Welcome to the Viking Therapeutics 2020 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 call is being recorded today, October 28, 2020. 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 Greg Zante, Senior Vice President of Finance. Before we begin, I would like to caution that comments made during this conference call today, October 28, 2020, 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 will now turn the call over to Brian Lian for his initial comments.

Thanks, Stephanie and thanks to everyone listening on the webcast or by phone. Today, we will provide an overview of our third quarter financial results, as well as an update on recent progress and developments with our pipeline programs and operations. I will begin with an update on our lead thyroid hormone beta receptor agonist program, VK2809. During the third quarter, we continued enrollment of patients in our Phase 2b VOYAGE study in biopsy confirmed non-alcoholic steatohepatitis and fibrosis. As of the end of the quarter, the majority of our U.S. clinical sites were open for patient enrollment. So, coronavirus-related disruptions continue to impact site operations. We are currently in the process of expanding the number of clinical sites in the U.S. and internationally and we continue to expect completion of enrollment in the first half of 2021. With respect to our second thyroid hormone beta receptor agonist, VK0214, during the third quarter, we achieved a significant milestone by advancing this compound into clinical development. In September, we announced the initiation of a Phase 1 trial to evaluate the safety, tolerability and pharmacokinetic profile of VK0214 in healthy subjects. Following completion of this study, we plan to initiate a Phase 1b study in patients with X-linked adrenoleukodystrophy. We are excited to be advancing this important program as patients suffering with X-ALD currently have no approved therapeutic options. I will provide additional detail on our development activities after we review our third quarter financial results. For that, I will turn the call over to Greg Zante, Viking’s Senior Vice President of Finance.

Thanks, Brian. In conjunction with my comments, I would like to recommend that participants refer to Viking’s Form 10-Q filing with the Securities and Exchange Commission, which we expect to file later today for additional details. I will now go over our financial results for the third quarter and first 9 months ended September 30, 2020 beginning with the results for the quarter. Our research and development expenses for the 3 months ended September 30, 2020 were $7.1 million compared to $5.3 million for the same period in 2019. The increase was primarily due to increased expenses related to our clinical studies, salaries and benefits and stock-based compensation partially offset by decreased expenses related to preclinical studies and services provided by third-party consultants. Our general and administrative expenses for the 3 months ended September 30, 2020 were $2.7 million compared to $2.2 million for the same period in 2019. The increase was primarily due to increased expenses related to stock-based compensation, salaries and benefits and insurance expenses partially offset by decreased expenses related to legal services and travel. For the 3 months ended September 30, 2020, Viking reported a net loss of $9.3 million or $0.13 per share compared to a net loss of $5.7 million or $0.08 per share in the corresponding period in 2019. The increase in net loss and net loss per share for the 3 months ended September 30, 2020 was primarily due to increases in research and development and general and administrative expenses noted previously as well as decreased interest income due to the decline in interest rates throughout the third quarter of 2020 as compared to prevailing interest rates during the third quarter of 2019. I will now go over the results for the first 9 months of 2020. Our research and development expenses…

Thanks, Greg. I will now provide an update on our recent development activities, beginning with our lead program, VK2809 for the treatment of NASH and fibrosis. VK2809 is an orally available small molecule agonist of the thyroid hormone receptor that possesses selectivity for liver tissue, as well as the beta receptor subtype. Clinical data to-date have demonstrated that VK2809 has compelling potency, selectivity, safety and tolerability profile that may provide benefits in a range of metabolic disorders including NASH. Our enthusiasm for this program stems in part from the results of our previously completed 12-week Phase 2 trial in non-alcoholic fatty liver disease and hypercholesterolemia. These data demonstrated that patients receiving VK2809 experienced statistically significant reductions in liver fat content as well as improvements in LDL cholesterol, achieving the study’s main efficacy objectives. On exploratory measures evaluating other plasma lipids, such as triglycerides, apolipoprotein B and lipoprotein A, treatment with VK2809 also resulted in significant reductions. Importantly, these results were achieved without any serious adverse events being reported among patients receiving a VK2809 or placebo. In the third quarter, additional follow-up data from this trial were presented in an oral presentation at the International Liver Conference, or EASL. The newly reported data demonstrated that patients treated with VK2809 experienced durable, statistically significant reductions in liver fat content that were maintained at week 16, 4 weeks after completion of the 12-week treatment period in the study. Specifically, VK2809 treated patients maintained a statistically significant 45% median reduction in liver fat content at week 16 compared to a 19% reduction among patients receiving placebo. Additionally, at week 16, 70% of VK2809 treated patients maintained the response, defined as experiencing a greater than or equal to 30% relative reduction of liver fat content from baseline. Notably, 100% of patients receiving 5 milligrams of…

Thank you. [Operator Instructions] Our first question comes from Joon Lee from Truist Securities. Please go ahead.

Hi, Brian. Thanks for taking – thanks for the updates and taking my question. I have a question on the additional data you presented at EASL, which I think is notable for more robust liver fat reduction in patients with higher baseline ALT whereas the placebo effects were suppressed in that higher ALT group. I am going to guess that the elevated baseline ALTs and more in line with the demographics that you are enrolling into Phase 2b VOYAGE? Was the powering of VOYAGE factoring in this data stratification specifically or was it based on all the patients that – effects you saw in all the patients in the earlier study? And the second question is that the durability that you saw at the 16 weeks does that change how you might strategize around your Phase B development plans given this durability in terms of the frequency of dosing? Thank you.

Hey, Joon. Thanks for the questions. As far as the subgroups that we looked at, in the 12-week study, that didn’t change our powering assumptions for the 52-week study. We were looking at overall assessments on histologic changes for the powering assumptions. We just thought it was really interesting when you look at pretty much every subset that we could identify that might represent higher risk or typical NASH phenotype that there wasn’t any difference in efficacy. And I think we had another slide in there about baseline liver fat as well and just seemed to be very consistent across ALT, BMI, baseline liver fat, hypertension all of those factors, so baseline glucose as well, so – but we didn’t use that for powering anything. And as far as your second question, what was your second question?

Durability.

Durability. Yes, no, we just think that that’s a pretty interesting, it’s useful scientific data for understanding the kinetics of liver fat changes. It doesn’t feed into our Phase 3 or future development plans, but it is a really interesting finding. It indicates you don’t necessarily need sustained dosing, you might be able to pursue an intermittent strategy that type of thing, but it didn’t really change anything. We expected there to be good durability based on the mechanism and the robustness of the initial signal.

Thank you.

Thanks, Joon.

The next question comes from Derek Archila from Stifel. Please go ahead.

Hey, guys and congrats on the progress and thanks for taking my questions. Just two from us. Just kind of thoughts on the recruitment right now, I know you are saying and still guiding to completing enrollment by the first half of 2021. I think having some conversations with some of your competitors did they seem to have more challenges with enrollment? So I just want to get a sense of how much does your timeline take into effect for kind of COVID and where we are in some of the kind of worsening conditions in the EU, where we think you are going to potentially open the site? So I just want to get your comments on that. And then second just give us a sense of your reg – the regulatory pathway in X-linked adrenoleukodystrophy and what that looks like and could we see data from that Phase 1b study sometime towards the end of 2021? Thanks.

Yes, thanks, Derek. As far as the enrollment in the Phase 2b study, I don’t want to understate the challenges. And so I didn’t mean to make it sound like we are having a super easy time with it. It’s really, really difficult. I think it’s difficult across the board for everybody, but when we look at the site operations, the screening pipeline, that sort of thing, we still think we can do this in the first half of 2021 and that could change if there are statewide lockdowns like we saw earlier this year, but we don’t see that right now. What’s really interesting in looking at the individual sites, they are maintaining pretty open operations despite the surges in certain parts of the country. And I think that weighs more on patient psychologies and then site operations now compared to back in March and April, but it’s very, very difficult. And we are still expecting to complete enrollment in the first half of ‘21 but very, very difficult As far as the registration path in X-ALD, we hope to get into patients in the first half of the year, provided we hit through the multiple dose portion of the ongoing study. And if things go well, it’s possible we would have data next year. I don’t know it’s possible we could be certainly later in the year. And then we plan to talk to the FDA about what the next steps look like. We would expect the endpoints and registration to be more functionally oriented, not biomarker oriented, but we won’t know for sure until we have those conversations.

Terrific. Thanks and congrats again on the progress.

Thanks, Derek.

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

Hi, this is Ryan on for Steve Seedhouse. Hey, Brian, I just want to get a timeline for presenting any additional data from the Phase 2a study, obviously, for the 16 week update or potentially a publication? And are you guys planning on having presenting any data this year?

Thanks, Ryan. No, we are not going to have anything at ASLD We do have a manuscript in preparation on the 12-week study. Most of the bigger journals are prioritizing COVID things right now. So, it has maybe slowed that process down a little bit, but we do intend to submit that in relatively near term. As far as additional data, no plans to-date to have additional data from that study, I think we have presented pretty much everything useful that we could present there, but maybe there could be some more in the publication.

Thanks, Brian.

Thanks.

The next question comes from Mathew Luchini from BMO. Please go ahead.

Hi, guys. Thanks for taking the questions and congrats on the progress. So, just a couple for me. I guess, first on the ex-U.S. sites that are going to be opening up. I think when we last connected on the last quarter update kind of like those were perhaps a little bit more near-term than just to kind of opening up this quarter. So, just wondering if there were any bottlenecks there that prevented those sites from actually coming online until it seems like the end of the year? And then secondarily on 0214 for the SAD/MAD data, should we expect that to – how should we expect that data to be communicated when it comes out would that be just press release? Are you holding enough for a medical conference of some sort? Yes, please on those two.

Sure. Hey, thanks, Matt. So on the ex-U.S. sites, yes, those have been slower than we had hoped to come online. Primarily due to administrative items, we had to submit a couple of documents. So, we had to correct a couple of typos in one document that required a more substantial resubmission of those documents than we had originally planned. It’s just but nothing major it was really pretty minor administrative stuff. And I don’t know, it’s hard for us to judge how much of that is just COVID related with delayed communication timelines between our regulatory liaison and the European regulatory agencies, but that could also play a little bit to those kind of slow timeline there. But I would say, we will be opening some European sites here imminently. So, I think we are on track there. As far as the VK0214 SAD and MAD data, we would hope to have some of those results in the first half of the year and good question on the disclosure strategy, I mean, minimally a press release, but depending on what the data look like, we might try to submit something to a later conference in 2021, but I think that will be driven on what we see if there is anything really exciting or interesting, we might want to save that for a conference, but I would say minimally, a press release, though.

Okay. And then just one last one, if I could, on the numbers, both operating expenses has been quite flat now two or three quarters this year. And I guess we had been expecting perhaps a little bit more of a step up as things had picked up with the Phase 2b, so just wondering how should we be thinking about at least maybe the last quarter of the year and anything you can say, loose or otherwise, as we start thinking forward to $21. With that, I will get back into queue. Thanks so much.

Hey, Matt. Greg, here. Yes, I think, yes, they have been a little bit flat, but we do expect them to continue to increase from here as the trial continues along. So, I think nothing to read into the flatness through this point, I think it will continue to pick up going forward here.

And we always try to be conservative on the estimates, but I think it’s certainly going to pick up.

Okay, great. Thanks guys for the questions and congrats on the progress.

Thanks, Matt.

The next question comes from Michael Morabito from Chardan Capital Markets. Please go ahead.

Hi, Brian. I just had a question, I want to know if there is anything put into place for the VOYAGE trial to treat patients who have endpoints during the trial test positive for COVID during the trial and if there is any kind of a protocol that you put in place for what would constitute rationale for excluding patients that have been affected by COVID, do you have anything like that in place?

Yes, thanks, Michael. It’s a great question. We treat COVID like you would treat the flu in this situation. If someone gets so sick that they can no longer participate or no longer are willing to participate, then they would discontinue, but that’s no different from pneumonia in this specific context – no different from pneumonia or some sort of injury that would preclude them from completing the study. So there is nothing COVID-specific in those discontinuation or withdrawal procedures, it’s just treated as another potential illness or injury that might lead to withdrawal.

Okay. Would you consider taking patients that have tested positive to potentially stratify in a post-op analysis after the fact?

Yes, I don’t know that there would be a meaningful number there, but I think we could certainly look at how those patients responded relative to the COVID-free patients, sure.

Okay, thank you.

Thanks.

The next question comes from David Bautz from Zacks. Please go ahead.

Hey, good afternoon everyone. Brian, we have heard other NASH companies talk about moving their compounds directly into a Phase 2/3 trial. And I was wondering if you could just remind us why you chose to go with a separate Phase 2 instead of Phase 3 instead of doing a combined trial?

Yes, thanks David. Well, the published guidance calls for a 12-month biopsy prior to Phase 3 unless you have got some compelling biological rationale to propose otherwise. And when we were planning the Phase 3, we had originally wanted to do a Phase 2/3, but then the guidance sort of suggested that might not be a good idea. We didn’t have long-term biopsy data as well. And I think most importantly and I think I have said on these calls before, we could not find a single KOL to support that plan. Maybe that’s different for other organizations, but that was certainly our experience. It was – there was no exception to that. It was absolutely 100% consistent. So, it sounds like a great idea. I wanted to do it, but at the end of the day, we didn’t have the biopsy data that the guidance called for and we had no real positive feedback from those who we proposed the structure to.

Okay. And for 0214, I understand you are in a PK study in healthy volunteers and I am just curious if there is some biomarker or other assay that you could look at to see if the drug is hitting the target in these individuals before you move into patients?

Yes, good question, David. So I think the target engagement evidence will come from changes to triglycerides and LDL cholesterol. We are also looking at some of the very long chain fatty acids, but it’s really unclear that those will generate useful data, because most healthy individuals have low levels of very long chain fatty acids. So, it’s not clear that you would see any change there. But we are looking at all those and I think that the target engagement will certainly be answered by the changes to LDL and triglycerides.

Okay, great. Thanks for taking the question.

Thanks, David.

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

Good afternoon and congrats and thanks for taking the questions. This is for the VOYAGE trials that you do have current [ph] arms, which is lower doses, what I am just trying to get is what might be the assumptions or expectations of this lower dose will provide to you versus the more higher dose which you have tested in the previous Phase 2a study?

Hey, thanks for the question. So, the dosing of the Phase 2b overlaps with the Phase 2a, on that higher dose, 10 milligram every other day or where we saw 58% or so, 57% reduction in liver fat. And as you look at those data, it seemed to us that all of those doses, just if we look at the totality of the data, they were all pretty similar. And so we felt that we had room to calm down exposures and likely still see some therapeutic benefit. And so to better understand the dose response, and to also identify the minimally effective dose, we added some of those lower doses. And so we would expect to see efficacy at the higher doses. Certainly, I think when you get down to 1 milligram it’s a little more questionable whether or not you will see a major effect there. But, we will certainly find that out in the study. But that was the reason for the spread of doses and coming down, the reason for the coming down in doses was just due to the fact that all those doses pretty much looked indistinguishable when in the totality.

Maybe just, [indiscernible] I mean, we have talked about RDR that there could be the option of at least contemplating maintain loading dose and subsequently with a loading dose whether this data, let’s say, next year first half of next year, how would that help you to think whether to design the subsequent trials or the Phase 3 trials in this regard although we certainly had that data yet?

Yes, it’s an interesting question. We had actually considered the sort of loading dose maintenance dose in the VOYAGE study. It was just a little complicated. Trial will be difficult enough as it was. So, we decided not to implement that sort of a design. I think in looking at Phase 3, if we were to choose something like that, I am not sure that we would do that, but we would want to know what the histologic benefit is from the lower doses. So, if you thought about starting somebody at a high dose for 12 weeks to induce a robust liver fat reduction then we transition them on to a lower dose. You would want to make sure that if you were to do that the low dose generates some histologic benefits and so we would need to see the longer term data there to make that call. But it is something we talked about here internally. And I think it’s a really interesting idea. I am just not sure that we will pursue it immediately.

Okay, great. Thanks a lot and again, congrats on the progress.

Thanks, Yale.

The next question comes from Jay Olson from Oppenheimer. Please go ahead.

Hey, Brian. Congrats on the progress. And thanks for taking the questions. I am curious if you could comment on some of the recent findings, suggesting that liver fat reduction as measured by MRI-PDFF is predictive of both NASH resolution and fibrosis improvement, and maybe comment on your target level of liver fat reduction in the VOYAGE study. And then on VK0214 I was wondering if you could comment on assuming your Phase 1 studies go well, how soon could you initiate a registrational study in X-ALD? Thank you.

Thanks, Jay. With the second question, we are not sure how soon we would be able to initiate a registration study. I mean, if everything went well, we would target a 2022 for that. But we would need to, have input from the FDA and have trial design everything. But that would probably be the timeframe. And with the first question on liver fat reduction, it just seems like the more data reported, the more supportive it is that the reduction in liver fat sort of indicates the resolution or at least a higher probability of resolution of Nash, and the regression and fibrosis. Now, I would say that’s most important for compounds that target liver fat, if it were a pure anti-inflammatory mechanism, you wouldn’t expect to see that and that might lead to a regression of fibrosis by some other means, but for compounds that reduce that lipotoxic load, the data, I mean, really seeing going back to the Flint study, the data seem to be supportive of the notion that when you have 26%, 28% or more reduction in relative liver fat content, you greatly increase the odds of histologic benefits on the other features.

Great. Thanks for taking the questions.

Thanks, Jay.

Next question comes from Andy Hsieh from William Blair. Please go ahead.

Great. Thank you for taking my questions. So Brian, I think last quarter, you mentioned about in the European region, you are looking at maybe 15 sites and you also gave kind of a breakdown between U.S. and EU, you said something closer to 4 to 1. So given the fact that I think you increased that projection from 80 sites to 90 sites in this quarter, would that ratio be roughly the same is that how we should think about kind of the geographic distribution?

Yes, I think the ratio will be pretty consistent. I don’t think there will be any overweights in ex-U.S. sites and underweights in U.S. as far as the additional sites. Now, I think it’s going to be pretty stable there.

Okay. And then for the EASL presentation, if you look at the weight loss at the end of the study, placebo was probably plus 1 and then across all the dosing arms is about minus 0.5 kilo. So, just curious about your interpretation of that, is that pretty clinically significant given the short treatment period or how do you think about that piece of data or what are you going to do with that data?

Yes, that’s a – it’s an observation that’s not lost on us. We have noticed it. The data, the ends are pretty small here. It’s obviously interesting to see, but I think when you look at this mechanism generally, you don’t really want to see weight loss at least in these sort of early studies, because weight loss is sort of a proxy for thyroid alpha activation. And so if you have a non-selective compound, you see a pretty pronounced weight loss. And so that was one of the reasons we were hoping not to see any significant weight loss, but we do, all of the arms do have this little delta from placebo. We will see in the VOYAGE study if that’s real or not, but we certainly noticed it and that’s – thanks for pointing that out.

I don’t know….

Yes, I don’t know it’s clinically significant, Andy, but we will see over a longer time period.

Yes, okay. Yes, fair enough. Cool. Thanks. Yes, thanks for taking my questions and congrats on all the progress this quarter.

Thanks, Andy.

[Operator Instructions] The next question comes from Scott Henry from ROTH Capital. Please go ahead.

Thank you and good afternoon. Brian, just a question on the 16-week durability of liver fat content reduction, how long would you typically expect a rebound to take place upon ending treatment? Just trying to get a sense of how to interpret 4 weeks in the context of when a patient’s liver would normalize?

Yes, it’s a good question. I don’t know that, that’s really ever been demonstrated in the literature, that’s why this was a really interesting check after 4 weeks. I know, it is also been done with one of the FGF analogs. And I think we see somewhat similar data on the kinetics of that liver fat returning. How long it would take? I don’t know, if you just do sort of linear extrapolation, it would suggest that it’s going to stay off for 4 to 6 months, could be longer, but don’t really know. And I don’t know if that’s been reported anywhere.

Okay. And will you look at data beyond 16 weeks with that trial? Will we get updates in the future?

No. For the 12-week study, the 16-week visit was the last visit.

Okay. And then shifting gears to the X-ALD program, the Phase 1 trial is certainly more involved than typical Phase 1, typically in healthy patients, hopefully it doesn’t hurt anyone. But this Phase 1a is randomized and placebo-controlled. Can you just give us a sense of obviously there is lot more effort going into this with the intent of getting more out of it? And I think you hit on this a little earlier, but what are the main markers that we should be focusing on when we do see that data?

Thanks, Scott. So, I don’t know that it’s anymore complicated, it’s maybe little more complicated in that stack design. So, we do a SAD and MAD sort of simultaneously with the MAD one cohort behind to the SAD, but that’s not an unheard of design and it’s that 8 patients or 8 subjects per cohort. It’s a pretty simple multiple ascending dose structure there. So it’s not highly unusual by any means. We will look at obviously safety, tolerability those sorts of things, but we will also be looking at thyroid hormone axis, the liver panel, everything that you would typically look at as well as some of the early potential signals of pharmacodynamic effect on LDL, Trigs, and the very long chain fatty acids. We wouldn’t expect to see much on the very long chain fatty acids, but we are still looking at them just out of interest.

Okay, great. Thank you for the color.

Thanks, Scott.

The next question comes from Julian Harrison from BTIG. Please go ahead.

Hi, thanks for taking my question and congrats on the steady progress. On the X-ALD Phase 1b data for next year, I am curious if you will be screening out AMN with cerebral evolving and if that’s the plan at first, at what point do you think you might be well informed enough to make a decision on whether or not to broaden development to this more severe subset? Thanks.

Thanks, Julian. Yes. So, we won’t be targeting patients with cerebral involvement. That’s a more serious phenotype and in the 28-day study, I think they are better off considering other options. We will target the adult male population with AMN and just monitor the markers. Moving forward, I don’t know, I think the cerebral cases are more common among children. And so I think that would be something that we would probably look at quite a bit further out than the registration study, which we probably target the same population as the 28-day study, which would be the more of the adult population.

Got it. Thank you. That’s helpful.

Thanks, Julian.

There are no more questions in the queue. 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. Have a good afternoon. Bye-bye.

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