CymaBay Therapeutics, Inc.
Q1 2018 Earnings Call Transcript

Published: 9 May 2018

[Operator:]

Good day, ladies and gentleman, and welcome to the CymaBay's First Quarter 2018 Financial Results Conference Call. At this time, all participants are in a listen-only mode. Following the formal remarks, we will open the call for your questions. Please be advised that the call will be recorded at the Company's request. It is also being webcast live on the Investors Section of CymaBay website at www.cymabay.com. Now I would like to turn the call over to Mr. Dan Menold, Vice President of Finance at CymaBay. Mr. Menold, please proceed.

[Dan Menold:]

Thank you, operator, and good afternoon, everyone. Earlier today, we issued a press release announcing our first quarter 2018 financial results and business update. You can access that release on our website under the Investors tab. Participating on the call today are Sujal Shah, Chief Executive Officer, Dr. Pol Boudes, Chief Medical Officer and Dr. Chuck McWherter, Chief Scientific Officer. They will provide an update on our financial position and clinical programs and review upcoming milestones before we open up the call for Q&A. Before we begin, I would like to remind everyone that statements made during this conference call, including the Q&A session relating to CymaBay's expected future performance, future business prospects, or future events or plans including future clinical plans are forward-looking statements as defined under the Private Securities Litigation Reform Act of 1995. Although the Company believes that the expectations reflected in such forward-looking statements are based upon reasonable assumptions, actual outcomes and results are subject to risks and uncertainties and could differ materially from those forecasts due to the impact of many factors. The Company assumes no obligation to update or supplement any forward-looking statements whether as a result of new information, future events or otherwise accept as required by applicable law. Participants are directed to the cautionary statements set forth in today's press release, as well as the risk factors set forth in CymaBay's Quarterly and Annual Reports filed with the SEC for factors that could cause actual results to differ materially from those anticipated in the forward-looking statements. This conference call is the property of CymaBay and any recording or rebroadcast is expressly prohibited without the written consent of CymaBay. At this time, I would like to turn the call over to Sujal.

[Sujal Shah:]

Thank you, Dan, and good afternoon, everyone. We've gotten off to a fast start in the beginning of the year, having successfully met several key clinical and operational objectives, and have exciting milestones ahead of us in the months to come. Today's call will focus on covering four of our most significant accomplishments since the beginning of the first quarter and close with major catalysts for the remainder of the year before taking question. Shortly after our presentation at the J.P. Morgan Healthcare Conference in January, we received significant inbound interest from institutional investors including existing and new potential shareholders looking for an opportunity to get behind the Company and our stated strategy to advance seladelpar with Primary Biliary Cholangitis or PBC and NonAlcoholic SteatoHepatitis or NASH. In February, we were able to successfully close on a widely placed common stock offering that raised $135.5 million in net proceeds. Including proceeds from the financing, cash, cash equivalents and marketable securities totaled $229.5 million at the end of the first quarter of 2018, which we believe is sufficient to fund our current operating plan into 2021. A full review of our Q1, 2018 financials is provided in our issued press release and filed 10-Q. A second key activity has been preparation for and meetings with regulatory agencies in the U.S. and Europe to discuss our planned Phase III study of seladelpar in PBC. Seladeplar is a highly potent and selective agonist of the nuclear receptor peroxisome proliferator-activated receptor delta or PPAR Delta. We believe that seladelpar is particularly well suited for the potential treatment of inflammatory liver diseases, including PBC. We have been pleased with the FDA and EMAs level of engagement and their recognition of the need for improved therapies for patients with PBC. We expect we will be in a position to provide an update on our regulatory discussion and Phase III study design before the end of the second quarter. And as previously disclosed, we intend on initiating Phase III in the second half of this year. That brings us to the third key highlight of this year, which I will ask our Chief Medical Officer, Dr. Pol Boudes to walk through in more detail. New 12-week and 26-week data from our ongoing Phase II study of seladelpar and PBC was featured in a late breaking presentation at the International Liver Congress 2018 hosted by the European Association for the Study of Liver Disease or EASL in Paris last month. This marks a third consecutive year in which data from our development program with seladelpar and PBC was featured in a late-breaker category of one of two Premier Annual Liver Meeting. Pol?

[Pol Boudes:]

Thank you, Sujal. As we have discussed on prior calls, our ongoing Phase II study of seladelpar in patients with PBC was expanded and extended first 12-week interim data readout in July of last year. After achieving proof-of-concept where dose is 5 milligram and 10 milligram once-daily demonstrated robust anti-cholestatic and anti-inflammatory effect with no drug-induced pruritus, through 12-week of dosing. The decision was made to expanding 12 months and extend those into 52 weeks to primarily support the overall safety data base for approval. The ongoing study also continues to provide us with a rich dataset around both the efficacy and safety of seladelpar and PBC. As Sujal mentioned, new 12 weeks and 26 weeks data from the ongoing study will feature at EASL International Liver Congress 2018 and you can find the medical poster presented at the Congress on our website as safety population in the data shared at EASL included 71 patients exposed to at least one dose of seladelpar of whom 53 received 12 weeks of treatment and 42 received 26 weeks of treatment. At baseline, mean alkaline phosphatase or AP was 358, 333, and 262 units per liter in the 2 milligram, 5 milligram, and 10 milligram groups, respectively. I will focus on four of the most important takeaways. First for AP, dose response of 12 weeks and dose deterioration beyond 12 weeks and responder rates, second, anti-inflammatory effects, third, the effect on clinical symptoms including pruritus, and four, overall safety. In the first part of the study, our objective was to measure the dose response between 2 milligram, 5 milligram, and 10 milligram. At 12 weeks, we observed a very nice dose response with change of AP of minus 21%, minus 33% and minus 45% in the 2 milligram, 5 milligram, and 10 milligram groups, respectively. With the focus on the two most efficacious doses of 5 milligram and 10 milligram, we further evaluated the effect of on dose titration and durability of response through 26 weeks. When we look further at the patient on the 5 milligram, we observed more than half had a response in AP lowering similar to 10 milligram, while others had more moderate reduction in AP. After the first 12 weeks dose titration was allowed for patients whose AP remained above normal, and at the level where additional AP lowering has the potential to reduce the risk of disease progression. At 26 weeks, we have the decrease in AP that were similar, of course, regimen with minus 45% for patients that stayed on 5 milligram, minus 43% for those that were titrated from 5 milligram to 10 milligram after week-12, and minus 43% for those receiving 10 milligram. At 23 weeks this decreases in AP led to 69%, 67% and 79% of patients across the three dose regimens, respectively meeting the responder criteria of AP less than 1.67 times the upper limit of normal, with at least a 15% decrease in AP from baseline and normal bilirubin. The responder rates made of these three criteria has been used as a primary endpoint for accelerated approval in PBC. Overall, 29% of patients had normal AP at week 26. We believe this profile around 18 weeks reduction responder rates and normalization positions seladelpar to potentially offer PBC patients improve efficacy of our existing second line treatment. The second key observation was highlighted by the rapid and robust decreases in turn transaminase signaling seladelpar clinically meaningful anti-inflammatory effect. At 12 weeks medium transaminase changes where our minus 9%, minus 28% and minus 35% in 2 milligram, 5 milligram, and 10 milligram groups respectively and decreases, we are maintain at 26 weeks in the 5 milligram and 10 milligram groups where decreases and transaminase where our minus 40% and minus 43% respectively. In addition to anti-cholestatic and anti-inflammatory effect or third takeaway from this results was a clear indication that treatment with seladelpar was not associated with drug-induced pruritus. Baseline median pruritus VAS was 19 and 37 in the 5 milligram or 5 milligram to 10 milligram deterioration and 10 milligram groups respectively and patients in a 10 milligram group that presented with a clinically relevant level of pruritus experienced consistent decreases during treatment approximately 24% at week 26 suggesting potential anti-pruritic activity. The lack of drug-induced pruritus with seladelpar maybe a key differentiator from a patients are ability of Ocaliva and the potential anti-pruritic activity will be further elucidated in our plain Phase III study. Finally, seladelpar was generally safe and well tolerated with no transaminase elevation safety signal. There were six serious adverse events and none were deemed related to seladelpar. We are planning for this ongoing Phase II study to which full enrollment before initiation of a Phase III study in the second half of the year. I would also like to remind you that in generally we announce the initiation of the long-term expansion study that offers patients in our clinical study, the opportunity to continue receiving treatment as we move forward in the development program. We've heard 30 patients reaching 52 weeks of dosing in the ongoing Phase II study of all enrolled in the longer-term extension study. We look forward to providing further updates on data from the ongoing Phase II study at future medical meeting. Sujal?

[Sujal Shah:]

Thank you, Pol. Our final update from the beginning of this year was the announcement made earlier today that we have now initiated screening. In a Phase IIb study of seladelpar in patients with NASH. As we have previously highlighted we believe that PPAR Delta mechanism maybe particularly well suited to treat NASH given its beneficial impact on glucose, lipid and sterile metabolism as well as suspect an inflammation and fiber genesis. On our prior call, we discussed, published result evaluating seladelpar in a mouse model of NASH and in patients with mix dyslipidemic that supported these effects that we believe should have benefit in NASH. The Phase IIb study that we initiated and announced today with a randomized placebo controlled parallel dose ranging study that is intended to enroll approximately 175 patients with liver biopsy proving NASH at specialized U.S. investigational centers. We intend to enroll non-cirrhotic NASH patients with similar disease level by growth of stage and background co-morbidity for example diabetes as has been studied recently by other sponsors. Seladelpar at doses of 10 milligram, 20 milligram and 50 milligram taken ones daily will be evaluated versus placebo in a 2

[Operator:]

Thank you. [Operator Instructions] Our first question is from Ed Arce with H.C. Wainwright. Please proceed.

[Jason Kolbert:]

Hi, thank you so much and congratulation. It's actually Jason Kolbert for Ed. I just want to talk with you a little bit about the powering assumptions that you're using on the study that you announced today. Can you walk me through kind of what the numbers will look like in each arm and how you came to those numbers and what proportion of patients do you think would experience a greater than 30% reduction in the MRI-PDFF at 12 weeks? Thanks.

[Sujal Shah:]

Appreciate. Thanks for the question. I'll start off and perhaps asked Chuck to provide some additional color. I think primarily we're powering the study really to assure the primary endpoint on the read and changing hepatic fat from baseline to 12 weeks through MRI-PDFF. Of course, we want to make sure that we have strong enough numbers at each dose to have proper dose ranging and also so that we can ultimately correlate and some fashion what we see in the MRI-PDFF with overall histology at 52 weeks. I think on the latter part of your question I think it's somewhat challenging for us to be able to project what will be see in the study of course I think we've had a number of sponsors with a number of different target observing 30% to 40% reduction in hepatic fat at 12 weeks I think those that's a benchmark at least that points toward the potential for meaningful histologic benefit both on NASH resolution as well as on fibrosis I think those become markers and guides for us to continue to evaluate. The potential for seladelpar both either as a single agent or as well as that potentially in combination with other target.

[Jason Kolbert:]

Makes perfect sense. Can you talk just a little bit about what the overall accuracy is of MRI-PDFF. And then I want to segue that to the timeline as you look towards your readouts at 12 weeks and 52 weeks?

[Sujal Shah:]

Yes, perhaps I'll answer the latter part of the question. Sorry Chuck and then I'll let Chuck talk specifically about the MRI-PDFF. I think in terms of timeline when you look at similar studies that have been conducted I think an appropriate estimation for a full enrollment would be about 12 months and that would ultimately put us in a position where we would expect to have the 12 week MRI-PDFF data in the second half of 2019.

[Jason Kolbert:]

Perfect. Makes sense. Okay. And then on the MRI-PDFF, how familiar are people with it? How accurate is that? How good is that?

[Chuck McWherter:]

Well, I'm just going to say that we have established a relationship with one of the leading MRI imaging company perspectum. And they have developed - they are using an advanced form of MRI-PDFF, the ideal technology. And the accuracy there is about 1%, so MRI-PDFF is actually broadly available throughout the western world. So it's actually a technology that is coming broadly into practice. So this is something that you are seeing in a number of - not only in the research study, but beginning to be used also in clinical practice. So it's something that's actually as you'll see from a number of sponsors that were example presented at EASL in last month and April. That's turned out to be a very significant technology in terms of assessing non-invasively the amount of tests however.

[Jason Kolbert:]

Makes perfect sense. I mean I go back to the old hep C days of biopsying patients, which you really don't want to do if you don't have to. Can you talk a little bit about the minimum proportion of patients with T2DM in terms of the trial?

[Pol Boudes:]

I can take this one. So what we are doing in this study is to allow patients with Type 2 diabetes mellitus. So it's difficult as of today to tell you exactly what will be the proportion, but I think we will finish up at least around 40%.

[Jason Kolbert:]

Okay, perfect Congratulations guys. Really great progress. Very exciting. Thank you on behalf of Ed.

[Pol Boudes:]

Thank you.

[Operator:]

Our next question is from Yasmeen Rahimi with ROTH Capital Partners. Please proceed.

[Yasmeen Rahimi:]

Thank you for taking my questions. Question one is focused on the NASH program, so can you tell us a little bit more about your dose collection? Specifically are there any sort of PK modeling differences when we think about the NASH population versus the PBC population?

[Sujal Shah:]

Yes, I'll start off. And Pol maybe can give us some color as well based on our experience, so we've grounded our assumptions here first of all to do a wide broad dose range in this study, again as we think about the potential for seladelpar as a single agent as well as in combination with other targets. So that's one basis for selecting a fairly broad dose range. If you look at our prior experience, as you recall we had conducted a study of seladelpar at 50 milligrams and 100 milligrams in patients with mixed dyslipidemia, it was an 8-week duration study in which we saw very beneficial effects across multiple metabolic parameters, decreases in LDL-cholesterol, triglycerides and such. And in that study we really saw a similar effect between 50 milligrams and 100 milligrams. So 50 milligrams ultimately with respect to some of the metabolic changes we saw in that study, I think is a justified basis for a high-end of the dose range. And then I think if you look at the data from our PBC experience particularly beyond just the anti-cholestatic effect observed, but when you look at the strong anti-inflammatory activity even at 10 milligrams and the consistency around which we saw response at 10 milligrams that really formed the basis for what we believe could be a low-end of the range to explore in the NASH population.

[Yasmeen Rahimi:]

Thank you. My second question is for Chuck, can you tell us a little bit more about the inclusion criteria building in on, what percentage of F1, F2, and F3 are you anticipating to enroll? And then secondly, what MRI-PDFF minimum requirement do you need? And then are you using spectrum multi-scan across all of your patient population are only in select one?

[Pol Boudes:]

This is Pol. Maybe I can take the second question which is the MRI-PDFF, so the threshold point inclusion in a trial is 10%, meaning that you have 10% of your liver which is actually made of fat. For spectrum, I mean this is what Chuck was alluding to. When you do MRI-PDFF, you have to use a technology that is very reproducible as Chuck mentioned. I mean it's very precise. But what is important also in the clinical trial is to use the control review of your data but also to train your [indiscernible] so that you get the best possible results and consistent evaluation of cross world. So that's exactly what we are doing with affect them and that's why actually we love to work with perspectum because they are very, very cautious about the quality of the data and especially the training of scientists. Now to come back to the first question, it's the same as with the question on IBC so it's a little bit difficult because but what I can tell you is the inclusion criteria, so we're going to enroll F1 to F3 meaning that we going to exclude patient that are F0 and we're going to exclude patient which are F4. Now the proportion of the patients that are going to be respectively in F1, F2, F3, I would not make a prediction at the moment, maybe you can look at - and look at the trials that have been done in similar population to figure out exactly how it's going to be. So I would not be comfortable today to give you a precise answer on that.

[Yasmeen Rahimi:]

Thank you. And if I may ask one last question, running the fact that placebo responses running quite high across by biopsy driven data, maybe why you select 25 patients in that placebo arm. Maybe some talks around that rather than keeping it at a higher number?

[Sujal Shah:]

So whether it maybe Chuck can comment after me. So the study is they well powered for MRI-PDFF that for sure. When you do biopsy, the number of patient's counts, so we think that with the way we are doing the trial where we get some very useful information, but what is also very important is the way you are doing the biopsy. So we are using and we are working with people who are extremely experienced in the reading of the liver biopsy because the viability that you're seeing including the viability in the placebo group can come also from the way you read the biopsy. So we have a very strict system in place and we have also - I think we have selected probably the best reader, you can think of for reading the biopsy. So we're pretty confident that the number we have in the trial are going to help us to figure out exactly what's going on - on the liver biopsy side of things and also to make correlation between the PDFF and the other criteria. Chuck, do you want to add anything on?

[Chuck McWherter:]

I think that covers and I think our primary examination in the study is really the first and foremost focused in on the non-invasive method look for metabolic effects as well as the markets that have been mentioned and then the develop histology correlation. I think one have to be possible or practical I should say in a study of this type with the patient numbers in hand. There are tradeoffs to be had and I think the patient numbers that we selected are going to allow us to at the end of the study be confident about making the decision for the future development at seladelpar. So once not looking necessarily or various the study within power that anticipate for the histology and power for the other end points in the histology at this time to inform the decision about where to go next.

[Yasmeen Rahimi:]

Thank you very much. And congratulations, again I'll jump back in the queue. Thanks.

[Sujal Shah:]

Thank you, Yasmeen.

[Operator:]

Our next question is from Jay Olson with Oppenheimer and Company. Please proceed.

[Jay Olson:]

Oh, hey, guys. Congratulations on all the progress and thank you for taking my question. Maybe to shift gears over the PBC for a moment, can you just talk about the reception to the data that was presented, EASL what kind of feedback from physician did you receive on that data?

[Sujal Shah:]

Thanks for the question Jay. I think for from our perspective we couldn't have had a better data set post last year's 12-week that was initially announced on the first 24 patients in the study I think we continue to Steve very strong durable response on AP as well as on inflammatory markers namely the drops and transaminase doubt to 26 weeks that both 5 milligrams and 10 milligrams we're very encouraging. A very nice dose response in the first part of the study after 12 weeks between 2.5 milligrams and 10 milligrams in fact as picturesque of a dose response curve as you could imagine. And so I think that overall response was one that continued to encourage us that there is real potential for seladelpar to offer patients both improved efficacy as well as potentially better tolerability. And the latter point really focusing in on the patient reported outcomes of pruritus as well as PBC 40 scale that's been used in PBC in particular to highlight the level of the fatigue that patients experience. I'll caution of course this is an open label study and so in order to appropriately access the effects of seladelpar on both pruritus as well as potentially on fatigue. You'd want to do so in a more robust fashion with the placebo compared or which is what we will in fact do in Phase III, but I think if you look at the trends observed in the dataset that we shared at EASL and continues to give us further encouragement that there may in fact be a potential to see anti-pruritic activity with seladelpar in PBC patients. And that certainly would continue to be a key differentiator versus existing second line treatment. And so all of these observations were really at the heart of the overall reception I'll say around the potential for seladelpar I think again it solidifies our plans to advance into Phase III in the second half of this year.

[Jay Olson:]

That's very helpful. And then I guess maybe just looking ahead to your Phase III study in PBC. Would you consider doing a biopsy sub-study in your Phase III study for PBCs similar to the study that was recently presented at EASL showing reduction in fibrosis or OCA?

[Sujal Shah:]

Maybe I'll make a couple of comments here. And then Pol, if you have some additional color to add. In the setting of PBC biopsy is not necessarily standard these days. The confirmation of diagnosis can and come really from a P levels as well as the present of anti-mitochondrial antibodies. So biopsy is not always necessary to confirm diagnosis. Nevertheless, we have had patients enrolled in our Phase II we would expect patients in Phase III to have had biopsies as well sometimes as confirmation of there disease at baseline and I think our goal primarily is to evaluate the effects on cholestatic as well as inflammatory markers and patient reported outcomes around clinical symptoms, but it wouldn't be unusual for us to collect biopsy where possible and where patients are amenable, and that would in fact obviously give us the opportunity to do some sub-analysis in the future.

[Jay Olson:]

Great. Thank you very much for taking the question.

[Sujal Shah:]

Thank you, Jay.

[Operator:]

Our next question is from Joseph Schwartz with Leerink. Please proceed.

[Unidentified Analyst:]

[Indiscernible] filling in for Joe. Questions on both NASH and PBC program, so with the initiation of Phase IIb NASH program and congrats on that progress. How are you thinking or how are your thoughts evolving around a strategic partnership with that program? Is there a certain inflection point you're looking towards? Or are you looking at a more broadly as opportunistic approach as opportunities may arise? And then second question is given what the seladelpar data was able to show in PBC, how are you thinking about potentially investigating a first-line PBC setting potentially as a concurrent to Phase III studies, when you embark on that later this year in the second half? And then last is sort of off topic here, but in the conference call earlier this morning, there was talk about OCA being pursued in PSC, and there is some chat about FDA's willingness to look at defined endpoint there. So given your magnitude of impact on how fast, how are you thinking about PSC as your potential label expansion strategy? Thank you.

[Sujal Shah:]

Thanks for the question. So first with respect to our overall strategy and NASH. I think currently given we're well funded to advance both in PBC and NASH. I think our objective in the near-term is to better understand the single agent activity of seladelpar. We recognized that treatment and NASH is very likely to include at least in some patients the potential to combine different therapies for the most optimal outcome for patients. And so we will continue to be observant and in dialogue as we think about strategic alternatives to expand beyond Phase II and NASH as we conclude this proof-of-concept study. Now I think with respect to your second question around PBC and first-line therapy. I'll say that currently first-line therapy of courses is Ursodeoxycholic Acid, which is generic also very well tolerated about 50% to 55% up to 60% of patients have an adequate response with an AP lowering below 1.67 times upper limit of normal. I think to go to a first-line setting would obviously require going head-to-head against UDCA. UDCA, I'll remind you also was approved on overall outcomes not accelerated approval which is the path that we have in front of us for being the preferred second line treatment alternative of choice. I think the latter is really our focus. That's where the clear unmet need is that patient population at risk for disease progression are those that are not adequately served with UDCA. Of course, we've had many thought leaders and physicians treating physicians for patients with PBC highlight an interest if you will in using if there was a safe and well tolerated second-line treatment alternative and using that potentially earlier in the treatment paradigm rather than waiting for a patient to be in responders to UDCA after 6 months to 12 months. I think that's a potential opportunity, but that's one in which I think you really think about and point to an opportunity to not only improve on the cholestatic markers, but also to overall improve on the clinical symptoms that you see in PBC, of course UDCA while it does get 50% to 60% of patients below 1.67 has not necessarily been shown to have any beneficial effects on pruritus. So there again, I think there's a potential of course to improve overall treatment alternatives for patients specifically in a second-line treatment setting as we're targeting, but potentially even beyond should there be an opportunity to demonstrate something in Phase III around pruritus. PSV certainly is an area of focus for us. We've been active internally with dialogue, with thought leaders, I think as the agency's, parameters around the study design as we do our own exploration into thinking about end points that would have meaningful benefit around overall outcomes in PSV. It will be an area that we continue to do some work and consider exploring in the future.

[Unidentified Analyst:]

Great, congrats on all the progress and thanks for taking our questions.

[Operator:]

[Operator Instructions] Our next question is from [Robin Garner with Life Science Advisors]. Please proceed with your questions.

[Unidentified Analyst:]

Hi, congratulations on all the success. Thank you for taking my call. Two questions for you. Can you talk about the rational for seladelpar and NASH and specific they speak the potential of the compound to improve, but the hepatic fat by MRI-PDFF and can you also speak to that 52 week endpoint, particularly as it relates to the histological end point?

[Sujal Shah:]

Yes, thanks for the question Robyn. Chuck, I'll ask you to perhaps address these two.

[Chuck McWherter:]

Yes, sure. So let's just start mechanistically PPAR delta and seladelpar as an agonist to PPAR delta has a strong impact across natural progression of fatty liver disease or NASH. So as effect on metabolic parameters that's been shown in the mouse model of albeit driven NASH to reduce liver fat, to improve insulin resistance and to be anti-inflammatory as well as antifibrotic. So across those parameters that's what really provided the impetus for us to bring barcode to the study that we announce today and particular point out that the reduction - not just in liver fat, but lipotoxicity, which drives implication in fibrosis with the characteristic that we found in our pre-clinical study. And so we're very intrigued to see if we can firstly produce the effect on low and liver fat, MRI-PDFF in the clinical study and then ultimately to see if that translate into reduction and implementation as well as in fibrosis using the non-invasive imaging methodology as well as the histology that will get it 52 week. In terms of I think if I understood your question around the 52 week plant for histology, there is not really an exact formula that one can follow in terms of the type point for that end point. You have other sponsors have used the time point that we bought in pruritus, last month this short of 12 weeks, another it has gone as long as 72 weeks and in fact the Phase III study for the currently underway with that a [indiscernible] using a 72 week end point. So to us, we are 52-day, and it was really strong end point to choose in terms of making sure that we had durable response, one that wouldn't be subject too much variability and one that we would confident it in terms of going forward. So that was really the basis for kind of shooting for 52-week endpoint as opposed to some earlier.

[Unidentified Analyst:]

Okay, great. Thank you.

[Sujal Shah:]

Thank you, Robyn.

[Operator:]

Ladies and gentlemen, we have reached the end of our question-and-answer session. I would like to turn the call over back to Sujal Shah for closing remarks.

[Sujal Shah:]

Thank you, operator. I'd like to thank you all once again for joining us today. Over the past two years, we've really continued to see the real potential for seladelpar, the only potent selective PPAR delta agonist in late stage development and its potential benefits across multiple liver diseases is something that that of course we continue to be very encouraged and enthusiastic about and we look forward to focusing further on advancing our development programs and ultimately providing you with timely updates in the near future. Thanks again.

[Operator:]

We have reached the end of our conference. You may disconnect your lines at this time. And thank you for your participation.