Good day, ladies and gentlemen. And welcome to the BioCryst Third Quarter 2014 Conference Call. At this time, all participants are in a listen-only mode. Later, we’ll conduct the question-and-answer session and instructions will follow at that time. (Operator Instructions). As a reminder, this conference call is being recorded. I would now like to introduce your host for today’s conference, Rob Bennett. Sir, you may begin.

Thanks. Good morning. And welcome to BioCryst’s third quarter 2014 corporate update and financial results conference call. Today’s press release and accompanying slides for this call are available on our website www.biocryst.com. At this time, all participants are in a listen-only mode. But we will open up the call later for your questions and instructions for Q&A will be provided then. Joining me on the call today are Jon Stonehouse, Chief Executive Officer of BioCryst; Tom Staab, Chief Financial Officer; and Dr. Bill Sheridan, our Chief Medical Officer. Before we begin, I’ll read a formal statement as shown on slide 2, regarding risk factors associated with today’s call. Today’s conference call will contain forward-looking statements, including statements regarding future results, unaudited and forward-looking financial information and company performance or achievements. These statements are subject to known and unknown risks and uncertainties, which may cause our actual results, performance or achievements to be materially different from any future results or performance expressed or implied in this presentation. You should not place undue reliance on the forward-looking statements. For additional information, including important risk factors, please refer to BioCryst’s documents filed with the SEC, which can be found on our company website. With that, I will turn the call over to Jon.

Thank you, Rob. Good morning, and thanks everyone for joining us today. The BioCryst team remains committed to building the small molecule, rare disease company and changing patient lives with oral drugs for the treatment of their disease. The majority of our efforts are on the advancement of our oral small molecule kallikrein inhibitors for the prevention of HAE attacks, with the goal of bringing normalcy to the lives of HAE patients and transforming the treatment of HAE. Activities are underway to get the OPuS-2 trial of 4161 up and running and we expect to dose the first patient before the end of this year. Bill will summarize the OPuS-2 trial design shortly. In addition, we remain on track to commence Phase I trials of our second generation Kallikrein inhibitors during the second quarter of 2015. We have also made significant progress towards improving the 4161 formulation. At this stage, we are becoming increasingly confident that we can reduce the pill burden per dose as we move toward the commercial formulation. Regarding BCX4430, the strategic value of this program is U.S. government stockpiling as a broad spectrum antiviral medical counter measure. The Ebola epidemic in West Africa has shifted our focus to Ebola virus disease. We are currently pursuing three important goals. First, determine a 4430 provides any antiviral effects or survival benefits in non-human primates infected with Ebola. Second, determine human safety and drug exposure in the Phase I healthy volunteer studies. Third, increase production of drug supply. As Bill will describe in more detail momentarily, the first study of 4430 in non-human primates infected with Ebola virus showed a prolongation of median survival with 4430, but no improvement in overall survival. A second study in a different non-human primate model will commence in November. The IND submission remains on track for this month and we are producing more drug to support the program. Finally, turning to our antiviral RAPIVAB for flu. There has been a lot of activity to be in a position to make RAPIVAB available in the U.S. during the upcoming influenza season, pending FDA approval. At this time, the status of our contract manufacturer has not changed. They continue to remain under a warning letter. An important next step is a successful general inspection of the plant, as this must be conducted in order to remove the warning letter status. It’s our understanding that the FDA inspection process is underway. That’s it for our general update and now I’ll turn it over to Bill who will discuss our programs in more detail.

Thanks Jon. In July, we presented the top line results of our OPuS-1 trial in hereditary angioedema. We are very pleased, this study was selected for oral presentation at the EADV conference in Amsterdam. Slide six provides some more granularity around patient reported attack rates by study period and randomization sequence and we’ve included in the presentation by study PI, Dr. Marcus Maurer. This analysis supports the robustness of the primary outcome in the study. We’re pleased to note that the design of our OPuS-2 study in HAE has been finalized following regulatory discussions and the protocol has now received U.S. Central IRB approval. Sites will be open for screening subjects in coming weeks in the United States. In the next few months, we expect that component or authority approvals, ethics committee approvals and site initiations will follow in the European countries targeted for the study. As shown on slide six, OPuS-2 is designed as a randomized parallel cohort placebo-controlled trial, taking two dose regimens of 4161, mainly 300 milligrams, three times a day and 500 milligrams three times a day. We plan to enroll approximately 100 subjects with HAE, randomized one to one to one across the three study arms. Each subject will receive 12 weeks of blinded study drug. The qualifying minimum attack rate has been liberalized compared to OPuS-1 but in other respects, the entry criteria are similar. OPuS-2 is powered at 90% to detect the benefit in reduction in angioedema attack rate as similar in magnitude to the proportional reduction seen in the OPuS-1 study. A full range of secondary efficacy measures will also be studied including quality of life and utility measures. We anticipate the trial will take about one year to complete through to reporting top-line results. OPuS-2 will use the soft gel product…

Thank you, Bill and good morning. Today I’d like to summarize the key elements of our third quarter and nine months 2014 financial results. As mentioned in prior quarters, our financial focus is on a single guiding principle, focusing our cash resources on the advancement of our core development programs to value-creating milestones and prudently managing expenses. Following our successful $107 million capital raise, I’m pleased to report our balance sheet is in a strong position and that we will remain very disciplined in deploying our cash. On slide 10, you see that revenue for the third quarter of 2014 was $3.2 million reflecting an increase from $2.4 million reported in the third quarter of 2013. This increase is the result of higher collaborative revenue from our BCX4430 development contract with NIAID, which has recently increased in value to approximately $29 million. The NIAID-related collaborative revenue more than offsets the decreased level of collaborative revenue under our BARDA RAPIVAB development contract as compared to 2013 following the conclusion of development activity in the June 30, 2014 expiration of that contract. Third quarter 2014 R&D expense was $13 million from $7.7 million in the third quarter of 2013. This increase was primarily associated with our HAE and 4430 programs, but was partially offset by decreased expenditures for RAPIVAB development due to the completion of development activity. General and administrative expenses for the third quarter of 2014 increased to $1.8 million compared to $1.6 million in 2013. The increase was due primarily to additional costs associated with RAPIVAB commercialization in order to make the drug available in the upcoming influenza season should it receive FDA approval. Moving below the operating line, we incurred $1.2 million of non-cash interest expense in the third quarter of 2014 and 2013. We also recorded a mark-to-market…

Thank you, Tom. So, in summary, what should you take away from today’s call? We’re well-positioned to reach important milestones from now to the end of next year, specifically before year-end, we expect to initiate the OPuS-2 trial in HAE patients; start a second non-human primate study; and a Phase 1 human safety study for 4430. And finally, we expect a decision by the FDA regarding our NDA for RAPIVAB by the PDUFA date. Looking out next year, we plan to complete a pre-clinical development of our second gen HAE compounds; file and IND; and move into Phase 1 safety studies during the second quarter of 2015. And finally and perhaps most importantly, we plan on reporting our results of the second gen Phase 1 in the third quarter and OPuS-2 by the end of 2015. We look forward to providing you with further updates as we reach these important milestone. So, that concludes our prepared remarks. And we are now ready to take your questions.

(Operator Instructions). Our first question comes from the line of Brian Abrahams of Wells Fargo Securities. Your line is open.

Hey guys, thanks for taking my questions. I wanted to drill down a little bit more on the OPuS-2 trial design. I was wondering if you could maybe talk a little bit about the rationale for using two different doses in that study. When I circle back and look at the prior data, I guess the 300 mg, the lower dose would equate to about 240 mg of the prior formulation; and I guess you tested a 200 milligram dose that where the targeted concentrations were -- I guess the concentrations were above your target range for a substantially shorter period of time as compared to the 400 mg and 800 mg doses. And so, just wondering the rationale for testing that dose and what gives you confidence that using 300 mgs TID will enable substantial sustained kallikrein inhibition?

Hi, this is Bill. I’ll start with a few points. Thanks for the question. So, I think let’s frame up the study first. So, this is a study that had two doses. The study will be successful if the 500 milligrams three times a day dose shows a statistically significant improvement compared to placebo regardless of what the 300 milligrams three times a day dose arm shows. If the 300 milligrams three times a day arm also shows an improvement, that’s very important to know. And it’s very helpful to understand what proportion of patients might benefit from a lower dose. So, obviously regulatory agencies are very interested in sponsors evaluating more than one dose, that’s written into the guidance documents in fact. And I think that as we go to the market, it’s helpful for us to know what the distribution of response look like. We are expanding the patient population and neutralizing the entry criteria. So, now the 24 subjects we had in OPuS-1 had very high attack rates than not typical of HAE patients. And as Dr. Maurer explained in our call discussing the OPuS-1 results, as we go to a broader patient population we may actually need less drug to get to enough total Kallikrein an additional level in the drug to be of benefit. So, I think they are doing good drug development reasons study of lower dose. And it’s a sensible thing to do at this stage.

Yes. I from a commercial perspective if we could develop lower doses affected in some patients because we know with the other prophylactic agents are out there that both physicians and patients play around with dosing. So, from a commercial perspective that would be very, very important to know.

Okay. That’s very helpful. That makes sense. And then, did you get any feedback from the FDA as to whether OPuS-2 could potentially be part of a regulatory -- registrational package. Could OPuS-1 and OPuS-2 serve as two randomized studies sufficient for approval or did you get any clarity or that really wait until we see results, and then you can go from there?

I think in general, it’s always good to see results as you’re making those decisions, but we take that feedback that two adequately well-controlled studies would be necessary for licensure. And so we’re designing OPuS-2 in a way that that would be one and for conservative planning purposes we believe that there will be another that will be necessary. Depending on what we see with OPuS-2 we may go back to the agency and bring forward if it’s really robust results we may say that this OPuS-1 could be adequate for filing, but again we’ll have to see that. I think we want to try to set expectations before that this is a division that follows the guidance very carefully. And so, therefore, I think for realistic purposes, we should assume that it’s OPuS-2 and another study.

Makes sense. And I assume that that’s nothing specific to 4161 and that’s really their view on the development for any new HAE drugs?

Yes. Yes, that’s correct.

Okay, great. I’ll hop back in the queue. Thanks again.

Our next question comes from the line of Charles Duncan of Piper Jaffray. Your line is open.

Hi guys. Thanks for taking the question. Congrats on the progress. I wanted to ask you a little bit more about OPuS-2 in part to get better understanding of the design. Bill, you said approximately 100 patients, 32 patients per arm. Can you share with us a little bit more color on what your baseline expectation is in terms of attack rate, but also in terms of the magnitude of benefit I think you’ve referred to it, but I didn’t catch an actual number. How did you power this study?

If we go back to the results of OPuS-1, the primary endpoint was adjudicated attack rates and we had an attack rate of 0.82 in the 4161 period compared to 1.27 and we discussed that in the previous call. So, the difference is about 0.45. So, if you think about that in a proportional sense, it’s 0.45 divided by 1.27 that gives you a percentage. So, we’re also able to look at the standard deviation of the attack rate in that study and I think that’s the reasonable thing to plan for parallel assumptions. And if you then go to slide 5, you can see that the standard deviation in the first period, which is if you like that can be viewed as a parallel design segment of OPuS-1, you can see the standard deviation on both placebo and 4161 was 0.7 and you can do the math and see what the proportion of that is. So, I think what we’re doing with the parallel calculations here is despite the fact that we’re expanding the population into a less severely affected group if you like and we may, we’re hoping Dr. Maurer is correct and that the benefit will be even better than we saw in OPuS-1, but we’re not counting on that. So, we’re planning to have enough patients in the study that we will hit an appropriate p value if we see a similar proportional affect comparing a drug arm to the placebo and with the pretty substantial standard deviation.

Okay. And that’s helpful. And then with regard to increased number of sites and increased number of patients to be enrolled, perhaps similar variability, what steps are you taking to reduce the likelihood of potential compounding variables with regard to those patients coming in and advertising a certain attack rate or whatever?

Right. It’s a good question, it reminds me of the old sore about why the bank robbers rob banks, because that’s where the money is. So, I think that with regarding to setting up clinical trials, you have to have patients with the disease that are going to getting events that you need to measure. So, we were very successful at doing that in OpuS-1. I think that there were two reasons for that. One is we were strict about the eligibility requirements and strict about documenting the patients actually had that attack rate. So, we’re taking the same type of approach in OpuS-1, it’s more diverse, because we are doing the study in both United States and we’re also expanding the number of countries in Europe; it was just Germany and the UK in OPuS-1, we’re going into more countries. So, patients will be able to qualify for the study either by having great medical records that really do tell us just like they did in OPuS-1 that the patient has the qualifying attack rate or if they are not adequate or don’t exist, then the patient will enter a screening running period and we’ll prospectively document if they’re having the attack rate to quality some sort of study. So, I think that that’s the number one thing that you have to have in order to run a study like this. The other aspects of operational execution, we’re going to pay just as much as attention as we get in OPuS-1 with regard to education of investigators and site personnel, site initiation visits and hands-on management of the study. So that will be to the same high standards.

Okay. And then my final question is regarding the duration of dosing, 12 weeks versus four seems like a good thing in terms of signal to noise. But I’m wondering if you have detected or have any reason to believe that there could be a difference in sensitivity to the drug over time, what do you anticipate in terms of that duration of treatment?

So, we didn’t -- yes, it’s interesting question and I absolutely agree that 12 weeks gives you more opportunity to see the attacks you need in order to detect the treatment effects. So, longer duration studies are very helpful in that regard. I think that in the biology of kallikrein, pre-kallikrein and contact activation and the way our drug works, we don’t see any reason to think that there would be a loss of effect over time or improvement in sensitivity to the drug over time. I think that what we’re trying to do here is to restore the normal phenotype of kallikrein inhibitory content in the blood. And I think we’ve made progress with our first generation content 4161. It looks like a real drug to us. And we’re actually very excited about implementing Opus-2. We’re not counting on an improvement in the way we plan the study.

Thanks for the added color, Bill. I’ll hop back in the queue.

Our next question comes from the line of Mario Corso of Mizuho. Your line is open.

Good afternoon. Thanks for taking my questions. A couple of things I wanted to ask about. In terms of the pill burden for 4161, I know there is no certainty yet, but if you could talk a little bit about how you see that looking or even a range of how that might look? And then in terms of OPuS-2, will there be an extension? Is there a design to get some longer term exposure from the study? And then thirdly, on peramivir, has there been any substantive FDA interaction besides waiting for an inspection that potentially could push the PDUFA out, say 90 days, or do you feel very certain that you’re going to see a decision in the next month? Thank you.

So I’ll take the pill burden one; Bill, you take the second one; and then, I’ll come back to the FDA RAPIVAB question. So, on the pill burden front, sort of the five capsules, three times a day for the 500 milligram and three capsules three times a day for the 300 milligram. As Bill mentioned, we have formulations where we have higher concentrations of liquid been able to be put into the capsule. And so getting back to the four capsules for the 500 milligram, I’m very, very confident we’ll get to that point and I think we can get even lower with that approach. And then we’re also exploring other technologies that could bring it down even further, too early to talk about at this point in time. But stay tuned. But we are really committed to bringing the capsule count down and so far, so good.

Yes. So with regard to the ability to have a rollover study, not at this stage, because the chronic toxicology to support that isn’t completed; it will be completed by the end of next year. Assuming that that supports the safety of chronic administration in people, they will be able to start to a long-term safety study. So, the opportunity for a rollover probably isn’t there and that would require a waiver of some type from the regulatory agencies.

So, with regard to your question about the interactions with the FDA there have been a bunch and as you probably know I think it’s from PDUFA 5, we now have a mid-cycle interaction, formal interaction with the FDA and then a late-cycle both of those have been completed. We’ve largely negotiated the labeling for the drug. And so, the big remaining issue is the manufacturing that we’ve been communicating all along. And as I said in my prepared comments, the inspection process is underway with our plant in our CMO, but we’re not in control of either the process or the timing, so I can’t give you a whole lot of insight beyond that. I mean the good news is with the amount of time left between now in our PDUFA date, at least the process is a routine process in terms of the inspection. Did I answer your question Mario?

Yes. Thank you.

Thank you. Our next question comes from the line of Steve Byrne of Bank of America. Your line is open.

Hey, Bill, I was wondering if you thought the reduction in bioavailability of the capsule formulation could have an increasing affect on the standard deviation of responses.

No, I think we’re going to hit the same exposure because of we’re giving more milligrams and the PK data from the relative bioavailability study supports that approach. So, I am not anticipating that that would have any influence on the standard deviation. I mean it’s certainly possible, but I’m not anticipating that.

Okay. And what are your thoughts about or at least considerations of perhaps a higher dose rather than a lower dose? Is that something that you consider notwithstanding the pill burden, but your comments on that and whether you think maybe a dose escalation study might also be worthy given the variability in responses maybe some individuals just need a higher dose because their particular bioavailability is lower?

Yes. We thought about that Steve after OPuS-1 and we beat that around quite a bit internally and with our experts and key opinion leaders. And the decision was given the robustness of the results and this just really high attack rate frequency population that we felt that the profile look pretty good with the dose that we had. You know from the Phase 1 that when you get up to much, much higher doses, I believe it was 800 milligrams that you start to see some side effects from the excipients and the formulation. So, don’t want to go to that. And then there is a saturable absorption mechanism. So, I think we’re at the point where we’re real comfortable that from the efficacy profile where we’ve got the high dose that we need. And at the end of the day, as I said earlier, physicians and patients may play around the dose again, but I’m less concerned about it on the upside than I am on the downside.

And then I had a question on the 4430 data in these macaques. Do you have any view on what might be limiting the efficacy and whether you just simply need to go higher doses or is it a dose frequency issue?

Yes, thanks for the question. I think it’s worth keeping in mind that this is just the first experiment. There is a nice review paper that came out this year that lists all of the monkey experiments published for of all the things that are being tried in either Marburg viruses or even Ebola virus disease models in monkeys. And for example, monoclonal antibody campaigns -- there is total of six experiments; three in cynomolgus monkeys and three in rhesus monkeys. So, it’s hard to answer every question in a single experiment in the BSL-4 facilities. The number of animals that you can put in those facilities is quite limited. It’s a huge amount of work to do each one of these studies. So, I think we’re happy that we’ve learnt something from the first study which is there does appear to be an effect. It’s statistically significant prolongation survival and an antiviral effect. You could be right that it might be simply be a matter of being on the cost of getting the right dose to maybe a higher dose will result in survivors. So that’s a typical hypothesis. So, we’ll be putting a higher dose regimen into the next study. The other interesting thing is that these models are really very aggressive. And up to the introduction of the monoclonal antibodies and 4430, there were no examples of experiments with survivors when the interventions were introduced more than -- after the first date. So, I think that we have very aggressive models the rhesus model seems to have slightly slower progression than the cyno model but in both cases, the rapidity of the disease is way faster than it is in humans. That to get an answer but I think that this having a result with a solid anti-viral effect and some survivors I think would give people grounds for hoping that there would be a treatment effect in human, the human disease is more slowly evolving and there is more time for the immune system to kick in.

And the mortality rate is different too.

Yes, that’s right. So, very, very rare to get a surviving monkey in the control groups in these experiments. And as you, obviously it’s a very bad outbreak, fortunately I guess there are survivals. And the survival rate in Africa is about -- it has been quite a good, about 30%. So, I think that they’re very, very high stress models. And we’ve taken the first step and we look forward to getting a lot more information from this study and also from completing the next study and let’s try to move the ball forward. And the goal here is to do better obviously.

And just one more from me on OPuS-2, what’s your (inaudible) and where you think the average attack frequency might be given the relaxed entry criteria?

We are not going to be very specific about the entry criterion, because I think just like you see, it’s so boring; we don’t want to have people try gain the system in terms of getting into a study. But now I think in 12 weeks, you can look back at the synchronized data and you could imagine that list study in the New England Journal would have had time results, even if the attack rate had been quite a bit lower than what was reported. So there is a good opportunity to see attacks. I mean you could take the example of OPuS-1. If we see a similar number of attacks spread out over 12 weeks that’s probably just fine, right?

Okay. Thank you.

Our next question comes from the line of Christopher James of Brinson Patrick Securities. Your line is open.

All right, thanks for taking my questions and congrats on the progress this quarter. My first couple of questions relate to OPuS-2. Just given the longer duration, the 12-week versus four-week, do you anticipate any issues with off-target effects? How do you think about the effects on bleeding time with the longer duration and new formulation?

Thanks for the question. So, I think we’ve answered the anticoagulant off-target effect question definitively already. As a former practicing hematologist, the prothrombin time is a very valuable assay and the we know from the accumulated non-clinical and clinical data now that the concentrations of the drug that we make to effect the prothrombin time is so far above what’s achievable with oral dosing of this drug in humans, so that’s a non-issue. And we’ve got hundreds of prothrombin time evaluations from the Phase 1 and OPuS-1; obviously we’ll continue to do them. But I am very, very confident that continued administration for any period whatsoever is going to be safe from the perspective of anticoagulant off-target effects. One of the reasons you go progressively from short duration to longer duration studies obviously is because you can’t predict the other potential off-target effects of new drugs; it’s part of the testing paradigm. So, we’ve built-in comprehensive safety evaluations of course, but there is nothing in the Phase 1 nor the OPuS-1 data that makes us worry.

Yes, and we’ve done the 13-week talks just to allow us to be able to do the 12-week study. And as Bill said in his remarks, we’re studying six to nine-month.

Great. That’s really helpful. And I know you won’t comment on the minimum attack rate for your entry criteria, but maybe can you discuss the distribution of patients, maybe with respect to the lower attack rate that you’re targeting I guess from the literature, what proportion of patients with a JED, I think fall within that range that you’re going to be targeting?

So, I think I don’t know the answer to that question. I think that what I can tell you is that we anticipate that finding patients for the study proportionally will be less of a chore than it was for OPuS-1. On the other hand, it’s still going to be chore, because it always is. So, it’s always a challenge to recruit patients into any sort of orphan disease indication study. Sometimes by the way it’s a challenge even in run of the mill conversations. So, we’re putting a lot of efforts into identifying the sites that have the patients and are enthusiastic about the study. In the U.S. we’ve worked very closely with the patient efficacy groups to understand how they might be able to help recruitment for the study and the like. So, I think that like last year at this time when we’re about to getting to OPuS-1, it’s always hard to predict exactly how enrollment will go. But we will put our best effort behind it and we feel comfortable in setting out the time line that we did on the call.

And Bill isn’t it safe to say that as our clinical program progresses, we’re going to move closer and closer to the general population of HAE patients.

Yes clearly, I think your average patient out there in the community, they might or might not qualify for the study. There are plenty of patients out there who have very, very infrequent attacks that’s way less frequent and back every three months. Clearly they are not going to be able to qualify for the study.

Great. That’s really helpful. Thanks for the clarity on that and congrats again on your progress.

Thank you.

Our next question comes from the line of Rahul Jasuja of Noble Life Science Partners. Your line is open.

Hey good morning guys. Thanks for taking my question. My first question really is a clarification probably stemming from my ignorance here. So, when moving from the hard gel to the soft gel capsules, was there an expectation that the bioavailability could be that much lower? Could you sort of explain that and what were the advantages you were expecting going to the soft gel?

Well, so the hard gel thing was really only a temporary maneuver to enable us to do the OPuS-1 study. And so we’ve been develop working on soft gel formulations and succeeded. So, I think that in order to get the stability we need, there were certain changes we had to make into the excipients in liquid formulation. Whenever you do that, you can’t predict the result in terms of bioavailability and you need to do a relative bioavailability study. So, I’m not sure I was anticipating one direction or the other. You just have to do the experiment and find out the answer. I’m not worried about the 20% difference in bioavailability, I think you can fix by giving more milligrams.

Yes. The important thing is that we know that we’re getting similar exposure to OPuS-1. That would have been done faster if we went into the study not knowing that and then we found out that we had less exposure.

If that’s the -- if that excipient mix soft gel type of combination progresses and we can make it more concentrated, we’ll continue to pay close attention to those types of issues to make sure that whatever the final dosage form used that we’re getting the exposure we need.

Okay, that’s fair. And then the other question I had was, the upcoming trial compared to the OPuS-1 study obviously has patients that have a lower attack rate, and then potentially we had discussed that that population versus the high attack rate could do better given the low bioavailability with 4161. But then facing the fact that compliance was really excellent in the 28-day study with the higher attack rate patients. How would you sort of address the issue of compliance with patients that maybe are less driven, have less attack rates, and also heterogeneity in the population given the low bioavailability?

Yes. I don’t think you should think that people are less motivated if their frequency of attacks is less frequent. One attack is bad, really bad. And so, I would say in general what we’ve heard from patients what we’ve heard from physicians is that these are, these patients across the board whether it’s profile of OPuS-1 or OPuS-2 or even less frequent attack. These folks are very, very discipline at managing their disease, I mean think about it the prophylaxis treatment right now is every three to four day an IV infusion. So yes, we’re not worried about the discipline of these patients managing their disease.

And so, I think that just I said expectations, the amazing compliance that we saw in OPuS-1 is how about to need again and again and again. So, I’m not necessarily -- I’m not counting on that. But what I’m counting on is the diligence of our team and the investigators and the study staff to help drive attention to detail around taking the medicines. So, we’re taking every measure that you can think of to remind the patients who graciously agree to coming to the study to take their randomized medicine. And we’ve built in the study visits that you can see on slide six to reinforce that message as well as to do usual safety and other required follow-up and supervision that driving -- taking the medicine in any study with an oral medicine is one of the top priorities in execution.

Okay. And then, the other sort of sub-question there was, I mean there was significant heterogeneity in patient response in the OPuS-1 study, and that was due to poor bioavailability. I am asking a tough question, but do you think that the response and the heterogeneity and response in this lower attack rate population would be expected to be any different; would there be -- would be more homogenous, I mean what are your thoughts?

Okay. So, you’ve mentioned the bioavailability couple of times. Just to be clear, I don’t know of any reason to expect any difference in the distribution in bioavailability between OPuS-1 subjects, OPuS-2 subjects or any other subjects with HAE for that matter or any other group in the population by the way. So, I think that we don’t have any biology or science that would suggest that the bioavailability would change from one group to the next to the next. I think that the heterogeneity in response and the heterogeneity in attack rate, we’ve built-in what we believe our conservative estimates. So that type of thing into the power calculation to the study. So, I feel very, very comfortable about getting -- targeting 32 patients par arm for statistical purposes. If we get out a blank piece of paper and cover up the right hand side of slide five and look at the left hand side, that’s 12 patients per arm. And we’re seeing a pretty profound difference. And we’re having three times that many approximately. So, I feel pretty good about the [type of those].

Okay, very good. Thanks. That’s helpful.

Thank you. Our next question comes from the line of Ed Arce of Roth Capital Partners. Your line is open.

Great, thank you for taking my question. Most of them have been asked, but I have a couple. First with OPuS-2, assuming that 500 milligrams three times a day is ultimately the right dose going forward into potentially another trial or registration and assuming as you said, you’re very confident in breaking down the pill burden at that dose down to four pills per day or four pills per three times a day, it seems we’re back essentially the 12 dose per day that we saw in OPuS-1. And I’m wondering if that ultimately stands as the final pill burden, how do you think about that in terms of the commercial effect? I grant that this is a disciplined group of patients, but just your thoughts on that.

Yes, I mean I think what’s really important here is this is not hypertension; this is not high cholesterol; this is not reflux or something like that. This is HAE attacks and preventing them. And I feel like sometimes it sounds like a broken record but I’ve talked to more patients and physicians, and there are people that don’t like needles, period in this space. And they’re worried about vein fatigue and whole bunch of other things. And so there will be a population, even if it’s five capsules three times a day, there will be a population. Now, I’m confident that we’re going to get that capsule countdown per dose, but I can’t just stress enough that the desire for an oral makes the willingness to take multiple times a day multiple capsules much better.

Okay, one other final question I guess is you expect OPuS-2 to run about a year. And so my question is, do you think it likely that we could expect top line results by the end of 2015 or would it more likely be early 2016?

We’re shooting for the end of 2015.

Okay, all right. Thanks.

Yes.

(Operator Instructions). Our next question is a follow-up from the Charles Duncan of Piper Jaffray. Your line is open.

Sorry, guys. My questions were all answered. Thanks.

And so, I’m showing no further questions in the queue at this time. I’ll turn the call back to Jon Stonehouse for closing remarks.

Great, thank you. We’ve been working hard over the last quarter, since our last call. And I think as you look at this call, it’s about how we’re setting ourselves up for next year. Next year is a very exciting year with important studies and programs advancing. I mean if you think about it, we were really and one clinical trial this past year and now we’re at multiple programs in the clinic next year. So, it looks like it should be a very exciting year for the company. And so, as always, we appreciate your interest in BioCryst. And have a great day. Thank you.