CymaBay Therapeutics Inc (CBAY) 2018 Q1 法說會逐字稿

Good day, ladies and gentlemen, and welcome to CymaBay First Quarter 2018 Financial Results Conference Call. (Operator Instructions)

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 the CymaBay's 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.

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 Investor's 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 program and review upcoming milestones before we open up the call for Q&A.

Before we begin, I'd 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 believe that the expectations reflected in such forward-looking statements are based upon reasonable assumption, actual outcome and results are subject to risks and uncertainties and could differ materially from those forecast due to impact of many factors. The company assumes no obligation to update or supplement any forward-looking statement, whether as a result of new information, future events or otherwise, except 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'd like to turn the call over to Sujal.

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 4 of our most significant accomplishments since the beginning of the first quarter and closed with major catalysts for the remainder of the year before taking question.

Shortly after our presentation at the JPMorgan 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 for both 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 proceed. Including proceeds from the financing, cash, cash equivalent 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 preparations for and meetings with regulatory agencies in the U.S. and Europe to discuss our planned Phase III study of seladelpar in PBC. Seladelpar 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 to the potential treatment of inflammatory liver diseases, including PBC. We have been pleased with the FDA and EMA's level of engagement and their recognition of the need for improved therapies for patients with PBC. We expect we'll be in a position to provide an update on our regulatory discussions 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 in 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 marked the third consecutive year in which data from our development program of seladelpar in PBC was featured in a late-breaker category of 1 of 2 premier annual liver meeting. Pol?

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 for our first 12-week interim data readout in July of last year. After achieving proof of concept where doses of 5- and 10-milligram once-daily demonstrated robust anti-cholestatic and anti-inflammatory effect with no drug-induced pruritus through 12 weeks of dosing, the decision was made to extend enrollments and extend dosing to 52 weeks to primarily support the overall safety database for approval. The ongoing study also continues to provide us with a rich data set around both the efficacy and safety of seladelpar in PBC. As Sujal mentioned, new 12-week and 26-week data for the -- from the ongoing study were featured at EASL International Liver Congress 2018, and you can find the digital poster presented at the Congress on our website. The safety population in the data showed that EASL included 71 patients exposed to at least 1 dose of seladelpar, of whom 53 received 12 weeks of treatment and 42 received 26 weeks of treatment. And baseline in alkaline phosphatase, or AP, was 358, 333 and 262 units per liter in the 2-, 5- and 10-milligram groups, respectively. I'll focus on 4 of the most important takeaways. First for AP, dose response at 12 weeks and dose titration beyond 12 weeks and responder rate; second, anti-inflammatory effect; third, the effect on clinical symptoms, including pruritus; and fourth, overall safety. In the first part of the study, our objective was to measure the dose response between 2, 5 and 10 milligrams. At 12 weeks, we observed a very nice dose response with changes in AP of minus 21%, minus 33% and minus 45% in the 2-, 5- and 10-milligram groups, respectively. With a focus on the 2 most efficacious doses of 5 and 10 milligrams, we further evaluated the effect of -- on dose titration and durability of response through 26 weeks. When we look further at the patient on 5 milligrams, we observed more than half has a response in AP lowering, similar to those on 10 milligrams, while others had a more moderate rejection in AP. After the first 12 weeks, dose titration was permitted for patient with AP remaining above normal and at the level where additional AP lowering had the potential to reduce the risk of disease progression. At 26 weeks, we observed decreasing AP that was similar across regimen, with minus 45% for patients that stayed on 5 milligrams, minus 43% for those that were up titrated from 5 to 10 milligrams after week 12 and minus 43% for those receiving 10 milligrams. At 26 weeks, this decreases in AP led to 69%, 67% and 79% of patients across the 3 dose regimens, respectively, meeting the responder criteria of AP less than 1.67x the upper limit of normal with at least a 15% decrease in AP from baseline and normal bilirubin. The responder rate made up of these 3 criteria has been used as the primary endpoint for accelerated approval in PBC. Overall, 29% of patients had a normal AP at week 26. We believe this profile, around AP reduction responder rate and normalization, positions seladelpar to potentially offer PBC patients improved efficacy over existing second-line treatments.

The second key observation was highlighted by the rapid and robust decreases in serum transaminases, signaling seladelpar's clinically meaningful anti-inflammatory effects. At 12 weeks, medium transaminase changes were minus 9%, minus 28% and minus 35% in the 2-, 5- and 10-milligram groups, respectively. And decreases were maintained at 26 weeks in the 5- and 10-milligram groups where decreases in transaminase were minus 40% and minus 43%, respectively. In addition to anti-cholestatic and anti-inflammatory effects, our third takeaway from these 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- to 10-milligram titration and 10-milligram groups, respectively. And patients in the 10-milligram group, a group that's presented with a clinically relevant level of pruritus, experienced consistent decreases during treatment, approximately 24% at week 26, suggesting potential antipruritic activity. The lack of drug-induced pruritus with seladelpar may be a key differentiation for patients' reliability of the Ocaliva and the potential antipruritic activity will be further illustrated in our planned Phase III study.

Finally, seladelpar was generally safe and well tolerated with no transaminase elevation safety signal. There were 6 serious adverse events and none were being related to seladelpar. We are planning for this ongoing Phase II study to reach full enrollment before initiation of our Phase III study in the second half of the year. I would also like to remind you that in January, we announced the initiation of a long-term extension study that offers patients in our clinical study the opportunity to continue receiving treatment as we move forward in the development program. The first 30 patients reaching 52 weeks of dosing in the ongoing Phase II study have all enrolled in the long-term extension study. We look forward to providing further updates on data from the ongoing Phase II study at future medical meetings. Sujal?

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 the PPAR delta mechanism may be particularly well suited to treat NASH given its beneficial impact on glucose, lipid and sterile metabolism as well as its effect on inflammation and fibrogenesis. On our prior call, we discussed published results evaluating seladelpar in a mouse model of NASH and in patients with mixed dyslipidemia that supported these effects that we believe should have benefit in NASH. The Phase IIb study that we initiated and announced today is 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, fibrosis stage and background co-morbidity, for example, diabetes, as has been studied recently by other sponsors. Seladelpar at doses of 10, 20 and 50 milligrams, taken once daily, will be evaluated versus placebo in a 2:2 to 2:1 randomization. The primary efficacy outcome will be the change from baseline in liver fat content at 12 weeks as measured by magnetic resonance imaging using the proton-density fat fraction method, or MRI-PDFF. Among the secondary measures of efficacy, most notable is the evaluation of histological improvement in NASH and fibrosis as assessed by comparing liver biopsy samples taken at baseline and 52 weeks. Additional important planned assessments include MRI-PDFF measurements at 26 and 52 weeks of treatment as well as the use of the latest available innovative technologies for biochemical markers and noninvasive imaging that reflect inflammation, fibrosis and liver health. We are very fortunate to have Dr. Stephen Harrison, medical director of Pinnacle Clinical Research and a world-renowned expert in NASH, as principal coordinating investigator for this study. We look forward to providing updates on our progress in this study in the near future.

Let me close by leaving you with a few thoughts about our key upcoming milestones that I believe will further drive value through the rest of 2018. We are expecting to conclude discussions with the FDA and EMA around the Phase III registration study for seladelpar in PBC in the coming weeks, which should allow us to provide you with an update on our plans before the end of the second quarter. We continue to plan for initiation of the Phase III study in the second half of this year.

As we approach the second half of 2018, we will also gather 52-week data from the ongoing Phase II PBC study. We believe this data from the ongoing Phase II study can further support the efficacy and safety profile of seladelpar as they potentially improve treatment alternative for PBC patients over current second-line treatments. We are planning to hold an analyst and investor R&D day in New York City before the end of the second quarter where we will provide updates on our progress in both PBC and NASH. We look forward to providing you with more details on this event in the coming weeks.

We view 2018 as another year in which we believe CymaBay can experience significant growth and advance even closer to our goal of bringing novel treatment alternatives to patients suffering from liver diseases with high significant unmet need. The transformation we have experienced in the past year with our development programs and/or financial position now gives us the opportunity to focus on execution, which we believe will continue to drive value throughout the year.

Thank you for joining us today. We would now be happy to take your questions. Operator?

(Operator Instructions) Our first question is from Ed Arce with H.C. Wainwright.

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?

Appreciate it, thanks for the question. I'll start off and perhaps ask Chuck to provide some additional color. I think, primarily, we're powering the study really to assure the primary endpoint on the read and change in 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 in 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 we'll see in the study, of course, I think we've had a number of sponsors with a number of different targets observing 30% to 40% reduction in hepatic fat at 12 weeks. I think that's a benchmark at least that points towards 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 potentially in combination with other targets.

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 time line as you look towards your readouts at 12 and 52 weeks.

Yes. Perhaps I'll add as a 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.

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

Yes. Go ahead, Pol.

No, no, go ahead, Chuck.

Well, I was just going to say that we have established a relationship with one of the leading MRI imaging companies that's Perspectum, and they have developed -- they're 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're 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 the sponsors, things that were, for example, presented at EASL in -- last month at April, that's turned out to be very significant technology in terms of assessing noninvasively the amount of fat in the liver.

Makes perfect sense. I mean I go back to 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?

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%.

Our next question is from Yasmeen Rahimi with Roth Capital Partners.

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

Yes, I'll start off, and Pol maybe can give 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 the study, again, as we think about the potential for seladelpar as a single agent as well as in combination with other target. 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 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, triglyceride and such. And in that study, we really saw similar effect between 50 and 100 milligrams. So 50, ultimately, with respect to some of the metabolic changes we saw in that study, I think is the justified basis for our 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 effects 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.

My second question is for Chuck. Can you tell us a little bit more about the inclusion criteria, zooming in on what percentage of F1s, F2s and F3s are you anticipating to enroll? And then secondly, what MRI-PDFF minimum requirement do you need? And then are you using Perspectum multiscan across all of your patient population or only in select ones?

Maybe I can take the second question, which is the MRI-PDFF. So the threshold for inclusion in the trial is 10%, meaning that you have 10% of your liver, which is actually made of fat. For Perspectum, 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 central review of your data but also to train your center so that you get the best possible results and a consistent evaluation across all the centers. So that's exactly what we are doing with Perspectum. 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 centers. Now to come back to the first question, it's the same as with the question on the IBC. It's a little bit difficult because -- well, what I can tell you is the inclusion criteria, so we're going to enroll F1 to F3, meaning that we're going to exclude patients that are F0, and we're going to exclude patients which are F4. Now the proportion of the patients that are going to be, respectively, in F1, F2 and F3, I would not make a prediction at the moment. Maybe you can look at the literature and look at the trials that have been done in similar populations 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.

And if I may ask one last question. Running the fact that placebo response is running quite high across biopsy-driven data, maybe why select 25 patients in that placebo arm, maybe some thoughts around that rather than keeping it in a higher number.

So what I -- maybe Chuck can comment after me. So this study is a well powered for MRI-PDFF, that's for sure. When you do biopsy, the number of patient 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 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 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 are 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 the...

Well, I think that covers it. And I think our primary examination in this study is really to, first and foremost, focus in on the noninvasive method, look for metabolic effects as well as the markers that have been mentioned. And then to develop a histology correlation, I think one have to be plausible 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 this study, be confident about making the decision for the future development of seladelpar. So one is not looking necessarily for various -- the study wasn't powered, let us put it this way, for the histology, it's powered for the other endpoint, and the histology is designed to inform the decision about where to go next.

Our next question is from Jay Olson with Oppenheimer & Co.

Maybe to shift gears over to PBC for a moment, can you just talk about the reception to the data that was presented at EASL? What kind of feedback from physicians did you receive on that data?

Thanks for the question, Jay. I think 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 see very strong durable response on AP as well as on inflammatory markers, namely the drops in transaminase out to 26 weeks at both 5 and 10 milligrams, were very encouraging. A very nice dose response in the first part of this study up to 12 weeks, between 2, 5 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, a scale that's been used in PBC, in particular to highlight the level of fatigue that patients experience. I'll caution, of course, this in open-label study. And so in order to appropriately assess the effects of seladelpar in both pruritus as well as potentially on fatigue, you'd want to do so in a more robust fashion with the placebo comparator, which is what we will, in fact, do in Phase III. But I think if you look at the trends observed in the data set that was shared at EASL, it continues to give us further encouragement that there may, in fact, be a potential to see antipruritic 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.

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 PBC, similar to the study that was recently presented at EASL, showing a reduction in fibrosis or OCA?

Yes. So maybe I'll make a couple of comments here and then Pol, if he has some additional color to add. In the setting of PBC, biopsy is not necessarily standard these days. So the confirmation of diagnosis can come really from AP levels as well as the presence 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 there's a confirmation of their disease at baseline. And I think our goal primarily is to evaluate the effects on cholestatic as well as inflammatory markers, the end 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.

Our next question is from Joseph Schwartz with Leerink.

Questions on both NASH and PBC programs. 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 it more broadly as an 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 endpoints there. So given your magnitude of impact on alk phos, how are you thinking about PSC as your potential label expansion strategy?

Thanks for the question. So first, with respect to our overall strategy in 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 a single agent activity of seladelpar. We recognize that treatment in 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 course, 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 1.67x 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 outcome, not accelerated approval, which is the path that we have in front of us for being the preferred second-line treatment alternative of choice. So I think the latter is really our focus. That's where the clear unmet need is. The 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 -- patients with PBC highlight the -- an interest, if you will, in using -- if there is a safe and well-tolerated second-line treatment alternative and using that potentially earlier in the treatment paradigm rather than waiting for patient to be in aggregate responders to UDCA after 6 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 1.67x, 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 the 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. PSC, 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 study design, as we do our own exploration into thinking about endpoints that would have meaningful benefit around overall outcomes in PSC, it'll be an area that we continue to do some work and consider exploring in the future.

(Operator Instructions) Our next question is from Robin Garner with Life Science Advisors.

Two questions for you. Can you talk about the rationale for pursuing seladelpar in NASH and specifically speak to the potential of the compounds to improve lipotoxic by MRI-PDFF? And can you also speak to that 52-week endpoint, particularly as it relates to the histological endpoint?

Yes. Thanks for the question, Robin. Chuck, I'll ask you to perhaps address these 2.

Yes, sure. So let's just start mechanistically, PPAR delta and seladelpar as an agonist. The PPAR delta has a strong impact across the natural progression of fatty liver disease to NASH. So as effects on metabolic parameters, it had been shown in the mouse model of an obese-driven NASH to reduce liver fat, to improve insulin resistance and to be anti-inflammatory as well as anti-fibrotic. So across those parameters, that's what really provided the impetus for us to bring seladelpar forward to the study that we announced today. In particular, I'll point out that the reduction, not just in the liver fat but lipotoxic disease, which drives inflammation and fibrosis with the characteristic that we found in our preclinical study. And so we're very intrigued to see if we can first reproduce the effect on lowering liver fat by MRI-PDFF in the clinical study and then, ultimately, to see if that translates into reduction in inflammation as well as in fibrosis using the noninvasive images -- imaging methodologies as well as the histology that we'll get at 52 weeks. And in terms of -- I think if I understood your question around the 52-week point for histology, there's not really an exact formula that one can follow in terms of the time point for that endpoint. We have -- other sponsors have used a time point, and we saw it in Paris last month, to sort of 12 weeks, but others have gone as long as 72 weeks. And in fact, the Phase III study that is currently underway with deoxycholic acid as well as (inaudible) are using a 72-week endpoint. So to us, we thought that 52-week was a really strong endpoint to choose in terms of making sure that we had a durable response, one that wouldn't be subject to as much variability and one that we could be positive in terms of going forward. So that was really the basis for kind of shooting for a 52-week endpoint as opposed to something earlier.

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.

Thank you, operator. I'd like to thank you all once again for joining us today. Over the past 2 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, 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.

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