Good afternoon and welcome to the Viking Therapeutics' Fourth Quarter 2018 and Year-End Earnings Conference Call. [Operator Instructions] Please note, this event is being recorded. I would now like to turn the conference over to Stephanie Diaz, Investor Relations. Please go ahead.

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, March 13, 2019, 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 listening on the webcast or by phone. Today, I'll provide an update of our key 2018 accomplishments, as well as an update on recent progress and developments related to our pipeline programs and operations. 2018 was a pivotal year for Viking as two of our clinical programs yield the best-in-class data and we raised sufficient capital to advance our pipeline to an important value inflection points. Last September, we announced the results of a Phase 2 study of our novel thyroid receptor beta agonist, VK2809, in patients with hypercholesterolemia and non-alcoholic fatty liver disease. This study achieved both its primary and secondary endpoints, demonstrating statistically significant reductions in plasma lipids as well as liver fat after 12 weeks of dosing. These data provide compelling evidence of VK2809 safety and efficacy and support our decision to proceed with further development of this program in the setting of nonalcoholic steatohepatitis or NASH. In 2018, we also reported additional results from a Phase 2 trial of our novel selective androgen receptor modulator VK5211 in patients recovering from hip fracture. This trial successfully achieved its primary and secondary endpoints, demonstrating VK5211's potent effect on muscle growth in this frail population. Underscoring the importance of the data from both our VK2809 and VK5211 clinical programs, each of these two studies was featured in podium presentations at international conferences in their respective areas. In addition, earlier stage results demonstrating VK2809's promise in reducing liver fat and inflammatory markers were featured in a podium presentation at a third major conference in September. We are proud to have received the recognition at these events as they validate our own enthusiasm for our programs and support our view that the depth, quality and productivity of our pipeline differentiates Viking from many of our competitors in the development stage biopharmaceutical space. Based on the success of our pipeline programs, we were able to significantly strengthen our balance sheet in 2018 through offerings of common stock that resulted in total gross proceeds in excess of $315 million. I'll provide additional comments on our 2018 accomplishments, but first we'd like to review our fourth quarter and full year financials. I'll now turn the call over to Michael 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-K filing with the Securities Exchange Commission which I expect to find later today for additional details. I'll now go on the financial results for the fourth quarter and fiscal year end of December 31 2018. Our research and development expenses for the three months ended December 31, 2018 were $5.1 million compared to $3 million for the same period of 2017. The increase was primarily due to increased preclinical study efforts, manufacturing expenses related to our drug candidates, use of third-party consultants and stock-based compensation, partially offset by a decrease in clinical study expenses. Our fourth quarter general and administrative expenses were $1 million, compared to $1.4 million for the same period in 2017. The increase was primarily due to increased expenses related to stock-based compensation, salaries and benefits, and legal and patent expenses. For the three months ended December 31, 2018, Viking reported a net loss of $5.2 million or $0.07 per share, compared to a net loss of $4.1 million or $0.14 per share in the corresponding period in 2017. The increase in net loss for the three months ended December 31, 2018 was primarily due to the increase in research and development expenses noted previously, partially offset by an increase in other income related to the increase in interest income. The decrease in net loss per share for the three months ended December 31, 2018 is primarily driven by the additional shares outstanding at December 31, 2018 versus those outstanding at December 31, 2017 given the additional shares issued by the company during 2018 primarily through equity offering. Our research and development expenses for the 12 months ended December 31, 2018 were $19 million compared to $13.7 million for the…

Thanks Mike. Viking was founded with a mission of advancing a pipeline of promising small molecules. Our goal today is the same as it has always been. And that is to maximize the value of these programs in parallel with maximizing their benefit to patients in areas of high unmet need. With support from investors, we have been fortunate to receive the financial resources necessary to conduct the clinical studies to establish proof-of-concept with our most promising metabolic and endocrine programs. In late 2017, we reported a positive outcome from a Phase 2 trial of our novel selective androgen receptor modulator, VK5211, in patients recovering from hip fracture surgery. As previously discussed VK5211 produce a significant improvement in muscle mass in these patients as demonstrated by the successful achievement of the trials primary and secondary outcome measures. We were therefore excited this past year in 2018 to follow this initial success with the completion of a Phase 2 trial of VK2809, our novel thyroid receptor beta agonist in patients with hypercholesterolemia and fatty liver disease. The results of this study provide compelling evidence of VK2809 efficacy in this setting and we are preparing for next steps to advance the program. As a reminder VK2809 is an orally available agonist 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 2 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 every day or placebo for…

[Operator Instructions] Our first question comes from Steven Seedhouse with Raymond James. Please go ahead.

Brian, just to clarify that I heard you correct, did you say that all is in 10 of 10, 5 milligram patients were responded or so had greater than 30% reduction in liver fat content?

All of them. That is 9 of the 10. One did not receive a second MRI, one of the - so when you look at the 12 who are additional randomized there was one placebo patient and one VK2809 who did not get a second MRI.

And I want to also just ask about adverse events in the Phase 2, study of VK2809. There seems to be some uncertainty amongst investors here and actually similar scrutiny of AEs and intercepts Phase 3 NASH study. So obviously pretty topical right now in this space. I believe with the update today you've reported that there were no serious AEs I think across any of the arms in the study but my question is just related to any great treatment emergent AEs. Could you just clarify if there was any imbalance in treatment or emergent hepatobiliary or hepatic AEs or separately in treatment emergent cardiovascular AEs across the treatment arms in either 5 milligrams or 10 milligrams in the Phase 2 study?

So we don't have the patient by patient data from all of the arms yet. The 5 mg efficacy data were just recently received. I think we'll be getting the safety data later this month should be before EASL. So I'm not going to be able to give a lot of granularity treatment emergent. Well, there are no treatment emergent serious adverse events, treatment emergent to grade them I just don't have that off the top of my head. There weren't any major trends associated with receiving VK2809 and I just recall in the overall adverse event numbers, the highest number was in the placebo arm and not in the treatment arms. Yeah. So I don't know if I can get too far into the details about all of the data in hand.

Maybe turning to VK5211 this arm, you just mentioned at the end of the call exploring some orphan indications there. So there are actually some recent data for an oral testosterone drug in novel, but looks like it can reduce liver fat by about 30% or 40% and that mechanism also reduces ALT in patients and yeah, Arun Sanyal and Stephen Harrison, just some experts are pretty high profile folks in this field out in the related press releases essentially saying that the data and the mechanism are promising and worth pursuing further. So you have your SARM. Obviously I'm wondering if you've just ever entertain the idea of running a 12-week MRI-PDFF study with that molecule to see if you have anything there in NAFLD or NASH?

It's a really interesting question. And the answer to that is prior to those data being reported no. But when we saw that I thought that was pretty interesting and when you actually look at the body composition in the 12-week study, you saw a gain in muscle and the reduction in the fat content, which is I mean we would support the thesis they activate the androgen receptor and you can see some leaning. But, we're not going to pursue that near term, but it's really interesting I think that's a, that's a really cool approach to it you know especially in certain subpopulations.

And maybe I just have two quick ones to wrap up here so. Are you going to show 6 - the 16-week MRI measurements that is on if - I mean, I think that's four weeks after you stopped dosing in the Phase 2 study. And if so, what's - do you know what the half-life is a VK2809 in the liver after you've reached steady state, is it cleared pretty quickly or does it hang around for a few days or weeks and even if you know you're not going to have 16-week data? I think you already presented some metrics ASOBs so just want to make sure I'm interpreting …

Yes. So…

… so, data in the context of drug levels correctly?

So I don't believe we have tissue specific half-lives, I don't think that was ever determined, but I could be mistaken I have to go back and check but I don't recall ever seeing that. We do have the 16-week data from the 10 mg every other day and the 10 mg daily. I think we'll be getting the 16-week data from the 5 mg at the end of the month or early next month, if possible we would include that in the EASL, but in the EASL presentation, but I'm not positive that will have it, hopefully we will.

Last one for me. So you indicated I think I was on the last earnings call maybe that the final report from the six-month road and primary GLP talks studies and the Phase 2 study report for VK2809, were expected maybe late 1Q or early 2Q so. I guess the question is do you have those reports now and would the filing of your IND I guess upcoming be a fair indication that there were absolutely no issues that arose in those studies that concerned either you or FDA?

Yes. A critically important question. It's something we're spending a lot of time on. So I'll say consistent with our prior comments, we're not going to give a lot of detail on the completed animal studies and that's consistent with the industry standards as well. Right now the timing is to submit all of the data the human as well as the animal data to the FDA and have a pre-IND meeting around mid-summer. Summertime is the timing it looks like. There's nothing we're aware of that will prevent us from proceeding into the next study as we've planned. And I guess that's as far as we should really go at this point. But we feel good today.

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

Two questions. On VK2809 do you have any guidance I know it's still being decided ahead of your FDA meeting but before the approximate size of the Phase 2b and then secondly for VK5211, can you disclose any potential types of indications you might be interested and as part of your partnering discussions how are they going number one, and are you considering any potential options to co-promote as the program develops? Thanks.

On the size of the VK2809 program, I think it will be a robust study and we don't know exactly how many arms will be in there and obviously that's going to be a critical driver of science, but I would say on the low-end 150 and it could be up from there. With VK5211 some of the orphan indications that might benefit from this mechanism would be some of the muscular dystrophy and some of the orphan other small opportunities where muscle impairment plays a role in disability. And we are having some of those conversations today. On the hip fracture side, I think the regulatory path here in the U.S. has just made it, I think challenging for future progress. I think potentially in Europe, but there is a little bit more flexibility on clinical endpoints but in the U.S. it looks very difficult today. Is that answers your questions. Sorry.

Just that the part about optionality in your discussions for partnering would you maybe look to have or have the desire to have a potential co-promote option as part of your discussions?

It's always an option. Maybe, I mean as we sit here today, we have 16 employees, so 17 employees, it is just not something that is feasible today. But I guess as we mature and progress that, that could be an option especially in the smaller allegations it's I think realistic if there is a disease that has a certain number of specialized treatment centers where everybody goes. I mean, that makes a practical for a small company, but larger indications, I think, it would be very difficult.

The next question comes from Edward Nash with SunTrust. Please go ahead.

Congratulations on 5 milligram daily. This is Fang-Ke Huang for Edward Nash. And the first question is just to clarify, I remember you mentioned that the duration for animal study is nine months and you try to do it for 12 months, is that correct?

Well, the duration of the rodent study was six months and then we did a six-month primate study and ongoing is a 12-month primate study.

And the second one is you mentioned that it potentially got tested for lower dose down 5 milligram in the Phase 2b. Can you just remind us historically what those just tested in maybe other trials not in natural trial, but what other tools has been tested and how low you can see you can be?

So in the 14 day Phase 1b study, the doses ranged from 0.25 milligrams a day up to 40 milligrams a day. And you began to see efficacy and really kind of see something happening 1 milligrams to 2.5 milligrams and that really kind of you would see it more clearly above five. Where we see the efficacy in the liver and this is maybe a function of the liver targeting technology. I think fair to say robust at 5 meg and so it would certainly suggest that below 5 mg, you would see some efficacy I think would be hard to argue otherwise looking at the data.

And then, the next one I want to think about. You mentioned that it going to in the Phase 2b trial, the duration can be up to a tough math. I think the company start demonstrating an improvement in histology in liver as short as 12 weeks. And do you think what is your current thinking in terms of the duration the Phase 2b and is possible they're going to run that trial for shorter than 12 month?

So you know the - a lot of prior studies have looked at, at nine months and you're right with other mechanisms there has been a histologic benefit as short as 12 weeks. I guess the way we're looking at this is the current guidance calls for a 12-month biopsy. Now some of our advisers are suggesting that nine months is still likely to be sufficient. But I think this is something that we would like to ask in the pre-IND meeting with the recommended duration. And I think also when you think of this [indiscernible] data mechanism you know it may take some time to generate some of the little more clarity around the anti-fibrotic endpoints and if that's - if that's true maybe 12 months is a little bit better to establish the efficacy signal. But we're kind of discussing and thinking about all of these questions right now.

That makes sense. The last one, I'm sorry. So the last one is around VK0214, is that also a prodrug and also own and targeted deliver?

So it's a prodrug that is cleaved in the plasma, it's not targeted to the liver. So it's cleaved by [indiscernible] and so it's a little bit more diffuse. And that's the reason we started looking at that in X-ALD is that it just feels like not a liver specific disease and therefore you don't necessarily need the deliver targeted prodrug technology. So it's a different prodrug. That said we've also looked at the free phosphonic acid and different salts of that free phosphonic acid. And those also look very, very interesting. So it's just got a different profile altogether. It's a little bit more selective, it's about anywhere from 25 to 45 to 1 beta over alpha, still single digit animal or KI. So a really, really, really interesting compound that I think you know as a potential future in X-ALD and you know hyperlipidemia every place we think it might work I think it could also work.

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

So the first question has to do with exposure and PK profile. Could you remind us is there a significant difference between dosing once a day 5 milligram versus every other day for the 10 milligram cohort?

They're actually pretty similar as you might expect when you look at the overall means but the Cmax is obviously higher with the 10 mgs every other day than it is with the 5 mg daily. But yeah anyway does that answer your question?

Yes. So the second question has to do with VK0612. You know I think the street is probably not as familiar with this program the fructose-1,6 bisphosphonate - bisphosphatase inhibitor. Do you mind reminding us the scientific rationale, I think on the website you said this is a Phase 2 ready asset and also data generated to date, is it a pro-drug designed selectively get activated and deliver and what's the strategy here?

So, this is what Viking, the original license for Viking was for VK0612, so it's a - it is a very, very special molecule to the company. So, it is a different pro-drug. It's not - it doesn't use the hep direct technology. It inhibits an enzyme called fructose-1,6-bisphosphatase which is the second to the last step in endogenous gluconeogenesis. And it is shown in two different studies in type 2 diabetics to result in a - I think a very robust reduction in fasting plasma glucose and those were 14-day study and a 28-day study, highly statistically significant up to 59 mgs per deciliter which if that held it would translate into a 1.5% to 2% reduction in A1c. We haven't been aggressively developing it. I think when we were starting the company, there was some hesitation on the part of investors to - for small company to look at type 2 diabetes, but it doesn't diminish our enthusiasm for the mechanism and the prior data and the safety profile of the molecule. And at some point I think it would be worthwhile to explore a 12-week study to really demonstrate that it provides A1C reduction that is predicted from the fasting plasma glucose effects.

So from a strategic perspective, so partnership is kind of out of the question here and I guess related to that and kind of a follow up to Steve's question earlier. Would it be - would you entertain the possibility of combining in a NASH setting with VK2809, just to address kind of the metabolic syndrome aspect of the disease.

So, it's - I mean, it's a good question. And just to go back for a second, the door is always open here. So partnership is not off the table for any of our programs. So we're always interested in discussing opportunities with partners. As far as combinations, I think we thought about a lot of different combinations with the game VK0612. And the potential benefit in NASH patients, I mean, that's might make sense. And I don't guess anything more than that right now.

The next question comes from Yale Jen with Laidlaw and Company. Please go ahead.

You guys going to present a five meg data at the EASL and you suggest that it's sort of robust. Also my question to you is that should the data be robust enough that you guys can contemplate any sort of possibilities such as you have a higher dose, loading dose and subsequent with the maintenance those kind of regimen. How would you think about these things in general?

We thought a lot about that. That's a great question, Yale. So for example if you start for three months on a higher dose and then reduce somebody to a very low maintenance dose given the potency and the liver selectivity that you know might make sense. And so it's just one of the elements that we're thinking about for the upcoming Phase 2b study. We haven't made any final decisions there, we do want to keep the study you know manageable and small enough to complete in a timely fashion. But you've asked an important question and it's possible that you can answer that question with a smaller shorter study rather than putting it into a longer Phase 2b.

And just in that regard what do you see the potential sort of economical or let's put this way, patient benefit or the payer any payer benefit or not if that's potentially a sort of regimen can be used or can be considered?

Well I think the patient benefits you know I think generally people would favor you know low doses. I think generally people would favor you know not initiating probably pharmacy if it's at all possible. So the benefits of a single agent that can be effective at the very low dose I think would resonate well with both clinicians and patients. When you talk about payers you know it sounds like the initial payer receptivity is going to be highest in fibrotic patients and this is something that a lot of people sort of overlook when they think of the thyroid beta mechanism. There are anti-fibrotic benefits to activation of the thyroid beta receptor. It's in the literature we've shown it in multiple studies of our own. We presented this at AASLD in 2017. We see a reduction in collagen load, we see a reduction in fibrosis, we see a reduction in a whole range of genes associated with fibrotic signaling. So the notion that a thyroid beta agonist is just a metabolic agent I think it is incorrect and the data show that there is a lot broader effect than just a metabolic benefit. And if you can show a benefit on fibrosis that looks like the first place the payers are going to be most eager to reimburse.

And maybe one more question here which is VK0241 in X-ALD. Do you have a general picture regarding the Phase 1 study that you're probably going to start very early next year or latest year in terms of patient size? Can you start to look into having patients now to gauge some sort of signal efficacy signals so anything you can talk about that potential Phase 1 study or Phase 2?

On the patient side so what we can say that there is sort of a single ascending dose that blends into or transitions into a multiple ascending dose study that transitions into a 28 day study in patients. And so as you get far enough along in your SAD you can begin the multiple ascending dose cohorts as you get far-left long there you can start to roll some patients in. And I think that that sort of one-stop study would be very efficient and very capital efficient really. We would look at a very long chain fatty acid changes at 28 days. And if we see something then we would consider you know what the next study might look like which could potentially be a registration study there.

Where these patients - will be the sample flown from the plasma or from other tissues?

It would be well just to show the proof of concept, we look at plasma. That would be the probably the easiest and most efficient way to demonstrate proof of concept.

The next question comes from Scott Henry with ROTH Capital. Please go ahead.

Just a couple of questions. First on VK2809 as we start to get some parameters around the Phase 2b, obviously that could change both the FDA meeting. But how should we think about the enrollment time period to enroll 150 patients?

So we'll adjust the number of sites commensurate with any changes in enrollment there. So we would we would hope that that would be close to a wash with the larger trial size. And I think when you look at some of the other you know studies of similar size, the precedent is out there for the enrollment timeline and the timeline to the initial liver data followed by histology data. So you know there have been some - some recent examples there in the competitive landscape that allowed you to map that out.

So it sounds like we should be thinking about greater things could change about - two year process from start to finish. Is that a reasonable way to think about the time table?

Well, I think it's possible maybe to go more quickly than that. Hard to know. But for example one recent Phase 2 study took about five quarters from initiation to the initial reading on liver fat and then around you know six to seven before the histology data were available. I don't think that's an unreasonable time frame. But again very hard to predict until we get the size and enrollment criteria identified.

And then just a modeling question, when we think about R&D, obviously the biggest lever for 2019, I mean it sounds like it should track kind of similar to Q4 for the beginning of the year and perhaps spike up in Q4 maybe a little bit in Q3, is that how we should think about the R&D trajectory in 2019?

I don't think that's unreasonable. You know that's - I think that's a fair statement, it's a relatively flattish for the first half of the year and then it should begin to pick up in the second half.

The next question comes from David Bautz with Zack Investments. Please go ahead.

So from a competitive standpoint, you are a little bit behind some of the other players in the field and in NASH. So I'm wondering what ultimately made you decide and to go with the Phase 2b and not to do a combined Phase 2b/3 trial?

I don't think the lag in timing is as big an issue as maybe it's being made out to and there are multiple examples of the best therapy coming in second, third, fourth, or fifth and taking a large share of the market. So, I think, the history of drug development is rife with those sorts of examples. For us in comparing the Phase 2/3 to the Phase 2 standalone, the feedback from clinicians and KOLs and really vendors was unanimous in favor of the Phase 2 relative to the Phase 2/3. And so despite the fact that you can put on paper this very streamlined and presumably less expensive trial that rolls from Phase 2 to Phase 3, if no one wants to enroll a patient in that type of study, it takes away the timeline and the cost savings. And we heard that - multiple times we heard NASH Doc saying, if I've got several trials to choose for enrolling my NASH patients this would be my last choice. And that was really important feedback and that helped to push us toward a Phase 2b.

The next question comes from Mayank Mamtani with B. Riley FBR. Please go ahead.

Just a couple from me, at the highest level just taking a step back, just about the mechanism thyroid hormone receptor agonist. I mean you have two IND that are different in indication and I'm assuming different groups in the FDA and then obviously we have the End-of-Phase 2 meeting also for a more advanced asset, is there anything from a framework standpoint that FDA looks for when it looks for the class? And then more specific to your agent have you ever disclosed the safety margin or in other words how high the animal studies you may have tested your dose and relative to that what do you have -- in humans, maybe that ratio have you talked about that?

We haven't. I'll say that in the prior 13 weeks studies in animals the doses didn't go high enough to really determine a safety margin and that was really it was a little bit of an issue because whenever you propose the study design you have to discuss your proposed exposure levels in humans and how those exposure levels you know relate to the exposure in animals where adverse events were observed. Up dose in both the prior rodent and primate studies would be the no adverse effect level. So it was you know just impossible to test with the margin. We are dosing I would say substantially higher to eliminate that question in any future evaluation of the margin. And so I think we [really] answer that question for the next study.

And any comment on the class and how maybe FDA historically has looked at it and maybe how that view may have evolved at the FDA's level?

We know that you know the FDA has looked at the class with particular focus on the known issues associated with less selective thyroid agonists. And those are issues related to cardiovascular safety and bone and cartilage safety. And so we know those are areas of particular interest to them and those are areas that we look particularly closely at in all of our studies

And then just one minor question about the Phase 2 study. As you think about the therapeutic window it looks like the 5 mg gets you very close to the every other day dosing. So, it's lot of the thinking and you commented on that before just go lower dose and if you're getting the similar therapeutic benefit that would sort of be the way to go or do you think to get an anti-fibrotic benefit which is where the system will pay for the value. You want to dose as high as you could potentially?

Yes. It's a - now this is an excellent question, and I don't know the answer. No. Is there some different in dose response between fibrosis and liver fat. I don't know the answer to that. If it - if there is you might argue for a higher dose. But if you are causing all of the downstream effects that impact fibrosis and fat reduction with the same dose then you wouldn't have to. But I don't know. We didn't see in prior animal studies any sort of a separation there between fibrotic benefit and liver fat benefit. And we know that when you reduce a person's body weight by for example 10% that NASH resolves and fibrosis improves. And I think we're in that range. So - but is there some different effects, I don't know. It's a great question.

Your next question comes from Caroline Palomeque with Maxim Group. Please go ahead.

I'm just wondering if you could give any more color on the Phase 2b protocol for 2809 as far as - is it safe to assume that you'll be focusing the endpoints on the approvable you know fibrosis and resolution?

So I think we would look at a whole host of exploratory endpoints there. You know fibrosis I mean I'm sorry. I'm sorry NASH resolution with that worsening of fibrosis and you know the proportion of patients who experience some improvement in fibrosis without worsening of an NASH. All of the above would be explored in the study. Yes.

And then just a question on your pipeline. Just so for VK2809 in the glycogen storage disease, just wondering if that will be moving into the clinic anytime soon.

No, it's a great question and I think there's a lot of promise in that indication. We decided towards the end of last year to really focus on NASH for the near term maybe at some future date we could revisit the GSD but right now I think the company's resources and focus are in our view most effective in the NASH indication today.

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 months. Thanks very much and have a great afternoon.

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