Esperion Therapeutics Inc (ESPR) 2015 Q2 法說會逐字稿

Good day, ladies and gentlemen, and welcome to the Esperion Therapeutic second quarter 2015 conference call and webcast.

(Operator Instructions)

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

Thank you, Christine. Hello, everyone, and welcome to the Esperion Therapeutic ETC-1002 program update and second quarter 2015 financial results call. I'm Mindy Lowe from Esperion, and with me today are Tim Mayleben, our President and CEO, Mary McGowan, Chief Medical Officer, Marianne Andreach, Senior Vice President of Strategic Marketing and Product Planning, and Rick Bartram, Vice President of Finance.

As a reminder, this conference call and webcast is being recorded. To access the playback, please go to the investor's section of Esperion's website at esperion.com. We issued a press release earlier, detailing the contents of today's call. A copy can be found at esperion.com within the investors' section.

We will begin with prepared comments from our team, and then we will open the call for your 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 if you'd like to speak with the team.

We will use slides for our presentation today. These slides have been posted on our website, and are available for those following along throughout today's live webcast. Our comments today will be governed by our Safe Harbor Statement, which in summary [says], that through the course of our presentation and discussion today, we may make certain forward-looking statements and actual results may vary materially. Now I would like to turn the call over to Esperion's President and CEO, Tim Mayleben. Tim?

Thank you, Mindy. Good afternoon, everyone. I'd like to welcome you to our call and thank you for joining us today, as we provide you with an update on the ETC-1002 development program, and review our second quarter 2015 financial results. Also on today's call, we'll take sometime to address a few topics you have been asking us about, leading up to and following the Investor Day, we held last Thursday morning.

I want to emphasize just one thing before I begin. Our enthusiasm around the 1002 program and its potential to benefit patients is unwavering. If approved, we see a clear place for 1002 as a new oral LDL cholesterol lowering drug. Recall that cardiovascular disease is still the number one cause of death in the US, and the cholesterol treatment market is very large, and it continues to evolve.

Despite the availability of a variety of therapeutic options, there remains a significant unmet medical need for the large number of patients who are still unable to reach targeted LDL levels. Based upon the results from our studies to date, we continue to see that 1002 is nicely differentiated from all the other current and potential future therapies. So in addition to the quarterly 1002 program updates and financial results, let me highlight a couple of topics we will cover related to 1002.

We have received several questions on the topic of the incremental LDL cholesterol lowering efficacy of 1002 on top of low versus moderate intensity statins. And so, I will discuss some additional insights from the Phase 2B 09 clinical study from a post hoc analysis of these results, which as most of you know would typically be disclosed in a peer-reviewed publication or presentation. We will also walk you through our insights into the very weak interactions that we have seen with 1002 and statins, and the implications or the lack of implications if you will, on the safety, tolerability and efficacy when 1002 is used in combination with statins.

Let me make one other initial comment. Our goal at Esperion remains the same, to thoughtfully, expertly, and rapidly develop and gain approval for 1002 for use in patients with hyperlipidemia and mixed dyslipidemia, those that are seeking additional oral therapies to lower their LDL cholesterol, and thereby to maximize the revenue potential for 1002 and the value of Esperion.

So let's shift gears now, and into get into today's agenda. I'd like to begin by highlighting the accomplishments of the Esperion team, and our progress with 1002 during the second quarter of 2015. In early June, if you recall, we submitted a complete response to the 240 milligram partial clinical hold. In mid June, Dr. Mary McGowan joined us as Chief Medical Officer, and Dr. Scott Braunstein joined our Board of Directors. In early July, approximately four weeks later, the 240 milligram partial clinical hold was removed. This now allows 1002 to be used at doses above 240 milligrams in clinical studies. Having said that, we plan to initiate a Phase 3 clinical program in the fourth quarter of this year, using the already optimized 180 milligram dose. In late July, we announced positive top line results from the Phase 2 014 exploratory safety study in patients with both hypercholesterolemia and hypertension, demonstrating robust LDL cholesterol lowering, and hsCRP lowering and importantly, neutral effects on blood pressure.

Last week we held our second annual Investor Day. And finally, I wanted to highlight that earlier this week, Ashley Hall joined our team as Vice President Global Regulatory Affairs. Most recently, Ashley was Global Regulatory Lead for Cardiovascular at Amgen, and oversaw the regulatory strategy and global filings for the evolocumab program, leading to the first approval of a PCSK9 inhibitor for LDL cholesterol lowering. Prior to that, Ashley was Vice President of Regulatory Affairs at Micromet, which was acquired by Amgen in March of 2002 -- I'm sorry, 2012. Ashley has a science background, and is an attorney by training. She's a very accomplished regulatory leader, and we are excited to have her join our team at this pivotal time in the development of 1002. I would now like to turn the call over to Rick, who will review the financial highlights from the second quarter of 2015.

Thank you, Tim. As of June 30, 2015, Esperion had approximately $314 million in cash and investment securities, and approximately $5 million in debt outstanding under our existing credit facility. We expect our current cash and investment securities to be sufficient to fund the Phase 3 development program, and our operations through the expected approval of 1002. R&D expense was $7.2 million during the second quarter of 2015, compared to $6.5 million for the second quarter of 2014. The increase was primarily related to R&D costs associated with the further advancement of 1002, and the completion of our Phase 2 development program.

G&A expense was $5.3 million during the second quarter 2015, compared to $2.7 million for the second quarter of 2014. The increase was primarily associated with increased stock-based compensation expense, public company operating costs, and our commercial strategy activities. Our net loss for the three months ended June 30, 2015 was $12.4 million or $0.55 per share, compared to $9.2 million or $0.60 per share in the prior year. We currently have 22.5 million shares of common stock outstanding, with another 2.6 million to be issued upon the exercise of options and warrants.

Looking forward, we estimate that cash used in operations for the full year 2015 to be approximately $42 million. We also expect to incur approximately $12.5 million of noncash expenses during the full year 2015, which primarily consists of stock-based compensation expense. We expect to end 2015 with approximately $290 million in cash and investment securities. As I mentioned earlier, we continue to expect our current cash and investment securities will be sufficient to fund 1002 through the completion of the Phase 3 program, and our operations through the expected approval of 1002. With that, I'll turn the call back over to Tim.

Thank you, Rick. For those of you listening, note that there are, as Mindy highlighted earlier, a few slides that we've made available in connection with our call today. But for those of you who can't access those, please don't worry. First of all, they'll be available to you later, and second, my comments should be clear enough that you won't have to have the slides in front of you to understand what we are saying.

So as I noted earlier, we have conducted some additional analyses of the data from our 09 add-on to statin study. Of particular interest, we did a post hoc analysis of the LDL cholesterol lowering, which compared low intensity statins with the moderate intensity statins, that is the incremental LDL cholesterol lowering. What you will see in the slides is, that there was no statistically significant difference in the reductions between the two groups, within the 180 milligram dosing arm, which is the dose that we are taking into our Phase 3 program. And you will see further, that it was 19% incremental LDL cholesterol lowering on the low intensity statins, and 25% incremental LDL cholesterol lowering on moderate intensity statins. While post hoc in nature, these data are very encouraging as we continue to plan for our Phase 3 using maximally tolerated statin therapy. Let me also highlight that the majority of patients in the 180 milligram dosing arm received moderate intensity statin therapy, as opposed to the low intensity statin therapies.

Now with respect to safety intolerability in the 09, I would like to remind you that we did not observe any increases in either CPK or liver function tests. As you know, increases in CPK indicate potential damage to muscle cells, and we didn't see any of that. There are no cases of elevated LFTs or liver function tests. We also looked very closely at muscle-related adverse events. Note that there was one report associated with the 120 milligram dose, and no reports of muscle-related adverse events for the 180 milligram dose. Compare that with the placebo group, which in effect was the statin alone, and there were seven muscle-related adverse events recorded. Regarding SAEs in the 09 study, there were two SAEs in the placebo group, one patient with noncardiac chest pain and one with gallstones, and single SAE in the 1002 180 milligram patient of ovarian adenoma. None, none, of these SAEs were considered by the clinical investigators to be related to study drug.

Now during our Investor Day last week, we discussed the safety database from our Phase 2 program for 1002. Of special interest from those data, of course, are the liver function tests or LFTs. We reported that 1.2% of patients who received 1002 in Phase 2 had elevations in their liver transaminase levels. For context, this percentage compares very favorably to that of both rosuvastatin or Crestor which is 1.1%, and alirocumab which is 1.7%. And these data are directly from those respective package inserts. So with all of these data in hand for 1002 and from our Phase 1 and Phase 2 studies, we look forward to our End-of-Phase 2 meeting next week, to discuss our plans for Phase 3.

Okay. The next topic is the question that some of you have raised, about the potential for a drug-drug interaction between 1002 and statins. And so, I want to take just a couple of minutes to try to put this in context for all of you. We neither want to underplay or overplay this, simply to provide you some context. As many of you know, some statins are metabolized through what's called the cytochrome P450 family of enzymes, specifically 3A4. 1002 does not inhibit the activity of 3A4. The active form of 1002, 1002 CoA is formed in liver cells, and does not circulate in the blood. As you will recall, we have reported that the statin levels in the peripheral blood can be raised on average by 70%. However, note that there are other drugs listed in statin labels for those of you that have looked, that are known to interact with statins, and increase statin blood levels by 400% to 500%, with some as high as 3000%. So how will we know if there is an issue with a 70% increase in statin levels? Well, as I highlighted earlier, we have been actively monitoring both liver function tests as well as CPK levels. And recall, as I highlighted earlier, that in our 09 study we did not see any increases in LFTs or CPK levels. We did not see any adverse events in the 09 study that could be related to this increase in statin levels.

We've characterized the effect of 1002 on statin blood drug level as a weak interaction. In our drug interaction study with statins, it appears that the increase in statin blood drug levels occurs within the first few hours of dosing, and then rapidly decreases. Statins in 1002 are excreted through different pathways, and neither drug accumulates. So I know this was a little bit complex, but because of this, we are comfortable with the use of maximally tolerated statin doses in our planned Phase 3 program. Of course, this will be discussed next week during our End-of-Phase 2 meeting, and we will discuss with you more in the future.

Now, before we open the call to your questions, let's turn our attention to key upcoming milestones for Esperion and 1002. First you have probably picked up on my earlier comments, that our End-of-Phase 2 meeting will be held next week. And then following the receipt of the meeting minutes and within 45 days, we plan to host a conference call and webcast to report on, and discuss the results of that meeting. We have also submitted for presentation our deepening scientific and mechanistic understanding of 1002, in particular the inhibition of ATC citrate lyase, which lowers LDL cholesterol like a statin, but with reduced potential for muscle related-side effects and the related liver specificity of 1002. The next few months should prove to be very eventful. With that, we will open the call to your questions. Christine, please poll for questions.

(Operator Instructions)

Jason Butler, JMP Securities.

Hi. Thanks for taking the questions, and appreciate all the additional information you have given this afternoon. First question, just focusing on the new data that you gave from the 09 study, acknowledging that the patient numbers are not large here, can you speak to whether you saw any differences between the different statins in this trial?

I don't think we have that level of detail, Jason. I think generally, the data that we reported is representative of what we saw across the different statins. There is nothing that stands out, if you will, on the different statins.

Okay. Great. And then I guess, pointing to the prior trial, 007 trial, in that trial I guess, the way we thought about that, is you viewed atorva low dose statin. In this analysis, you are including atorva as a moderate dose. Can you just help us understand how you classified the different statin doses into low and moderate intensity? And if you for example switched tolerant to the low intensity would there be any -- I guess what I am asking is there sensitivity analyses here, if you move different statin doses around, is the data still robust?

Yes, I will ask Mary to comment.

What we decided to do for this analysis was utilize the AHA ACC guidelines to inform us as to what we should refer to as low intensity statin therapy, and moderate intensity statin therapy. So the low intensity statin therapy will be statin therapy that includes simvastatin 10, pravastatin 10 and 20, lovastatin 20, [luvastatin] 20 and 40, and pitavastatin1 milligram. In our studies, we had only four statins, atorvas, simvas, rosuva and prava. Our moderate intensity statins, I will just include those that we included. Moderate intensity statins are defined as atorvastatin 10 and 20, rosuvastatin 5 and 10, simvastatin 20 and 40, and pravastatin 40 and 80. So this is what we used, because this is in the literature.

Okay. Great. But again just to ask the question -- I guess in clinical practice do you view atorva 10 as low or moderate? And then if you looked atorva 10 as low in this analysis, would you have seen a difference?

There were so few patients, but I will tell you that atorva 10 I would consider it to be a moderate intensity statin and atorva 10, really only had a muscle ache or muscle AE in the 10-milligram group in placebo --not.

Jason, you were asking about the efficacy?

Yes, please.

Yes, so the efficacy of atorva 10 would fall into the moderate intensity because that's 30% to 50%, or 30% to less than 50%. Atorva 10 classically lowers LDL about 38%.

Okay. Helpful. Thank you very much, and thanks for taking the questions.

Thank you, Jason.

Your next question comes from the line of Jessica Fye from JPMorgan. Your line is open.

Hey, guys. Just a question on the communication after your End-of-Phase 2 meeting. I just want to make sure I understand when we could expect an update. Are you not going to wait for minutes to communicate to the street i.e., could we hear an update in August? Is that what you are saying.

No, I am sorry if I misspoke, Jess. We have been saying consistently that we will wait for the meeting minutes to communicate the outcome of the End-of-Phase 2 meeting.

Okay. Got it.

We expect those within 45 days.

Okay. So second half of September kind of.

Yes, I think that's the right time frame to think about.

And then, since we are going to get the Amgen label between now and then, is there anything that you are watching for in that label? I think they ran sort of a broader clinical program. Are you expecting any differences between their indication and that for [Praluent]?

It's a good question, and I think our official answer is we'll find out on the 27t, with everybody else.

Okay. Thank you.

Yes.

Your next question comes from the line of John Eckard from Barclays. Your line is open.

Hi. Thanks for taking the question. I know there is so much focus on US right now, which obviously is legitimate. But when it comes to oral drugs like ETC, I guess when we look at Zetia, when it comes to ex US opportunity, what do you see as relevant global opportunity ex US verses US? Is there a drug such as like Zetia that can be used as a comp to see how such a drug is used in other parts of the word?

Thanks for the question, John. Marianne, can you respond?

Sure. Thanks for the question, John. As we think about what we can expect outside the US, so I think as we have mentioned before, we are going to -- we have initiated some dialogue in Europe and we thought about that. Ezetimibe is approved and used throughout Europe. It's something that we are certainly paying attention to as you suggested, because when you look at statins for example, most if not all are genericized at this point, and all referenced priced. And as we look at, ezetimibe, it actually is a good comp for us to start with. So we definitely agree with you.

I guess, two things. One thing I notice is ezetimibe last year, almost like 45% of the sales were outside of the US Is this, how does is -- if you are willing to say, how does this come into the thought process, when you talk broadly with partners in the past? I mean, are they -- does everybody really just care about US first, and they'll figure out the rest later? Or does the profile of the drug outside the US, is that critically important to their process as well?

So, John, this is Tim. So without standing in the shoes of potential partners, I would just say generally that the ex US opportunity is viewed generally, in this therapeutic area as being almost of equal value over the long term as US opportunity. And I think if you look at the revenue generated by LDL cholesterol lowering drugs, obviously oral LDL cholesterol lowering drugs, I think the revenue would generally support that as well, the revenue generated by the drugs would support that.

Do you feel that the PCSK9s over in Europe, especially since they have a relatively broad label or broader than Praluent's label here, could that change the impact of small molecule drugs in Europe at least in the future?

It's a very interesting question. Marianne, do you have any initial thoughts?

That is a great question, John, and it's something that we have thought about a bit. If you think about this, we talk about in the US focusing here, that we're going to now have a new class of large molecule injectable biologics.

Well, think about Europe too, into which, the one thing we recognize about Europe relative to the US, is there seems to be a higher degree of cost containment, when it comes to the purchase and utilization of pharmaceutical products. So I think when you look at Europe, the number of prescriptions written for statins is about equal to that of the number of prescriptions written here in the US So that shows us right away, there is a large group of patients. We know patients aren't necessarily all being treated to goal, but there are certainly opportunities for new therapies. How Europe and the individual countries are going to look at reimbursement and access relative to the large molecule injectable biologics remains to be seen. But it certainly could change the face of treatment in Europe, and could potentially have benefits for an oral small molecule like ETC-1002 following them on to the market in Europe.

If I can just make a comment. This is Mary McGowan, John. In my clinical practice and in the practice of my peers, and I work in cholesterol metabolism, it is very frequent for patients to request an oral agent above an injectable. It is very, very hard to convince patients to initiate an injectable agent when there are oral agents they haven't yet tried.

Thanks. Tim, if somebody hits themselves with a knife is that an AK event (laughter)? Just in case, we hear of anymore of those? No. Okay. (laughter) I'll get back in queue.

Thank you.

Your next question comes from the like of Michael Yee from RBC Capital Markets. Your line is open.

Hi guys. Thanks. A couple questions, in your analysis that you showed there in slide 3, is there any thought as to the dose response that you see with the low intensity statin, versus why the difference in [dose] response verses the modern intensity statin? I am just trying to understand those numbers, what that might be.

Mike, I think it's very tempting both to us and probably to you as well to what I will say is to read too much into these results. First as we highlighted it's post hoc analysis. I think one of the concerns that we had heard expressed, and again I think this analysis nicely deflects that concern, was that we would see a diminution in either the incremental LDL cholesterol lowering of ETC-1002, as you dosed higher with statins. I think what this analysis does is, show that is not happening. And again, if you read -- are tempted to read too much in it, you can even say that maybe there is a signal to the opposite. That's why I say, we are trying to be very balanced, because first of all it's a post hoc analysis. It's not pre-specified. And as I think Mary highlighted earlier, the numbers overall are small. But as we said, it's encouraging. It's encouraging.

Yes. The point is that there is not a difference in totality.

That's right. I think that's the right way you look at it.

FDA, the upcoming announcement post your End-of-Phase 2 meeting is there any chance that the FDA asks you to run some form of a Phase 2/3 study with maximally tolerated or high intensity statins? What do you think the chances are of that happening?

It's a very good question. We don't know. We don't think so, and the reason we -- again, we don't know for sure. But the reason that we feel comfortable as I said in our prepared comments, is as we've gone from low intensity statins to moderate intensity statins, we continue to see the efficacy, and we don't see any change in any of the safety or tolerability aspects. And I think that's one of the reasons. If we had seen something, we might -- we and others might be concerned about us going to the high intensity statins. But given this very attractive safety intolerability profile that we have seen, we don't think so. We think it's the next natural progression is to study these patients, and of course they'll be monitored in our Phase 3 program. So but we'll see. We'll certainly report back on that if that's the case.

Okay. Last question is regulatory. In the US, if Amgen gets the same label as generally, regeneron, in terms of secondary prevention, will that change your view on your ability to have primary and secondary, given that they had a very balanced population of that? And then in Europe, same question, but more positive is that, following along on the other question, do you believe that their broad label there, just makes regulatory bar easier, because of -- I mean, they even call it statin intolerance? So two different sides of the [Atlantic]?

Right. You may have heard me say last week, we want to banish both broad and narrow from our lexicon, and instead really focus on the patient population. So I think to your question about the PCSK9 label, keep in mind that I think -- and we have done some further analysis of this. But I think the estimates that we have seen are 8 to 10 -- represents 8 million to 10 million patients in the US; And even if we, again just to put this in perspective, even if we think about just an oral LDL cholesterol lowering therapy, that represents roughly a $16 billion to $20 billion market opportunity.

I'm good with it. I just want to understand if it would change your thinking, because clearly they ran a broader population of mixed patients, and if they don't, maybe it's going to be class (inaudible) label, maybe it's not. I just want to understand it. I agree (inaudible). I just want to understand if that changes your mind?

I think we will learn -- I am not trying to be evasive, although I think you are going to -- you may think that. But I think we're so close to being informed by our End-of-Phase 2 meeting, that I don't want to speculate when I know we are going to have this information in a matter of weeks. That is both our End-of-Phase 2 meeting as well as the Amgen label as you said.

Okay. Then on the Europe side, sorry, that was it, just the Europe side, is the hurdle lower, because of the label they gave them there, including statin intolerance? Do you see that opposite?

I will ask Marianne to comment, if you don't mind, Marianne.

No problem, Tim. Mike, it's interesting to see the difference. I think that as we continue moving forward, the idea that we already know that ezetimibe has the specific indication in Europe, specifically in France for statin intolerance. So we knew that from a regulatory perspective, there could be a difference in how they look at programs. So as we move forward in our planning with respect to Europe, and where we intend to seek scientific advice, I think that will truly help guide us in what we are thinking about. But seeing what's already happened to date with the PCSK9s certainly really helpful to us, as we think about what the European opportunity might truly look like.

Thank you, guys.

Thank you, Mike.

(Operator Instructions)

Your next question comes from the line of Andrew Peters. Your line is open.

Hey guys. Thanks for taking my questions, and thanks again for all the clarity on the call. I just wanted to touch on something that you mentioned last week at the Analyst day, the potential for running a concurrent Phase 2 studies that can read out next year, along with the Phase 3 program. I was hoping for a little bit more detail on today's call. So can you outline your thoughts on additional kind of clinical work beyond the scope of the Phase 3 plan right now, and potential timing around those? Thanks.

Yes, thanks, Andrew. So yes, I think we have talked about the fact that we have interest in what I will say, is further expanding the profile of ETC-1002 by looking, for example -- and I will just give you one for example, is looking at ETC1002 in a defined Phase 2 study on what we have referred to as triplet therapy, triplet oral therapy, looking at 1002 plus a statin and plus ezetimibe. And really the goal there for example, would be to characterize the total LDL cholesterol lowering of the three oral drugs combined. And of course you know continuing to evaluate safety and tolerability profile. So that's just one for example. I think we're very much in the evaluation and discussion phases of that. And I think as you guys know we try to be as transparent with you all as possible, but our immediate focus as you've -- or our maniacal focus as you have heard us say, is really on the End-of-Phase 2 meeting and successfully executing on the launch of the Phase 3 program. So I think on our call in November, we'll have more details, Andrew, for you and others, about not only the details about those studies, but also as you requested the timing of those studies as well.

Great. Thanks. And a quick question on the potential cardiovascular outcomes trial. You kind of gave your initial thoughts on the potential size of one at the analyst day. I just wanted to see if -- how your financial guidance could potentially change, if FDA suggested a larger outcome study would be needed, in terms of guidance for sufficient cash through an NDA? Thanks.

Sure. So maybe I will just take the opportunity, Andrew, with your question about the [CD] outcomes trial, just to remind folks that what we suggested is our initial estimate is that we would include about 12,500 patients in our cardiovascular outcome study. And that we're thinking about the initiation of that in late 2016 or the first half of 2017. I think some folks have raised the question of whether the size of that cardiovascular outcomes trial is adequate or not, especially in the context of other CD outcomes trials that are currently being run by other LDL cholesterol lowering drugs, ranging from 18,000 to perhaps 30,000 patients in the case of one of the [CEPT] inhibitors. But I would just point everybody, for context to one of the CEPT inhibitor outcomes trials that is ongoing, called the ACCELERATE trial, and just highlight that that study includes -- it's at clintrials.gov -- includes about 12,000 patients. It has a very good definition of an end point, as well in that study. And of course that study has been deemed adequate by the regulators, and the -- what is it -- imitation is the sincerest form of flattery. We have looked at that study, and we think that it is a very efficient and appropriate study to consider for ETC-1002 as well. We have not, we have not, Andrew, looked at what the financial impact would be of a larger study, simply because we've got this very relevant, very appropriate comparator in the ACCELERATE study.

Great. Thanks.

Your next question comes from the line of Chad Messer from Needham & Company. Your line is open.

Great. I wanted to thank you guys for giving the best data-driven answer you could have, to the question of statin interaction. Those post hoc kind of analyses aren't perfect, but as one of the people who was asking questions about that, that's probably about all you could have done, And just thanks for being so responsive on that.

Sure.

Thank you.

As we look forward to the End-of-Phase 2 meeting, and I know this team's been in front of the FDA quite a few times and has experience with this kind of thing, how confident are you that we'll get a pretty clear answer? Not asking you to speculate on what the answer is. But just this isn't a FPA negotiation or anything, it's just End-of-Phase 2 meeting, a clear answer on what CBOT requirements are? Do you think it will be pretty black and white, or is there a chance that there would still be some gray zone?

Chad, it's a very good question. And I think I will just highlight something that I said earlier, which is that this summer has, I think if it has revealed nothing else, it has revealed that we are in what appears to be an evolving landscape, I think as we highlighted the initial advisory committee meetings, and then the recent label for another LDL cholesterol lowering drug, proved to be somewhat surprising. Again, although as I said, the overall market opportunity has not changed. But it certainly appears that there has been some evolution. And having said that, we feel very confident in our team's ability to navigate that, especially as I highlighted earlier with Ashley joining our team and having some very recent and relevant experience leading a similar effort. So more to follow, when we report on the End-of-Phase 2 meeting result, but I hope those comments were at least a little helpful.

Yes, thanks. That is helpful. Obviously, hoping we have the answers that investors want, and not necessarily something gray. But life is what it is, and we'll have, what we have, when we have it. Thank you.

No, and I think, just one other comment, Chad, which is that I think sometimes, the worst thing is the uncertainty. And again, having the End-of-Phase 2 meeting and being in the position to communicate those results is the great thing. So we are definitely looking forward to the meeting, and even more so looking forward to communicating the results.

Great. Thank you.

Your next question comes from the line of Vamil Divan from Credit Suisse. Your line is open.

Guys, this is [Ligwal] calling in for Vamil. Most of our questions have actually been asked, and one follow up question regarding comments between interaction between ETC-1002 and statins. I know you guys classified as 70% as weak interaction. Is that something that the FDA has issued guidance on, or is that more of your view on the actual interaction?

Yes, that's a good question, Lee. I think the answer is that it, is a relative term, not a great term because weak verses strong, et cetera, there are some limitations to its use. That's why we have generally referred folks to the percentage levels or the multiple levels. So as I said earlier, we are seeing a 0.7 increase versus a 4 to 5 times increase with other drugs on the labels, or even as high as 30 times. We refer to those as 400% or 500% versus the 70%. So it's -- you're right. It is an imprecise term, but it is a relative term, relative to the other interactions that you see on the labels. That's really all we were trying to do is to provide some context, and yes.

That's great. Just a follow up on that question. I know you provided a great level of information today. I just have one question about whether the interaction between low intensity verses moderate intensity statins change as you get to a higher levels? Is it the same 70%,or do you see any change in terms of that interaction?

Right, so in a drug-drug interaction study, you don't. That's not one of the outcomes that you can derive. So we believe it will be the same. And again, our belief is based on tremendous experience, not only obviously in developing LDL cholesterol lowering drugs like Lipitor, which our team did, but -- which many in our team did. But also obviously the involvement in the development of ETC-1002.

Okay. Perfect. Thank you. Appreciate it.

You're welcome.

We will now conclude the Q&A portion of the call. As mentioned earlier, please e-mail Mindy at MLOWE@esperion.com if you have any questions from today's discussion. Now I would like to turn the call back over to Tim Mayleben for closing remarks.

I want to thank you for joining our call today, and for your continued interest in 1002, and your support of the Esperion. I also want to extend my thanks to each Esperion colleague. We wouldn't be here without their hard work and their passion to bring 1002 through development and approval. As you have heard me say before, we are truly blessed by all of their efforts. We look forward to continuing to update you on our progress throughout the rest of this very exciting year. Thank you.

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