Esperion Therapeutics Inc (ESPR) 2014 Q2 法說會逐字稿

Good day, ladies and gentlemen, and welcome to the Esperion Therapeutics second-quarter 2014 conference call.

(Operator Instructions)

I would now like to introduce your host for today's conference, Ms. Mindy Lowe with Esperion. You may begin.

Thank you, Andrew. Good day, everyone, and welcome to the Esperion Therapeutics second-quarter 2014 earnings call.

I'm Mindy Lower from Esperion, and with me today are Tim Mayleben, our president and CEO, Roger Newton, our chief scientific officer, Marianne Andreach, our vice president strategic marketing and product planning, and Rick Bartram, our controller. We are also joined by the newest member of our team, Narendra Lawlani, Esperion's executive vice president of research and development and chief operating officer.

As a reminder this call is being recorded. To access the playback of this website, please go to the investor section of Esperion's website at www.Esperion.com. I would like to remind callers that the information discussed on the call today is covered under the safe harbor provision of Private Securities Litigation Reform Act. I caution listeners that the Company's management will be making forward-looking statements.

Actual results could differ materially from those stated or implied by our forward-looking statements due to the risks and uncertainties associated with the Company's business. The forward-looking statements are qualified in their entirety by the cautionary statements contained in today's press release and the Company's SEC filings. The content of this conference call contains time sensitive information that is accurate only as of the date of this live broadcast, August 12, 2014

Esperion undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this conference call. We issued a press release earlier today detailing the content of today's call. A copy can be found at www.esperion.com within the investors section. We will begin with prepared comments from our teams, and then we will open your call for the questions.

Following today's call, the management team will be available for any follow-up questions. Please e-mail me directly at MLOWE@Esperion.com, and I will schedule 15 minutes for you and the team.

Now I'd like to turn the call over to Esperion president and CEO, Tim Mayleben. Tim?

Thank you, Mindy.

I hope you are all enjoying the summer, and I would like to welcome you all to our call and thank you for joining us today as we provide you an update on the second quarter of 2014. Before we get started, I wanted to provide a brief introduction of Dr Narendra Lawlani, who as Mindy mentioned, is Esperion's new executive vice president of research and development and chief operating officer.

For those of you who may not remember, Narendra worked with Roger, Marianne, and others on the development of Lipitor at Warner-Lambert Parke-Davis. He was part of the original Esperion, where he was vice president of drug safety until its acquisition by Pfizer in 2004 and most recently chief scientific officer at Cerenis Therapeutics. We are very happy to have Narendra back with the Esperion team, and we welcome his deep drug development experience and key insights as we advance the development of ETC-1002.

As many of you know, we held our inaugural analyst day two weeks ago. A lot of material was covered during almost three and a half hours of presentations by several of the world's leading experts in their fields. The half-day session has been very well received, and we have heard from many of you that you came away with both new insights and answers to many of your questions.

With that in mind, and for those of you that were not able to attend or watch the webcast yet, I want to start today's call by providing just a few highlights from that event. Next, I will provide a brief update on the 1002 development program and remind everyone of the key dates for our upcoming results and milestones. Rick will review highlights from the second quarter 2014 financial results, and then we will open the call or your questions.

Let me start with highlights from our analyst day, Dr. James McKenney kicked off the event by reviewing the long history of LDL-cholesterol as a biomarker. He then provided really a history lesson in LDL-cholesterol management reminding us that 1985 marked the inception of the NCEP, or the national cholesterol education program and also the adult treatment panel one guidelines, which were the first ever LDL-cholesterol guidelines.

He also reminded us that there has been a 60% reduction in deaths from cardiovascular disease over these past 30 years, really since the initiation of NCEP. But even with all that progress, cardiovascular disease is still the number one cause of death in the US today, and LDL-cholesterol is the number one modifiable lipid risk marker, which is why we are focused with 1002 on lowering LDL cholesterol.

Finally, he reviewed and provided a perspective on the 1002 development program to date, which includes seven completed, phase I and phase IIa clinical trials. Dr McGovern, Dr Mark McGovern took the podium and reviewed Esperion's three ongoing phase II clinical trials of 1002 and importantly, provided some context both as a physician, and as a very successful lipid drug developer for each of our ongoing clinical trials. For the first time, he also summarized our initial thoughts on the phase III program for 1002 in statin intolerant patients.

Next, Dr. Jamie Unterberg spoke about statin intolerance from a practicing physician's standpoint. He emphasized that statin intolerance is a real problem, and his best estimate is that 10%, 10% of patients who have taken a statin are statin intolerant. This is based not only on what he has seen in his own patients, but also his review of the medical literature.

A video on statin intolerance featuring Dr Paul Thompson, who you should probably remember from the AHA last year, and is from Hartford Hospital, is an expert in statin intolerance. And he was featured in this video, along with two patients from Dr Thompson's practice, who are statin intolerant, and, for the first time as we like to say, help to put a face on statin intolerance. I encourage you to watch the video if you haven't had a chance to see it yet.

After a short break, Dr Greg Steinberg and Esperion's Steve Pinkoski outlined the novel first in class dual mechanisms of action of 1002. For the first time for analysts and investors, they revealed the more than 40-year history of ATP citrate lyase as a validated target for atherosclerosis research and the more recent and intensive research into AMP kinase as a validated target. They also spoke about the relevance of this research to atherosclerosis and LDL-cholesterol and its translation to our clinical results.

And, finally, Dr Peter Libby, the world's leading experts on inflammation and cardiovascular disease spoke about the importance of inflammation in atherosclerosis, and why lowing hsCRP, a key risk marker of inflammation is so important to the management of cardiovascular disease risk. Of note, only statins and 1002 have been shown to consistently lower both hsCRP and LDL-cholesterol.

As I highlighted during the analyst event, interest in 1002 is continuing to build, and we think there are a number of reasons for that. First, 1002 is novel, and it's first in class, and we are way ahead of anyone else in development. As I mentioned, ACL and AMPK are well-validated drug targets. 1002 is an oral once daily pill in a bottle, which is the standard of care in all of the successful LDL lowering therapies, where convenience of dosing and ease administration have always been important in this area.

The thing you have to remember about this disease is that unlike diabetes, for example, patients with high LDL cholesterol or atherosclerosis typically don't feel bad if they don't take their medication. So convenience of dosing is important.

1002 is a small molecule with low relative cost of goods. And this is important in what we are seeing as an increasingly economically constrained payer environment. The phase I and phase IIa data for 1002 have been very promising. 1002 lowers LDL cholesterol by 27% to 40% and hsCRP by a similar amount, the only drug other than a statin to consistently do both. 1002 has been very well tolerated, especially notable in statin intolerant patients. And 1002 is in a late stage clinical development program.

Unlike many therapeutic indications, LDL-cholesterol is a well-validated biomarker and 1002 lowers LDL cholesterol 27% to 40%. With LDL-cholesterol lowering therapies, what you have to remember is that what you see from an efficacy standpoint in phase I and phase IIa is what you see in phase IIb and III. The path to FDA approval with LDL-cholesterol lowering is well trodden, plus 1002 lowers hsCRP similar to a statin, and from a safety standpoint has demonstrated positive effects on blood pressure, another very well accepted biomarker for lowering cardiovascular disease risk.

Finally, as we heard at the analyst day, statin intolerance is real, and it's a huge and growing problem. So, let me walk through some numbers for perspective. You have heard us say 70 million people in the US have high LDL cholesterol levels or hypercholesterolemia.

Approximately half, or 35 million people need to take therapies to lower their LDL-cholesterol levels and correspondingly reduce their risk of cardiovascular disease. Now we are the first to acknowledge because of our history in this therapeutic area that most patients can take a statins, but with those numbers, and up to 10% of patients not being able to tolerate a statin at any dose, and many others only able to tolerate statins at a low to moderate dose, that don't get them to their LDL cholesterol-lowering goal, this is an estimated 2 million to 7 million patients.

Statin intolerant patients and their physicians, which as you heard us say are most typically the lipidologists and specialized cardiologists need new alternative inexpensive oral therapies that can provide them statin-like or 30% to 40% lowering of their LDL cholesterol and hsCRP levels, but without the side effects that they experience with statins. We experienced the 1002 can fill that need.

We believe that 1002 can be that alternative, and we believe that 1002 is the right drug in development for LDL-cholesterol lowering at the right time for this statin intolerant patient population, a patient population that has high unmet needs and deserves more effective, better tolerated oral therapies. Let me shift gears now and briefly update you on the 1002 development program. Our largest clinical trial, the 349 patient phase IIb 08 statin intolerance study has completed last patient last visits, and our CRO has begun the trial wrap of activities.

We are on target to report top line results from this study in early October. Our second phase IIb clinical trial, the 132 patient 09 add-on to statin study will complete screening and randomization of patients this quarter. Now, this is a few weeks behind where we had hoped to be, and as a result, we are now projecting the 09 top line results will be available in Q1 of 2015, rather than the very end of -- I'm sorry, the very end of Q4 2014.

Finally, our third ongoing phase II clinical trial, the 144-patient 014 study in patients with both hypercholesterolemia and hypertension was initiated earlier this quarter. Enrollment has started out well, and top line results are expected to be available in Q2 of 2015. Shifting gears once again to the non clinical front, we told you in May that the long-term safety reports were complete, and we can now tell you that they have been submitted to the FDA at the end of June.

Finally, I'm pleased to report that we are on target to complete and submit reports from our two-year carcinogenicity studies to the FDA in December of 2014. These are important milestones in the continuing development of 1002, and all of them serve to continue to enhance the value of the 1002 program. The bottom line is this, we grow ever more confident that 1002 could play an important role in cost-effectively and conveniently providing LDL-cholesterol lowering to patients with hypercholesterolemia and a history of statin intolerance, a patient population with a very high level of unmet medical needs.

I will now turn the call over to Rick for review of the financial highlights from the second quarter. Rick?

Thanks, Tim.

As of June 30, 2014, Esperion had approximately $67 million in cash and investment securities and approximately $5 million in debt outstanding under our new credit facility. Our net loss for the six months ended June 30, 2014 was $17.1 million compared to $11.2 million in the prior-year comparative period. The change is primarily related to increases in R&D costs for the advancement of 1002 in the 08 and the 09 studies and increases in public company operating costs.

We currently have 15.4 million shares of common stock outstanding, with another 1.8 million to be issued upon the exercise of options and warrants. Lastly, I want to make a few final comments are those of you with final -- financial projection models for our business. As we reported earlier today, EPS for the three and six months ended was a loss of $0.60 and $1.11 per share respectively.

We expect our R&D costs for the remainder of the year to be approximately $18.5 million. We expect our G&A cost for the remainder of the year to be approximately $5 million. We also estimate our full-year EPS will be a loss of approximately $2.60 per share. As we stated on our last earnings call, we continue to expect that our current cash, cash equivalents and investment securities will be sufficient to fund our operations into early 2016.

With that, I'll turn the call back over to Tim.

Thanks, Rick.

Before we open the call to your questions, let me just highlight a few of the key dates, or reiterate a few of the key dates for the month ahead. In early October -- in early October of 2014, we will report top line results from the phase IIb 08 clinical trial in statin intolerant patients. In December -- December 2014, we will submit the two-year carcinogenicity reports to the FDA.

In Q1 of 2015, we will report top line results from the phase IIb 09 add-on to statin clinical trials. And in Q2, 2015, we will report top line results from the phase II 014 clinical trial in patients with hypercholesterolemia and hypertension. As you can tell from our comments today, Esperion will continue to report very meaningful data from the 1002 development program each quarter over the next year.

We will now open the call to your questions. Andrew, if you would, please poll for questions.

Certainly.

(Operator Instructions)

I'm showing our first question or comment comes from the line of Mr Jason Butler with JMP Securities. Your line is now open, sir.

Hi, thanks for taking the questions and congratulations on the progress this quarter. Just a first question on enrollment in the 009 study. Anything -- any more color there that you can give in terms of have you had any challenges specifically enrolling patients, or is it simply that your estimates were just a little on the aggressive side for the enrollment period.

This is Tim, Jason. Thanks for your question. I will start out and Narendra, if you want to add anything, please do. But the bottom line is that in any of these trials, we make estimates in terms of the number of patients and screen failure rates and number of centers we need to accomplish our goal over a certain time frame, an enrollment goal over a certain timeframe.

And in our case, I think in the 09 study, we started out with perhaps too few centers. We started out with, I think, about 30 -- 25, 30 centers. We subsequently bumped that up to about 40 centers and have experienced much better enrollment by the increased number of centers.

But I think -- again, I think our estimates perhaps were a little bit more aggressive and again, it's not a huge delay, but because of the timing, the original timing of the 09 results, I think we have pretty consistently said by the end of the fourth quarter, 2014, any slippage in the timeframe was going to push the results into the early part of the first quarter of 2015. And that's exactly what we are seeing.

So we have seen much better enrollment. Like I said, we got off to a little bit of a slow start by not having an of centers and estimating a screen failure rate that was a little bit on the lower side compared to what we actually experienced, and so that is the result. And that may be more detail than you were even looking for, but that is the bottom line.

That's helpful. Thanks a lot, Tim. And then just on the study in hypertensive patients, can you just give us a little bit more color on the rationale for that study and the data that you have so far that supports why you think 1002 can be useful in that patient population?

Sure. Thanks again for that question, Jason.

As we have been saying, we are not, we're definitively not developing a hypertensive drug. So maybe to start out with that definitive statement. To take folks back to the phase IIa program, clinical program, we did a safety analysis of blood pressure in the phase I and phase IIa results.

When we look at the phase IIa results retrospectively, a retrospective analysis, we noticed that not only were we not worsening blood pressure in these patients, but in patients that had higher levels of blood pressure, not necessarily hypertensive, but that had greater than normal levels of blood pressure, we were actually reducing systolic blood pressure in a statistically significant manner.

So as is common when you see a retrospective analysis and you are doing good drug development, we turn that into a prospective hypothesis, and that is the hypothesis that we are testing in the 014 study to look specifically at patients that not only have hypertension but also hypercholesterolemia. As you may recall, Dr Mark McGovern had reminded us that the overlap for those two conditions is something on the order of about 45% to 50%. So they are co-morbid conditions in many patients.

So we look at blood pressure as a safety -- measure of safety. It's also of course one of the most well validated and well accepted biomarkers for cardiovascular disease risk. That is if you lower blood pressure, it is well accepted among thought leaders and FDA that you are also lowering cardiovascular disease risk.

And so we think in the case of 1002, if we can show, as we did retrospectively, if we can show prospectively that ETC-1002 lowers blood pressure in this co-morbid population that that is a -- an exclamation point if you will, on the safety that we've seen so far in the 1002 development program.

Great. Thanks a lot for the color there, Tim.

Yes, thank you for the question, Jason.

And the next question or comment comes from the line of Mr Jonathan Eckard with Citi.

So thanks for the introduction, and, Tim, I don't want to distract from your programs by talking about other programs, such as PC SK9s, but I would like to know when we have details from the IMPROVE-IT trial and when we have details from some of these PC SK9 trials, what are the things that you are most looking forward to, not with regards to competitive landscape, both with regards to regulatory kind of reception -- broader landscape type of things.

What are some of the findings, the bigger picture findings you're hoping to learn from both IMPROVE-IT and some of the PC SK9 data?

That is a great question. Marianne, can I ask you to take initial crack at that question?

Sure, Tim. Thanks. We are paying a lot of attention to IMPROVE-IT as well as the PC SK9 trials that will be reporting out between now and the end of the year. As you probably saw today, it was announced that the IMPROVE-IT results are going to be presented at the American Heart Association, as well as a study from Sanofi Regeneron on their PC SK9 in patients with statin intolerance.

So we look at those studies with -- as you would suspect, a high degree of interest. IMPROVE-IT is a study that is out there to test the hypothesis of the addition of a ezetimibe to a statin. So we are able to learn more about what we might possibly see when you put those two therapies together and whether or not the additional LDL cholesterol-lowering provided by ezetimibe actually would translate into clinical outcome reduction.

No one knows if that happens. We will see that and learn that from the results of the study. From the PC SK9 perspective, especially thinking about the study that Sanofi, Regeneron is presenting, it is clear from the title of the talk that is going to be given at AHA that the design of this is different from other statin intolerance studies that we have seen before in that they have an active, control arm of a statin in the study. So it will be interesting to see not just the efficacy in that study, but the safety perspective and thinking about then what that is going to mean going forward for companies getting indications specifically to reduce elevated LDL cholesterol in patients with hypercholesterolemia who have a history of statin intolerance.

That's great. Thanks.

One other thing, Jon, I just wanted to mention to build on what Marianne was saying. I think one of the things that we always try to remind folks, we think that 1002 is well differentiated from, for example, the PC SK9s that are in development today, because we keep saying it's an oral therapy in the tradition of all the successful LDL cholesterol-lowering therapies in the history of the world.

That is one point of emphasis. I think, secondly that we lower both LDL cholesterol and hsCRP, and then finally, that in a payer constrained, what we're seeing as an increasingly economically payer constrained environment, that relatively lower-cost small molecules, we think will always have a place in the treatment armamentarium for physicians.

And then, from a regulatory standpoint, we always, again, folks on the team have been around long enough to remember that the LDL hypothesis that lowering LDL cholesterol leads to lowering of cardiovascular disease risk is not just the -- it's has not just been the statins, but there have been other therapeutic alternatives that have provided that same data to support that when you lower LDL cholesterol, you also get a reduction in cardiovascular disease risk.

And so we like to remind folks that we are in statin intolerant patients by definition not testing the same hypothesis that IMPROVE-IT is, which is on top of a statin, or some of the other recent trials, whether it's AIM-HIGH or HP S2-THRIVE, all of which were testing a different hypothesis than the one that we are testing in statin intolerance patients, which is primarily LDL lowering in a patient population that has a very high level of unmet medical need as demonstrated by the very high baseline LDL levels you've seen not only in our trial, but in the trials -- the other statin intolerant trials that have been done in this therapeutic area.

So we try to differentiate that the hypothesis that we are testing is different than perhaps what the PC SK9 sponsors are going or any of the recent trials have done, which is always been testing this hypothesis -- hypothesis of incremental LDL cholesterol-lowering on top of a statin. That is clearly not our focus with statin intolerance.

Perfect and then one question is that some of the other, again the PC SK9 in their design of their statin intolerance trials, it seems like in their definition of statin intolerance they have been doing a little bit of backpedaling with regards to what they initially did versus the FDA's definition of statin intolerance. I was wondering, could you outline a little bit of the nuances of your trial design statin intolerance, because you have both statin tolerant and intolerant patients.

Could you maybe articulate some of the potential benefits of including both of those populations and how the findings from this trial could provide you a little bit more insight than maybe somehow the other statin intolerant trials have been designed.

It is a very interesting question. I appreciate you bringing it out, Jon.

So again just to take folks back, so in our 08 study, as Jon mentioned, we are including both statin intolerant and statin intolerant patients in the same study. As far as we can tell from reviewing the literature, this has never been done before. That is looking at both statin tolerance and statin intolerance.

And I just want to highlight that the definition of statin intolerance that we are using is the one that has been promulgated by FDA and has been provided not only to us, but our understanding is to others that are developing therapies in this space, as well. And that is failure on two or more statins, one at the lowest approved dose, secondary to muscle pain and muscle weakness, with that muscle pain and muscle weakness dissipating with the cessation of therapy.

So that is the FDA's definition of statin intolerance. So coming back to the 08 study, we are looking at patients that meet that definition, 50% of the patients in the trial meet that definition, the other 50% of the patients are just hypercholesterolemic with no evidence of statin intolerance. And the value of that is for the first time to see in the same trial whether patients who are statin intolerant respond the same or different to our therapy or our therapy or the active control, which is ezetimibe, or the combination of the two.

So we will get some insight into the difference between those two patient populations, or if there are any differences, Jon. And again, because the study has never been on before, the hypothesis has never been tested, we don't know, the world doesn't know, we are going to find out, and the world is going to find out. I think the other benefit of the trial design is, in our case at the phase IIb study, it's specifically looking at the 120 mg dose and the 180 mg dose of ETC-1002, and then looking at those same doses in combination with ezetimibe.

In the case of the trial, we will get some insight into the doses that we should use in our phase III program and -- which is again a dose range-finding experience that we are going through in the phase IIb program. So we will get insight into dosing levels for the phase III program.

All very helpful. Thank you very much.

Thanks for the question, John.

Our next question or comment comes from the line of Mr. Brian Klein with Stifel. Your line is now open, sir.

Hi, this is Colleen Mackey in for Brian Klein. I have a question for you all about the safety data, the long-term chronic toxicology data and the carcinogenicity data. Just wondering if we will be able to see it before you submit it to the FDA?

And then to follow up with that, I know that you said that at your analyst day that one of the key objectives for your phase III program will be coming up with a safety database. So wondering if you are using these results to start that process, inform that process, and how you might structure the database? And in general, what your thoughts are there going into phase IIIb?

Sure.

Colleen, I will take the last question first and then, Narendra, I'll ask you to respond to the first question after I finish on the last one. So just to remind folks, at the end of our phase IIa program, our human safety database was approximately 300 patients, 317 patients on drug for periods up to 12 weeks and up to 240 mg. We said by the end of our phase IIb program, we will have approximately 750 to 800 patients who will have been on drug, and we will have more than tripled the exposure.

So by the -- that is the patients who have drug exposure. So by the end of our phase IIb program and the end of phase II meeting, we will be bringing a substantially, a substantial, quite a substantial human safety database to our end of phase II meeting. As I said 750 to 800 patients on drug for periods as long as 12 weeks. In fact, most of the patients will have been on 12 weeks of therapy.

And then we will continue to build on that safety database in our phase III program. I think Dr. McGovern at the analyst day, as you had referenced records, had given some indication of what the phase III program would look like, and we are not being real specific about numbers at this stage, Colleen, simply because that will all come clear as a result of our end of phase II meeting with FDA.

But we are experienced lipid regulating drug developers. That's what we have on the team. We certainly understand what the requirements are. We certainly understand what the history is. And so I think we have a good feeling for what that is, and as we get closer to our end of phase II to meeting, we should have better estimates for you.

With that, let me turn it over to Narendra to comment on the nonclinical.

Thanks, Tim. As mentioned earlier, we have submitted (inaudible) drugs to the FDA in June, and we are going to be submitting longterm carcinogenicity studies in December of this year. We are not not expecting to have any discussions before end of phase II meeting FDA. Until then, as the program will continue as planned.

All right and our next question or comment comes from the line of Mr Jason Cantor with Credit Suisse.

Yes, this is Jeremiah filling in for Jason. Thanks for taking our questions. Regarding the meeting with the FDA -- in the phase II meeting with the FDA, what events do you need to complete in order to schedule that. Is that just -- is studies 14 the last gating event and do you have a final date in hand to do so?

Thanks for the question, Jeremiah. Narendra, do you want to take that one as well?

Yes, right now we are planning end of phase II meeting towards the end of second quarter next year. For b, for this particular meeting, the main focus is going to be on what kind of phase III clinical plan we want to have for approval. In order to achieve that we have completed several phase IIa and phase IIb studies.

Finally, 08 and 09 will be included in this, and we will definitely bring up human [base] of up to 014 study also in this meeting. Along with that, we will definitely discuss all the non clinical studies that have been completed to date to support development of this program. And we are confident that with this package together we will make progress to move the program into phase III.

As a follow-up to that, whenever the FDA is considering lifting a clinical hold, do they traditionally communicate that at the meeting, or is that something that follows some time after the meeting?

At this time I don't think we can make any -- we cannot speculate how they are going to communicate, but we are planning to have the [additions] address by that meeting.

And this is the last question regarding study 008, in regards to the combo arms 1002 with Zetia, I know they are relatively small numbers, but is there a certain threshold that would pique your interest and make you just pursue that type of regimen further?

Jeremiah, this is Tim. I would say that there are two, well, not just two, there are multiple factors that we will consider as we explore that potential for combination. First, I think we want to recognize that this initial look is very exploratory. As you noted, the numbers are quite small, 20 to 30 patients in each of those arms. So a total of 50 to 60 patients of combination therapy. So, we will be looking at those numbers. But, again, we view them as exploratory.

I think the other thing we are keeping our eye on, of course, is the acceptance exogenously of Zetia or the continued acceptance of Zetia. It is, as you and all of us know, it has become the standard of care for statin intolerant patients, in some part because there are, as we have been saying, there are just not very good options to statins available in the market today.

So we will keep an eye on the market. We will certainly keep an eye on how the dialogue around Zetia when the IMPROVE-IT results come out and then the results from this exploratory arm, as well.

More to follow on that, but we are definitely looking for additional data. We are very data-driven on these kinds of things, so we will be looking for additional data on multiple fronts to help inform that decision.

Thank you for taking questions.

Thanks, Jeremiah.

I'm showing no further questions or comments at this time. With that, we will now conclude the Q&A portion of the call. As mentioned earlier, please e-mail Mindy Lowe at MLOWE@esperion.com to schedule a follow-up call with Management if there are any questions from today's discussion. Now I would like to turn the call back over to president and CEO, Mr. Tim Mayleben, for closing remarks.

Thank you, Andrew. I want to thank everybody for joining the call today and for your continued interest in 1002 and Esperion. As we've been saying, the next several months will be very eventful, and we look forward to continuing to update you on our progress. Thank you again.

This concludes today's conference call for Esperion Therapeutics. You may now disconnect.