Viking Therapeutics, Inc. (VKTX) Earnings Call Transcript & Summary

Hi, everyone. Thanks for joining day 1 of our UBS Global Healthcare Conference. My name is Sriker Nadipuram, and I'm an associate on the U.S. pharma SMID cap biotech team here at UBS under senior analyst, Navin Jacobs. And with that, it's my pleasure to welcome Brian Lian, CEO of Viking Therapeutics, to present on the company. Brian, take it away.

Great. Thanks very much, and thanks to UBS for the opportunity to present. We really appreciate it. I'll be making some forward-looking statements during the presentation today. I would encourage anybody listening to this presentation or viewing the slides to refer to the Securities and Exchange website -- Securities and Exchange Commission website for the most current information on the company. Moving to Slide 3. I'll take you through the Viking story today. So we're a San Diego-based company, focused on novel therapeutics for metabolic and endocrine diseases. We have clinical programs that we believe have demonstrated best-in-class efficacy data in several different clinical areas. The program that has generated a lot of interest for us is our metabolic disease program, and it's highlighted by VK2809, which we're developing for nonalcoholic steatohepatitis or NASH. It's a novel, selective thyroid beta receptor agonist. In a Phase II trial in patients with NAFLD and hypercholesterolemia, we demonstrated a significant reduction in liver fat content as well as plasma lipids. And we're currently conducting a Phase IIb study in patients with biopsy-confirmed nonalcoholic steatohepatitis, and we call this the VOYAGE study. We have a second program focused in the rare disease arena, and this is highlighted by a compound called VK0214, another selective thyroid receptor beta agonist that, in animal models, has shown a very nice improvement in biomarkers for a disease called X-linked adrenoleukodystrophy. And right now, we plan to bring that into the clinic later this year. We have other pipeline programs focused on musculoskeletal and metabolic disorders, but I'll be focusing primarily on VK2809 and VK0214 today. Slide 4 is just a snapshot of the pipeline, where we sit today, VK2809 in Phase IIb for NASH, VK0214 moving into the clinic with an IND planned in the next couple of months. And then other programs include our musculoskeletal program, VK5211, a selective androgen receptor modulator. VK0612 is a fructose bisphosphatase inhibitor for type 2 diabetes. And then VK1430 is a DGAT-1 inhibitor that has shown some interesting data in hypertriglyceridemia. Moving to Slide 5 and into Slide 6, I'll talk more now about our VK2809 program. This is a member of a proprietary family of small molecule thyroid hormone mimetics that have shown tissue and receptor subtype selectivity. And many of these molecules have demonstrated potent lipid reductions in both animals and humans. They're built on unique chemical scaffolds that we think should provide a wider safety window versus some of the legacy approaches toward this receptor. And generally, when you think of the thyroid beta receptor, you can think of it as having a broad biologic activity. Some of the larger markets that could be addressed with this mechanism include the NASH market, hypercholesterolemia or dyslipidemia. But there are also some orphan indications that might benefit from the mechanism, and we're looking at X-linked adrenoleukodystrophy. As I mentioned a moment ago, we have 2 molecules, VK2809 and VK0214, in development. They're both oral, amenable to once-daily dosing. VK2809 is in the Phase IIb study in NASH, and VK0214 is set to move into the clinic ultimately for X-linked adrenoleukodystrophy. Moving to Slide 7, a brief overview of the thyroid hormone receptor. These are nuclear hormone receptors, and you can think of 2 major subtypes of this receptor. The beta receptor is expressed in the liver and brain, and it serves as a -- the way we think of it is a master regulator for lipid metabolism. The alpha receptor is expressed in skeletal muscle and cardiac tissue, and it plays a role in basal metabolic rate and heart rate contractility and that sort of thing. So in the lipid setting, the goal is to be very potent on the beta receptor and very silent on the alpha receptor, and that's where these molecules seem to do reasonably well. We move to Slide 8. We think this is a particularly exciting target for the setting of fatty liver diseases, NASH in particular. And when you look across the top of the slide there, you can see the progression from a healthy liver to cirrhosis passing through NASH. And the reason the beta receptor is interesting here is that we know it plays a role in lipid metabolism. We know that agonism at beta receptor results in systemic and liver-specific effects. The receptor is localized to the liver and with limited expression outside the liver. And we've seen from multiple models in vivo that activation of the beta receptor provides an anti-fibrotic benefit. And then finally, we know from several different clinical studies that there seems to be a correlation between reducing liver fat and improving other histologic features of NASH. So we think an agent that reduces liver fats and improves systemic lipids as well as antagonizes fibrotic signaling could provide a very nice benefit overall to patients with NASH. Moving to Slide 9. What is unique about this molecule, if you look at the left-hand side of Slide 9, upper left, is the actual chemical structure of VK2809. If dosed as a prodrug, and VK2809 itself has no activity on either thyroid hormone receptor, but following oral administration, if you go down the arrow there, you can see the conversion into a molecule denoted VK2809A, and that's the potent thyroid receptor beta agonist. That cleavage is mediated by an enzyme called cytochrome P450 3A4, which is primarily expressed in the liver. And so the result of this is that you get a chemical delivery of an active thyroid agonist into the tissue of greatest interest with limited activation outside of the liver. Some of the qualitative data for this effect are shown on the right-hand side of the slide. This is a rat that was dosed with radiolabeled VK2809, and you can see where radioactivity shows up highest is in red, and lower is in blue. And you can see that the radioactivity seems to localize in the liver relative to other tissues. And so we think this selective activation and differentiated underlying chemistry makes VK2809 a very selective compound, and it reduces the risk of ex-hepatic systemic side effects. Moving to Slide 10. We have evaluated this compound in multiple animal models of fatty liver disease, and what Slide 10 shows are some data from a model of diet-induced NASH. These are animals that are raised on high cholesterol, high fructose diet for around 35 weeks. And at that point, they're biopsied to confirm that they have not only NASH but also fibrosis. And only those animals with NASH and fibrosis are brought into the study. In this experiment, dosing was 8 weeks daily. And after 8 weeks, we evaluated the liver of the animals. And what the graph shows on the right-hand side are fat content. So triglyceride content was reduced 70% after 8 weeks of daily dosing with VK2809. Cholesterol content was reduced 65%. Total liver lipid content was reduced approximately 80%, and the NAFLD activity score was reduced approximately 40%. So a very nice improvement in lipids and steatosis and NASH activity score -- NAFLD activity score. Moving to Slide 11. We also looked at fibrosis in this same set of animals, and what we see after 8 weeks of daily dosing on fibrosis was a 50% reduction, type 1 collagen, a 60% reduction. And then hydroxyproline was reduced by 46% after 8 weeks. So it supports the thesis that this selective activation of thyroid beta produces a broad metabolic benefit beyond simple steatosis reduction. If we move to Slide 12, what we see are some gene expression data from the same cohort of animals. And what we can see here is a benefit on suppression of collagen III, collagen I, alpha-SMA, autotaxin and galectin-1. And these gene expression changes seemed to correlate with the improved fibrosis that were observed -- data that were observed in the same animals. So it seems to align nicely with the observed histology. We also looked at changes in genes associated with lipid metabolism and insulin sensitivity, and we saw improvement in those genes as well, which would seem to align with the benefits we saw in steatosis. So overall, very nice profile of expression aligning with the observed histology in the experiments. Slide 13 shows some data from the early clinical experience with VK2809. When we licensed this program, it had been through 2 Phase I studies, a single-ascending dose study and a multiple-ascending dose study. These are some data from the multiple-ascending dose study. It was a 14-day study in healthy volunteers with mild hypercholesterolemia. And what the graph shows is the effect on LDL cholesterol that's shown in the green bars. And what was observed is about a 35% to 40% reduction in LDL cholesterol at the higher doses. The blue bars show the effect on triglycerides after 14 days, and a nicer effect on triglycerides relative to cholesterol was also observed. So an encouraging early set of data, excellent safety and tolerability after 14 days. There are no SAEs. And these results, combined with the animal data, supported the decision to move into a Phase II study in NAFLD. What Slide 14 shows is the design of the Phase IIa study that we conducted. This study enrolled patients with nonalcoholic fatty liver disease and elevated LDL cholesterol, randomized them into 4 different arms: placebo, 5 milligrams daily, 10 milligrams every other day and 10 milligrams daily, for a 12-week treatment window. The primary end point here was change in LDL cholesterol relative to placebo. And the secondary end point, which was really the de facto primary for most people interested in this study, was the change in liver fat by MRI-PDFF after 12 weeks. Exploratory end points looked at other lipids and, importantly, changes in atherogenic proteins like Lp(a) and apo B. Moving to Slide 15. This slide shows the effect on LDL cholesterol. This was the primary end point in the study. And we were gratified to see that after 12 weeks, there was a significant reduction in the LDL cholesterol. It tended to be placebo-adjusted between 15% and 20%. So we're very happy with that nice reduction in plasma lipids. Moving to Slide 16, though, is the effect on liver fat. And what the graph on Slide 16 shows is the relative reduction in liver fat content. And so when we look at the placebo patients, this was pretty consistent with what's observed in the literature, approximately 9.4% relative reduction in liver fat content. The 5 -- the VK2809 patients receiving 5 milligrams daily experienced a 53.8% reduction. Patients receiving 10 milligrams every other day experienced a 56.5% relative reduction, and then the 10 mg daily arm experienced approximately a 60% relative reduction in liver fat content. If you look at the blue box on the left-hand side, it shows the maximal reductions observed after 12 weeks. And the highest single reduction was actually in someone in the 5-milligram daily arm, who experienced a 78% relative reduction in liver fat content. Moving to Slide 17. This is just a nice image of the liver of 2 patients who were randomized in the study. The top 2 images here show liver scans for a patient who received placebo. And so if you look at the upper-left image here, the scale of liver fat is along the bottom of each image. And this person had approximately a 20% liver fat content in their entire liver. Following 12 weeks of dosing, you can see -- if you move to the upper-right image, you can see very little change in the blue color. Really, they received placebo -- received no benefit. And if you look at the data for this person on the -- in the table there, subject a, you can see that the person -- the absolute change was a 2.3% increase for a relative change of 11.4%. So placebo obviously did nothing. If we look at the bottom 2 images, you can see on the lower left, this is a patient who started this study at about a 25% liver fat content overall. After 12 weeks of exposure to VK2809 at 10 milligrams per day, you can look on the right-hand side, you can see the liver. Not only has the color changed dramatically darker, but you can almost see that the size has been reduced via the removal of liver fat. And this person overall experienced a 75% reduction in liver fat content. So a nice graphical representation of benefit from the drug on liver fat. If we move to Slide 18, this slide summarizes the relative reductions -- I mean, sorry, the patients who are characterized as a responder. And responders in this study were defined as patients who experienced at least a 30% relative reduction in liver fat content. The reason that's an important cutoff in NASH is that there seems to be a higher probability of experiencing additional histologic benefits once 30% liver fat reduction is achieved. And so the responder rate is an important metric for success for metabolic targeting agents in NASH studies. Placebo patients, I believe they have a cohort here that showed a 16.7% response rate. 5-milligram daily cohort showed a 100% response rate. The n is small there, but all of these patients experienced at least a 30% reduction in liver fat content. 10 milligrams every other day, approximately 77% response rate. And then 10 milligrams daily showed a approximately 91% response rate. When we combine these cohorts, the overall response rate was 88%. And we also then looked at the proportion of patients in this study who experienced at least a 50% reduction in liver fat content, and 70% showed at least a 50% reduction. So very encouraging data. As far as we know, that's the highest response data that have been reported by an oral agent in development for NASH. Moving to Slide 19. Here's a couple of data points from the exploratory end point on atherogenic protein. The left-hand graph shows the change in Lp(a) after 12 weeks. It's a little bit bumpy there, but we think that this will smoothen with a larger n in the upcoming study, but anywhere from about 17% to 35%, 36% reduction in Lp(a). If you move to the right-hand graph, the effect on apo B at 12 weeks is 18% to the low 20% range. What's important about all of these lipid changes, LDL, triglycerides, which were also significantly reduced, as well as the atherogenic proteins, is that most patients from NASH actually die from a cardiovascular-related event or complication. And so to have an agent that not only improves liver health but also improves the global cardiometabolic profile of a patient is extremely important. And it's really a differentiating feature for this mechanism relative to some of the other mechanisms in development. And we think it improves the odds of success in a Phase III trial, where one of the long-term approval end points includes a mortality end point or a mortality component. Moving to Slide 20, looking at the safety and tolerability profile. Through 12 weeks of dosing with VK2809, there were no SAEs observed in this study. And as a matter of fact, to date, there have been no SAEs reported in any VK2809 study that has been completed. Looking at ALT and AST levels, we saw a reduction after 12 weeks relative to placebo, and patients who enrolled with a higher baseline ALT seemed to benefit more on ALT and AST after 12 weeks. There were no other changes to other liver function tests, direct bilirubin, indirect bilirubin, alkaline phosphatases or INR, after 12 weeks of daily dosing. And no clinically meaningful changes in other markers that you might want to look at in a study like this. So the thyroid axis was not changed. The cardiovascular markers on -- looking at cardiovascular toxicity, troponin, CK-MB, NT proBNP, those were unchanged. And vital signs as well, blood pressure, heart and heart rate and weight were unchanged. And finally, excellent tolerability, this is a very well-tolerated molecule. We see no GI impact whatsoever, and the actual GI and nausea events were actually lower in treated versus placebo. Moving to Slide 21. So the way we think about this study, looking back on it, we saw a robust reduction in liver fat on MRI-PDFF in NAFLD patients after 12 weeks of oral dosing. Nearly 90% of patients receiving VK2809 experienced at least a 30% reduction in liver fat content, including everyone who received a 5-milligram dose. And more than 2/3 experienced at least a 50% reduction in liver fat content. So we're very excited about the efficacy data on liver fat. We see a significant broader impact on cardiometabolic health with the reduction in LDL, triglycerides and atherogenic proteins. And then finally, very encouraging safety and tolerability, no SAEs, and we saw discontinuations well balanced across all cohorts in this study. So where we sit today, if we move to Slide 22, we've seen in Phase I promising safety, a very predictable PK profile, no surprises there, and robust lipid-lowering effects. The 12-week study that we just described demonstrated potent liver fat reductions. We see no drug-drug interaction when VK2809 is co-administered with atorvastatin, and we feel that this profile supports further development in biopsy-confirmed NASH. And to that end, we initiated late last year a 12-month study called the VOYAGE study. It's a Phase IIb study in biopsy-confirmed NASH, and that is outlined beginning on Slide 24. So the VOYAGE study is a multi-arm, dose-ranging study. Patients with biopsy-confirmed NASH will be randomized into 1 of 5 arms: placebo, 1-milligram VK2809 dose per day, 2.5 milligrams of VK2809 per day, 5 milligrams of VK2809 every other day, and 10 milligrams of VK2809 every other day. The primary end point in this study will be a change in liver fat as assessed by MRI-PDFF at 12 weeks, and the secondary end points will look at changes in histology after 12 months of exposure. Some of the key inclusion criteria are highlighted on Slide 25. So these patients have to have biopsy-confirmed NASH with an NAS of at least 4. Liver fat content, it has to be at least 8%, and we're targeting primarily F2 and F3 fibrosis. Up to 25% of patients can have F1 fibrosis. But if you have F1, you have to have another risk factor along with the F1. Primary end point here is change in liver fat at 12 weeks, and secondary and exploratory end points will all look at histology at 12 months. So some of the closing comments for VK2809. We're often asked, how does this stack up competitively with over 40 NASH programs in development in Phase II or later? What makes this a special compound compared to the competition? And we think there are several basic but really important elements here that separate VK2809. First, it's oral. We think that, given all things equal, most patients would prefer an oral versus other routes of administration. Secondly, we're liver-targeted. We are truly liver-targeted. We're not liver-targeted that's -- because that's where the beta receptor is. We're liver-targeted because the drug is chemically cleaved in the liver and activated in the liver, and that's where the beta receptor is. So you get a much higher concentration of drug in the liver. We see a potent reduction in liver fat content. And we know historically when patients lose weight and experience liver fat loss, that correlates with NASH resolution and improvement in fibrosis markers. We see improvement in systemic lipids, and we think that improves the overall metabolic profile. We don't see elevations in other lipids that might require a polypharmacy approach from early on in the study. We can treat it as a single agent. And then finally, well-tolerated, we see no tolerability issues to date and a very clean safety profile, so no GI or pruritus or anything like that. So we're really excited about the profile here to date. And the more we see from the emerging landscape, the more confident we are that this is a very competitive molecule. And we look forward to continuing the VOYAGE study and reporting those data when they're available. I'll move now into our rare disease program highlighted by VK0214, if we go to Slide #28. We're looking at a rare disease called X-linked adrenoleukodystrophy, which is an orphan neurodegenerative disorder. It's X-linked, meaning it's carried by women, but primarily manifested in men and boys, although women in the fifth and sixth decade of life also do begin to manifest some forms of X-ALD. There's no cure, no approved therapy. And you can think of the disease as having 2 large but very heterogeneous buckets. The most severe form is called cerebral ALD, and this is characterized as a rapidly progressive inflammatory demyelination, results in disruption of the blood-brain barrier. And it tends to affect younger patients, typically under the age of 12. Although if you can make it through adolescence, there is another window of risk that happens in the 20s and 30s. It presents clinically as a deterioration in speech and behavior in kids. It's often misdiagnosed as ADHD, but it's rapidly progressive, and patients often become vegetative within 3 to 5 years. The more common form of ALD is called adrenomyeloneuropathy, and the big difference here is that there's no brain involvement and no inflammation. It seems to affect motor neurons and the spinal cord, affects nearly all adult patients. So it's -- penetrant in adults is 100%. It's considered the default manifestation of ALD, and this clinically presents as a progressive loss of motor skills. Most patients become wheelchair-bound, and leg paralysis is fairly common. Moving to Slide 29, highlight of the pathogenesis of X-ALD. It's believed to result from a mutation in gene for a transporter called ABCD1, which is shown in this cartoon here. ABCD1 serves as a shuttle for very long-chain fatty acids that are brought into the peroxisome and metabolized and discarded. If you have X-ALD, any number of mutations renders the ABCD1 transporter poorly functional or nonfunctional, and that results in an accumulation of very long-chain fatty acids, which is believed to contribute to the onset and progression of disease. What makes the thyroid beta agonist approach interesting here is that, if you look at the lower right part of Slide 29, it's been shown that when you agonize the thyroid beta receptor, you stimulate an improvement in expression of ABCD2 and 3, which may mitigate some of the very long chain fatty acid elevations and downstream effects that result from nonfunctional ABCD1. And so what we did early on here, we've done several different experiments in vitro and in vivo. What Slide 30 shows is some highlights from experiments we've done in ABCD1 knockout mice. This is a model that is intended to mirror the biochemical profile of patients with X-ALD. And so these mice develop high levels of very long chain fatty acids. And what we did in this work was we exposed animals to VK0214 orally, and we assessed their changes in very long chain fatty acids. And when we look across here, these graphs on Slide 30, what you can see, what appears to be a nice and progressive reduction in very long chain fatty acids over time. A key question from this work was, do you see an effect beyond plasma? Because it may be really important to see the reduction in tissue as well. And so moving to Slide 31, we assessed liver, spinal cord and brain following exposure to VK0214. And we see a nice significant reduction in very long chain fatty acids in the spinal cord and brain. So overall, encouraged by this profile. It suggests potential benefit in both the AMN and the cerebral form of the disease. And with this program, where we sit today, is we are rapidly approaching an IND filing, which we expect to file around the middle of the year. And then we'll move into a clinical development pathway where it's a single-ascending dose study in healthy volunteers, followed by a multiple-ascending dose study in healthy volunteers, followed by a 28-day Phase Ib study in patients with X-linked adrenoleukodystrophy. And we hope to start that study as soon as the IND is cleared. And that summarizes the pipeline. If we go to Slide 32, just a quick recap of where we are financially. We ended the first quarter with approximately $270 million in cash and equivalents. We think that will get us through the next several clinical catalysts that are important for the company. And the burn, I think, is very manageable at this point. We're a pretty small organization. We have 18 employees, and we've, I think, operated really, really efficiently given the clinical accomplishments that have been made. Moving to Slide 33, just a wrap-up slide. So we're focused at Viking on novel therapeutics for metabolic and endocrine diseases. Our metabolic disease program is highlighted by VK2809, which is a selective thyroid beta receptor agonist that we're developing for NASH in Phase IIa. This molecule demonstrated a potent reduction in liver fat as well as plasma lipids, and we're currently conducting a Phase IIb study we call the VOYAGE study in biopsy-confirmed NASH. Second program is VK0214, another selective thyroid beta agonist that we're developing for X-linked adrenoleukodystrophy, and we expect to bring that compound into the clinic later this year. And then we have a pipeline of other programs that I didn't talk about today, but those programs target musculoskeletal and other metabolic disorders. So I'll stop there. Thanks very much to UBS for the opportunity to move through the story here. And happy to take any questions.

Thanks very much, Brian. I guess I'll kick off. We've gotten a few questions in from investors. This one is actually on one of the pipeline assets you just mentioned at the end. So they have a question on, what is the FDA proposed end point for VK5211? Have you advanced interest in partnerships? So if not, why not are you focused on partnerships?

So we are focused on partnerships there. We've not given a lot of updates. We've -- it's taken longer than we've wanted there, but there has been a fairly sustained level of interest in that program. It's certainly not sitting in a backroom here at Viking. The FDA -- we had a Type C meeting with the FDA in 2018. And what the FDA suggested was if we were looking at hip fracture in a registration trial with VK5211, that we would need to show a benefit on function and quality of life. And both of those are challenging alone. But to show them together in the same study, it's probably going to take a larger study than we're comfortable conducting and maybe a little longer than we would be comfortable conducting. And so we think a study of that nature is best handled by a larger partner. And so that's where that program is. We will not be pursuing that further in the hip fracture indication.

Got it. Okay. So a couple here on -- going back to NASH. So in which -- like specifically looking at the profile of your drug, in which group do you see the greatest opportunity in terms of fibrosis score, F1, F2, F3, et cetera?

Yes. It's a good question. I mean we'll have to look at the data. What we know from diet studies and bariatric surgery studies is that when someone loses at least 10% of their body weight, there seems to be an improvement in fibrosis as well as the rate of resolution of NASH. We think when we look at our liver fat content reductions, the absolute change is in that 8% to 10% range. So it's -- and we're requiring patients to have at least an 8% liver fat content in the VOYAGE study. So how does that translate to each particular subset of fibrosis? It's not clear. It will probably depend on each individual patient's profile. But I think it's very difficult to predict what would be the most likely population to receive benefit. I think it's certainly plausible that all would receive benefit from this mechanism.

Got it. Okay. Here's another one. So especially relevant with Intercept's PDUFA and AdCom coming up, but what feedback have you heard from regulators about the MRI-PDFF? I see that you've included biopsy in your Phase IIb. But in terms of primary end point, it looks like you're relying on the MRI-PDFF. So what feedback have you gotten? Do you think that you'll be able to make a biopsy -- a fibrosis improvement claim using MRI-PDFF data?

Yes. So this is a Phase II trial. We're not going to be filing for approval following completion of this study. To go into Phase III today, a 12-month biopsy study is required per FDA guidance. So what we know, and I think everybody knows, is that MRI-PDFF is not an approvable end point. But it is a very interesting predictor of improved histologic benefit, and that's been demonstrated time and time again. We think that we designed this study to be very similar to other studies, Phase IIb studies in NASH, looking at liver fat changes initially, followed by histologic benefits at a later time. So there's nothing really different about our study relative to many other studies that have been conducted in Phase IIb in NASH.

Got it. That makes sense. And you spoke about -- here's one on competition. You spoke about the competitive -- how competitive the NASH space is. This question is specifically about if semaglutide gains a NASH indication, how do you think VK2809 will be positioned in a market such as that? And do you see VK2809 as something that can be -- will mostly be used as monotherapy? Or do you see it potentially as something that will be like a base -- a backbone for combo therapy?

Yes. It's a great question. The answer is we don't know just yet. Semaglutide, there was some data from semaglutide maybe a couple of weeks ago from a 72-week study that showed the highest NASH resolution rates ever reported. I thought the data looked fantastic. But it was a little curious that there wasn't a real discussion of a fibrosis benefit. Maybe there are changes in markers that suggest some benefit there, but didn't seem to be highlighted in the initial disclosure. We think that, that may be an appropriate therapy for some patients. VK2809 might be appropriate for others. The market is pretty heterogeneous as far as patient presentation. So we think that there's certainly room for multiple mechanisms to coexist. We think that there is nothing we've seen that matches our overall cardiometabolic profile when you combine liver fat and plasma lipid benefits and tolerability. So -- and we also think that -- I mean, the data from semaglutide were injectable. We have not yet seen any oral data from semaglutide, and those exposures are somewhat different. The oral dosing is going to have to go up quite a bit to achieve the same exposures that were observed in that study. So unknown yet if the oral version there will be successful, but we think VK2809 is competitive in either scenario. And we think combining those 2 mechanisms or a thyroid beta agonist with any number of mechanisms might make a lot of sense.

Great. That's all the questions we have for now. So I just want to thank you for joining, and thanks for coming. I appreciate it. Thank you, everyone.

Thanks a lot. Nice to talk to you, and happy to follow up. If anybody has questions, we're always available. So thanks for the opportunity.

Thanks, Brian. Bye.

Okay. Thanks. Bye-bye.