Good afternoon, ladies and gentlemen. Welcome to the Enanta Pharmaceuticals Second Quarter Financial Results Conference Call. My name is Ronnie, and I will be your conference operator today. All lines have been placed on mute to prevent any background noise. After the speakers' remarks, there will be a question-and-answer session. [Operator Instructions]. Thank you. I will now like to turn the call over to Carol Miceli, Director of Investor Relations. Please go ahead.

Thank you, Ronnie, and welcome to Enanta Pharmaceuticals' fiscal second quarter financial results conference call. The news release with our financial results was issued this afternoon and is available on our Web site at www.enanta.com. You can also listen to the webcast or the replay by going to the Investors section of our Web site. On the call today is Dr. Jay Luly, President and CEO; Paul Mellett, our Chief Financial Officer, and other members of our senior management team. Before we begin with our formal remarks, we want to remind you that we will be making forward-looking statements including plans and expectations with respect to our licensed product and our product candidates and financial projections, all of which involve certain assumptions, risks and uncertainties that are beyond our control and could cause our actual developments and results to differ materially from these statements. A description of these risks is in our most recent Form 10-K and other periodic reports filed with the SEC. In addition, Enanta does not undertake any obligation to update any forward-looking statements made during this call. I'd now like to turn the call over to Dr. Jay Luly, President and CEO.

Thank you, Carol. Good afternoon, everyone, and thank you for joining us today. I’m pleased to report on Enanta results and to update you on our progress in our R&D efforts. Enanta remains in a very strong position to expand and to execute on our pipeline. Our cash position of $246 million and recurring revenue stream from our successful HCV collaboration with AbbVie allow us to fund our business operations and R&D initiatives for the foreseeable future. Our HCV protease collaboration with AbbVie continues to progress with Enanta participating in AbbVie’s lead HCV regimens with our protease inhibitor paritaprevir and also contributing a second protease inhibitor ABT-493 to AbbVie’s latest investigational HCV regimen currently in Phase 3 trials. AbbVie’s initial HCV regimens continue to provide substantial royalty flow to Enanta. Enanta received $30 million in royalties for the first half of our fiscal year and we’re continuing royalty payments flowing to Enanta this year. Let’s shift to ABT-493, our second protease inhibitor. ABT-493 is advancing toward an NDA filing as part of AbbVie’s next generation HCV co-formulated regimen made up of ABT-493 and ABT-530, which is AbbVie’s second NS5A inhibitor. This pangenotypic, all oral, only daily ribavirin free HCV treatment continues to demonstrate very high cure rates in HCV patients often and as little as eight weeks of treatment. Last month, exciting new data from the SURVEYOR 1 and 2 studies using this 2-DAA co-formulation were reported during the EASL meeting in Barcelona. The data demonstrated that 97% to 98% SVR12 was achieved with only eight weeks of treatment in genotypes 1, 2 or 3 HCV patients without cirrhosis. In patients with genotype 3 HCV with compensated cirrhosis, also known as Child-Pugh A one of the most difficult to treat populations, 100% SVR12 was achieved with 12 weeks of treatment…

Thank you, Jay. I'd like to remind everyone that Enanta reports on a fiscal year schedule, our fiscal year ended September 30, and today we are reporting results for our second fiscal quarter ended March 31, 2016. Enanta ended the quarter with approximately 246 million in cash and marketable securities as compared to 209 million at our September 30, 2015 fiscal year-end. We expect that these cash resources will be sufficient to meet our anticipated cash requirements for the foreseeable future. Revenue consisted of 13 million of royalty income earned on AbbVie’s net sales of paritaprevir containing regimens. Milestone payments, royalties and other payments from collaborations have varied significantly from period-to-period and we expect that variability to continue. I do want to note that this quarter is the first in our new royalty year under our AbbVie agreement for purposes of determining applicable royalty tiers. The amount of VIEKIRA sales allocated to paritaprevir, particularly whether they are sales of 3-DAA or 2-DAA regimens containing paritaprevir as well as the net sales adjustments and the annual royalty tiers under our agreement are all factors that contribute to the amount of actual royalties we earn on AbbVie’s HCV sales. Any of these factors could change in subsequent quarters. For example, if AbbVie's sales include a higher percentage of 2-DAA regimen sales such as those in Japan, then our royalties would increase even if AbbVie’s total HCV sales stay the same. Moving on to expenses. Research and development expenses were 9.1 million and 5.4 million for the second fiscal quarters ending March 31, 2016 and 2015, respectively. The increase in the recent three-month period was due primarily to increased preclinical and clinical costs associated with our wholly-owned R&D programs. We expect that our R&D expenses will continue to increase in fiscal 2016 as we continue our cyclophilin inhibitor clinical trials, advance our NASH program into the clinic and increase our R&D capabilities. General and administrative expense was 4.4 million for the quarter ended March 31, 2016 and 3.4 million for the comparable quarter in 2015. The increase in G&A in the three-month periods is due primarily to higher stock-based compensation expense as well as additional expenses to support our expanding operations. We incurred a net loss for the second quarter of 1.6 million as compared to a net income of 28.7 million in the second quarter of 2015. During the three months ended March 31, 2016, the company increased its estimate of its annual effective tax rate for fiscal 2016 from 27% to 31.5%, primarily due to lower projected research and development tax credits. This resulted in an income tax provision of 1.55 million despite a pre-tax loss for the quarter as the entire catch-up is recorded in the current quarter. Further financial details will be available in our Form 10-Q for this fiscal quarter. I’d now like to turn the call back to the operator and open the lines up for Q&A. Operator?

[Operator Instructions]. Your first question comes from the line of Geoff Meacham with Barclays.

Hi, guys. This is Evan Seigerman on for Geoff. Thanks for taking the questions. So just a quick question regarding just some recent HCV guidance that we saw published, I think it was last week. So do you believe that – I’m just wondering how this impacts your development strategy for 494, the cyclophilin inhibitor? Does this even apply?

Well, the guidance doesn’t particularly bear on those factors with regards to some of the words that were in there. Again, it’s a draft guidance. I think where it might potentially apply to us down the road would be if we’re in combinations with other DAAs.

Okay. And then kind of just following up with the cyclophilin inhibitor and we saw data from yours and data from Scripts at EASL. I’m just wondering if you can help me better understand kind of some of the benefits and drawbacks of each approach?

When you say with regards to Scripts?

Scripts research had a cyclophilin inhibitor that they presented data on. It was PS003.

Yes, I don’t have that information right in front of me. I know they did have a poster I think that talked about some effects on the ability to re-infect cells after they had been exposed to cyclophilin inhibitors and so forth. But that is a little bit different than our molecules and what we’ve been pursuing. So I can’t specifically make a comparison between the two. We haven’t tested the other agent. But what we have shown pretty convincingly is really interesting pangenotypic activity, very uniform pangenotypic activity from a potency perspective across GT 1 through 6 and amazingly, good activity against all the RAVs. In fact, you can see a little bit of that data in the corporate presentation that we posted last week showing on NS5A resistance-associated variants, which is where many of the problems with current therapies are encountering here with the NS5A RAVs. So we wind up pretty much every NS5A that’s on the market or in development, line them up and compared all the resistance mutation that they have issues with and our cyclophilin inhibitor pretty much knocks them down as though they were wild type across every mutation that we’ve seen, so whether that’s NS5A or NS5B or also protease. So what we’ve been really focusing on is establishing that really strong high barrier to resistance mechanism. We’ve been flushing it out with regards to being pangenotypic and again, we’re pretty much done with Phase 1. We’re just nearing the end of that and we’re on track to again get in patients next quarter, so we’re very excited to get going on that so that we can get some combinations to really prove that principle that we’ve seen pre-clinically.

Great. Thanks for taking the questions.

Thank you.

Your next question comes from the line of Brian Skorney with Robert Baird.

Thanks for taking the questions. I guess one kind of off of the prior question in terms of the revised draft FDA guidance. Do you think that there’s any risk in terms of the timeline for ABT-493 approval? I don’t think there’s currently outside of a Japanese study, a head-to-head study with the 493 base regimen. And then I have one on the FXR agonist after.

Okay. Thanks, Brian. So there are other head-to-heads. So the Japanese studies that you mentioned are head-to-head trials, comparator trials, endurance 3 in genotype 3 is also a comparative study. So again, and AbbVie’s had extensive discussions with FDA all along the way into Phase 2 meetings and throughout the design of Phase 3 and they feel pretty comfortable with those discussions and the fact that, again, the comparator trials that are ongoing.

Okay. And then in terms of the FXR agonist, I was just wondering if we had the OCA FDA AdCom this quarter and I was just wondering if you guys had any takeaways from that AdCom, anything you learned from the OCA preclinical profile and where you think you’re asset might potentially be able to differentiate?

Yes, so not a lot of learnings I would say from that AdCom. It was obviously a fairly straightforward one for Intercept. There didn’t seem to be a lot of controversy and there was a unanimous vote at least in PBC going forward with recommendation. So I think what we continue to do is focus on the potency and activity. Again, with our first agent we’ve tried to make it very, very selective across all other nuclear receptors and really dialed out TGR5, which is another receptor that FXR agonist can sometimes bind to – that has been at least implicated pre-clinically in pruritus. I don’t know if that’s a situation. I think people are going to be sorting a lot of that out clinically. But we’ve been doing a lot of characterization. Not a lot of it unfortunately yet has been put out there into the public domain for some variety of reasons. Some of its competitive and some of its we’re still working up final data out of several different models. So, we will be putting out more information later this year and we are reiterating our target of being in the clinic later this year as well.

Great. Thanks.

You’re welcome.

[Operator Instructions]. Your next question comes from the line of Jessica Fye with JPMorgan.

Hi, guys. This is Ryan on for Jess. I appreciate you taking the questions. Maybe going to 494, the cyclophilin inhibitor, as you progress towards moving into the proof of concept, maybe taking a step back, as you think about the mechanism of action, I think you were talking earlier about how it had pretty good activity against some of the NS5A RAVs. Is that your expectation that it would pair well using a NS5A or what mechanisms do you think are most promising in terms of the combination to pair the agent with?

Sure. So we actually have looked at combinations with very mechanism of action and have generated a lot of interesting data combination wise showing activity to mild synergy depending upon the mechanism and the combination. So we feel like every combination partner is possible. As you know, we have a Phase 2 ready NS5A ourselves called EDP-239 that we finished proof of concept study on. But we’re actually thinking that to marry our cyclophilin inhibitor with another really high barrier of mechanism would be on the most intriguing things I think in terms of new combinations to come forward. So to that end, we do like the new mechanism which also has a pretty high barrier. I think cyclophilins are probably higher. To say it another way, if we could achieve what we wanted to achieve without having a NS5A in the regimen, I think that’s what we’ll try to do. We can make it as simple as a 2-DAA regimen. If we need extra horsepower as it turns out, once we do the clinical studies and determine we could use a little bit more power, then we certainly have a NS5A that we can add to the mix. But right now we want to try to make it as simple as possible and as high a barrier to resistance as possible.

Okay. And would you have some data to present possibly, like a medical conference later this year?

I think that’s very likely.

Great.

We’ll be aiming to put some data out later this year.

Okay. Thanks for taking my questions.

You’re welcome.

There are no more questions at this time. I’d like to turn the call back over to Carol Miceli.

Okay. Thank you everyone for joining us today. If you have any additional questions, feel free to give us a call in the office. Thank you.

Thank you for participating in today’s conference call. You may now disconnect.