Welcome to the Viking Therapeutics 2022 Second Quarter Financial Results Conference Call. At this time, all participants are in listen-only mode. Following management’s prepared remarks we will hold a Q&A session. As a reminder, this conference call is being recorded today, July 27, 2022. 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, Viking’s CFO. Before we begin, I would like to caution that comments made during this conference call today, July 27, 2022, 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 thanks to everyone dialed in by phone or listening on the webcast. Today, we will review our financial results for the second quarter of 2022 and provide an update on recent progress with our pipeline programs and operations. During the second quarter, we continued to advance each of our three clinical programs. With respect to our lead compound, VK2809, we continued enrollment in the Phase 2b VOYAGE study, targeting patients with biopsy-confirmed NASH and fibrosis, and we expect to complete enrollment in this study in the second half of the year. We also continue to enroll subjects in a Phase I trial of our newest clinical program evaluating VK2735, a dual agonist of the glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide receptors. We are eager to evaluate the results from this study, and we expect to report the initial data later this year. Finally, with respect to our second novel thyroid hormone receptor beta agonist, VK0214 for the treatment of X-linked adrenoleukodystrophy, as discussed on our last call, the FDA earlier this year had requested the completion of an in vivo study prior to continued dosing of patients in a Phase 1b study of this compound. During the second quarter, we successfully completed the requested study, submitted the results to the FDA, and were recently informed that the trial may proceed as planned. We are currently in the process of resuming the study and look forward to reporting results in 2023. I will provide further detail on our operations and development activities after we review our second quarter 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-Q filing with the Securities and Exchange Commission, which we expect to file later today. I will now go over our financial results for the second quarter and first six months ended June 30, 2022, beginning with the results for the quarter. Our research and development expenses for the three months ended June 30, 2022 were $13.5 million, compared to $12.8 million for the same period in 2021. The increase was primarily due to increased expenses related to manufacturing for the Company’s drug candidates, clinical studies, stock-based compensation, and salaries and benefits, partially offset by decreased expenses related to preclinical studies and services provided by third-party consultants. Our general and administrative expenses for the three months ended June 30, 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. For the three months ended June 30, 2022, Viking reported a net loss of $17.4 million, or $0.23 per share, compared to a net loss of $15.4 million, or $0.20 per share in the corresponding period in 2021. The increase in net loss and net loss per share for the three months ended June 30, 2022 was primarily due to the increase in research and development expenses and general and administrative expenses noted previously, compared to the same period in 2021. I will now go over our financial results for the first six months of the year. Our research and development expenses for the six months ending June 30, 2022 were $26.1 million, compared to $24.3 million for the same period in 2021. The increase was primarily due to increased expenses related to manufacturing for the Company’s drug candidates, stock-based compensation, salaries and benefits, and clinical studies, partially offset by decreased expenses related to preclinical studies. Our general and administrative expenses for the six months ending June 30, 2022 were $7.8 million, compared to $5.4 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. For the six months ending June 30, 2022, Viking reported a net loss of $33.5 million, or $0.43 per share, compared to a net loss of $29.4 million, or $0.38 per share in the corresponding period in 2021. The increase in net loss and net loss per share for the six months ended June 30, 2022 was primarily due to the increase in research and development expenses and general and administrative expenses noted previously. Turning to the balance sheet at June 30, 2022, Viking held cash, cash equivalents, and short-term investments totaling $169 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. During the second quarter, we continued to advance our clinical pipeline focused on the development of best-in-class or first-in-class treatments for serious metabolic diseases. Our lead compounds, VK2809 for NASH and fibrosis, and our new program evaluating VK2735 for metabolic diseases, both advanced according to plan during the quarter. In addition, we recently announced the removal of a clinical hold on our study evaluating VK0214 in patients with X-linked adrenoleukodystrophy. I will begin with an update on our lead compound VK2809. VK2809 is an orally available small molecule agonist of the thyroid hormone receptor that is selected for liver tissue as well as the beta isoform of the receptor. This is currently being evaluated in our Phase 2b VOYAGE study in patients with NASH and fibrosis. Data generated to-date suggests VK2809 has the potential to be a best-in-class treatment for NASH and fibrosis. We have previously announced data from a 12-week Phase 2a trial of VK2809 in patients with hypercholesterolemia and non-alcoholic fatty liver disease. This trial successfully achieved both its primary and secondary endpoints and demonstrated significant reductions in liver fat and plasma lipids. The results from the Phase 2a trial included data showing that dosing 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% reduction in liver fat content, including all patients receiving five milligrams per day, the lowest dose in the study. In addition, patients receiving VK2809 experienced improvements in plasma lipids such as LDL cholesterol, triglycerides, and atherogenic proteins. These results are of particular importance as VK2809's lipid-lowering effects suggest a potential cardiovascular benefit. This key feature represents a significant point of differentiation when compared to other drugs and mechanisms in development that have been shown to increase plasma lipids and potentially cardiovascular risk. Patients treated with VK2809 in the 12-week study also experienced durable reductions in liver fat, with the majority of patients remaining responders four weeks after completion of dosing. Finally, the study 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 the VK2809-treated versus placebo patients. Based on these promising results, we initiated the VOYAGE study, a Phase 2b study designed to evaluate VK2809 in patients with NASH and fibrosis. VOYAGE is a randomized, double-blind, placebo-controlled multicenter 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 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 assessed by hepatic biopsy after 52 weeks of treatment. During the second quarter, enrollment in VOYAGE continued at both U.S. and ex-U.S. sites, and we remain on track to complete enrollment in the second half of this year. Moving to our dual agonist program, earlier this year, we announced the initiation of a Phase 1 trial of our newest pipeline compound, VK2735. VK2735, which was developed internally at Viking, is a dual agonist of the Glucagon-Like Peptide-1 or GLP-1 receptor and the Glucose-Dependent Insulinotropic Polypeptide or GIP receptors. Based on data to date, we are excited about this program and the potential for this mechanism to be applicable across a range of metabolic disorders. Initial data from our dual agonist program were presented last November in two posters at ObesityWeek, the annual meeting of the obesity society. These posters highlighted the improvements in metabolic profile observed among diet-induced obese mice treated with our compounds as compared to control cohorts. Specifically, weight loss, glucose control, and insulin sensitivity were all enhanced following treatment with our dual agonists, compared to the effects observed following treatment with the GLP-1 mono-agonist semaglutide. When administered at the same dose for the same period of time, we observed reductions in liver fat content that were generally larger among animals treated with our compounds relative to the liver fat reductions observed among animals treated with semaglutide. These results suggested that the addition of GIP receptor activity improved upon the effects achieved through activation of the GLP-1 receptor alone. In January of this year, we announced the initiation of a Phase 1 clinical trial of VK2735. The Phase 1 trial is a randomized double-blind placebo-controlled single ascending and multiple ascending dose study. The single ascending dose portion of the study will enroll healthy adults, while the multiple ascending dose portion of the study will enroll healthy adults with a minimum body mass index of 30 kilograms per meter squared. The primary objectives of the study include an evaluation of the 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 weights and liver fat content after four weeks of once-weekly administration. During the quarter, enrollment continued in both the SAD and MAD portions of the study and we expect to report the initial data from this study in the fourth quarter. I will wrap up with an update on VK0214, Viking’s second orally available small molecule thyroid hormone receptor beta agonist in clinical development. We believe VK0214 has the potential to be a first-in-class treatment for X-linked adrenoleukodystrophy or X-ALD. X-ALD is a rare and often fatal metabolic disorder characterized by a breakdown in the protective barriers surrounding brain and nerve cells. The disease is caused by genetic mutations that impact the function of a proximal 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. Our rationale for advancing VK0214 into the clinic was based on the observation that the thyroid hormone beta receptor plays an important role in regulating the expression of very long chain fatty acid transporters. Multiple models have shown that improved and potentially normalized very long chain fatty acid metabolism can be achieved through increased expression of compensatory transporters. Because VK0214 is a potent agonist of the thyroid hormone beta receptor, we believe it may provide therapeutic benefit in the treatment of X-ALD. Early data from nonclinical studies have supported this rationale with VK0214 demonstrating the ability to stimulate the expression of the key compensatory transporter of very long chain fatty acids and reduced plasma levels of very long chain fatty acids in an animal model. Last year, we reported the results of a randomized double-blind placebo-controlled single ascending and multiple ascending dose Phase 1 study of VK0214 in healthy volunteers. The study was successful, with VK0214 demonstrating dose-dependent exposures, no evidence of accumulation, and half-life consistent with anticipated once daily dosing. After 14 days of treatment, subjects who received VK0214 also experienced reductions in LDL cholesterol, triglycerides, apolipoprotein B, and lipoprotein A. Many of these lipid reductions achieved statistical significance, though the study was not powered to demonstrate statistical significance on lipid assessments. VK0214 also demonstrated encouraging safety and tolerability in this study, among more than 100 subjects enrolled, no serious adverse events were reported, and no treatment or dose-related signals were observed for vital signs or cardiovascular measures. No gastrointestinal disturbances such as diarrhea or nausea were reported even at doses of 125 milligrams daily, the highest dose evaluated in the study. Shortly after the conclusion of the Phase 1 study, we initiated the Phase 1b study of VK0214 in patients with the Adrenal Myelin Neuropathy or AMN form of X-ALD. AMN is the most common form of X-ALD, affecting approximately 50% of those with the disease. Clinical manifestations include progressive leg weakness, incontinence, and sexual dysfunction. The Phase 1b 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 unblinded review of preliminary safety, tolerability, and pharmacokinetic data, additional dosing cohorts may be pursued. In January of this year, we announced this trial had been placed on clinical hold by the FDA. The agency requested completion of an additional preclinical study prior to the continued dosing of patients. This request was not due to any findings from ongoing or previously completed studies. Rather, the FDA informed us that it considered the trial to be a Phase 2 trial rather than a Phase 1b. As such, regulatory guidance required that a rodent genotoxicity study be completed prior to initiation. During the second quarter, we successfully completed the requested study and submitted the results to the agency. Following the review, we received an authorization to resume the study as planned, and we are in the process of doing so now. We expect to report the results from this trial in the first half of 2023. Finally, as we expand and advance our clinical pipeline, we continue to carefully manage our financial resources. We entered the second quarter with approximately $170 million in cash, which we believe provides the runway to advance each of our clinical programs into later stage development. In conclusion, as we look to the next 12 months, we anticipate multiple important catalysts from our clinical pipeline. Between now and year-end, we expect to announce the initial data from the Phase 1 study of our newest clinical compound VK2735, our internally developed program targeting dual activation of the GLP-1 and GIP receptors, with potential applications in a range of metabolic disorders. We also expect to announce completion of enrollment in the VOYAGE Phase 2b study evaluating VK2809 in patients with NASH and fibrosis, and we remain on track to announce in the first half of 2023 the results from our Phase 1b study evaluating VK0214 for the treatment of X-ALD. By any measure, next year will be a pivotal year for Viking. As we highlighted on our year-end call in February, Viking has transformed over the past several quarters from a company with one clinical program to a company with three active clinical programs across a range of indications, with important data expected from each within the next 12 months. The breadth and depth of our clinical and preclinical pipeline represent an important evolution from a single program company into a diversified biopharmaceutical company with programs across multiple important indications. In our view, the data we expect to report in the upcoming quarters will serve to strengthen Viking’s position as a leader in the development of novel, class-leading therapeutics for the treatment of metabolic disorders. This concludes our prepared comments for today. Thanks again for joining us. And we will now open the call for questions.

Our first question will come from Steven Seedhouse with Raymond James. You may now go ahead.

Great, and thanks for taking the question. I want to ask a few on VK2735. Just first, in the Phase 1, are you going to look to generating data in diabetics at some point or just the healthy volunteers and obese but otherwise healthy volunteers? And then in the initial data release later this year are you going to, do you think, have data from optimized doses by then or just some low-dose cohort?

Hi Steve. So I think the protocol is requiring people to be non-diabetic; they are healthy volunteers. Although in the MAD portion of the trial, they do have to have an elevated BMI. As far as the data we will report, right now, the timeline shows that we should be able to report the data from all of the planned cohorts. If we were to add additional cohorts that might push a full read of the data out a little bit. But we certainly plan to announce everything we have on the timelines that looks like we will be able to right now.

And then a pharmacology question. It is just, I think a lot of folks are trying to figure out what you know, how this molecule is going to stack up against other GLP-1 agonists? And it is not clear to me, I guess, why does appetite seem to be so good relative to some others. But one hypothesis is like the relative potency on GLP-1 receptor versus GIP receptor, like is it lower potency on the GLP-1 receptor? So I’m just wondering if you screened a bunch of molecules; you had this data in the DIO mouse model? I’m curious if you think that dynamic of just fine-tuning the relative potency on the two targets is important. In your hands, how have you thought about optimizing that for your molecule and ultimately VK2735 that you chose to advance to the clinic?

Yes, this is an interesting question. I think it is really difficult to predict what the binding affinities on each receptor are given each change. What we found is that the more you tune in GIP activity, the lower the weight loss tends to be. The more you tune into GLP-1 activity, as long as you still have the GIP activity, you see sort of an optimized blend of the two. So it seems like, and this is just in our hands, it seems like you want to lead with GLP-1 activity and then layer on the GIP, because when we do the reverse, it just seems like the efficacy is not there to the same degree.

Okay. And then last question in the Phase 1, is it too soon in the first month to see any drug antibodies manifesting? Because there is just some weird data for others in this class where based on the design of that molecule, like almost half the patients had them, but the weight loss was actually more pronounced when they did, so they certainly weren’t neutralizing. And I just, I don’t know what to make of that. I’m just curious if it is a relevant observation or something to look into in such a short Phase 1?

Yes. Well, we are looking at it. And I think your observation is sort of what we have seen in the literature as well. And that is the anti-drug antibody levels don’t seem to have any relevance; you think they should have some relevance, but they don’t seem to have relevance. And so I don’t know why that is, and there may be examples of these classes of compounds having some impact from anti-drug antibodies, but we haven’t seen it, we will look at it. I think maybe we want to see a little bit longer treatment window to really see the full extent of the anti-drug antibody effect, but we will look at it and see what it says sort of looks like.

Thanks for taking the questions.

Sure. Thanks, Steve.

Our next question will come from Joon Lee with Truist Securities. You may now go ahead.

Good afternoon. This is [indiscernible] filling in for Joon, and I appreciate the opportunity to ask questions. My first question is about 2735. From the upcoming Phase 1 data, what data points would significantly impact your decision to pursue the development of 2735 for either obesity or Prader-Willi syndrome? I also have a follow-up.

Yes. It is a good question. It will be in that neighborhood. I think we are leaning towards the weight loss indications. But we will have to make the decision once we see the actual data. We do have several compounds sort of percolating here in development at different stages preclinically. And so as you look forward, a few quarters you might envision a program that targets a large indication and a program that targets a smaller indication, sort of analogous to what we are doing with the thyroid beta receptor portfolio where we have got VK2809 in the larger NASH indication and VK0214 in the smaller X-ALD indication. So if things progress similarly in the dual agonist arena, we might be able to have an opportunity to look at two programs, one in a large indication like obesity and one in smaller indications like Prader-Willi syndrome, but it is too early to definitively make those sorts of assignments right now we will have to see what the data looks like.

Okay. Thank you. And my second question is, all Altimmune is working on a GLP-1 glucagon dual agonist. What are some of the disadvantages or advantages of glucagon as an add on to the GLP-1 mechanism versus GIP?

Well, I think questions around other companies' compounds might be better directed toward those companies. I think the dual agonists GIP and GLP-1 or glucagon and GLP-1; they both seem to have effects. They have different receptors and pathways, obviously, but they both seem to have promising effects on weight loss and metabolic control. But, I’m not super close to their program, so it is hard to do a critical analysis and compare and contrast sort of comment on them.

Alright. Thank you sir.

Thanks.

Our next question will come from Joe Pantginis with H.C. Wainwright. You may now go ahead.

Hey guys, good afternoon. Thanks for taking the question. I guess a couple of logistical questions. As the 0214 study looks to get started, just curious if there are any meaningful changes either to design or the, say the numbers of centers that any centers dropped out, were you able to add new ones, et cetera? Thanks.

Thanks, Joe. Yes, we have added some sites now in Europe, maybe five or six across Europe. And we haven’t had any significant discontinuations since the hold. I don’t think we have had any notable discontinuations. Maybe one site discontinued, but we didn’t expect a lot of contributions from that particular site. So overall, we are going to restart screening here very shortly. And hopefully, we will have enrollment resuming at a better trajectory than we had seen with just the U.S. sites.

Got it. And then for 2809, just wanted to check in on your supply preparation should the VOYAGE study be successful for next stages?

Yes. Thanks. We are in the process of making registration batches of VK2809, which would utilize the tablet formulation for Phase 3 trials. And those have to be prepared for an end of Phase 2 meeting, which we anticipate after we have a successful conclusion of the VOYAGE study. So all of that is going on in the background, and it is all going according to plan with few disruptions really.

Got it. And then maybe I'm trying to game the timing of VOYAGE or predict the timing of VOYAGE here. So I guess I would ask the question the following way. What percentage of the patients already enrolled in the study have reached the 12-week follow-up endpoint or are you willing to disclose that?

I actually don’t know how many have reached the 12-week endpoint. A big percentage, but I don’t know the number. I mean, yes.

No, no sure I get it. okay, thanks a lot guys.

Yes. Thanks, Joe.

Our next question will come from Andy Hsieh with William Blair. You may now go ahead.

Great. Thanks Brian for taking my question. So another question for VK2735. Assuming everything checks out in the Phase 1b study, as you kind of think about mid-stage or later-stage programs, looking at the kinetics of weight loss, you don’t really see a plateau of weight loss until maybe six to nine months. So would that be kind of a minimum duration of a potential Phase 2 program then independent of which indication you are looking for?

Yes, that is a great question. Our Phase 2 program, because we are going pretty quickly with this program, is really one of the limiting factors is the tox package availability, and the next tox package generally do have a 14 to 28-day tox, and then 13-week tox, and then the chronic tox. The next program duration is probably going to be dictated by the 13-week tox, which will be available later this year. And then we will start as soon as possible after that the chronic tox, which would allow us to do much longer studies.

Got it. And one question, kind of derived from Steve’s question as well. Would it be reasonable to assume that kind of based on these programs, even for late-stage trials, you’ll probably carry a couple of doses just to really see the dose response?

Yes, I think that is very reasonable to assume different people will tolerate different dose levels, and different people will need different levels of efficacy. So, it stands to reason that you would take more than one dose into later stage development, yes.

Got it, okay. And my final question has to do with manufacturing. So, obviously, you are very well versed when it comes to small molecule 5211 sodium rate hormone agonists. And these compounds are basically small peptides. So regarding the complexity for manufacturing these drugs, can you kind of talk about that and also maybe the cost associated with manufacturing for clinical trials supply?

Yes. So, we are virtual, so we don’t have any of that ability in-house, the manufacturing ability. So we do contract with global vendors on manufacturing, and we leave it to their expertise to optimize the synthetic routes for these compounds. And then we contract with other formulation vendors to develop the optimal formulations for the compounds. We have got the in-house expertise on formulation development and that sort of thing; we just don’t have the labs. As far as the cost of goods, right now, it doesn’t look like these will be prohibitively expensive to manufacture. They are not super difficult molecules to manufacture; they are peptides, and that is a well-established manufacturing process. So we wouldn’t expect there to be any sort of a disproportionately high level of cost.

Great. That is very helpful. Thank you so much, Brian.

Thanks a lot, Andy.

Our next question will come from Jay Olson with Oppenheimer. You may now go ahead.

Hey Brian, thanks for taking the questions. For VK2809, we were curious if you think there is still any value in having a consensus panel of three liver biopsy readers since we now know that approach did not change the interim results of intercepts and regenerate study, or do you think the industry can go back to a single biopsy reader?

Yes, this is an interesting question, Jay. So I think that the trend really is to this three-reader panel, and I don’t know if that is going to get reversed because of the reanalysis of the REGENERATE study. We are using two when necessary in the Phase 2b study, and we would anticipate probably a three-reader panel just because of the greater comfort that I think people and the FDA might have around more eyes on the slides. But your point is, I mean, right on, is it necessary? I don’t know. I mean, these are all highly trained pathologists; I guess, consensus is better than just a single person. But is it really necessary? I’m not sure.

Okay. Understood. And then also related to 2809, do your interactions with the FDA suggest that achievement of NASH resolution only is sufficient for an accelerated approval, or do you think the FDA might also require fibrosis improvement?

Well, to my knowledge, the guidance hasn’t changed. So either of those is sufficient for an efficacy claim under subpart H is the surrogate that is allowed. So until there is a change in guidance, that is our assumption. We haven’t received any communication or anything like that that would suggest otherwise. I think it is better to have both, but if NASH resolution is still acceptable, it seems that it is, then I think that should be okay under subpart H.

Okay, thank you. And then maybe if I could sneak in one last question on 2735. Can you talk about what the most efficient way would be to expedite the clinical development of that program? And, for example, would you be looking for a partnership?

Yes, so it is, I think that philosophy there will be really is the same as with all of our programs. We are always open to discussing partnering opportunities. It seems like the greatest inflection in value for that program will be after a Phase 2 study to demonstrate a longer-term signal efficacy and safety and tolerability as well. So that would be the most likely and appropriate time to engage partners prior to a large Phase 3, but we are always open to those discussions. So to the extent we can have them and they would make sense for the company and our shareholders, we would certainly pursue something but I would anticipate something after or more serious discussions after Phase 2.

Great. thanks for taking the questions.

Thanks, Jay.

Our next question will come from Justin Zelin with BTIG. You may now proceed.

Hey, Brian, this is someone stepping in for Justin. I have two questions for you. First, could you comment on the enrollment pace for VOYAGE over the last quarter and any significant changes you've observed in screen failure? Secondly, could you provide more details on 2735, specifically regarding the number of sites? I know you plan to include it on clinicaltrials.gov, but how many sites are you aiming for in 2735? Thanks.

Yes, as far as the cadence for VK2809, no significant changes one way or another in cadence over the last few months. It is a little lumpy. Sometimes you have a great week, sometimes you don’t have as good a week, but it has been pretty consistent through the last several months. With the VK2735 comp, and I think clinicaltrials.gov is accurate there. So I don’t think there is any update necessarily there.

Great. it sounds good. Thank you.

Thanks.

Our next question will come from Yale Jen with Laidlaw & Co. You may now go ahead.

Thanks, Brian for the questions. You mentioned earlier that you could potentially increase more - for VK2735 in the fourth quarter of this year, so I’m just curious what may be the gating factors or decision points for that.

I think I missed one of the early words there, we could increase the-.

Maybe more than the dose cohort than you are currently scheduled.

Yes. So in both the SAD and the MAD portion, you dose up and look for any reason to stop escalation. And with this mechanism, you would anticipate that to be tolerability-related. So if you have better tolerability, you might find a reason to dose higher. We don’t know one way or another right now. But if we were able to dose higher because tolerability was really good, then that might extend the timeline a little bit, but no visibility into that currently.

Okay. Well, maybe one more question here, which is, again, to read out VK2735 maybe in the fourth quarter of this year, what should your investment anticipate, what type of biomarker or any other things could be reported at that meeting?

So it is a Phase 1, so we will be looking at safety and tolerability, and PK profile after single and multiple doses. The pharmacodynamic endpoints will look at plasma glucose and insulin, body weight changes. And we are also doing MRI-PDFF on these subjects to assess changes in liver fat content. So all of those will be, I think, points of interest in the initial dataset.

Okay. Great. Thanks a lot. I appreciate that and congrats on the progress.

Thanks a lot, Yale.

Our next question will come from indiscernible with Maxim Group. You may now go ahead.

Hey everyone. Thanks for taking our question. Just two very quick questions. On VK0214, are you now considering potentially reading out any interim results? Or are you just going to wait for the full top-line data? And two, are you making any study protocol amendments saying how you have this pause?

For the first question, no, it is a small study; we indicated when we first received the hold that we consider this to be probably about a six-month delay. And so we would originally anticipated data toward the end of this year. And with the six-month delay, it kind of pushes that into the first half of next year. As far as protocol amendments, no anticipated protocol amendments at this point. No.

Alright, thanks a lot.

Thanks.

This concludes our question-and-answer session. I would like to turn the conference back over to Stephanie 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.

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