Viking Therapeutics Q1 2023 Earnings Call Transcript

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Provided by Quartr
April 26, 2023

There are 11 speakers on the call.

Operator

Welcome to the Viking Therapeutics First Quarter 2023 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 and A session. As a reminder, this conference call is being recorded today, April 26, 2023. I would now like to turn the conference over to Viking's Manager of Investor Relations, Stephanie Diaz.

Operator

Please go ahead, Stephanie.

Speaker 1

Hello, and thank you all for participating in today's call. Joining me today is Brian Lien, Viking's President and CEO and Greg Zanti, Viking's CFO. Before we begin, I'd like to caution that comments made during this conference call today, April 26, 2023, will contain forward looking statements under the Safe Harbor provisions 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 I'll now turn the call over to Brian Lynn for his initial comments.

Speaker 2

Thanks, Stephanie, and good afternoon to everyone dialed in by phone or listening on the webcast. Today, we'll review our financial results for the Q1 of 2023 and provide an update on recent progress with our clinical programs and operations. The Q1 of 2023 was an exciting time at Viking with important progress announced across multiple clinical programs. With respect to VK2809, our lead thyroid hormone receptor beta agonist for the treatment of NASH and fibrosis, early in the quarter, we announced completion of enrollments in our Phase 2b voyage trial and we expect to announce top line data from the primary endpoint in this study in the Q2 of 2023. With respect to our newest clinical program, the dual GLP-one and GIP receptor agonist VK2735 for the potential treatment of metabolic disorders, Last month, we announced data from our first clinical study of this compound, a Phase 1 single ascending dose and multiple ascending dose study in healthy volunteers.

Speaker 2

As we'll discuss in a few minutes, the results were encouraging with mean weight loss of up to 18 pounds observed following 28 days of treatment. We plan to initiate a Phase 2 study of VK-two thousand seven hundred and thirty five in patients with obesity in mid-twenty 23. In addition, we announced the initiation of a new clinical study to evaluate a novel oral formulation of this compound. With respect to our 3rd ongoing clinical program, the novel thyroid hormone beta receptor agonist VK0214, our Phase 1b trial evaluating this compound for the treatment of X linked adrenoleukodystrophy continues to enroll and we expect to report the results from this study in the second half of the year. Late in the quarter, we also completed the successful public offering of common stock, raising gross proceeds of approximately $288,000,000 I'll provide further details on our operations and development activities after we review our Q1 2023 financial results.

Speaker 2

For that, I'll turn the call over to Greg Zanti, Viking's Chief Financial Officer.

Speaker 3

Thanks, Brian. In conjunction with my comments, I'd like to recommend that participants refer to Viking's Form 10 Q filing with the Securities and Exchange Commission, which we expect to file today. I'll now go over our financial results for the Q1 ended March 31, 2023. Our research and development expenses for the 3 months ended March 31, 2023 were $11,000,000 compared to $12,600,000 for the same period in 2022. The decrease was primarily due to decreased expenses related to clinical studies, preclinical studies and third party consultants, partially offset by increased expenses related to salaries and benefits, stock based compensation and regulatory services.

Speaker 3

Our general and administrative expenses for the 3 months ended March 31, 2023 were $9,500,000 compared to $3,700,000 for the same period in 2022. The increase was primarily due to increased expenses related to legal and patent services, Stock based compensation and salaries and benefits. For the 3 months ended March 31, 2023, Viking reported a net loss of $19,500,000 or $0.25 per share compared to a net loss of 16,100,000 or $0.21 per share in the corresponding period of 2022. The increase in net loss and net loss per share for the 3 months ended March 31, 20 was primarily due to the increased general and administrative expenses noted previously, partially offset by increased interest income compared to the same period of 2022. Turning to the balance sheet.

Speaker 3

At March 31, 2023, Viking held cash, cash equivalents and short term investments totaling $135,700,000 compared to 155 $500,000 as of December 31, 2022. The company's Q1 2023 cash balance does not account for the completion of a public offering of common stock, resulting in gross proceeds of approximately $288,000,000 that was completed at the end of the first quarter And closed on April 3, 2023. Pro form a including this offering, our end of quarter cash, Cash equivalents and short term investments were approximately $406,000,000 This concludes my financial review, And I'll now turn the call back over to Brian.

Speaker 2

Thanks, Greg. As mentioned in my opening comments, the Q1 of 20 23 was an exciting time at Viking. In recent weeks, we announced positive data from a Phase 1 study in healthy volunteers with our newest clinical program, the The dual incretin receptor agonist VK-two thousand seven hundred and thirty five. These results, which I will discuss in more detail shortly, Have served to broaden our presence in metabolic diseases and diversify our pipeline, further increasing the value of the company. We are very pleased to begin the Q2 from a position of clinical momentum, financial strength and optimism for upcoming data.

Speaker 2

I'll now provide an overview of progress with our clinical 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 selected for liver tissue as well as the beta isoform of the receptor. Prior 12 week Phase IIa trial evaluating VK2809 in patients with hypercholesterolemia and non alcoholic fatty liver disease Successfully achieved both its primary and secondary endpoints, demonstrating significant reductions in liver fat and plasma lipids. Cohorts treated with VK2809 experienced up to 60% mean relative reductions in liver fat content and 88% of patients receiving VK2809 Experienced at least a 30% relative reduction in liver fat content. Importantly, the reductions in liver fat were durable With the majority of patients remaining responders 4 weeks after completion of dosing.

Speaker 2

This study also demonstrated the promising safety and tolerability 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 We believe DK2809's activation of the thyroid hormone beta receptor provides unique therapeutic benefits for patients with NASH. Perhaps one of the most important additional benefits of this compound It's its ability to reduce plasma lipids including LDL cholesterol, triglycerides and atherogenic proteins, all of which have been correlated with increased It is important to note that a number of studies evaluating other NASH development programs have demonstrated elevations in these lipids following treatment. In contrast, patients in Viking's 12 week Phase IIa study experienced robust reductions in these lipids suggesting that VK2809 May offer a cardioprotective benefit. We believe VK2809's broad lipid lowering properties combined with its safety, excellent tolerability, Significant liver fat reduction and oral route of administration establish it as a best in class therapeutic for the treatment of NASH.

Speaker 2

Based on the promising results from our Phase IIa trial, the company initiated the VOIDGE Phase IIb study. This trial 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 VOAGE study will evaluate changes in liver fat from baseline to week 12 in patients treated with VK2809 As compared to patients receiving placebo, secondary and exploratory objectives include the evaluation of histologic changes Assessed by hepatic biopsy after 52 weeks of treatment. During the Q1, we announced completion of enrollment in the VOAGE study We look forward to sharing top line results including the trial's primary endpoint during the Q2 of this year.

Speaker 2

I'll now turn to our newest clinical program highlighted by a compound called VK-two thousand seven hundred and thirty five, which we believe has the potential for the treatment of various metabolic This order such as obesity, NASH and certain rare diseases. VK-two thousand seven hundred and thirty five is a dual agonist of the glucagon like peptide 1 or GLP-one receptor and the glucose dependent insulinotropic polypeptide or GIP receptor. Initial in vivo data from our dual agonist program demonstrated improvements in weight loss, glucose control and insulin sensitivity among diet induced obese mice following treatment with Viking's compounds as compared to a GLP-one mono agonist 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 those observed Based on these in vivo and other preclinical data, We initiated a Phase 1 single ascending dose and multiple ascending dose clinical trial of VK-two thousand seven hundred and thirty five. The single ascending dose portion of the study enrolled healthy men and women and evaluated escalating single doses of VK-two thousand seven hundred and thirty five.

Speaker 2

The multiple ascending dose portion enrolled healthy men and women with a minimum body mass index of 30 kilograms per meter squared. In the multiple ascending dose portion of the study, subject received VK2735 once weekly for 28 days. During the Q1, we were pleased to announce the results from this study with VK-two thousand seven hundred and thirty five demonstrating promising safety, Tolerability, a predictable PK profile and positive signs of clinical benefit. Key takeaways from the single ascending dose portion of the study Were that single doses of VK-two thousand seven hundred and thirty five were safe and well tolerated and that the compound's PK profile demonstrated favorable characteristics in humans. Following single subcutaneous doses, VK-two thousand seven hundred and thirty five demonstrated a half life of approximately 170 to 250 hours, A Tmax ranging from 75 to 90 hours and excellent therapeutic exposures.

Speaker 2

In the 28 day multiple ascending dose portion of the study, VK-two thousand seven hundred and thirty five demonstrated encouraging safety and tolerability and positive signs of clinical activity. All cohorts receiving VK2735 demonstrated reductions in mean body weight from baseline ranging up to 7.8%. Cohorts receiving VK2735 also demonstrated reductions in mean body weight relative to placebo ranging up to 6%. Statistically significant differences compared to placebo were maintained or improved at the day 43 follow-up time point 21 days after Last dose of VK-two thousand seven hundred and thirty five was administered. Importantly, VK-two thousand seven hundred and thirty five demonstrated And 99% of gastrointestinal related adverse events were also reported as mild or moderate.

Speaker 2

In addition, all cohorts treated with VK-two thousand seven hundred and thirty five demonstrated improvements in plasma glucose levels relative to placebo, Though not all cohorts achieve statistical significance. We believe the tolerability data from this study indicate that higher doses may be achieved with Longer titration windows and we plan to evaluate further dose escalation in subsequent studies. Turning to our future plans for VK-two thousand seven hundred and thirty five. Based on the positive results generated in the Phase 1 study, we plan to initiate a Phase 2 trial Concurrent with the announcement of the Phase I data just described, We also announced the initiation of a Phase 1 clinical study to evaluate an oral tablet formulation of VK-two thousand seven hundred and thirty five. We believe the tablet formulation represents a significant potential expansion of the program's overall value and utility.

Speaker 2

In vivo data to date suggests that therapeutic plasma levels of VK-two thousand seven hundred and thirty five may be achieved via oral dosing, And we expect both the subcutaneous formulation and the oral formulation to provide unique benefits to patients. The ability to select either The oral study is an extension of the Phase 1 study discussed a moment ago. This portion of the study is a randomized, double blind, Placebo controlled study in healthy volunteers who have a minimum body mass index of 30 kilograms per meter squared. Subjects will receive daily oral doses for 28 days. Primary objective of the study is to evaluate the safety, Tolerability and pharmacokinetics of VK-two thousand seven hundred and thirty five following 28 days of oral dosing.

Speaker 2

Exploratory endpoints include changes in body weight and plasma glucose. We believe the results from this study could potentially be available in the second half of twenty twenty three. I will now provide an update on our 3rd clinical candidate VK0214. This is Viking's 2nd orally available small molecule thyroid hormone And it is currently being evaluated in a Phase 1b clinical trial in patients with X linked adrenoleukodystrophy or X ALD. X ALD is a rare and often fatal metabolic disorder.

Speaker 2

Patients with X ALD have genetic mutations that Impact the function of a peroxisomal transporter of very long chain fatty acids. When transporter function is impaired, Patients are unable to efficiently metabolize very long chain fatty acids and the resulting accumulation of these compounds is believed to contribute to the onset and progression of X In a prior Phase 1 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 receive VK0214 experienced reductions in LDL cholesterol, triglycerides, apolipoprotein B And lipoprotein A. VK0214 also demonstrated an encouraging safety and tolerability profile With no serious adverse events reported and no treatment or dose related signals observed for GI side effects, vital signs or cardiovascular measures. Following these favorable results, Viking initiated the Phase 1b study of VK0214 in patients with the adrenomyeloneuropathy or AMN form AMN is the most common form of X ALD affecting approximately 50% of patients.

Speaker 2

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, tolerability and pharmacokinetics of VK0214 administered once daily orally for 28 days. The study also includes an exploratory assessment of changes in plasma levels of very long chain fatty acids. This study continues to enroll and we expect to report the initial results later this year. Moving to other corporate updates.

Speaker 2

Late in the Q1, we completed a successful public offering of common stock raising gross proceeds of approximately $288,000,000 We were happy to see the receptivity and enthusiasm from investors and are grateful for their support as we continue advancing our pipeline programs. As Greg mentioned earlier, pro form a for the offering, our end of quarter cash balance was approximately $400,000,000 This enables the company to further invest in pipeline programs, Both existing and new and places Viking in a position of strength in discussions with potential corporate partners. In conclusion, the Q1 of 2023 proved to be an exceptional quarter for Viking. We announced completion of enrollment in the Voyage study VK2809 in patients with NASH and fibrosis and we expect to report data for the primary endpoint of this study later this quarter. We also announced the first human data from our dual GLP-one GIP receptor agonist VK2735 demonstrating promising safety and tolerability And exciting reductions in body weight.

Speaker 2

We look forward to initiating a U. S. Phase 2 study in obesity in mid-twenty 23. We also further expanded the reach of this program by announcing the initiation of a study using an oral tablet formulation From which we expect to report results toward the end of the year. With our VK0214 program, We continued enrolling our Phase 1b study in patients with adrenomyeloneuropathy and we anticipate reporting data from this study later in the year.

Speaker 2

Finally, we significantly strengthened our balance sheet in the quarter through a successful offering of common stock, which resulted in proceeds of over 280,000,000 Our current runway extends well beyond each of the clinical catalysts outlined here. We feel fortunate and grateful to be in the position we're in and look forward to providing additional updates as they're available. This concludes our prepared comments for today. Thanks again for joining us. And we'll now open the call for questions.

Speaker 2

Operator?

Operator

Thank you. We will now begin the question and answer session. This first question comes from Steve Seedhouse with Raymond James. Please go ahead.

Speaker 4

Great. Thanks so much for taking the questions. I had a few on the oral formulation of the GLP-one GIP. 1st, just, you haven't shared any preclinical data. So wanted to ask In general, if the expectation would be you could get to sort of exposure and ultimately efficacy levels that would be equivalent to the injectable or What specifically would be the expectations in terms of potency of what you could achieve at peak in humans?

Speaker 4

And then also With that compound, is this something that would lend itself to like a titration schema as well or you're essentially Looking at flat doses in the Phase

Speaker 2

1? Hey, Steve. Thanks for the questions. With the exposures, yes, I don't think we expect the exposures to achieve the same level that are observed with The subcu formulation, maybe I'll be proven wrong, but I don't think we'll get there. It's almost a different product.

Speaker 2

I would consider the oral formulation maybe For someone who first doesn't want to start with an injectable or for someone who maybe has a BMI 32 to 34 or something that Might be adequately addressed with an oral formulation or potentially in a maintenance setting where you start with the subcu and then So there are a lot of different ways that it could be used, but my own guess is that we probably won't see the same exposures With the oral? The same question? Titration. Oh, titration, yes. So yes, we will titrate In the upcoming study.

Speaker 2

So the first cohorts flat dosing and subsequent cohorts will titrate up.

Speaker 4

Okay. So it's just one dose of one tablet dose that you just give multiple pills, I guess, In that case

Speaker 2

That's right.

Speaker 5

Yes.

Speaker 2

Yes. The first cohort is 2.5 mgs and that's flat. And then From there, they dose up. I mean, 1st week will be 2.5, and then the remaining 3 weeks would be a higher dose. And then as you go on in through the cohorts, you kind of titrate up per week.

Speaker 4

Okay. Couple more, just because really interesting program, obviously. You mentioned maintenance dosing as one option. That's obviously just given how many people in the next Decade are likely to be gravitating towards using cretins. I imagine there'd be some enormous Group of patients coming on or having been on injectables, I'm curious if you're going to gather that type of maintenance data In the Phase 1, can you take patients that you already treated with the injectable and start them on oral and see how they do?

Speaker 4

And then I just One more in the program after if I could. Thanks.

Speaker 2

Yes. No, thanks. In this study, we're really just trying to see if the formulation will provide Exposures and what levels compare to the subcu. So I think in the future those transition type studies It would be really important and really interesting, but this is just the first one and we're just going to see how the exposures turn out.

Speaker 4

Okay. And then the Phase 1, I think you guys were for the injectable, at least you were collecting MRI PDFF data and there may be some other Biomarkers in there that weren't ready for the initial top line. So can you just comment on, you have the guidance in place for the oral data. Should there is there any other data either from the clinical injectable study Beyond the top line that you've already announced that would be coming here near term that we should keep an eye out for? Thanks.

Speaker 2

Yes. Thanks, Steve. We'll probably be reporting more data a little bit later in the year, potentially at Obesity Week. But we don't have any near term nothing imminent there. You're right.

Speaker 2

We did have a number of biomarkers in liver fat in the study.

Speaker 5

All right.

Speaker 4

Thanks, Brian.

Speaker 2

Thanks, Steve.

Operator

Thank you. And our next question today comes from Joon Lee with Truist Securities. Please go ahead.

Speaker 6

Hey, thanks for taking our questions and congrats on the progress. What really stood out from the healthy volunteer study of VK-two thousand seven hundred and thirty five was how clean the tolerability profile was. So is

Speaker 2

Hi, June. Thanks. Yes. So I don't really know. It was a small study, so you could argue that maybe we're just looking at small numbers.

Speaker 2

What was interesting with the tolerability was that there wasn't really a dose related change in tolerability as you went up. I think the highest dose cohort actually had Really, really good tolerability, better than some of the earlier cohorts. So, mechanistically, I know people have talked about arrest and recruitment Being one thing that might lead to improved tolerability, if you can have a Sustained effect on GLP-one without arrest and recruitment, you could see maybe An increase in efficacy without necessarily issues with nausea, but I don't know. Otherwise, I don't know that mechanistically there's anything That would explain it.

Speaker 6

Fair enough. And both Lilly and Nova have historically done Head to head trials of their GLPs, at least for diabetes. Do you have any plans to do a head to head trial of VK 2,735 against other obesity drugs?

Speaker 2

Yes, great question. I think it's a really good idea as we move further through the program, but this upcoming Phase 2 will not have an active comparator in it. It's just placebo. But I do think that's something important For the future, just to see how they compare.

Speaker 6

Thanks for taking our question.

Speaker 2

Thanks, June.

Operator

Thank you. And our next question today comes from Annabel Samimy with Stifel. Please go ahead.

Speaker 7

Hi. Thanks for taking my question. So I wanted to ask about the titration period that you're considering Phase 2, I mean, already, it looked like you had some good tolerability. It looks like you have some very good weight loss already within 28 weeks. So I guess, I'm wondering why you would want to push that further, and what kind of titration schedule might we be looking at?

Speaker 7

So I guess that's the first question. And is this the same exact molecule as 2,735? Are you changing the balance GLP-one or GIP in any way as you go into the oral if you don't have the same, I guess, targeted exposure? And then I have one more follow-up.

Speaker 2

Yes. It's the same molecule, Annabel, in the oral and the subcu. And We're titrating in the 28 day study really because we've not dosed with this compound before, so we don't know if there are any differences in Tolerability and we're doing fewer cohorts. So in the subcu, we did have the first two cohorts were flat dosing and then we titrated. And here the first cohort is going to be flat and then we titrate.

Speaker 2

Nothing obvious that suggests we have to titrate. And to your point, I think the tolerability was really, Really promising in the subcu, but it's just its first study. And we know that GLP-one agonism is tied to And GI side effects. So we just want to try to control for that as best as possible.

Speaker 7

I guess To be more specific, why do you feel like you need to go higher on the dosing, if you've sort of attained some pretty competitive Results as it is with good tolerability.

Speaker 2

In the oral that you're talking about?

Speaker 7

No, in the injectable for Phase 2.

Speaker 2

Oh, and injectable. Yes, we're going to go up to 15 milligrams because the 10 milligram was very well tolerated and Maybe the 15 milligram cohort to the 28 day study, but that was the reason we were Considering adding that 15 milligram cohort to the 28 day study, but we decided to just Stop the study here and put that into the Phase 2 and we'll titrate up to it. But I don't think there's anything I don't think we're necessarily pushing With increasing the dose to 15.

Speaker 7

Okay. And then if I can ask on VK2809, I mean you have some Pretty good validation from a competing program. But I guess some of the KOLs we spoke to, one of the things that they brought up was that they were a little bit surprised That there was not just NASH reduction, but they also were able to shift fibrotic improvement as early as year 1. So how do you really think about this? And would you expect the same for yourself if your Seemingly superior liver fat reduction holds up in voyage.

Speaker 7

How are were you surprised with the fibrotic effect within 2 weeks given that it's more of a downstream process from the fat reduction?

Speaker 2

Well, I don't know. I think that yes and no, I guess. I mean, the fibrosis improvement endpoint is a traditionally a more difficult Endpoint to show improvement on. But we know that the mechanism demonstrates in animal models reduction in Collagen load and improvement in fibrosis. And whether or not that secondary to fat reduction, I don't think we know and haven't seen that published anywhere.

Speaker 2

So We weren't totally surprised. I guess you could argue that it's too short a window and this is more a metabolic targeting mechanism. Everything we've seen in animals suggests that it should actually do both. It should help with NASH resolution and improve fibrosis.

Speaker 7

Okay, great. And if I can squeeze in one more, any thoughts about how long this $406,000,000 will take you out to?

Speaker 3

Yes. Hi, Annabel. Certainly, we're covered, as Brian mentioned earlier, well beyond all the catalysts in our Three development programs. We wouldn't point to an exact year, but certainly well beyond 2 years out and well beyond.

Speaker 7

Okay, great. Thank you.

Speaker 2

Thanks, Annabel.

Operator

Thank you. And our next question today comes from Jay Olson at Oppenheimer. Please go ahead.

Speaker 8

Hey, congrats on all the progress and thank you for the update. Maybe just to follow-up on VK2809. 2,809. Can you just talk about what we should expect to see In the top line results besides MRI, PDFF, will we see change in LDL cholesterol And then I guess can you just talk about sort of the GI tolerability of VK2809? It seems like that's a potentially important feature for your molecule.

Speaker 8

And then I had a follow-up if I could please.

Speaker 2

Sure. Thanks, Jay. With the initial data, we would plan to have the liver fat by MRI PDFF And then lipid panel, so likely LDL, trigs and if we get the atherogenic proteins, Lp and APOB, we'd report those as well, As well as safety and tolerability. The GI profile to date has been excellent. We haven't really seen anything different from placebo.

Speaker 2

And there's no reason to think that we would see differences in the population, but we don't have the data, so we can't say for sure yet. But there's nothing that would lead us to believe that there Any sort of a GI signal with the compound, it's exceptionally well tolerated.

Speaker 8

Okay, great. Thank you. That's super helpful. MRI, PDFF and any other endpoints that we should be watching, including safety and tolerability, And then what you would see as the most important differentiating points from resmetirom that would be great. Thank you.

Speaker 2

Yes. Thanks, Jay. Well, I think the internal hurdle that we're using is a 30% mean reduction in liver fat. If we can see The treatment groups showing a 30% mean reduction, that would be our Success hurdle. Obviously, higher is better.

Speaker 2

We saw really nice reductions in the Phase 2a study. I'm not sure I would expect that level of efficacy in this study just because it's a larger study and you often see a penalty when you go into larger populations. But if we see 30%, I think there's a lot of precedent that suggests that translates to a higher probability of histologic benefit. I think there's plenty of room for multiple of the same mechanism to coexist in NASH. I think there will be Differentiation among products and they're probably switching.

Speaker 2

I think our tolerability profile is outstanding and our efficacy has been Exceptionally strong so far. So I think we're comfortable with where we would be competitively.

Speaker 8

Excellent. Thank you so much for taking the questions and we'll look forward to seeing the results.

Speaker 2

Thanks very much, Jay.

Operator

Thank you. And our next question today comes from Andy Hsieh with

Speaker 9

So Brian, you mentioned a couple of times about the activities in liver fat, at least in the preclinical model from these dual agonist Candidates, including 2,735. So I'm curious if that was by design or it's An observation that you just observe as you advance these candidates from preclinical to clinical settings?

Speaker 2

Yes. It's thanks, Andy. It's I think the liver fat change from this mechanism because there are no receptors In the liver, is probably most tied to weight loss and Insulin sensitivity, improving insulin sensitivity. So I don't think there's necessarily A direct effect on liver fat, it's more tied to weight loss. But In animals, we did see really interesting data, typically generally always better Then a GLP-one mono agonist and comparable to better than another dual agonist.

Speaker 2

So we're really excited about the potential there. I think that the models we looked at were generally the diet induced obese mouse. So, if you're Skinnier or your body weight is lower, liver fat is lower, you probably wouldn't see as large an effect since the effect is driven by weight loss, but Pretty interesting characteristic.

Speaker 9

Got it. We've gotten some questions from investors about Relative contribution of weight loss from either fat or lean body mass, do you have a good handle from the Phase 1 Study about the proportion that's the observed weight loss is coming from?

Speaker 2

We don't. We didn't Do any DEXA scans in this study, so we don't have the relative change in weight. We do from the animals, we saw predominantly A reduction in fat and not muscle. But I think it's been shown in other studies When you lose a certain amount of weight, you do start to cut into muscle. But we didn't see that in The animal studies that we conducted and we unfortunately just didn't look at it in this study.

Speaker 9

Great. Is that something You'll look at in the Phase 2 study?

Speaker 2

Not currently, no. It's a 13 week study. So we don't have a plan to DEXA scans in the upcoming study. It might be something we'd look at in a longer term study.

Speaker 9

Got it. Got it. That's helpful. And then maybe lastly for the oral formulation versus subcu, could you kind of help us think about the amount In terms of dosing from these two formulations on a relative sense?

Speaker 2

Yes. The oral will push up a little bit higher. We're going I think the plan is to go to 20 milligrams with the oral, so not a huge amount higher Then the currently planned dose for Phase 2 in the subcu.

Operator

Our next question comes from Yale Jen with Leibaugh and Company. Please go ahead.

Speaker 5

Good afternoon and thanks for taking the questions and congrats on all the progress Just a quick question. First one probably is a little bit half beating. In terms of SG and A in Q1, that seems It's been higher than prior quarters. Should we anticipate that to be a normal? Is this generally a one time situation?

Speaker 2

Yes. Thanks, Yale. That's primarily due to it is not something you should expect to see moving forward. That's really due to timing of some legal expenses and those should be reduced moving forward and you wouldn't expect The runway moving forward.

Speaker 5

Okay, great. And a follow-up question here, again, about the 2,735 Phase 2 study, could you give us sort of overall a view about what you anticipate to do for that study? Anything you can review in terms of the study design?

Speaker 2

Yes. The Study design is a 13 week study with flat dosing in the lowest dose cohorts and then titrated dosing In the higher dosed cohorts, the top dose right now is targeting 15 milligrams And we'll do stepwise titration up there. It's 13 weeks in duration. So you'd be at the top dose for, I think 3 to 4 weeks at the end there. Primary endpoint will be change in body weight.

Speaker 5

And how big the study might be in terms of

Speaker 2

Yes, we haven't disclosed that, but I would say 150 or so or 100 to 150 would be the target there.

Speaker 5

And great. That's very helpful. Maybe the last question here Is that you mentioned that about with the cash in hand, you might also contemplate Some additional pipeline expansions, I know you want to be focused, but nevertheless, was there anything in your mind that could be Excluded and going forward? Yes.

Speaker 2

We have a lot of things we're working on, but we I haven't disclosed, but we typically spend time in an area as little money as possible on Some of these nascent programs and the ones that show promise we bring forward. I think 2,000 735 is a good example of that. And As things mature appropriately, we'll have more to say about them.

Speaker 5

Okay, great. Thanks a lot. Again, congrats.

Speaker 2

Thanks a lot, Ian.

Operator

Thank you. And our next question today comes from Justin Zelman with BTIG. Please go ahead.

Speaker 10

Hi, thanks for taking the question and congrats on all the progress. Maybe just a follow-up on the Phase 2 for the dual agonist Here, you mentioned 13 weeks of active dosing. Will you continue to follow-up the patients past the 13 weeks? And For further longer term data, would we have to look towards another study here?

Speaker 4

And I have some follow ups.

Speaker 2

Yes. To answer the second question, yes, I think longer data would come from a subsequent study of 26 weeks or longer. Not that that's the next study, but we plan to get through this study first. The follow-up period in this study, I believe, is 4 weeks. So you come back, I think well, multiple times you come back after the 13 week treatment period, but I think the last follow-up said week 17 And Mary Anne is nodding in agreement here, Mary Anne Mancini, our COO.

Speaker 2

So, anyway, that's the duration.

Speaker 10

Great. And from the Phase 1 data, did you notice anything in the PKPD profile that suggests that It might be different from what we've seen with the tirzepatide compound. I'm just curious if there was anything that appeared in that data set yet or is it too early to tell?

Speaker 2

Yes. It's really hard to make those comparisons because the obviously they weren't head to head in the population That we've seen published for the tirzepatide compound is just a different population than we looked at. We do see, I think, Later Tmax, longer half life, and I think our exposures are improved. But again, very difficult to make those sorts In the absence of a head to head data set.

Speaker 10

Great. And I'll ask one last question. Further down the road, do you see any potential to run a combination with the 2,809 and the dual agonist potentially in a NASH study?

Speaker 2

Yes. It's not something we've talked much about. But if we were to do something like that, I think We talk about it if and when we have data on it.

Speaker 10

Great. Thanks for taking my questions.

Speaker 2

Thanks, Jeff.

Operator

Thank you. And our next question today comes from naz Rahman with Maxim Group. Please go ahead.

Speaker 8

Hi, guys. Thanks for taking my question. Just really quickly on the oral. What gives you confidence on the Timing of the initial data for second half of twenty twenty three, like are you guys seeing any potential competition Any issues recruiting patients with all the, I guess, various GLP-one studies ongoing?

Speaker 2

Yes. We think we can get the data in the second half. We feel confident about that. Luckily, obesity is the largest market ever. So, we shouldn't have problems with recruiting, but, I don't know, we haven't had many Competitive issues at this point.

Speaker 8

Right. How many sites are there? And for this study, are all the sites also in Australia?

Speaker 2

Yes. It's actually an extension of the earlier study, the single ascending dose and multiple ascending dose study. It's the same site. It's a single site in Australia. The Phase 2 study will be here in the United States.

Speaker 8

Got it. Are you seeing like, I guess, like faster rates enrollment or I guess like higher Rate of interest versus when you initially started your injectable studies?

Speaker 2

I think it's maybe too early to say there. I don't know the answer to that question. All right.

Speaker 8

Got it. Thank you for taking my questions.

Speaker 2

Thanks, Nat.

Operator

Thank you. And ladies and gentlemen, this concludes our question and answer session. I'd like to turn the conference back over to Stephanie Diaz for any closing remarks.

Speaker 1

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.

Operator

Thank you. This concludes today's conference call. We thank you all for attending today's presentation. You may now disconnect your

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Earnings Conference Call
Viking Therapeutics Q1 2023
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