Welcome to the Viking Therapeutics Fourth Quarter and Full-year 2022 Financial Results Conference Call. At this time, all participants are in a listen-only mode. Following management’s prepared remarks, we will hold a question and answer session. As a reminder, this conference call is being recorded today, February 8, 2023. I would now like to turn it over to Viking’s Manager of Investor Relations, Stephanie Diaz. 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 Greg Zante, Viking’s CFO. Before we begin, I would like to caution that comments made during this conference call today, February 8, 2023, will contain forward-looking statements under the safe harbor provisions of the U.S. Private Securities Litigation Reform Act of 1995, including statements about Viking’s expectations regarding its development activities, timelines, and milestones. Forward-looking statements are subject to risks and uncertainties that could cause actual results to differ materially and adversely, and reported results should not be considered as an indication of future performance. These forward-looking statements speak only as of today’s date, 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 good afternoon to everyone dialed in by phone or listening on the webcast. Today, we will review our financial results for the fourth quarter and full-year 2022 and provide an update on recent progress with our clinical programs and operations. 2022 was an exciting year for Viking as we expanded our development pipeline and advanced each of our three clinical programs. With respect to VK2809, our lead drug candidate for the treatment of NASH and fibrosis, we recently announced completion of enrollment in our Phase IIb VOYAGE trial, and we expect to announce top line data from this study in the second quarter of 2023. In addition, the Phase I trial evaluating our newest program, the dual GLP-1 and GIP receptor agonist VK2735 for the potential treatment of metabolic disorders is continuing. We expect to report the initial data from this trial later this quarter. And finally, the Phase Ib clinical trial evaluating VK0214 for the treatment of X-linked adrenoleukodystrophy also continues to enroll, and we expect to complete this study later this year. Our clinical advancements have significantly strengthened Viking’s position as a leader in the development of novel class-leading therapeutics for the treatment of metabolic disorders, and we look forward to reporting data from each of these three clinical programs this year. I will provide further details on our operations and development activities after we review our fourth quarter and full-year 2022 financial results. With that, I will turn the call over to Greg Zante, Viking’s Chief Financial Officer.

Thanks, Brian. In conjunction with my comments, I would like to recommend that participants refer to Viking’s Form 10-K filing with the Securities and Exchange Commission, which we expect to file shortly. I will now go over our results for the fourth quarter and full-year ended December 31, 2022, beginning with the results for the quarter. Our research and development expenses for the three months ended December 31, 2022, were $16.2 million compared to $9.8 million for the same period in 2021. The increase was primarily due to increased expenses related to preclinical studies, manufacturing for the Company’s drug candidates, clinical studies, stock-based compensation, and salaries and benefits, partially offset by decreased expenses related to third-party consultants. Our general and administrative expenses for the three months ended December 31, 2022, were $4.1 million compared to $2.7 million for the same period in 2021. The increase was primarily due to increased expenses related to legal services, stock-based compensation, and salaries and benefits, partially offset by decreased expenses related to third-party consultants. For the three months ended December 31, 2022, Viking reported a net loss of $19.6 million or $0.26 per share compared to a net loss of $12.4 million or $0.16 per share in the corresponding period in 2021. The increase in net loss and net loss per share for the three months ended December 31, 2022, was primarily due to the increase in research and development and general and administrative expenses noted previously compared to the same period of 2021. I will now go over results for the 2022 full fiscal year. Our research and development expenses for the year ending December 31, 2022, were $54.2 million compared to $45 million for the same period in 2021. The increase was primarily due to increased expenses related to manufacturing for the Company’s drug candidates, preclinical studies, salaries and benefits, and stock-based compensation, partially offset by decreased expenses related to third-party consultants and clinical studies. Our general and administrative expenses for the year ending December 31, 2022, were $16.1 million compared to $10.7 million for the same period in 2021. The increase was primarily due to increased expenses related to legal services, stock-based compensation, salaries and benefits, and insurance, partially offset by decreased expenses related to professional services and third-party consultants. For the year ending December 31, 2022, Viking reported a net loss of $68.9 million or $0.90 per share compared to a net loss of $55 million or $0.71 per share in the corresponding period in 2021. The increase in net loss and net loss per share for the year ended December 31, 2022, was primarily due to the increase in research and development and general administrative expenses, as noted previously. Turning to the balance sheet. At December 31, 2022, Viking held cash, cash equivalents, and short-term investments totaling $155 million compared to $202 million as of December 31, 2021. This concludes my financial review, and I will now turn the call back over to Brian.

Thanks, Greg. 2022 was an exciting year for Viking as we expanded our development footprint and made continued progress with our existing clinical programs. Over the past 12 months, Viking not only advanced its two existing clinical programs but building on our expertise in metabolic disorders, we announced the addition of a new internally developed clinical program with VK2735. I will now provide an overview of our progress with each of these three programs, beginning with our lead compound, VK2809, for NASH and fibrosis. VK2809 is an orally available small molecule agonist of the thyroid hormone receptor that is selective for liver tissue as well as the beta isoform of the receptor. We believe activation of the thyroid hormone beta receptor provides unique therapeutic benefits for patients with NASH and that the data to date point to VK2809 as a best-in-class therapeutic for this indication. Data from the Company’s prior 12-week Phase IIa trial in patients with hypercholesterolemia and nonalcoholic fatty liver disease support the promise of VK2809. This trial successfully achieved both its primary and secondary endpoints, demonstrating significant reductions in liver fat and plasma lipids. Further, the trial demonstrated that cohorts treated with VK2809 experienced up to 60% mean relative reductions in liver fat content, and that 88% of patients receiving VK2809 experienced at least a 30% relative reduction of liver fat content. Importantly, the reductions in liver fat were durable, with the majority of patients remaining responders four weeks after completion of dosing. This study also demonstrated the promising safety and tolerability profile of VK2809. No serious adverse events were reported, and the rate of GI disturbances such as nausea and diarrhea was lower among VK2809-treated patients when compared to patients treated with placebo. Perhaps one of the most distinguishing features of VK2809 is its unique effect on plasma lipids, including LDL cholesterol, triglycerides, and atherogenic proteins, all of which have been correlated with cardiovascular risk. Various studies evaluating other NASH development programs have demonstrated elevation of these lipids following treatment. By comparison, patients in Viking’s 12-week Phase IIa study experienced robust reductions in these plasma lipids, suggesting that VK2809 may offer a cardioprotective benefit. For all of these reasons, we believe VK2809’s broad lipid-lowering properties combined with its safety, excellent tolerability, and significant liver fat reduction establish it as a leading drug candidate for the treatment of NASH. Following successful completion of our Phase IIa trial, Viking initiated the VOYAGE study, a Phase IIb trial designed to evaluate VK2809 in patients with biopsy-confirmed NASH and fibrosis. VOYAGE is a randomized, double-blind, placebo-controlled, multicenter international trial designed to assess the efficacy, safety, and tolerability of VK2809 in patients with biopsy-confirmed NASH and fibrosis. The target population includes patients with at least 8% liver fat content as measured by magnetic resonance imaging proton density fat fraction, as well as F2 and F3 fibrosis. Up to 25% of patients may have F1 fibrosis provided that they also possess at least one additional risk factor. The primary endpoint of the VOYAGE study will evaluate the change in liver fat content from baseline to week 12 in patients treated with VK2809 as compared to patients receiving placebo. Secondary objectives include the evaluation of histologic changes by hepatic biopsy after 52 weeks of treatment. Earlier this quarter, we announced completion of enrollment in VOYAGE, and we look forward to sharing top-line results, including the trial’s primary endpoint during the second quarter of this year. I will now provide an update on our newest clinical candidate, VK2735, for the potential treatment of various metabolic disorders, such as obesity, NASH, and certain rare diseases. VK2735 arose from our internal research, leveraging our in-house metabolic expertise to design and evaluate new compounds with promising therapeutic potential. This compound is a dual agonist of the glucagon-like peptide-1, or GLP-1 receptor, and the glucose-dependent insulinotropic polypeptide, or GIP receptor. Initial data from this program presented at the Annual Meeting of the Obesity Society in 2021 demonstrated that GIP receptor activity improved upon the metabolic effects achieved through activation of the GLP-1 receptor alone. Specific findings included improvements observed in weight loss, glucose control, and insulin sensitivity among diet-induced obese mice following treatment with Viking compounds as compared to a GLP-1 monoagonist when administered at the same dose for the same period of time. In addition, the observed reductions in liver fat content were generally larger among animals treated with our compounds relative to the liver fat reductions observed among animals treated with a GLP-1 monoagonist. In 2022, Viking announced the initiation of a Phase I clinical trial of VK2735. This trial is a randomized, double-blind, placebo-controlled, single ascending and multiple ascending dose study. The single ascending dose portion of the study is designed to enroll healthy adults, while the multiple ascending dose portion is designed to enroll healthy adults with a minimum body mass index of 30 kilograms per meter squared. Primary objectives of the study include an evaluation of safety and tolerability of single and multiple doses of VK2735 delivered subcutaneously, as well as the identification of doses suitable for further clinical development. The trial will also evaluate the pharmacokinetics of VK2735 following single and multiple doses. Exploratory pharmacodynamic assessments include evaluations of changes in body weight and liver fat content after four weeks of once weekly administration. This study is ongoing, and we expect to report initial results later this quarter. Our third clinical candidate is VK0214, which is currently being evaluated in a Phase Ib clinical trial in patients with X-linked adrenoleukodystrophy or X-ALD. VK0214 is Viking’s second orally available small molecule thyroid hormone receptor beta agonist in clinical development. X-ALD is a rare and often fatal metabolic disorder caused by genetic mutations that impact the function of peroxisomal transporter of very long chain fatty acids. As a result of the mutations, transporter function is impaired, and patients are unable to efficiently metabolize very long chain fatty acids. The resulting accumulation of these compounds is believed to contribute to the onset and progression of clinical signs and symptoms in patients with X-ALD. In a prior 14-day Phase I study in more than 100 healthy volunteers, VK0214 demonstrated dose-dependent exposures, no evidence of accumulation, and a half-life consistent with anticipated once-daily dosing. Subjects who received VK0214 experienced reductions in LDL cholesterol, triglycerides, apolipoprotein B, and lipoprotein A. This study also demonstrated VK0214’s encouraging safety and tolerability. No serious adverse events were reported, and no treatment or dose-related signals were observed for GI side effects, vital signs, or cardiovascular measures. Following completion of the Phase I study, Viking initiated the Phase Ib study of VK0214 in patients with the adrenomyeloneuropathy or AMN form of X-ALD. AMN is the most common form of X-ALD affecting approximately 50% of those with the disease. The Phase Ib trial is a randomized, double-blind, placebo-controlled multicenter study in adult male patients with AMN. The primary objectives of the study are to evaluate the safety and tolerability of VK0214 administered orally once daily for 28 days. The study also includes an evaluation of the pharmacokinetics of VK0214 in AMN patients as well as an exploratory assessment of changes in plasma levels of very long-chain fatty acids. Pending a blinded review of preliminary data, additional dosing cohorts may be pursued. This study continues to enroll, and we expect to report the initial results later this year. Turning to financials. Our balance sheet remains strong. And as Greg discussed, we completed the year with approximately $155 million in cash. We currently anticipate that our overall R&D expenses in 2023 will be approximately in line with our 2022 R&D expenses. We believe our current cash resources provide sufficient runway to advance each of our clinical programs into later-stage development. In closing, I wish to emphasize the significant transformation that has taken place at Viking over the past couple of years, which accelerated in 2022. Building on our initial success with our lead program, VK2809, Viking has evolved from a company with a single clinical program to a company advancing three distinct clinical candidates for a range of metabolic indications. In 2023, we expect to report clinical data from each of these three programs. With respect to VK2809 for the treatment of NASH and fibrosis, we have now completed enrollment in our Phase IIb VOYAGE trial, and we expect to report initial data in the second quarter. Our Phase I study evaluating the dual GLP-1 GIP agonist VK2735 is ongoing, and we expect to report the initial data from this study later this quarter. And our Phase Ib trial evaluating VK0214 in X-ALD patients continues to enroll, and we expect to report data from this trial later this year. This concludes our prepared comments for today. Thanks again for joining us, and we will now open the call for questions.

We will now begin the question-and-answer session. Our first question will come from Joon Lee of Truist. Please go ahead.

Thanks for taking our questions and for the updates. According to clinicaltrials.gov, the target enrollment for the healthy volunteer study for 2735 is 80 subjects across six cohorts in Part A and five cohorts in Part B. Have you now exceeded your target enrollment and/or maybe added more cohorts? I’m just asking because the estimated completion date is stated as December. Thank you.

Hey Joon, thanks for the question. No, we haven’t added any additional cohorts. It is just a little slower than we would like, but we haven’t prolonged anything.

And you are still enrolling or have you now completed enrollment for the healthy volunteer study?

We haven’t said what we have said is we will have the results this quarter. But keep in mind that the trial is 28 days of treatment, and then there is, I believe, a 60-day follow-up window. So there is a long window there.

Okay and one last question. Are you enrolling both male and female for the multi-dose portion, or is it just men?

It is both.

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

Good afternoon, thanks a lot for taking the questions. Just wanted to ask a couple, first on 2735. So the decisions on dose escalation based on the SRC meetings, I guess they are looking at safety and laboratory data. I just wanted to confirm, is that laboratory data that goes into the dose escalation decision, just all safety or would it include something like serum triglycerides to assess pharmacodynamic activity?

No, it is pretty much a safety-driven determination. They have PK as well, but it is pretty much safety and not really any pharmacodynamic measures on efficacy.

Okay. And just to parlay a question. So did you end up fully enrolling five cohorts in the MAD portion or was it less than five cohorts ultimately?

Well, we haven’t said exactly how many have been. It is ongoing now. So yes, we just haven’t disclosed that.

Okay. Maybe on the pharmacology of that molecule, I’m curious, there are a lot of folks digging in, including us on relative activity across these two receptor targets. Can you comment on if you look at the GLP-1 activity in isolation, and compare that to native GLP-1 activity. Are you more or less or equipotent versus the native peptide specifically on GLP-1? I’m just trying to isolate that variable.

Yes. That is a good question. I think most of these compounds, not just ours, but most of them are less potent on GLP-1. I think the one we looked most at on that receptor was semaglutide, and we are pretty similar to semaglutide. I don’t recall the numbers off the top of my head, but we are pretty close on that.

Okay. Yes. And to hepatitis as well. So that is interesting. Okay. And then just on TR Beta, obviously, lots of focus on that mechanism these days. We have been getting questions again lately on just the dose selection in the VOYAGE study. So I was hoping you could just articulate what key aspects or aspects of the therapeutic window for this mechanism. Are you trying to optimize by testing a series of doses, including lower doses than in the prior Phase IIa study?

Yes, yes. So the prior 12-week Phase II study, when we looked at all of the data, the efficacy data, the changes in lipids, those kinds of things. There were three cohorts, 5 mg a day, 10 mg every other day, and 10 mg daily. And we looked at all the data; they all looked pretty similar. And so it suggested that we were sort of on the far right of the dose response curve. Maybe that is incorrect, but that is certainly what it looked like to us. And so we felt that we had room to come down in dose. And we know that the FDA always likes to have a handle on what the minimally effective dose is. And so we looked back at prior studies and what looked like was that 1 mg dose when you look at the Phase I data it starts to look like it is affecting lipids. And so we thought that would probably be the minimally effective dose. And we then dosed up from there to include a top dose of 10 mg every other day, which was overlapping with the 12-week study. And we thought that was largely equal to the 5 mg daily and the 10 mg daily. And we just spread it out between those, but that was kind of the rationale.

Thanks Brian. Thanks for the questions.

Thanks Steve.

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

Hey guys, good afternoon, thanks for taking the question. Brian, I don’t think it is too early to ask this question, but as you look towards a potential Phase III for 2809, obviously, the clinical trial community has been gaining in their understanding and traction with TR beta on two different fronts with two different assets. So I guess with the other asset being a little more mature, how would you consider or what kinds of things are you considering to handle regarding, say, competition for patients to enroll into your pivotal study?

Well, I think that there are enough patients out there to enroll Phase III studies even if there is an approved agent with the same mechanism. And we have seen that in the diabetes space in the past with multiple approved GLP-1s; there are still trials enrolling GLP-1 agonists and plenty of other indications that share those characteristics. So I mean NASH is hard to enroll under any circumstances, but I don’t think competition will be a significant problem there. It is just a hard side to enroll anyway.

Sure, very helpful, thank you.

Thanks Joe.

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

Hey, this is someone on the line for Jay. Congratulations on the progress. I have a couple of questions. First, regarding 2809, in the Phase IIa study, you indicated that the toxicity or gastrointestinal adverse events were actually lower in the treatment groups. Could you remind us if this is related to the liver-targeting property of 2809 and how we should anticipate gastrointestinal tolerability in the Alzheimer's study? Additionally, do you see a potential to combine 2809 with all GLP-1 in the future? I also have a follow-up question about 2735.

Yes, to answer the second question first. Yes, I think 2809 could be combined with a variety of different compounds and oral GLP-1s could be one of those. With respect to the GI tolerability, we just haven’t seen anything like that in any of the prior studies. And I don’t know that it is necessarily because it is liver-targeted; just something we haven’t seen.

Okay, thanks and for 2735, maybe just following a previous question. I know there was like a few dose cohorts were initiated maybe in the second half of last year. So just wondering, for the upcoming readout, should we expect to see data from all cohorts or only some of the cohorts? Thanks.

Yes. We hope to have the data from all of the cohorts. It has been, I know it has been slower than everybody would like, including us, the holidays kind of broke that up a little bit as well. And then we had a couple of cohorts that got split. And since it is a Phase I unit, it is not necessarily available to have patients come in the next day if they miss a day. So that has just dragged out some of the cohorts. But we do believe we will have the data this quarter from all the cohorts.

Okay. Thanks again for taking the question.

Thanks.

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

Thanks for taking our question. So obviously, there is a lot of movement in the NASH space recently. Just curious about your thinking in terms of the correlation between liver fat reduction or the magnitude of that and leading to fibrosis from a histological perspective?

Yes. Thanks, Andy. I think it is fairly well-established correlation between reduction in liver fats and improvement in overall histology, including fibrosis, and that has been shown in pharmacological studies but also in weight loss studies. But there are exceptions. There are some mechanisms that have been shown to reduce liver fat and haven’t resulted in other histologic improvements. And I don’t know why that is. But most of them would appear to show that when you reduce liver fat, particularly above 30% relative reduction, you have higher odds of success on NASH resolution and fibrosis improvement.

Got it. That is helpful. Going on to the 2735 program, maybe as a whole, looking at your in-house compounds, as you anticipate the readout from the Phase I SAD/MAD study and also indication selection. I’m just curious about kind of the potential to advance other assets, right? There are, I forgot, maybe half a dozen or so development candidates that you presented. And I’m curious if there is any sort of special unique characteristics that might be good for a specific indication, same thing for 2735, anything that you saw there that would position you well for potentially rare disease versus other bigger metabolic diseases?

Yes. That is a good question, Andy. We have looked at a whole bunch of these, and we continue to explore different peptides. And we have sort of a scoring system that we have used, and that has helped guide us to make some decisions on which compounds to prioritize. And that kind of that is kind of the early part of the discovery work. And then we look at the in-vivo data, PK, and efficacy models to help prioritize. As far as the indications to select, I think just globally, when you look at the opportunities for the mechanism, it is NASH, diabetes, obesity, and then a couple of smaller indications. And we would like to view the opportunities kind of like we look at with the thyroid beta agonist where we have got 2809 and a bigger opportunity, NASH, and then VK0214 in the orphan indication. I think if we were able to parallel that with the dual agonist, and we had something in a large indication and a different molecule in a smaller indication, that would be ideal. And I think we will be pursuing that as we move forward.

Great, thanks for answering all of our questions.

Thank you, Andy.

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

Good afternoon and thanks for taking the questions. In terms of 2735, we understand that, obviously, after the data release, you will make some additional decisions, pending that outcome. But nevertheless, would you give me a top sort of view what you and possibly anticipate to do after the data release in this quarter? Thank you.

Yes. Thanks, Yale. Well, we would hope to pursue an IND in the U.S. following completion of this study. And so we would hope to pursue that sometime around the midyear time point and then proceed from there. And we will have more information and details around the plans for Phase II once we release the Phase I data.

Okay, great. Thanks and I appreciate it.

Thanks, Yale.

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

Thank you and good afternoon. Just a couple of questions. First, spending in the quarter was a little higher than earlier in the year. How should we think about spending in 2023 relative to 2022? And perhaps the cadence throughout the year as far as the quarters?

Hey Scott, I think we did make the comment, Brian did in the earlier comments that our R&D expenses will be pretty consistent. We expect in 2023 versus 2022 in total for the year. So I think those drive most of our spending; the R&D expenses do. So I guess we could think about our spending lining up pretty closely with our R&D expenditure. So if we are - we look at that pretty consistently, I think.

Okay. And consistent through the year as well, any trends we should factor in?

No, I would say pretty evenly throughout the year, just looking at the plans ahead. So yes, I would say pretty evenly.

Okay. Great. That is helpful. And Brian, sort of a big-picture question. Clearly, the valuation of the company has changed over the last months. Does that impact your strategy with some of these assets going forward just in terms of development, perhaps how long you keep them and the options that are available to you?

Scott, well, not really. We have always said that when we look at some of these large indications like NASH, it would be preferable to have a larger party involved in Phase III and beyond. And that is still our preference. I think as the market cap changes, you might have more opportunities to do things yourselves. But that doesn’t change our preference to have a partner involved in later-stage studies.

Okay. Great and final question, just with regards to 2735. Obviously, obesity is a very hot indication right now in significant market. Is there anything in your safety profile or your expected safety profile that would make it better or worse than similar agents out there? I mean, diabetes is certainly a more straightforward market, but obesity. Just wondering how it compares to other similar class agents.

Yes, I think on tolerability, it is a challenge to differentiate. If you modulate the GLP-1 receptor because it is hard to extricate efficacy from nausea with that mechanism and so I think the plus is that clinicians and patients both are aware of that titration seems to help, and it is generally transient. It happens early. And if you can get through the first month or two of dosing, then you are probably past most of those tolerability issues. And I think there is receptivity to - or at least acceptance of tolerability issues if you are confident that you are going to lose weight, and that is the big differentiating feature of these agents is they just induce profound weight loss. So I think it is hard to separate on tolerability when you have this mechanism, but I think it is okay given the familiarity and most patients will accept it if they know they are going to lose weight.

Okay. Thank you for taking the questions.

Thanks Scott.

The next question comes from Justin Zelin of BTIG. Please go ahead.

Hey guys, thanks for taking the question and congrats on the progress. I will add a question on 2735. So obviously, you are going to be looking at safety, tolerability, PKA, and PD here. Do you think that you will be able to see some signs of efficacy in four weeks here or do you think you will probably need to look at a longer time period on drug to start seeing some weight loss?

Hey Justin, that is a great question. I think 28 days is really hard to see weight loss in. So we are going to be looking most at tolerability, PK informing us for what sort of regimen we take forward into a Phase II study. When we look at the potential pharmacodynamic measures, body weight is of the greatest interest of people. And I think the hurdle we are really looking at there is if we can show efficacy that looks similar to a GLP-1 monoagonist, I think that would be pretty exciting. And generally, that is in the sub-2% range, 1% to 2% over 28 days. We feel that would be exciting because we know that we are hitting GIP and we know in the animals, we see a clear separation from GLP-1 monoagonist, and we believe that that is going to augment the activity of GLP-1, but we just don’t know whether or not that is going to be fully observed or observable in a treatment course as short as 28 days. So we are trying to be pretty conservative on the expectations for efficacy there since it is such a short study.

Great that makes sense for me. Thanks for taking the question.

Thanks Justin.

The next question comes from Naz Rahman of Maxim Group. Please go ahead.

Hi guys, thanks for taking my question. And I had a few, but I will focus on 0214 kind of shifting a little bit. What the data expected later this year, could you just kind of walk us through what you are sort of hoping to see in the study or what you are looking for?

Yes. With this study, we are going to be looking - it is a Phase Ib study. So we will look at safety and tolerability and PK in the patient population. We saw really encouraging tolerability and pharmacodynamic effects in a shorter study in healthy volunteers, but they didn’t have adrenoleukodystrophy. So we will look at PK and see if there are any differences. And on the pharmacodynamic side, we will look at changes in very long chain fatty acids, which are believed to contribute to the course of disease in these patients. Those will be the main areas of focus.

Just could you remind us, are you looking at any notable biomarkers in these patients?

Yes. I think very long chain fatty acids would be the key biomarker we would be looking at there.

Okay. Got it. On the study line, could you also remind us if you plan on enrolling the third cohort in the study?

Oh, the third dosing cohort. Well, we have three cohorts now. It is a placebo and then 20 and 40. And when we have enough data to make a decision, we may or may not add a higher dose cohort.

Got it. And when you release the data, are you going to release the data from the cohort separately or are you just going to wait until you have data from all three cohorts?

It is a parallel design. So we would really solve the data together.

Okay, got it. Thanks for answering my questions.

Thanks, Naz.

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 great afternoon.

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