all that, I'd like to turn the call over to Mike Kishbauch, President and CEO of Achillion.

Michael D. Kishbauch

Thanks, Glenn. Good morning, everyone, and thanks for getting together with us today. As Glenn noted, we have reported this morning our second quarter and 6-month 2012 financial results for Achillion and also provided last evening, as promised, updated Phase II trial results and the first SVR results generated on sovaprevir. So again, before going any further, let me just tell everyone that sovaprevir or, as we numerically referred to it since its discovery, ACH-1625 is the recently generated generic name and branded generic name for our next-generation protease inhibitor. Therefore, we will be referring to 1625 as sovaprevir, going forward. And for those of you who may have trouble remembering the name, sovaprevir is spelled S-O-V-A-P-R-E-V-I-R. Someone said to us sovaprevir can simply be abbreviated SVR. It sounds a little blip, I guess, but if it helps you remember, there it is.

So for those joining us today who may not be as familiar with Achillion or our therapeutic focus, Achillion is dedicated to generating in-house, potentially best-in-class protease inhibitors and NS5A inhibitors for the treatment of Hepatitis C. Hepatitis C, as I'm sure most of everyone on this call is now aware, is a very real and devastating disease and that is only recently being recognized for a full extent of the population infected with this virus with upwards of 5 million Americans and maybe 30x that number infected worldwide. This is a very significant unmet medical need and market opportunity. With all of the development activity in this space, we at Achillion have worked and will continue to work tirelessly to advance the best possible compound that can be used in combination to treat this disease. With the initial SVR -- or cure rates we reported last night for our lead protease sovaprevir, we're genuinely gratified to know that patients with HCV are actually being cured with this drug now. Those results have also helped to set the stage, so to speak, for upcoming studies to evaluate the future treatment approach to HCV all-oral interferon-free regimens. As we will discuss this morning between our portfolio of protease inhibitors, which includes sovaprevir as well as ACH-2684, along with our second-generation NS5A inhibitor ACH-3102, we are poised, we believe, to begin all-oral trials for HCV this year, hopefully on the way to curing HCV without the use of interferon.

So during the first half of 2012, we've successfully achieved the milestones we laid out previously but also set ourselves up for a very busy back half of 2012. So the agenda for this morning consists of 2 -- 3 presentations. The first is from Mary Kay Fenton, Achillion's CFO, who will review our financial results to date from the guidance, going forward. And then second, Dr. Milind Deshpande, our President of R&D and Chief Scientific Officer, will walk you through our pipeline and specifically address 3 items: first, the Phase II SVR data we reported last evening on sovaprevir; second, a discussion of ACH-3102, our pan-genotypic NS5A inhibitor and how it's differentiated from the first-generation compounds that are in development; and then third, a review of the upcoming milestones for the remainder of this year and into 2013.

So with that, I'll turn the discussion over to Ms. Fenton for a brief review of our financials. Mary Kay?

Mary Kay Fenton

Thanks, Mike. And good morning, everyone. Thank you for joining us.

As you know, this morning, we announced earnings for both the second quarter and the 6 months ended June 30, 2012. In that announcement, we reported a net loss of $11.5 million for the 3 months ended June 30, 2012, and $20.7 million for the 6 months then ended.

Research and development expenses were $9 million in the second quarter of 2012 and $17.9 million in the first half of 2012, increased slightly from the same period in 2011, resulting from ongoing clinical development work on sovaprevir as well as ACH-2684, our additional protease inhibitor, as well as the initiation of clinical testing several months ago on ACH-3102, our second-generation NS5A inhibitor.

Revenue for the 6 months ended June 30 was $2.5 million compared to $121,000 for the same period in 2011. Recall that the primary driver for this variance in revenue is related to the recognition of $2.5 million in deferred revenue in the first quarter of 2012 under our past collaboration with Gilead Sciences.

Looking forward to the remainder of 2012, we are maintaining our previously provided guidance on operating cash use that averages just under $11 million per quarter, with some quarters throughout the year being slightly higher and others somewhat lower, depending on the timing of clinical trial initiations and patient enrollment in those trials.

Importantly, you'll note that our cash balance of $60 million at the end of the second quarter will fund our operating plans throughout this year and through 2013, which has been our operating plan since early last year. R&D expenses for 2012 will approximate $38 million, consistent with past guidance. And our net loss per share that we anticipate for the annual period will range from $0.65 to $0.70 per share.

Please note that, at the close of business today, we will file with the SEC both our complete quarterly report on Form 10-Q as well as a registration statement on Form S-8 that simply registers shares previously approved by shareholders at our June annual meeting. And those -- and that registration statement is solely related to our employee stock incentive plan.

And with that brief review, I'll pass it back to Mike.

Michael D. Kishbauch

Thanks, Mary Kay. So moving forward to the second item on this morning's agenda, I'd like to ask Dr. Milind Deshpande, our Chief Scientific Officer, to review the SVR data reported this morning on sovaprevir and then discuss ACH-3102 and our upcoming 2012 and 2013 milestones.

One additional preface point, if I may. Some of you will be aware that we have scheduled a formal R&D Day, or Analyst Day, as they're sometimes called, for September 27 of this year. This event will feature 2 of the key opinion leaders in the field as well as a rather comprehensive exposé of our study plans going forward and updated analysis of multiple compounds in the Achillion pipeline. Therefore, I'll ask you to consider this regularly scheduled quarterly call today as a kind of an interim step on the way to a much more detailed event next month. We'll update you on what's new today and provide our current perspective on recent events in the field and then invite you to tune in, in a few weeks for an even more substantive exchange.

So, Milind?

Milind S. Deshpande

Thank you, Mike. And thank you, all, for joining us on the call today. As Mike mentioned, yesterday, we disclosed the SVR full results on sovaprevir for the treatment of genotype 1 treatment naïve HCV patients. To remind everyone, sovaprevir is a linear [indiscernible] protease inhibitor.

A Phase II study was initiated last summer and enrolled a total of 58 patients into one of the previous arms where patients were randomized to receive either 200 milligrams, 400 milligrams or 800 milligrams of sovaprevir in combination with interferon and ribavirin for 12 weeks, followed by an additional 12 or 36 weeks of pegylated interferon and ribavirin, depending on their response after 12 weeks of triple therapy.

Patients are stratified based on their IL28B status. All patients completed triple therapy with sovaprevir in March of this year and, as we reported back in April of 2012, 94% to 100% of patients achieved cEVR. Last evening, we reported our SVR rates for patients assigned to receive an additional 12 weeks of pegylated interferon and ribavirin based upon the response viral treatment criteria. In all, 39 patients were assigned to 24 weeks of therapy. Note that the remaining 14 patients are continuing to receive a full 36 weeks of peg/riba and we will have those results after the New Year.

SVR4 rates in subjects assigned to 24 weeks of treatment were 90%, 85% and 100% for the 200-milligram, 400-milligram and 800-milligram dose groups, respectively. One subject in the 400-milligram dose group had viral rebound at week 20 while receiving peg/riba; and 2 subjects, 1 each in the 200- and 400-milligram dose groups, experienced viral relapse before SVR4.

We are very pleased with the results to date from this Phase II study with sovaprevir. All 3 doses tested 200, 400 and 800 milligrams are comparable with respect to efficacies. Subgroup analysis suggests that all doses were effective regardless of genotype 1a versus 1b, IL28B subtype and pre-existing variants at amino acid position 80 of NS3 protease.

Our clinical virology conducted with HCV automate [ph] samples from segment 1 show lack of mutations at amino acid loci 155, 156 and 168, which are known to confer high level of resistance to NS3 protease inhibitors. Based on the PK/PD analysis from the study as well as from older [ph] studies, the in vivo EC50 for sovaprevir is 0.4 nanograms per ml. The mean trough concentration observed for the 200-milligram dose of sovaprevir is 22 nanograms per ml, thus exceeding the in vivo EC50 by 55-fold. Robust trough concentrations observed at sovaprevir may explain the high SVR rates across all 3 dose groups.

Lastly, as we have discussed before, the difficult patient population in the study consisted predominantly of genotype 1a, IL28B, non-CC patients, and many of the patients had a high body mass index and high viral load at baseline.

These SVR rates, combined with its resistance profile, with potential for drug-drug interactions, once-daily dosings without boosting with ritonavir, suggests that sovaprevir may provide an optimal profile for combination with other DAAs to create an oral regimen for cure of HCV.

I also want to mention some other achievements we made in the first half of 2012 with sovaprevir. First and foremost is the completion of 6- and 9-month toxicology. These nonclinical studies provide high safety margins for continued development of sovaprevir. We have also completed development of a commercially viable tablet formulation that will be used in all future clinical studies. The formulation work led to a new tablet that has improved absorption and diminished full effect. The PK data obtained from a relative viability study will be used in conjunction with other clinical data to select go-forward goals for combination studies. We look forward to providing additional details on upcoming combination development program, including our gold selection when we host everyone at our R&D Day on September 27 in New York City.

Moving on to ACH-3102, our second-generation pan-genotypic NS5A inhibitor. We successfully advanced this model compound from first synthesis into the clinic, a process which took just under one year, and continue to make rapid progress towards proof-of-concept results in HCV-infected patients. And a NS5A inhibitor that provides a high barrier to resistance will play a critical role in combination therapy. NS5A inhibitors produce very rapid and pronounced decline in HCV RNA, but the first-generation compounds have been limited by the rapid emergence of resistance observed in a clinical setting. ACH-3102 is a second-generation NS5A inhibitor that has the same potent effect in vitro against wild-type HCV, but it also has significantly improved activity against the known single as well as double mutations that are frequently seen with other NS5A inhibitors. By optimizing 3102, we believe that this NS5A inhibitor could become a cornerstone of HCV therapy by providing potent antiviral activity and a high barrier to resistance.

We initiated Phase I studies during the first half of 2012 and are pleased to report that this compound has progressed very well. To date, doses of 2,000 milligrams have been administered in the single ascending dose portion. Doses from 25 to 75 milligrams have been administered for 14 days with healthy volunteers. To date, 3102 has been safe and well tolerated, and based upon its final clinical profile, it is more certainly a once-daily drug. With the progress made in healthy volunteer segments, we are now poised to begin the HCV infected Phase I study which will evaluate doses up to 3 milligrams -- to 300 milligrams for antiviral activity.

Combination of protease inhibitor and NS5A inhibitor has achieved sustained viral response in genotype 1b nonresponders. We have improved on virology profile of ACH-3102, as compared to other NS5A inhibitors, so that we may have achieved cures not only in genotype 1b but also in genotype 1a.

Finally, looking forward to the remainder of 2012, we will report proof-of-concept results on ACH-3102 during the third quarter. Also, during this period, we plan on completing a drug-drug interaction study evaluating sovaprevir and ACH-3102. The results from the DDI study and the proof-of-concepts results for 3102 will check the necessary boxes to initiate a 12-week combination study evaluating sovaprevir plus 3102 for the treatment of genotype 1 HCV-infected patients. An initial readout from this trial will be provided during the first quarter of 2013.

With that update, we all look forward to seeing you in person next month at the R&D Day. And I will now turn it over to Mike for concluding remarks.

Michael D. Kishbauch

And all right, thanks, Milind. And with that review, I'll take just a few moments before addressing questions to review the bigger HCV picture and where Achillion's optimized portfolio of homegrown compounds kicked in, including the backdrop of recent events in the field.

Regardless of what class an HCV compound is classified to occupy, whether it's a protease inhibitor, an NS5A inhibitor, nucleoside or something like an entry inhibitor, the important attributes of the individual compounds supersede class designation. The compound has to be safe, well tolerated, have efficacy and improved barrier to resistance, be conveniently administered and be combinable with other HCV compounds. So again, that's the big 6, as we think about it: safety, tolerability, efficacy, resistance profile, convenience and combinability. Within each of the therapeutic classes in development today, there are many examples of agents that do not fit all of these criteria and a select few that do. So our goal at Achillion, which many of you have heard me say over and over again, is to generate potentially best-in-class agents that do meet these criteria. And we believe sovaprevir, ACH-2684 and ACH-3102 all naturally fit the bill today.

So looking forward, our primary goal remains the initiation of an all-oral interferon-free combination of our internally developed assets to treat and cure HCV. By the end of the year, we will initiate our first combo study evaluating sovaprevir and ACH-3102 to achieve this full. Something else we've observed and we've been acutely aware of during the last year advancing this portfolio is that all HCV patients are not created equal. Aside from differences in genotype, there are profound variations across the millions of patients infected with this virus. This variability means that there will not be a "one size fits all" approach for HCV for many, many years. As an example, current estimates indicate that nearly 30% of HCV patients are soradic [ph], 30% potentially increasing as HCV patients wait for treatment. This is a segment of HCV patients that potentially are significantly underserved where compounds may not perform in this sizable segment as they do in healthy segment naïve patients. And this for us highlights the fragmented HCV market as well as a variety of intriguing development approaches. Other examples include patients with bridging fibrosis, co-infection with HIV, no responders, et cetera.

So in addition to advancing our portfolio, as we had described this morning, we remain focused on the bigger picture in ensuring that we can differentiate and tackle as many of these market segments as possible with our portfolio of competence. I'll also note that this topic, the real world of HCV patients and the market opportunities associated with it, is something that will be discussed further at our R&D Day next month.

So this view of the market, combined with the substantial SVR rates reported last evening for sovaprevir and the upcoming proof-of-concept results we expect on ACH-3102, means that Achillion is well positioned to accelerate our development programs into the overall arena and begin reading out combo results during the early part of next year.

Thanks again for your attention. And Ally, I'll turn it back to you, and would now like to open things up for your questions.

Question-and-Answer Session

Operator

[Operator Instructions] Our first question comes from Tom Russo of Baird.

Thomas J. Russo - Robert W. Baird & Co. Incorporated, Research Division

Congrats on the further validation for 1625. A question first for Milind, and then maybe one for Joe. On the combo trial that you're going to be kicking off later this year, are there any considerations to include a 24-week arm, just in case? And will you have coverage for that for the study? And then if all goes well in the Phase II combo study, when would you be in position to start Phase III?

Milind S. Deshpande

Tom, I'll answer the question regarding the trial design for combination of 1625 and 3102. We have completed all the necessary non-clinical studies with 1625. That will allow us to use that compound for more than 3 months. With 3102, we have completed 3-month tox studies and the 6-month tox studies are in progress. And if we decide to dose the combination for greater than 12 weeks, we will have all the supporting data we need to conduct a longer-term treatment duration. And I think we will make the decision whether to have a 24-week arm or not based on the data that you see with 3102 from the proof-of-concept study. And so at this point, that decision is open. We will have all the necessary tox data to do a 24-week study, but whether or not we go up to 24 weeks will depend on the information we get from the 3102 study -- ongoing study.

Thomas J. Russo - Robert W. Baird & Co. Incorporated, Research Division

Okay. And then maybe for Joe. The field has obviously been re-scrambled a bit over the past few weeks with the updates from Vertex and Idenix and Roche and Gilead. Can you share whether you're seeing any impact from all this yet on the BD front and then maybe your current strategy and outlook with regard to cross-company collaboration?

Joseph Truitt

Yes, sure, Tom. So on the BD front, I'll just classify things as they've been over the last couple of years as active. And beyond that, we can't really go into any specifics. But as far as cross-company collaborations, from an Achillion perspective, we believe now that our portfolio and the individual compounds in it -- have advanced to the point where there is a lot of interests in trying to look a cross-company -- across companies and identify compounds that may be good fits, in particular as we look at some of the more difficult-to-treat populations that Mike pointed out earlier. Our base plan is to continue to move our own portfolio, forward it to address as many of these populations as we can. But we certainly remain open to and are engaged in lots of different dialogues regarding different mechanisms to put in combination with our portfolio.

Operator

Our next question comes from Rachel McMinn of Bank of America Merrill Lynch.

Rachel L. McMinn - BofA Merrill Lynch, Research Division

I guess I wanted to ask more from a regulatory perspective, Milind, how much -- I guess, how much safety data is required for combination studies. And I know that you're not really in a position or not ready to disclose what dose you're taking forward, but if I look at the 1625 data, we're talking about 20 patients if you decide to go with the highest dose. If you went with the lowest dose, you're looking at 60 patients worth of 12 weeks of exposure. And I'm just wondering to what extent -- have you had regulatory discussions to make sure that that's enough data in order to carry 3102 forward with 1625 in your next combo study?

Milind S. Deshpande

Thanks for the question, Rachel. We believe that, with 1625, we have enough exposure and enough number of patients at the 3 dose groups that we have tested to conduct another 12-week combination study. With 3102, one of the reasons why we completed 14-day dosing in healthy volunteers is that, that is a minimum requirement to conduct a 12-week trial in HCV patients. So in terms of the requirement for conducting a study in combination of 1625 and 3102, we have the adequate safety data for 1625 as well as for 3102.

Rachel L. McMinn - BofA Merrill Lynch, Research Division

So -- and this is based off of recent discussions with the regulators. I guess where I'm coming from is, given a lot of the recent HCV molecules that have encountered safety issues during Phase II, you want to make sure that you have extensive -- or maybe it just comes down to design -- in the way that you design this upcoming combo study that you have an even bigger arm with 1625 without 3102 to kind of phase out the safety data. Can -- maybe, can you just help us understand what that design would look like so we can understand how much safety data you're walking away from in this next study?

Milind S. Deshpande

And so in terms of the doses for 1625, Rachel, I'm inclined at this point to say that, most likely, we will proceed either with the 200- or the 400-milligram dose group. So that gives us a -- and the fact that we have dosed 1625 at the 800-milligram dose, with that expands the safety database for the lower-dose groups. In terms of 3102, when we look at the nonclinical profile for 3102 and the exposures that we achieved in our nonclinical studies, that gives us a very robust margin for -- very robust safety margin for our clinical exposures for 3102 as well. And again as I mentioned, we have dosed now 3 doses of 3102 up to 14 days in healthy volunteers. And the outcome of those studies was very benign, meaning we have not seen anything in terms of safety for 3102. So in terms of the trial design for the combination study, again, it will be an exploratory trial with maybe 2 arms of the study where we will explore 3 different doses of 3102 in combination with 1625. And we'll monitor with the adequate monitoring because this is the first combination study that we will be conducting with sovaprevir and 3102. I think this is pretty standard. And I understand, because of the safety issues that we are seeing in some of the Phase II trials that are currently ongoing, we are very aware of the safety issues that -- based on the profile that we have seen for 1625 as well as for 3102. And I think we have enough data to support conducting a 12-week or the 24-week trial with these 2 agents.

Rachel L. McMinn - BofA Merrill Lynch, Research Division

And then just so I'm clear: You're going to include ribavirin in the combination study, or you would not?

Milind S. Deshpande

That's correct. We will include ribavirin in the study.

Rachel L. McMinn - BofA Merrill Lynch, Research Division

Okay. And then can you just -- Sorry, one last question for me. You had mentioned that you plan to test 300-mg dosing for 3102, but I think you said you tested 25- to 75-mg in your 14-day study, so can you help us understand why you think you need to get to doses that high?

Milind S. Deshpande

Yes. So the dose -- the 3 doses that we are testing for our proof-of-concept are 50, 150 and 300. And based on the PK characteristics that have emerged for 3102 and taking into account the potency and the trough concentrations that we need to maintain throughout the study, we believe that we can achieve those trough concentrations with a dose of 75 milligrams or lower. And again, these are based on fairly robust modeling that was done internally. But since we are doing the -- this is the first time we are testing 3102 in HCV-infected patients, I think it behooves us to explore a variety of doses. And so we at -- we have a fairly sound rationale based on PK/PD modeling that suggests that 75-milligram dosing or lower will be applications. But as I said, this is the first time we are testing 3102 and it is for that reason we want it to go up to 300 milligrams.

Operator

Our next question comes from Ted Tenthoff of Piper Jaffray.

Edward A. Tenthoff - Piper Jaffray Companies, Research Division

I guess a lot of my questions have been answered, but maybe kind of going back to the 30,000-foot view. Mike, you touched on this a little bit. But with kind of the recent developments, in particular the Bristol trial suspension, how do you see the landscape changing? And with respect to this data, I know it's just out, but how do you see kind of your combination sitting into the HCV world as it's evolving?

Michael D. Kishbauch

I'll start and then I'll have Joe Truitt pop in behind me, Ted. So let's -- here's how I'd address your questions. So let's stipulate at the outset that the guys who end up launching earlier in this decade, whether that's Gilead, Abbott, whoever, will enjoy a first mover advantage. Wish I have that advantage. But pending any surprises, don't bet against surprises in this field, I probably don't have that first mover advantage and I'd probably be a click behind. That said, however, when you look at the multidimensional matrix that surrounds this category featuring colleague therapy with 2 or 3 classes of compound; IL28 status; resistance profiles; a whole raft of co-morbidities, patients who in the real world can be pretty colorful and may not, probably will not, behave like the clinical trial; geographic variability, and then throw in some economic issues, just for a little spice, the idea that this market will reduce to a simple kind of win-play-show formula and/or evaporate quickly is a serious reach on a good day, in my view, and grossly inconsistent, by the way, with the commercial models of the major developers who number double figures or more. Bottom line, and this is a restatement of what we've said all along, there will be a solid handful of combinations that will compete for patients over a time period that may span a couple additional decades. And I think we can be among those squarely in the mix. Parenthetically, the events, that you referred to, just last week illustrate once again that stuff will happen on the development front. There will be surprises, major and minor, because this is drug development. And our job, frankly, is to keep our heads down and execute. And to the extent we can do this against a portfolio that includes multiple compounds that are likely complementary to one another, I like our position. And Joe, do you want to piggyback on any of that?

Joseph Truitt

Yes. Ted, just to -- some additional thoughts there. As we've spent a fair amount of effort really trying to understand the commercial landscape not only in the U.S. and Europe but globally, one of the things that certainly appears is a highly segmented patient population. There really isn't a standard HCV patient, and therefore, we view the world as going to need a number of different regimens to try to address these different populations. Some of the populations we've pointed out today are certainly the larger segments and we're going to be targeting those with our portfolio. But I think, if you can see it in some of our competitors out there, you'll see them taking different combinations forward against different patient populations, but we believe that that's exactly what should happen and will happen and that therefore will lead to a number of different combinations being on the market in the future. And this will come in waves that won't all be wrapped up in one simple FDA approval in the mid-decade timeframe. This will take some effort and some continuing development. One of the other things that I'd like to point out to you, Ted, is that the other thing that shows up pretty consistently in all of our work, in all of our market research is that, when you speak to payers, patients and physicians, there are certain things they're squarely focused on and those tend to be effectiveness or SVR, resistance profile, safety, tolerability, ease of dosing, the duration that you're going to use and, I think, importantly, cost effectiveness of what we'll be able to deliver to the market. What does not show up is a specific -- a desire for one mechanism of action. So what -- and I think what we see is that -- as long as we can deliver those attributes in whatever we put into our combination, that we'll be just fine when we get to the commercialization of the combination. And so far, Achillion's portfolio, based on what we're seeing, is certainly matching up very nicely against these attributes that I outlined. And just so as you look at the market, we're not the only ones that are pursuing that path. There are others that are also -- have similar combinations in development. But that's really, I think, a quick summary of how we look at it.

Edward A. Tenthoff - Piper Jaffray Companies, Research Division

That's very helpful. And I like the fact that you guys have the follow-on compounds, too, just in case we do hit on these safety flags.

Joseph Truitt

And the other thing I'll piggyback on, and here I'm going to refer back to Rachel's comment/question, Ted, is that I think one is ill-advised to blithely ignore what's going on in the field when there are mishaps and assume they will or won't have any regulatory impact. I think she's dead right. And frankly, here again, companies have different approaches to the management, to the regulatory function. In our case, my friend Dr. Shah, sitting to my left here, tends to favor an approach that feels like almost constant dialogue with the agencies. Some people submit stuff and then sort of step back and wait for the response. And Gautam has a different approach. It doesn't mean it's right, doesn't mean it's wrong, but it's something we're comfortable with. And over his tenure at Achillion, I think we have tended to get hit with fewer surprises from a regulatory standpoint than perhaps some of our colleagues. It doesn't mean you can't get hit with a late-breaking curveball, that does happen, but I feel like we're a little less vulnerable to kind of tectonic shifts in regulatory view than perhaps some because of the way we conduct business in [indiscernible].

Operator

Our next question comes from Brian Abrahams of Wells Fargo.

Brian Corey Abrahams - Wells Fargo Securities, LLC, Research Division

Congrats on progress. Nice to see you had good SVR data for sovaprevir, and 3102 moving along well. Milind, a question for you regarding 3102. You've talked in the past about the drug's activity versus the typical NS5A-resistant variance being greater than what you see for the first-generation NS5A inhibitors. Can you talk us through what the practical clinical implications of this might be and where that might make the most difference when you combine it with a direct-acting antiviral? Could you potentially get away with lower doses, better odds of eliminating ribavirin, shorter duration? How might we see this play out? And then I had a follow-up question.

Michael D. Kishbauch

Thanks. So this is Mike. Brian, thanks for that question. By the way, you win the pool for the first analyst to properly pronounce sovaprevir, so [indiscernible]. Milind, go ahead.

Milind S. Deshpande

That's a great question. And I love that question because I think it really highlights the key differences between 3102 and some of the limitations that we have seen with NS5A inhibitors. And as I mentioned in the call, one of the key characteristics of NS5A inhibitors in general is that we see a very rapid and pronounced decrease in HCV RNA, the Phase I decline, as it is characterized in terms of viral kinetics. So RNA -- NS5A inhibitors have that very sharp, rapid decline in HCV RNA in the first 24, 48 hours of treatment. And the issue with NS5A inhibitors -- I think, the third-generation NS5A inhibitors is the rapid emergence of resistance. And at this point, I would like to separate out genotype 1b versus genotype 1a because the profile of NS5A inhibitors across these 2 subtypes is very, very different. In genotype 1b, multiple mutations come up but the key mutation that come first, resistance to NS5A inhibitors in genotype 1b, is the Y93 mutation. And genotype 1b, the variance at Y93 are -- have a reasonable replication capacity. And so when we look at the resistance profile for NS5A inhibitors in 1B, the key mutation to look at is Y93 as a single mutation, and the second mutation that is seen very frequently is a double mutation that has L31 M/V mutation in combination with the Y93 mutation. And so a single mutation at 93 and a double mutation in combination with mutation at 31 confirms high level of resistance in genotype 1b. What we see with 3102 is that there is maybe a 3 to 4 forward [ph] shift in 350 at best [ph] with the single as well as the double mutations. In fact, we have not been able to generate resistant mutations with 3102 at concentrations that are greater than 200 mg or more, which is, as you can imagine, it's a fairly low concentration in terms of trying to generate resistance. At the same concentration with -- for example, with BMS-052, we see resistance at Y93 as well as a double mutation that has L31 V/M plus Y93 mutations. So this is a very clear difference between 3102 and other NS5A inhibitors in genotype 1b. And the other question, what are the clinical implications of this? We have already seen good data with NS5A inhibitor plus ribavirin in genotype 1b, going back to the first study that was done by BMS in genotype 1b no responders. So clearly, you had difficult-to-treat patient population and BMS-052 in combination with ribavirin worked well. So we believe that 3102 in combination with ribavirin will deliver much better responses in genotype 1b, as compared to BMS-052. Now moving on to genotype 1a, as I mentioned earlier, the profile of NS5A inhibitors in genotype 1a is very, very different, as compared to 1b. It is different in several different ways. First of all, the resistance mutations that come up are a lot more extensive in 1a, as compared to 1b. You see mutations like amino acids at 28, 30, 31, 58 and 93. And we see these mutations come up in less than 2 weeks of treatment with an NS5A inhibitor. What we see with 3102 is that we address all the mutations extremely well, as compared to other NS5A inhibitors. One of the key mutations to focus on is the L31 green mutation where for other NS5A inhibitors you will see a full shift of, at least, 200- to 300-fold or up to a thousandfold difference. With ACH-3102, that difference is maybe three- to fourfold again. So a significantly better profile for 3102 in genotype 1b as well as in genotype 1a. Again, the clinical significance of this, I think we will see a more robust activity in combination with the PI and ribavirin against genotype 1a as well as genotype 1b, which I think it's probably a difficult task for NS5A inhibitors that do not cover the L31, as well as mutations at 28, 30, 31, 58 and 93. So a long answer, but I think it's a very, very important question for NS5A inhibitors because the potency is not really an issue, it is how well these compounds are in terms of suppressing emergence of resistance.

Brian Corey Abrahams - Wells Fargo Securities, LLC, Research Division

Milind, that's very helpful. And then just one more quick follow-up, then I'll hop back in the queue. How long does 3102 take to reach steady state? I'm just trying to get a sense of how we'll be able to contextualize the viral suppression results you'll report next month relative to other NS5A inhibitors and whether this trial will be long enough to enable clear comparisons on viral suppression.

Milind S. Deshpande

Yes, all right. Well, again a great question. The PK data that is emerging for 3102 is such that we are seeing a prolonged half life for 3102. So I guess your question refers to the trial design that we have embarked upon for the proof-of-concept study. As I mentioned earlier on the call, we are exploring 3 doses of 3102, 50, 150 and 300 milligrams, and we are administering a single dose of 3102. Based on the prolonged half-life, we believe that we will exceed the target trough concentrations with these doses for at least up to 5 days. So even though we are dosing 3102 only once, we are providing trough concentrations that will exceed our target for at least 5 days.

Operator

Our next question comes from Katherine Xu of William Blair.

Y. Katherine Xu - William Blair & Company L.L.C., Research Division

Everyone, so I'm just curious about the 3102. So did you stop at 75 milligrams for the 14-day study in the southeast, or you are still going to escalate higher to kind of cover what you have in the HCV patients?

Milind S. Deshpande

So for the 14-day study, we started out with the 25-milligram dose and we have accelerated up to 75 milligrams. So [indiscernible].

Y. Katherine Xu - William Blair & Company L.L.C., Research Division

In HCV patients, you are going for higher, right? So I'm just wondering -- it should -- you're not doing higher dose as you need healthy issues along tiers [ph] anymore?

Milind S. Deshpande

Oh, so -- sorry, I misunderstood your question. So I guess you're asking about the proof-of-concept study in HCV-infected patients?

Y. Katherine Xu - William Blair & Company L.L.C., Research Division

Yes.

Milind S. Deshpande

Yes. So again, based on all the PK/PD modeling that we have done, we are targeting a trough concentration of about 100 nanograms per ml. And we believe that, at steady state, we can achieve that trough concentration with doses that are less than 75 milligrams of 3102. But again, in response to Rachel's question, as I said, even though we have a high level of confidence in our modeling, this is the first time that we are taking 3102 in HCV-infected patients. And I think it is important for us to see the dose response, starting with a low dose of 50 going up to 300 milligrams. I don't think that we will require 300 milligrams to achieve steady state, but I think it is best explore these doses in the first proof-of-concept study that we have undertaken.

Y. Katherine Xu - William Blair & Company L.L.C., Research Division

Okay. So as I'm doing the tone change with regard to strategy and the views on the landscape -- but I might be mistaken. I just want to make sure that I understood it. So previously, I think that the key goal here is to develop pan-genotypic combinations that would be as broadly applicable as possible to the patient population. And then today, we've heard it repeatedly, the sizing of the patient population up into different sections and then, of course, getting approved for different populations. We understood that as well, but I just thought there was a tone change. I mean, I just want to see, is that true, and is the assumption correct?

Michael D. Kishbauch

I don't think there is a tone change, Katherine. Joe, you can piggyback on top of me here. But I think -- fundamentally, I think you're right. When -- in the category that's fond of saying a broad application for one's combinations or individual products makes a heck a lot of sense. I think what we're reflecting in some of our comments, and I think this will be probably elucidated in fair fashion at the R&D Day next month, is that as we learn more about our compounds and, frankly, go to school on the learning of some others in the field as well, some segmented approaches have emerged that we might ultimately consider worth studying. And so I think what we want to do is piggyback on top, if you will, the omnibus strategy to try to reflect the study program that reflects the learnings of those particular segments that we think could be important, soradics [ph] being one infant, probably others as well.

Joseph Truitt

Katherine, it's Joe. I think we'll continue to -- we're certainly going to pursue, and you'll see that in our trial design, we're going to go after the genotype 1 naïve population and as well as looking at the -- on the no responders. But there are certainly -- the size of this market and the global nature of it is so large that there's other opportunities out there beyond that, that are very significant. And so that's what we're addressing that there probably won't just be one combination that will be ideal for every single patient population across the globe and by segment.

Y. Katherine Xu - William Blair & Company L.L.C., Research Division

So last one is just housekeeping. What is the criteria on the eRVR for the sovaprevir study that you just reported on? [indiscernible] 2012?

Milind S. Deshpande

Truly you have -- so the criteria for eRVR was undetectable at week 4 as well as undetectable at week 12. And however, there was one patient in the 200-milligram dose group, 2 patients in the 400 and 2 patients in the 800 who strictly did not meet the criteria for eRVR. And just to give you one example: There was one patient in the 400-milligram dose group who was undetectable at week 3, detectable at week 4 and 5 but still less than 25 and undetectable at week 6. So technically, this person did not meet the criteria for eRVR but achieved undetectable at -- of week 3 and continued to be undetectable from week 6 forward. So it was a judgment call that we had to make based on the virology that we were seeing whether or not to add this patient to response-guided treatment.

Operator

Our next question comes from Brian Skorney of Brean Murray.

Brian Skorney - Brean Murray, Carret & Co., LLC, Research Division

I guess my first one is just kind of relating to the patients that we don't have full data on yet. By my count, I guess there's 14 patients that hadn't clearly dropped out but are getting 12 plus 36. And so I guess my question is, is that right? Have any of those patients been lost to follow-up yet or dropped out? And have you seen any of those patients rebound while on peg/riba so far?

Milind S. Deshpande

We have not locked that data set. So you can imagine, before we come to any conclusions into these data, we have to -- clearly, the data sets, we have to make sure that we have the right information, lock the data set and then analyze it. So we will not do that until all patients have completed their 36 weeks of dosing of peg/riba. At this point, we are probably, about 50% who have completed dosing, but we have not analyzed the data.

Brian Skorney - Brean Murray, Carret & Co., LLC, Research Division

Got you. And then, Milind, you were discussing the EC50s for wild-type genotype 1 and the concentrations you're getting in terms of nanograms per ml at the 200 mg dose. I wonder, can you just walk us through the EC50s to 1625 for relevant subtypes, including PI-resistant strains, as well as the other genotypes? And also, what the concentration of 1625, is at the 400- and 800-mg dose? I'm just trying to determine what fold concentration of drug you could be getting that could be relevant for inhibiting non-wild-type GT-1.

Michael D. Kishbauch

Yes. So to answer the first part of your question, the way we get the in vivo EC50 is based on the PK/PD modeling that happens after we will get the antiviral response, as well as the PK. And we did this exercise after a monotherapy with 1625. We did a similar exercise after we dosed 1625 in combination with peg/riba for 4 weeks. That was the segment 1 study. And then we went through a similar analysis after we had the data for 12 weeks of study. And the conclusions are very consistent. So we evaluated 2 models to derive the PK/PD relationship and the first model was based on viral kinetics where you take into account the viral reproduction and the efficacy of the drug. And the second model was pretty standard, which is the Emax model. And both these models give us an in vivo EC50 of 0.4 nanograms per ml. This is more potent. The EC50 is lower than the EC50 that you see in your standard replicon assay. In the standard replicon assay, the EC50 for 1625 against genotype 1 is about 10 nanomotors. So you are looking at a greater potency of 1625 as more than what was predicted in the replicon assay. And so that's the first part to your question. The second part is, what are the concentrations for different dose groups? So for the 200-milligram [indiscernible] dose group, the mean trough concentration in this segment 2 study was 22 nanograms per ml. For the 400-milligram dose group it was 72 nanograms per ml. And the 800-milligram dose group, it was 689 nanograms per ml. So as I said earlier on the call, we far exceed the in vivo EC50s, the trough concentrations far exceed the in vivo EC50s for 1625. How does this compare to activity against the key resistant mutations as well as across genotypes? I don't have the numbers in front of me for all the resistant mutations, but at least for the key resistant mutations at 155, 156 and 168, these concentrations again exceed those EC50s that have been seen in the replicon assays.

Brian Skorney - Brean Murray, Carret & Co., LLC, Research Division

And what about for genotypes 2, 3, 4, 5?

Milind S. Deshpande

So on genotypes 2, 4, 5 and 6, the activity is very similar to genotype 1, so the EC50s are very similar. For our genotype 3, the EC50 is higher, and that's the reason -- if you recall, we did a study with 1625 against genotype 3 and saw reasonable activity. But we won't have a group PK/PD model for the activity against genotype 3.

Brian Skorney - Brean Murray, Carret & Co., LLC, Research Division

And so I guess that kind of leads just to what your thoughts are in terms of looking at 1625 plus 3102 and a potential pan-genotypic combo regimen.

Milind S. Deshpande

We are certainly going to explore that. And I think a combination of 1625 and 3102 will work really well. For NS5A inhibitors in general, I think the key genotype to look at is genotype 2b. And for the reasons that I was articulating earlier, the natural variant in genotype 2b is a -- and we're pioneering -- are a very new sort of new losing [ph] which is typically seen in genotype 1a or 1b as the natural amino acid. And as we have seen with other NS5A inhibitors, they lose significant potency against the L31 mutations. So I think a signature study or -- the key issue with NS5A inhibitors in genotype 2 is going to be robust activity against genotype 2b. I think 3102, based on the potent activity against L31, will do well in genotype 2. We have not seen any differences in genotype 3. So a combination of 3102 and 1625, I think, will perform well across all genotypes but that's an experiment that we are certainly going to do sooner than later.

Operator

[Operator Instructions] Our next question comes from Matthew Harrison of UBS.

Matthew Harrison - UBS Investment Bank, Research Division

Maybe if I could try and follow up on Rachel's question about safety populations. When you're talking to companies about cross-company collaborations, what's the size of the safety data they expect -- those potential partners are looking for? And how do you think about when you'll have adequate -- or do you already have adequate safety to meet the criteria that they're looking for?

Joseph Truitt

This is Joe. I'll take that question. Yes, when we -- the biggest issue that people want to see is they want to make sure that your -- that you have your 3-month tox work done. That's always important. And then they want to see -- I mean, they want to make sure that you've met the minimum criteria in the patient safety so that they can feel comfortable putting the drugs into combination from a safety perspective. And both ACH-3102 and sovaprevir and, for that matter of fact, ACH-2684 have all met those minimum objectives. So anyway, we've met the minimum threshold across and have not really run into that as an issue.

Operator

Our next question comes from Phil Nadeau of Cowen and Company.

Philip Nadeau - Cowen and Company, LLC, Research Division

Milind, could you go into a little bit more detail on the 6- and 9-month preclinical tox that you've done for 3102? Did you see any toxicities at all no matter what the dose and maybe would like to share with us the multiple of expected human exposure that you went up to at the highest dose? That would be great.

Milind S. Deshpande

So the 6-month study was done in the rag [ph]. The 9-month study was done in the don [ph]. And just to give you a perspective on what the safety margins are, in the clinical studies with 1625, the AUCs that we see at the efficacious doses are -- for the lowest dose, there are around 10 to 15 microgram hour per ml. And so if you compare the AUCs that are required for efficacy to the AUCs that we got at the Noel [ph], we see at least a 10- to 15-fold safety margin. And for a 6- or a 9-month study, that is a very, very robust margin. Oh, is it -- was your question 1625 or 3102?

Philip Nadeau - Cowen and Company, LLC, Research Division

3102, yes.

Milind S. Deshpande

Oh, sorry. So anyway, I gave you the information on 1625. For 3102, we have not completed the 6- and 9-month study. So far, we have completed 3-month studies in rag and don [ph]. And again, the AUCs that we expect at the efficacious dose are around 8 microgram hour per ml. And in terms of the AUCs that we see at the Noel [ph], we are in excess of 100 microgram hour per ml, so again, fairly robust safety margins. And the 6-month studies are ongoing. They should be completed by first quarter of next year.

Operator

Our next question comes from Nathan Cali of Noble Financial.

Nathan Cali - Noble Financial Group, Inc., Research Division

Congrats on the progress. We're looking forward to the combination studies. Just a quick question. When moving from patients at cEVR to patients assigned to 12 weeks, there was a little bit of difference in the numbers and I'm just trying to understand what those differences were in the 200-mg and 800-mg dosing regimens. I would assume that it should have been 12 patients instead of 10 in the 200 and then 14 instead of 17 patients instead of 14 in the 800-milligram dosing regimen, based upon what we saw from the selection criteria.

Milind S. Deshpande

I'm -- I can walk you through the patient disposition in the 200- and the 800-milligram dose group, and then let's see where we come out after that. So there were 19 subjects in the 200-milligram dose group. 1 subject withdrew consent at week 5 due to mood swings and due to abscess. So there were 18 subjects who completed 12 weeks of treatment, okay? Of the 12 -- so of the 18 subjects who completed 12 weeks of treatment, 12 subjects were assigned to 24 weeks of treatment and 6 subjects were assigned to full 48 weeks of treatment. Was that -- is that clear?

Nathan Cali - Noble Financial Group, Inc., Research Division

Yes.

Milind S. Deshpande

So, okay. So of the 12 subjects who were assigned to 24 weeks of treatment, 10 subjects completed 24 weeks of treatment. And of the 10 subjects who completed 24 weeks of treatment, 9 subjects achieved SVR4.

Operator

Our next question comes from Heather Behanna of JMP Securities.

Heather Behanna - JMP Securities LLC, Research Division

Congrats on the sovaprevir data. Just a question on the disposition of the patients, the 1 rebound and the 2 relapses. If you could give us any color on their -- if they're a 1a or 1b or what their IL28B status was, that would be great.

Milind S. Deshpande

Sure, sure. So in the 200-milligram dose group, there was one patient who relapsed. And the characteristics of that patients -- patient were that patient was genotype 1a TT, body mass index was 27, the baseline viral load was 5.94 logs. So a high baseline viral load and 1a TT genotype. In terms of the patient who had the rebound in a 400-milligram dose group, that patient was genotype 1b CC and the baseline viral load was 6.24 logs, so very high baseline viral load. And we are still following-up that patient. There is a possibility that there might be a compliance issue after the patients stopped taking 1625 because this patient was undetectable from week 2 all the way through and then we saw a breakthrough at week 20. So we are calling that patient to see if there were any compliance issues. The patient who had relapse in the 400-milligram dose group, that patient was genotype 1a R28 BTT [ph]. This patient had a baseline viral load of 6.19 log and a body mass index of 24. So these are the baseline characteristics for these 3 patients.

Operator

Our next question comes from Howard Liang of Leerink Swann.

Howard Liang - Leerink Swann LLC, Research Division

What do we know -- or I guess, what can you tell us about the metabolisms of sovaprevir and 3102?

Milind S. Deshpande

Sovaprevir is metabolically very stable. We see very little metabolism for sovaprevir. It is eliminated through the bile mostly unchanged. It is not a substrate for any of the major CYP isoenzymes and it is not an inhibitor or an inducer of any of the CYP isoenzymes. For 3102, a similar story, it is very stable. It is not a substrate for any of the major isoenzymes, nor it is an inhibitor or an inducer of any of the CYPs.

Operator

Our next question comes from Ravi Mehrotra of Credit Suisse.

Koon Ching

This is actually Koon, asking questions in behalf of Ravi. I -- the first question is -- you mentioned you have initial data in early 2013. Just want to know what you will be presenting or what you'll be announcing. Would it be SVR data? Would it be partial SVR data from patients recruited? And then my second question is -- we've seen some -- obviously, we've seen some data from other PIs. Just want to get your comments on why you think -- how does 1625 compare? And why do you think it could serve as the anchor to a interferon-free regimen?

Milind S. Deshpande

What we'll be announcing first quarter of next year is RVR from the combination trial. In terms of the comparison of sovaprevir to other protease inhibitors, I think, based on the SVR4 data, I think it is fair to say that we are at the high end of SVR4s that were reported for other PIs. I hope that this trend will continue and we will see very robust SVR8 as well as SVR12. And the distinguishing characteristics of 1625, as we have talked earlier on this call, I think, in terms of potency, it has done well. One interesting characteristics of 1625 that has emerged and we will confirm as we do additional studies with 1625 is that we have not seen a high level of resistance in [indiscernible] 1625, i.e., we have not seen variance at 155, 156 or 168. It is clearly a once-daily drug. It does not require boosting with ritonavir to achieve once-daily dosing. And as I was answering Howard's question, it has a very attractive profile in terms of combination with other DAAs because it is not a substrate inhibitor or inducer of any of the CYP isoenzymes.

Operator

Our next question comes from Akiva Felt of Wedbush.

Akiva Felt - Wedbush Securities Inc., Research Division

I have a follow-up question about the new sovaprevir data. The -- any additional details about the 2 relapses? I mean, were these patients followed up weekly or just at week 4? Did you get a sense of the relapses that were early or late? Or anything else notable?

Milind S. Deshpande

No. So these patients had their end-of-treatment visit. And after that, they came to the clinic for their end-of-treatment plus week 4 visit. So that was their SVR4. There were no intermediate viral loads that were determined. And I think I've already described the baseline characteristics for these subjects.

Operator

Our next question comes from Jason Kolbert of Maxim.

Jason Kolbert - Maxim Group LLC, Research Division

I'm not going to ask you any questions about viral resistance, I promise, but I would like to change gears a little bit and ask Joseph Truitt a question on business development. We know that the window is very tight. There's a tremendous push. And certainly, I respect what you're saying, which is that we don't know what the final evolution of therapies are going to be like. But here you are sitting with a QD pan-genotypic protease inhibitor. I can think of a company out there that's got a TIDPI [ph] that's trying to anchor a regimen, and it just doesn't make sense. Help me understand from a deal-making point of view: How long you think the window is to come up with a partnership or a combination so that you can still be competitive in terms of the timeline? How much heat is there out there to make a deal?

Joseph Truitt

Yes, there are 2 aspects to your question, Jason. One has to do with timing, one has to do with really the more provocative issue that you raised. And look, as we've indicated on previous occasions, again that we're acutely aware of the strategic activity history in HCV and the resulting speculation regarding potential transactions for the company, look, we remain confident in the stand-alone prospects for Achillion and are focused on developing our existing portfolio. But at the same time, our Board is obviously focused on maximizing value for our shareholders. And so we'll continually evaluate our strategic alternatives with that in mind. Having that said, we can't comment on the rumors, speculation or prospects of a specific transaction occurring. As regards your question on timeframe, frankly, I -- my earlier diatribe about the fact that this market is going to evolve over a period of time, there will be changes. Frankly, it puts me in a position to speculate that this notion of a window of opportunity that will narrow and eventually close, it just doesn't apply to this market, there will be changes. There will be opportunities that don't appear to be present today that will emerge later on. There will be others that seem obvious today that will close up later on. But in a market that is as complex as this and which will continue to evolve over a period of not years but possibly a couple of decades, I think the -- any company like ours has got to make the best decision rather than the expedient decision. And again, I think that's where I would leave it.

Operator

I'd now like to turn the conference back over to Mr. Mike Kishbauch for any closing remarks.

Michael D. Kishbauch

All right, good deal. I think we'll close it up at this point. And thank you, guys, for tuning in. Obviously, we're looking forward to providing updates later in the quarter on 3102 and also looking forward to seeing everyone next month at the Inaugural R&D Day in New York City. At that point, we look forward to spending time to dig into each of our compounds, set the stage for initiating the all-oral interferon-free proprietary regimen for HCV by the end of the year. And also, it goes without saying, after the call this morning, management team is here and available in the office to answer any follow-up questions that arise, so feel free to reach out to Mary Kay or Glenn Schulman.

And again, thanks for joining us. Good day to all.

Operator

Ladies and gentlemen, this does conclude today's conference. You may all disconnect, and have a wonderful day.

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