Viking Therapeutics, Inc. (VKTX) Q3 2018 Earnings Report, Transcript and Summary

Welcome to the Viking Therapeutics’ 2018 Third Quarter Financial Results Conference Call. At this time, all participants are in a listen-only mode. Following management’s prepared remarks, we will hold a Q&A session. [Operator Instructions] As a reminder, this conference call is being recorded today November 7, 2018. I would now like to turn the conference over to Viking’s Manager of Investor Relations, Stephanie Diaz. Please go ahead, Stephanie.

Hello and thank you all for participating in today's call. Joining me today is Brian Lian, Viking's President and CEO, and Michael Morneau, Vice President of Finance and Administration. Before we begin, I'd like to caution that comments made during this conference call, today, November 7, 2018, will contain forward-looking statements within the meaning of the Securities Act of 1933 concerning the current beliefs of the Company, which involve a number of assumptions, risks, and uncertainties. Actual results could differ from these statements, and the Company undertakes no obligation to revise or update any statement made today. I encourage you to review all of the Company's filings with the Securities and Exchange Commission concerning these and other matters. I'll now turn the call over to Brian Lian for his initial comments. Brian?

Thanks, Stephanie. And thanks to everyone dialing in and listening on the webcast. Today, I'll be providing an update on recent progress and developments related to our pipeline, programs and operations. The third quarter was a particularly exciting period for Viking as both of our lead clinical programs achieved key milestones. During the quarter, we reported positive data from a Phase II trial of our novel thyroid receptor beta agonist VK2809, in patients with elevated LDL-cholesterol and non-alcoholic fatty liver disease. This trial achieved both its primary and secondary endpoints, demonstrating statistically significant improvements in plasma lipids and liver fat content. We look forward to presenting these results at the upcoming meeting of the American Association for the Study of Liver Diseases. Also during the quarter, the results from a previously completed Phase II study of our novel selective androgen receptor modulator VK5211, in patients recovering from hip fracture were presented at the oral plenary session of the Annual Meeting of the American Society for Bone and Mineral Research. We believe the selection of these data for this prestigious session highlights the potential of VK5211 in the fracture recovery study. In addition, in early October, the results from a study of VK2809 an in vivo model of glycogen storage disease were highlighted during the oral plenary session of the Annual Meeting of the American Thyroid Association. These results highlighted further evidence of VK2809 beneficial effect on inflammation and fat metabolism, which we believe are relevant to a variety of liver diseases, including NASH. Finally, we strengthened our balance sheet during the quarter through an offering of common stock, putting us on solid financial footing to further advance our pipeline program. I'd like to begin today's call with a review of our third quarter financial results after which I will provide an update on our most recent corporate development. I'll now turn the call over to Mike Morneau, Viking’s, Vice President of Finance and Administration to discuss our financial results. Mike?

Thanks Brian. In conjunction with my comments, I’d like to recommend that participants refer to Viking’s 10-Q filing with the Securities and Exchange Commission, which we expect to file later today for additional details. I’ll now go over the financial results for the third quarter and first nine months of 2018. Our research and development expenses for the three months ended September 30, 2018 were $5.7 million compared to $3.5 million for the same period in 2017. The increase was primarily due to increased manufacturing expenses related to our drug candidate, preclinical study efforts, use of third-party consultants and stock-based compensation partially offset by a decrease in clinical study expenses. Our third quarter general and administrative expenses were $1.7 million compared to $1.2 million for the same period in 2017. The increase was primarily due to increased expenses related to stock-based compensation, salaries and benefits, professional services, insurance expenses, legal and patent expenses, and franchise taxes. For the three months ended September 30, 2018 Viking reported a net loss of $6.6 million or $0.11 per share compared to a net loss of $6.1 million or $0.22 per share in the corresponding period in 2017. The increase in net loss for the three months ended September 30, 2018 was primarily due to an increase in research and development expenses noted previously, partially offset by decreased expenses related to the change in fair value of the debt conversion feature liability and an increase in interest income. Our research and development expenses for the nine months ended September 30, 2018 were $14 million compared to $10.7 million for the same period in 2017. The increase was primarily due to increased expenses related to preclinical study efforts, manufacturing related to our drug candidates, use of third-party consultants and stock-based compensation partially offset by a decrease in clinical study expenses. Our general and administrative expenses for the nine months ended September 30, 2018 were $5.2 million compared to $3.9 million for the same period in 2017. The increase was primarily due to increased expenses related to stock-based compensation, salaries and benefits, professional services, insurance, legal and patent expenses, and franchise taxes. For the nine months ended September 30, 2018 Viking reported a net loss of $16.8 million or $0.32 per share compared to a net loss of $16.5 million or $0.67 per share in the corresponding period in 2017. The net loss for the nine months ended September 30, 2018 was consistent with a net loss for the corresponding period in 2017 primarily due to the increase in research and development expenses noted previously offset by an increase in other income related to the decrease in the fair value of the debt conversion feature liability as well as an increase in interest income. Our balance sheet at September 30, 2018 showed cash, cash equivalents and investments totaling $304.2 million. As of October 31, 2018 Viking had 71,459,857 shares of common stock outstanding. This concludes my financial review and I'll now turn the call back over to Brian.

Thanks Mike. During the third quarter, we made multiple announcements highlighting data from our development programs, which we believe serve as an important reminder of the breadth and depth of the value drivers in our pipeline. I'll summarize the highlights now. In September, we were pleased to announce positive topline results from a 12-week Phase II study of VK2809, our novel thyroid receptor beta agonist. As a reminder, VK2809 is an orally available agonists of the thyroid hormone receptor that possesses selectivity for liver tissue, as well as the beta receptor subtype, suggesting promising therapeutic potential in a range of lipid disorders, including non-alcoholic steatohepatitis or NASH. Our Phase II trial was a randomized, double-blind, placebo controlled parallel group study designed to evaluate the efficacy, safety, and tolerability of VK2809 in patients with non-alcoholic fatty liver disease and elevated LDL-cholesterol. Patients were randomized to receive 10 milligram oral doses of VK2809 every other day or 10 milligrams of VK2809 everyday or placebo for 12 weeks. The trial's primary endpoint evaluated the effect of VK2809 on LDL-cholesterol after 12 weeks compared to placebo. The secondary endpoint, which for many was the endpoint of greatest interest assess the change in liver fat by MRI proton density fat fraction after 12 weeks. Other endpoints assess changes in atherogenic lipid, safety and tolerability. We were pleased to report in September that the study successfully achieved its primary and secondary endpoint. With respect to the trials primary endpoint, the results demonstrated that patients receiving VK2809 experienced statistically significant reductions in LDL-C compared with the placebo-treated patient. In addition, VK2809-treated patients experienced statistically significant improvements in other lipids, including the atherogenic proteins, apolipoprotein B and lipoprotein A. While we are happy to achieve our primary endpoint, results for our secondary endpoint are potentially even more important for the future development path for VK2809. As we reported in September, topline results demonstrated that patients receiving VK2809 experienced unprecedented reductions in liver fat content compared with other oral agents. Specifically patients receiving VK2809 dosed at 10 milligrams every other day for 12 weeks experienced a median relative reduction in liver fat content of approximately 57% from baseline as assessed by MRI-PDFF. Patients receiving VK2809 doses of 10 milligrams daily experienced the median relative liver fat reduction of approximately 60% from baseline. By comparison, patients receiving placebo experienced a median relative reduction in liver fat content of approximately 9%. The magnitude of these effects, particularly at these low doses is very encouraging. To our knowledge, this magnitude of liver fat reduction is unprecedented among oral agents and development for NASH today, so no head-to-head studies had been conducted. We believe these results at these relatively modest doses support our view that VK2809 unique liver targeting features provide differentiated benefit on this important measure of efficacy for NASH. Trial also included the responder analysis, which was intended to assess whether the observed reduction in liver fat may predict broader clinical benefit. Patients were characterized as responders if they experienced a greater than or equal to 30% relative reduction in liver fat content. This threshold is of interest as multiple studies have demonstrated that one liver fat is reduced by 30% percent or more, a corresponding increase in the odds have improved overall histology is also observed. Our responder analysis of our data revealed encouraging results, among patients treated with VK2809 dosed at 10 milligrams every other day, approximately 77%, demonstrated at least a 30% reduction in liver fat content. Among patients treated with VK2809 dose of 10 milligrams per day, approximately 91% demonstrated at least a 30% reduction in liver fat. We also performed an additional responder analysis looking for patients whose liver fat was reduced by half or 50% over the course of study. We coined the term super responder to define this population and found the exercise intriguing because a 50% relative reduction is substantially larger than the 30% at which histology has been shown to improve. In this analysis, approximately 67% or two-thirds of all patients who received VK2809 in this study experienced at 50% or greater reduction in liver fat. This outcome is compelling as we believe it confirms not only the depth, but also the breadth of the signal observed in this study. Starting to safety, VK2809 was shown to be safe and well tolerated in this study. No serious adverse events were reported among patients receiving VK2809 or placebo. The overall numbers of adverse events were relatively evenly distributed across treatment arms. So numerically, there were slightly more observed among patients randomized to placebo. Finally, VK2809 was shown to be extremely well tolerated in this study. We're encouraged by the safety and tolerability profile, display it thus far, particularly in light of the potent pharmacodynamic effects demonstrated in the efficacy measures. Overall, we believe these results point to a best-in-class therapeutic profile for VK2809. Following our receipt of the results, we submitted a late-breaker abstract for presentation at the Liver meeting, which is the Annual Meeting of the American Association for the Study of Liver Diseases. In October, we are notified of abstracts acceptance and we're happy to say that our presentation will be part of the Late-Breaking Oral Abstract Session I, which will take place on Monday, November 12 in San Francisco. In addition, we were informed that our abstract has been nominated for inclusion in the best of AASLD, which serves to highlight contributions of particular important at each annual meeting. Given these results, we're in the process of preparing for next clinical steps with VK2809, which we anticipate will involve a study in patients with biopsy-confirmed NASH. The design of that study is a topic of intense focus at the company and we are working diligently with our advisors on the best path forward. At this point, we plan to file an IND and initiate the next clinical study in 2019. As we proceed with the planning and implementation of next steps for VK2809 in NASH, we had also been evaluating our efforts in the area of glycogen storage disease. As a reminder, as we've discussed in prior updates, VK2809 has demonstrated impressive efficacy in vivo models of GSD Ia. In this work, VK2809 produce substantial reductions in liver fat content as well as improvements in inflammation and on autophagy, which are characteristics that support the compounds potential benefit in both GSD Ia and NASH. However, given the efficacy signal that was observed in our recent Phase II study, we have decided to focus our efforts more closely on the development of VK2809 for NASH. As a result, we plan to defer additional clinical work in GSD Ia. I want to emphasize this does not imply any lack of enthusiasm for VK2809 potential benefit in this important setting. It merely reflects our belief that the focus required to successfully execute a program in NASH will not allow us at this time to dedicate the attention required to effectively manage a clinical program in GSP Ia. I'd now like to turn to Viking’s other orphan disease program, which is evaluating our small molecule thyroid receptor agonists VK0214, as a potential treatment for X-linked adrenoleukodystrophy or X-ALD. X-ALD is a devastating disease caused by a defect in peroxisomal transporter called ABCD-1. These patients are often characterized by the accumulation of very long chain fatty acids in plasma and tissue. Sustained elevations in very long chain fatty acids are believed to contribute to the severe cerebral and motor neuron toxicities commonly observed in the disease. Activation of the thyroid beta receptor is believed to stimulate the metabolism in very long chain fatty acids, providing a potential therapeutic benefit. VK0214 is an orally available small molecule thyroid receptor agonist that possesses selectivity for the beta receptor subtype and may therefore represent a potential pharmacologic approach to the disease. Last year, we and our collaborators at the Kennedy Krieger Institute completed a 25-week study evaluating VK0214 in an animal model of X-ALD. The result of this study showed promising effects on markers of disease, notably an improvement in very long chain fatty acid levels in both plasma and tissue. We're currently conducting IND enabling work for this program and plan to file an IND to conduct a proof of concept study in 2019. I’ll now provide an update on VK5211 our novel selective androgen receptor modulator for musculoskeletal disorders. As a reminder, VK5211 is designed to selectively stimulate muscle and bone formation with reduced activity in peripheral tissues such as skin and prostate. Following surgery to repair hip fracture, many patients experience a loss of bone and muscle at accelerated rates placing them at increased risk of further morbidity, refracture and prolonged disability. For these reasons, hip fracture is a serious medical condition and as our population continues to age we believe the incidence of hip and other fracture injuries will continue to increase. It is our belief that VK5211 may represent an important treatment option for these patients by stimulating the formation of muscle and bone thereby improving musculoskeletal health and facilitating recovery from the injury. Topline data from our Phase II study in-patients recovering from hip fracture were announced in November of last year. The results showed the trial successfully achieved its primary endpoint demonstrating statistically significant dose-dependent increases in lean body mass, less head, following treatment with VK5211 as compared to placebo. The study also achieved important secondary endpoints demonstrating statistically significant increases in appendicular lean mass, as well as total lean body mass for all doses of VK5211 compared with placebo. In addition, though not powered for significance, endpoints assessing physical functions also showed numerical trends favoring treatment arms. Importantly VK5211 also demonstrated encouraging safety and tolerability in this study with no drug-related serious adverse events reported. During the third quarter Viking was notified that the results from our Phase II study were selected for presentation as part of the oral plenary session at the annual meeting of the American Society for bone and mineral research. In addition, we were informed that our abstract had been awarded the Most Outstanding Clinical Abstract Award by the ASBMR Conference organizers. The study results were presented on September 30 and we were honored to have received such a prominent position at this important meeting. We believe that this recognition speaks about the quality of the data generated as well as the potential for VK5211 to offer a much needed treatment option in this setting. During the second quarter, we submitted request to the FDA for Type C meeting to discuss the potential regulatory path forward for VK5211 in hip fracture. Later in the third quarter we received written answers to the questions posed in our Type C meeting briefing package. These comments provide useful input for further development of VK5211 hip fracture. As we've indicated on prior calls, in our view, any subsequent studies of VK5211 in orthopedic indication would be best executed by partner, particularly one with an existing bone or musculoskeletal franchise. We continue to explore partnering opportunities that will allow us to optimize the value of VK5211 and move the program forward in the most efficient manner possible. We will provide updates on these activities as warranted. I'll now wrap up with some comments on a recent corporate activity. During the third quarter following the announcement of positive Phase II data for VK2809, we completed a successful offering of common stock which resulted in gross proceeds of approximately $176 million. This financing provides us with the funds needed to aggressively advance our pipeline programs and provides a financial runway that we expect will it extend beyond 2020. We are grateful to the investors who participated in this offering and we wish to thank all of our investors for their continued support as we move forward. In conclusion, during the third quarter, we announced Phase II data indicating that VK2809 holds tremendous promise as a potential therapeutic for fatty liver diseases such as NASH. We look forward to presenting these results in just a few days. Also during the quarter, we’re honored to have the Phase II data from our VK5211 program presented at the ASBMR Annual Meeting and recognized as the most outstanding clinical abstract by the conference organizers. We continue to explore partnering opportunities for VK5211. And finally, we are continuing to build our clinical pipeline by advancing our VK0214 program for X-ALD. We currently planned to file an IND and initiate a proof-of-concept trial for this program in 2019. These assets combined with our exceptional team and the support from our investors have positioned Viking for further success in the clinic and with potential partners. This concludes our prepared statements for today. Thanks again for joining us. And I'd now like to open the call for questions. Operator?

We will now begin the question-and-answer session. [Operator Instructions] The first question comes from Edward Nash of SunTrust Robinson Humphrey. Please go ahead.

Hey, thank you for taking my question. This is [indiscernible] on for Edward Nash. The first question I want to ask is regarding your program for NASH, and previously you indicated you’re going to have a meeting with FDA. I just want to know the progress regarding the meeting? And have you thinking change in terms of where they're going to do a Phase II, III trial? Or are you going to do a Phase IIb trial? And I have a follow-up.

Yes, sure. Thanks for the question. So we're actually evaluating both approaches right now and haven’t made any decisions, a lot of input in that decision. But we would plan to file an IND to proceed in the biopsy-confirmed NASH sometime in the first half of next year.

Great. And my second question is on the VK0214. So there – are the company now developing ex-vivo gene therapy for the disease? And just want to know that how are we going to position 0214 in the context of that devolvement? Thank you.

Yes, thanks. So that's primarily being developed for the childhood cerebral form of the disease. And we would probably be targeting the adult population that presents with the adrenomyeloneuropathy form of the disease. So there wouldn't be in our view, any sort of a major competitive issue there. What we've also seen is that certain individuals who have successfully been treated with bone marrow transplant actually go on to develop AMN later in life. So although it's considered curative early, there are incidences of people developing AMN. So that would actually assist in the market for the adult population. I hope that makes sense.

Thank you so much. And congrats on the progress.

Thanks.

The next question comes from Steven Seedhouse of Raymond James. Please go ahead.

Thanks for taking the question. Brian, you mentioned plans obviously for NASH, IND in 2019. I think the Street at this point is cognizant of – some of the ongoing long-term preclinical toxicology studies for 2809 being a gating factor for that NASH trial. Just curious if you're going to announce or present those preclinical data once they're analyzed and update the Street on the status of that and any subsequent FDA meeting?

Yes. Steve, thanks for the question. So probably not. Companies typically don't announce their GLP doc studies. I mean, the whole goal of those studies is to generate a toxicity signal. So people just don't publish that, announced that, so unlikely I think the next steps here would be to file the IND and proceed forward.

Okay. So the IND filing I guess is the [indiscernible] detail I guess that we will be looking for. That's helpful. And then just – I mean, could you just remind us why those animal toxicology studies, why they hadn't been conducted prior to this year? And did it have to do with switching of indications to NASH for 2809 and those studies just not being required for the previous indication?

No, no. To be totally honest, we couldn't afford them. So we have always been somewhat capital constrained and as soon as we had the sufficient funding to move forward with them, we got them underway. But it was difficult with a balance sheet, does thin as it was for so long with us to plan out studies that may or may not have been completable with the runway. So that's the answer.

Got it. Okay, that’s pretty clear. And just lastly, so you mentioned on the last – on the call that you had following your Phase II data, obviously you're presenting those data AASLD, we're all looking forward. To that presentation, but you had mentioned another abstract that you submitted a describing the liver safe – the aggregate liver safety data for 2809. It looks like that that didn't end up in the late-breaker line up. I'm just curious if you have plans to present or announced those data elsewhere, sort of near-term either at Investor conferences, maybe early next year or a Medical meeting, or if not, are you able to share any of – just key conclusions or take homes that otherwise might have been presented at the meeting that are now?

Yes. Yes, so liver safety be in the presentation on Monday. But this was a sort of a comprehensive look at all of the multiple dose studies at VK2809. And so we had hoped that it would have been accepted, but it doesn't it doesn't necessarily fall under the description of a late-breaker. So I think had we submitted it under the normal timeframe, might have been a different response. But I don't know, I think the idea there might be to submit it for Easel. And that that submission deadline is toward the end of November.

Okay, great. Looking forward to the presentation in a couple of days here. Thanks.

Okay. Thanks Steve.

The next question comes from Joe Pantginis of H.C. Wainwright. Please go ahead.

Hi, all. Good afternoon. Thanks for taking the question. Brian, just wondering, I know you had mentioned on the last quarterly call or even not think it was the 2809 call that you might provide a further details or the results of the Type C meetings. So I'm just curious if you can provide any of the answers that the FDA provided to you guys. I know you were looking at potential composite endpoints, various structural or functional types of endpoints, quality of life, et cetera. So can you provide any of the answers?

Yes. It's a great question, Joe. We haven't provided a lot of information. We are providing all of that to the parties that are interested in learning that information. But there were no real surprises in the FDA feedback. In a perfect world, I think muscle mass would have been an approvable endpoint for Phase III. But we had always expected that was a long shot and that the FDA was likely to require something along the lines-of-function and quality-of-life, patient-reported outcomes, and that's really a sort of the global feedback. It was a more that to proceed and hip function and quality of life would probably be the more important endpoints and muscle would be an important surrogate, but not necessarily an approvable endpoint, so no surprises, but, anyway, yes.

Got it. That's fair. Thank you. And then just quickly for 0214, what are some of the remaining gating factors with regard to ongoing IND enabling studies to get to the filing?

Yes, so we're working on the formulation there. We're working on the 28-day talks and then all of the other reproductive – all the other stuff that goes into the IND. So, all ongoing today, but it’s a lot of work, all invisible pretty much, but a lot of work, right.

Right, great. Thanks, Brian.

Yes, thanks Joe.

The next question comes from Andy Hsieh of William Blair. Please go ahead.

Hey guys. Thanks for taking my question. Just one following up on Steve's question earlier. I think before you kind of frame the extra poster presentation in terms of safety as a presentation on the panel review. So the way that I understand it is – there's a panel outside of DSMB made evolve liver experts you kind of adjudicate all the safety events? Is that I'm going to be a part of the oral presentation or is that part will be completely reserved for the Easel presentation next year.

So I'm not sure. It's a good question. Thanks again, I don't know that we ever characterized it as a poster to adjudicate liver safety. It was a comprehensive view of prior studies. It is a comprehensive review of prior studies. During the run up to the data presentation, we did convene a panel of NASH and a drug induced liver injury experts to walk through all of the Phase II data, but this poster included not only the Phase II data, but also the 14 day data and any prior multiple dose study. So I'm sorry if I that was a miss communicated certainly wasn't at a poster written by the panel not at all. It was asked one of the panelists actually was a coauthor on it though. But we would plan to submit that for Easel.

Gotcha. Yes, the apologies for my confusion. So related to that, regarding the IND for 2809, I believe on the last call you talked about the two tox studies, one in rodent and then one in primate. So is the rodent study almost completed? I'm just trying to get a sense of, what's completed, what's not and in terms of the more refined timing.

Yes. So both the six-month primate, rodent studies are going to be completed this quarter and we would likely receive the audited study reports sometime late first quarter, early second quarter. That's kind of the broad timing there.

Great. Okay. Well congratulations again and all. I guess I'll see you on Monday.

Okay. Thanks.

[Operator Instructions] The next question comes from Yale Jen of Laidlaw and Company. Please go ahead.

Good afternoon, Brian. Thanks for taking the questions. I'm not going to steel a lot of thunder for the AASLD presentation. But could you talk a little bit about the favorable context of the data to be presented at that meeting later this month?

Thanks Yale. Did you say the framework of the data?

Probably would be – there is a lot of topline data have been presented earlier at these press release, so what other sort of additional aspect we should be looking into at a presentation one to anticipate to be there?

Yes, sure. So the primary endpoint data haven't been detailed previously. The lipid changes haven't been detailed previously. And then the AE profile hasn't really been detailed, so we'll have some more information on those. But it is a pretty short presentation, 15 minutes total. But they are pretty typical for Phase II oral presentation.

Okay. That's very helpful. And I know you are not going to provide a lot of details regarding the meetings – the FDA meetings regarding 5211, but you’ll also talk about composite endpoint. Is there additional sort of colors you can share regarding the endpoint or the prosperity be included in this composite endpoint or aspect to be included in the endpoint?

Yes. Well, it's kind of going back to my earlier answer. We did receive some feedback, but the FDA never gives you a detailed recipe for approval in these sorts of communications. They did suggest that function and quality of life were more important for registration than simply muscle. But there was no – well we're not going to provide a lot more detail and communication there. But generally the FDA does not provide specific endpoints in this sort of setting. You would have to propose then the trial and come back to them. But if a function and quality of life seem to be the umbrella areas that they're most interested in.

And I assume that what sort of expectation to eventually having a partner – you would like to have the partner also to have a greatest thing in terms of – in the next discussion with agencies. So ultimately it will be a better collaboration in that regard. Would that be fair?

Yes, I think we would let the partner a design the study, but we've certainly used what we know about the molecule to assist in that design along with the FDA feedback. But I think the partner would probably drive the process.

Okay, great. Thanks a lot. Appreciate it. And I look forward to the presentation later on.

Thank you.

The next question comes from Caroline Palomeque of Maxim Group. Please go ahead.

Thanks for taking the question and congratulations on all the progress so far. Just wondering with a lot of programs sitting in the clinic in 2019, I was just wondering what the trends might look like in R&D expense, because I think in the past you'd said that you expect them to remain flat, but just wondering what we might be – how you might be seeing R&D in the next year or so?

Yes. So we expect it to be pretty consistent over the next two to three quarters and then begin to tick up the second half of next year. I'll let Mike for any additional color there yet.

Yes, no that's fair. Over the first – at least first half of the year is expect to be consistent and then after that we’ll start to see some uptick.

Okay, great. And then just a quick follow-up on the 2809, just wondering if you could add any more color on trial design or will you just announce the trial design when you do the IND in the first half of 2019? Will there be any kind of prior announcement?

Well, I think as soon as we get our heads around what the end points might look like in both options and we're thinking about a Phase IIb is a standalone, which is very traditional. You'd have a biopsy confirmed endpoint after nine months or 12 months or a Phase II/III where you may have some early interim that allows you to narrow dose and proceed from there. And that's a much complicated design that we have not worked out all of the details that we're focused on understanding that right now. So I think as soon as we have a good view of the pros and cons of both approaches that we would communicate what the next steps are.

Great. That's helpful. Thanks Brian. Thanks, Caroline. End of Q&A

This concludes our question-and-answer session. I would like to turn the conference back over to Stephanie Diaz for any closing remarks.

Thank you again for your participation and continued support of Viking Therapeutics. We look forward to updating you again in the coming month. Have a great afternoon. Bye-Bye.

The conference has now concluded. Thank you for attending today's presentation. You may now disconnect.