Viking Therapeutics - Earnings Call - Q1 2022
April 26, 2023
Transcript
Speaker 0
Welcome to the Viking Therapeutics First Quarter twenty twenty three 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, 04/26/2023.
Speaker 1
I would now like to turn
Speaker 0
the conference over to Viking's Manager of Investor Relations, Stephanie Diaz. Please go ahead, Stephanie.
Speaker 2
Hello, and thank you all for participating in today's call. Joining me today is Brian Lian, 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, 04/26/2023, 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'll now turn the call over to Brian Linn for his initial comments.
Speaker 3
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 2023 and provide an update on recent progress with our clinical programs and operations. The 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 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 one single ascending dose and multiple ascending dose study in healthy volunteers.
As we'll discuss in a few minutes, the results were encouraging with mean weight loss of up to 18 pounds observed following twenty eight days of treatment. We plan to initiate a Phase two study of VK280735 in patients with obesity in mid-twenty twenty three. In addition, we announced the initiation of a new clinical study to evaluate a novel oral formulation of this compound. With respect to our third 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 that we plan to use for the continued advancement of each of our programs through key clinical milestones.
I'll provide further details on our operations and development activities after we review our first quarter twenty twenty three financial results. For that, I'll turn the call over to Greg Zanti, Viking's Chief Financial Officer.
Speaker 4
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 first quarter ended 03/31/2023. Our research and development expenses for the three months ended 03/31/2023 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.
Our general and administrative expenses for the three months ended 03/31/2023 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 three months ended 03/31/2023, 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 three months ended 03/31/2023 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.
At 03/31/2023, Viking held cash, cash equivalents and short term investments totaling a 135,700,000.0 compared to $155,500,000 as of 12/31/2022. The company's Q1 twenty twenty three 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 04/03/2023. Pro form a including this offering, our end of quarter cash, cash equivalents and short term investments were approximately $4.00 $6,000,000 This concludes my financial review and I'll now turn the call back over to Brian.
Speaker 3
Thanks, Greg. As mentioned in my opening comments, the 2023 was an exciting time at Viking. In recent weeks, we announced positive data from a Phase one study in healthy volunteers with our newest clinical program, the dual incretin receptor agonist VK2735. 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 second quarter from a position of clinical momentum, financial strength and optimism for upcoming data.
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 twelve week phase 2a 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 eighty eight percent of patients receiving VK2809 experienced at least a 30% relative reduction in liver fat content. Importantly, 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 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. We believe VK2809's activation of the thyroid hormone beta receptor provides unique therapeutic benefits for patients with NASH. Perhaps
Speaker 5
one of
Speaker 3
the most important additional benefits of this compound is its ability to reduce plasma lipids including LDL cholesterol, triglycerides, and atherogenic proteins, all of which have been correlated with increased cardiovascular risk. 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 twelve week Phase 2a study experienced robust reductions in these lipids suggesting that VK2809 may offer a cardio protective 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. Based on the promising results from our Phase 2a trial, the company initiated the VOYAGE Phase 2b 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 eight percent liver fat content as measured by magnetic resonance imaging, proton density, fraction as well as F2 and F3 fibrosis. Up to twenty five percent of patients may have F1 fibrosis provided that they also possess at least one additional risk factor. Primary endpoint of the VOYAGE study will evaluate changes in liver fat from baseline to week twelve 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 fifty two weeks of treatment.
During the first quarter, we announced completion of enrollment in the VOYAGE study and we look forward to sharing top line results including the trial's primary endpoint during the second quarter of this year. I'll now turn to our newest clinical program, highlighted by a compound called VK2735, which we believe has the potential for the treatment of various metabolic disorders such as obesity, NASH, and certain rare diseases. VK2735 is a dual agonist of the glucagon like peptide one 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 Vikings 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 among animals treated with a GLP-one mono agonist.
Based on these in vivo and other preclinical data, we initiated a phase one single ascending dose and multiple ascending dose clinical trial of VK2735. The single ascending dose portion of the study enrolled healthy men and women, and evaluated escalating single doses of VK2735. The multiple ascending dose portion enrolled healthy men and women with a minimum body mass index of thirty kilograms per meter squared. In the multiple ascending dose portion of the study, subject received VK2735 once weekly for twenty eight days. During the first quarter, we were pleased to announce the results from this study with VK2735 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 VK2735 were safe and well tolerated, and that the compound's PK profile demonstrated favorable characteristics in humans. Following single subcutaneous doses, VK2735 demonstrated the half life of approximately one hundred and seventy to two fifty hours, a Tmax ranging from seventy five to ninety hours, and excellent therapeutic exposures. In the twenty eight day multiple ascending dose portion of the study, VK2735 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 forty three follow-up time point, twenty one days after the last dose of VK2735 was administered. Importantly, VK2735 demonstrated encouraging safety and tolerability following repeated dosing. Ninety eight percent of observed adverse events were reported as mild or moderate, and ninety nine percent of gastrointestinal related adverse events were also reported as mild or moderate. In addition, all cohorts treated with VK2735 demonstrated improvements in plasma glucose levels relative to placebo, though not all cohorts achieved 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 VK280735. Based on the positive results generated in the Phase one study, we plan to initiate a Phase two trial in patients with obesity in mid-twenty twenty three. Concurrent with the announcement of the Phase one data just described, we also announced the initiation of a Phase one clinical study to evaluate an oral tablet formulation of VK2735. We believe the tablet formulation represents a significant potential expansion of the program's overall value and utility. In vivo data to date suggests that therapeutic plasma levels of VK2735 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 subcutaneous or oral dosage forms of VK280735 creates attractive potential treatment options and further extends the reach of this important program. The oral study is an extension of the Phase one 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 thirty kilograms per meter squared. Subjects will receive daily oral doses for twenty eight days.
Primary objective of the study is to the safety, tolerability, and pharmacokinetics of VK VK2735 following twenty eight days of oral dosing. Exploratory endpoints include changes in body weight and plasma glucose. We believe the results from this study could potentially be available in the 2023. I will now provide an update on our third clinical candidate VK0214. This is Viking's second orally available small molecule thyroid hormone receptor beta agonist, 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. Patients with XALD 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 ALD. In a prior phase one 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. 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 adrenal myeloneuropathy or AMN form of X ALD. AMN is the most common form of X ALD affecting approximately fifty percent of patients. The phase one b 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 twenty eight 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. Late in the first quarter, 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 program, both existing and new, and places Viking in a position of strength in discussions with potential corporate partners. In conclusion, the 2023 proved to be an exceptional quarter for Viking. We announced completion of enrollment in the VOYAGE study of 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. We look forward to initiating a US phase two study in obesity in mid twenty twenty three.
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 adrenal myeloneuropathy, and we anticipate reporting data from this study later in the year. 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. Operator?
Speaker 0
Thank you. This first question comes from Steve Seedhouse with Raymond James. I
Speaker 1
had a few on the oral formulation of the GLP-one GIP. First, just you haven't shared any preclinical data. So I wanted to ask in general if the expectation would be you could get this 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? And then also with that compound, is this something that would lend itself to like a titration scheme as well? Or are you essentially looking at flat doses in the Phase one?
Speaker 3
Hey, Steve. Thanks for the questions. With the exposures, yeah, I don't think we expect the exposures to achieve the same level that are observed with the SubQ formulation. Maybe I'll be proven wrong, but I don't think we'll we'll we'll get there. It's almost, you know, a a different product.
I would consider the oral formulation maybe for someone who first doesn't wanna start with an injectable or for someone who maybe has a BMI, you know, thirty two to thirty four or something that, you know, might be adequately addressed with an oral formulation or, you know, potentially in a maintenance setting where you start with the sub q and then and then transition on. So there are lot of different ways that it could be used, but my own guess is that we probably won't see the the same exposures with the with the oral. Same question? Titration. Oh, titration.
Yeah. So, yeah, we we will titrate in the upcoming study. So the first cohorts flat dosing and and subsequent cohorts will will titrate up.
Speaker 1
Okay. So it's just one dose of one tablet dose that you just get multiple pills, I guess, in that case?
Speaker 3
That's right. Yeah. Yep. Yep. The first, the first cohort is two and a half mgs, and that's flat.
And and then, from there, they, they dose up. I mean, first week will be two and a half, and then the remaining three weeks would be a higher dose. And then as you go on in through the cohorts, you'd kinda titrate up per week.
Speaker 1
Okay. Couple couple more, just because it's really interesting program, obviously. You mentioned maintenance dosing is one option. That's obviously just given
Speaker 6
how
Speaker 1
many people in the next, you know, decade are likely to be gravitating towards using creatins, I imagine there'd be some enormous group of patients coming on or, you know, having been on injectables. I'm curious if you're gonna gather that type maintenance data in the phase one. Can you take patients that you already treated with the injectable and start them on oral and see how they do? And then I just have one more in the program after if I could. Thanks.
Speaker 3
Yeah. No. Thanks. In this study, we're really just trying to see if the formulation will provide exposures and, you know, what what levels compare to the sub q. So I think in the future, you know, those transition type studies would be really important and really interesting, but this is just the first one, and we're just gonna see how exposures turn out.
Speaker 7
Okay. And then
Speaker 6
the phase one, I think
Speaker 1
you guys were for the injectable, at least you were collecting MRI PDFF data, and there were maybe 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 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 3
Yeah. Thanks, Steve. We'll probably be reporting more data a little bit later in the year potentially at ObesityWeek. But we we don't have any any near term, you know, nothing imminent there. But you're right.
We did have a number of biomarkers in liver fat in the study.
Speaker 1
Alright. Thanks, Brent.
Speaker 3
Thanks, Steve.
Speaker 0
Thank you. And our next question today comes from Joon Lee with Truist Securities. Please go ahead.
Speaker 5
Hey. Thanks for taking our questions, and congrats on the progress. You know, what really stood out from the healthy volunteer study of VK280735 was how clean the tolerability profile was. So is that a is that just a function of the study being a small Phase one study, or is there some mechanistic hypotheses as to why two seven three five may be better tolerated and with possibly better weight loss? And I have a follow-up.
Thank you.
Speaker 3
Hi, June. Thanks. Yeah. So It was a small study, so you could argue that, maybe we're we're just looking at, small numbers.
What was interesting with the tolerability was that there wasn't really a dose related change tolerability as you went up. I think the 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 a sustained, effect on on GLP one, without, arrest and recruitment, you you could see maybe an increase in efficacy without necessarily, issues with nausea, but I don't I don't know. Otherwise, I don't know that mechanistically there's anything obvious that would explain it.
Speaker 5
Fair enough. And, you know, both Lilly and Novo have historically done head to head to head trials of their GLPs, at least for diabetes. Do you have any plans to do a head to head trial of v k three two seven three five against other obesity drugs?
Speaker 3
Yeah. Great question. I think it's a it's a really good idea as we move further through the program, but, this, upcoming phase two 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 5
Thanks for taking my question.
Speaker 3
Thanks, June.
Speaker 0
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'm I'm I I wanted to ask about the the titration period that you're considering for phase two. I mean, it looked like you had some good tolerability. It looks like you have some very good weight loss already within twenty eight 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? So I guess that's the first question. And is this the same exact molecule as two thousand seven hundred thirty five? Are you changing the balance between GLP-one or GIP in any way as you go into the oral if you don't have the same, I guess, target exposure? And then I have one more follow-up.
Speaker 3
Yeah. It's the same molecule, Annabel, the oral and the sub q. And we're titrating in the twenty eight day study really because we've 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 sub q, we did have the first two cohorts were flat dosing, then we titrated.
And here the first cohort is gonna be flat and then we titrate. But nothing, obvious that suggests we have to titrate. And to your point, I think the tolerability was really, really promising in the in the sub q, but it's just, you know, it's first study. And we we know that GLP one agonism is tied to nausea and and, GI side effects, so we just wanna, you know, try to control for that as best as possible.
Speaker 7
I I guess, you know, to be more specific, why do you feel like you need to go higher on the dosing if you've sort of attained some of some pretty competitive results as it is with good tolerability?
Speaker 3
In the in the oral
Speaker 6
that you're talking about?
Speaker 7
No. In the, in the injectable for phase two.
Speaker 3
Oh, in the injectable. Yeah. We're gonna go up to, to fifteen milligrams because, the ten milligram was very well tolerated, you know, maybe the fifteen will work better. We we won't know, until we get there, but, that was the reason we were considering adding that, fifteen milligram cohort to the twenty eight day study, but we decided to just, you know, stop the study here and and put that into the phase two, and, we'll titrate up to it. But I I don't think there's anything, I don't think we're necessarily pushing anything with, with increasing the dose to fifteen.
Speaker 7
Okay. And then if I can ask on VK2809. I mean, 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 surprised that there was not just NASH reduction, but they also were able to show fibrotic improvement as early as year one. So how do you really think about this, and would you expect the same for yourself if your you know, seemingly superior liver fat reduction holds up in voyage?
You know, how are were you as surprised with the fibrotic effect within fifty two weeks given that it's more of a downstream process from the fat reduction?
Speaker 3
Well, I I don't know. I think that yes and no, I guess. I mean, the the fibrosis improvement endpoint is a traditionally a more difficult, endpoint to show improvement on. But we know that the mechanism demonstrates in in animal models, reduction in collagen load and improvement in fibrosis. And whether or not that's secondary to fat reduction, I don't think we know and haven't seen that published anywhere.
So we weren't, you know, totally surprised. I I guess you could argue that, you know, it's too short a window, and this is more a metabolic targeting mechanism. But 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 4
Yeah. Hi, Annabel. You know, certainly, we're we're covered, as Brian mentioned earlier, you know, well beyond all the catalysts in our, three development programs. You know, we we wouldn't point to an exact year, but certainly, well beyond, you know, two years out and and well beyond.
Speaker 7
Okay. Great. Thank you.
Speaker 6
Thanks, Annabel.
Speaker 0
Thank you. And our next question today comes from Jay Olson at Oppenheimer. Please go ahead.
Speaker 8
Oh, hey. Congrats on all the progress, and thank you for the update. Maybe just to follow-up on VK2809. 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 levels?
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. And then I had a follow-up if I could, please.
Speaker 3
Sure. Thanks, Jay. The with the initial data, we would plan to have the liver fat by MRI PDFF, and then, a lipid panel. So, you know, likely LDL, trigs. And, if we get the atherogenic proteins, Lp and ApoB, we'd those as well, as well as, you know, safety and, and and tolerability.
The GI profile to date has been, excellent. We haven't really seen anything, different from placebo. And there's no reason to think that we would see differences in the, in the Voyage population, but, we we don't have the data, so we can't can't, say for sure yet. But there's nothing that would, lead us to believe that there would any be any sort of a GI signal with the compound. It's exceptionally well tolerated.
Speaker 8
Okay. Great. Thank you. That's super helpful. And then if you could maybe help us frame for investors what a best case scenario might look like with regards to 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 ResMeder on, would be great. Thank you.
Speaker 3
Yeah. Thanks, Jay. Well, I think the the internal hurdle that we're using is a 30% mean reduction in liver fat. If we can see, you know, treatment groups showing a 30% mean reduction, that that would be our success hurdle. Yeah.
Obviously, higher is better. We saw really nice reductions in the phase two a study. I'm not sure I would expect that level of efficacy in this study just because it's a larger study, and you you often see a penalty when you go into larger populations. But, you know, if we see 30%, I think there's a lot of precedent, that suggests that translates to a higher probability of, histologic benefit. I I think, you know, 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. 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 3
Thanks very much, Jay.
Speaker 0
Thank you. And our next question today comes from Andy Hsieh with William Blair. Please go ahead.
Speaker 9
Okay. Thanks for taking my question, and congratulations on all the achievements this quarter. 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 two thousand seven hundred thirty five. So I'm curious if that was by design or it's an observation that you just observed as you advance these candidates, from preclinical to clinical settings.
Speaker 3
Yeah. It's thanks, Andy. It's it's I I think the liver fat change from this mechanism because there are no receptors in the liver is is probably most tied to weight loss and, you know, insulin sensitivity, improving insulin sensitivity. So I don't think there's necessarily a a direct effect on liver fat. It's more tied to to to weight loss.
But in animals, we we did see really interesting data. Typically, you know, generally always better than a than a GLP one mono agonist and comparable to better than another a dual agonist. So we're we're really excited about the potential there. I think that, you know, the the models we looked at were generally the diet induced obese mouse. So if you're if you're, you know, skinnier or your your body weight's lower, liver fat's 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, you know, relative contribution of weight loss from either fat or lean body mass. Do you have a good handle from the phase one study about the proportion that's, you know, the observed weight loss is coming from?
Speaker 3
We don't. We didn't, do any DEXA's DEXA scans in this study, so we don't have the relative change in weight. We do from the animals, saw predominantly a reduction in fat and and not muscle. But I think, it's been shown in in other studies that when you lose a, you know, certain amount of weight, you do start to start to cut into to muscle. But, we didn't we didn't see that in any of the the animal studies that we conducted.
And we unfortunately just didn't look at it in the study.
Speaker 9
Great. Is that something that you'll you'll you'll look at in the phase two study?
Speaker 3
No. It's a thirteen week study, so we don't have a plan to do DEXA scans in the in the upcoming study. It might be something we'd look at in a in a longer term study.
Speaker 9
Got it. Got it. That's 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 on a relative sense?
Speaker 3
Yeah. The, the oral will push up a little bit higher. We're going I think the plan is to go to twenty milligrams with the oral, so not a huge amount higher than the currently planned dose for phase for for the the phase two and the subcu.
Speaker 9
Got it. Okay. Awesome. Well, thanks for answering all all our questions.
Speaker 6
Thanks a lot, Andy.
Speaker 0
Our next question comes from Yale Jen with Laidlaw and Company. Please go ahead.
Speaker 6
Congrats on all the progress so far. Just a quick few quick questions. The first one probably is a little bit housekeeping. In terms of SG and A for first quarter, that seems significantly higher than prior quarters. Should we anticipate that to be a normal this is generally a one time situation?
Speaker 3
Yeah. Thanks, Yo. That that's, primarily due to it it is not something you you you should expect to see, moving forward. That's really due to timing of some, some legal legal expenses, and, those should be, reduced, moving forward, and you wouldn't expect to be the the runway moving forward.
Speaker 6
Okay. Great. And, a follow-up question here, again, about the 2735 phase two study. Could you give us, sort of over or a a view about what you anticipate to do for that study? Anything you can review in terms of the study design?
Speaker 3
Yeah. The study design is a thirteen week study with the flat dosing in the the lowest dose cohorts, and then a titrated dosing in the higher dose cohorts. The top dose right now is targeting fifteen milligrams, and we'll do a stepwise titration up there. It's thirteen weeks in duration, so you'd be at the top dose for, I think, three to four weeks at the end there. The primary endpoint will be change in body weight.
Speaker 6
And how big the study might be in terms of size?
Speaker 3
Yeah. We haven't disclosed that, but I I would say, you know, a hundred and fifty or so or or, you know, one to a hundred to a hundred and fifty would be the the target there.
Speaker 6
And great. That's very helpful. Maybe the last question here is that that you mentioned that about, with the cash in hand, you might also contemplate some additional pipeline expansions. I know you wanna be focused, but nevertheless, was there anything in your mind that could be explored and going forward? Yes.
Yeah. We have a lot
Speaker 3
of things that we're we're we're working on, but we we haven't disclosed. But we we typically spend time in in an area as as little money as possible on some of these, nascent programs and the ones that show, you know, promise we we bring forward. And I think, two seven three five is a is a good example of that. And, you know, as as things mature appropriately, we'll we'll have more to say about them.
Speaker 6
Okay, great. Thanks a lot. And again, congrats.
Speaker 3
Thanks a lot, Yale.
Speaker 0
Thank you. And our next question today comes from Justin Zelen 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 II for the dual agonist here. You mentioned 13 of active dosing. Will you continue to follow-up the patients past the thirteen weeks? And you know, for further longer term data, would we have to look towards another study here?
And I have some follow ups.
Speaker 3
Yeah. To answer the second question, yeah, I think longer data would come from a, you know, a subsequent study of, you know, twenty six 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, believe, is four weeks. So you come back, I think, well, multiple times you come back after the thirteen week treatment period, but I think the last follow-up said week seventeen.
And Mary Anne is nodding in agreement here, Mary Anne Mansini, our COO. So, anyway, that's the duration. Great.
Speaker 10
And and from the phase one data, did 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 dataset yet or is it too early to tell?
Speaker 3
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 than we looked at. We we do see, I think, a later Tmax, a longer half life, and I think our exposures are improved. But again, very difficult to make those sorts of comparisons in in the absence of a head to head dataset.
Speaker 10
Great. And I'll ask one last question. Further down the road, see any potential to run a combination with two thousand eight hundred and nine and the dual agonist potentially in a NASH study?
Speaker 3
Yeah. 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 the questions.
Speaker 3
Thanks, Jeff.
Speaker 0
Thank you. And our next question today comes from Nas Raman with Maxim Group. Please go ahead.
Speaker 8
Hi, guys. Thanks for taking my question. Just really quickly on the oral. What kind of what gives you confidence on the timing of the initial data for second half twenty three? Like, are you guys seeing any potential competition or any issues recruiting patients with all the, I guess, various GLP one studies ongoing?
Speaker 3
Yeah. We think we can get, the data in the second half. We feel confident about that. Luckily, obesity is, you know, 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 and for this study, are all the sites also in Australia?
Speaker 3
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 II 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, rates of interest versus when you initially started your injectable studies?
Speaker 3
I think it's maybe too early to say there. I don't know the answer
Speaker 8
All to that right. Got it. Thanks for taking my questions.
Speaker 3
Thanks, Nas.
Speaker 0
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 2
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.
Speaker 0
Thank you. This concludes today's conference call. We thank you all for attending today's presentation.