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

Wonderful. Thank you, guys. It is wonderful to see you all here today. Thank you so much for taking the time. It is my privilege to have the Viking team here with me. I've got Gregory and Brian, CEO and CFO of the company. This is a particularly interesting and exciting time in the world of cardiometabolic obesity and kind of all the places that you guys play in. And so undoubtedly, there's lots of questions and lots of things that everyone wants to dive into. For those of you who don't know me, my name is Courtney Breen. I am the U.S. biopharma lead analyst here at Bernstein. So think about -- a lot about all the large-cap names, but also all the companies that are coming in to look to compete with many of those large-cap names or partner with them over the years. So we're going to spend a bit of time with the Viking team walking us through some presentation materials, and then we'll dive into Q&A. Just a reminder, we do have the Pigeonhole app available. So if anyone has any questions, please feel free to put those through on Pigeonhole, and I'll be happy to integrate them into the Q&A at the end. So with that, I will hand over to you to walk through some of these presentation slides.

Great. Thanks, Courtney. Thanks also to Bernstein for the opportunity to participate. We've got a great schedule, and it's good to see you all today. I'll make some forward-looking statements. I'd refer anybody listening to this presentation or viewing these slides to the Securities and Exchange website -- Commission's website for the most current information on Viking. So happy to walk through the story. We're developing novel therapeutics for metabolic and endocrine diseases. We have multiple clinical programs that have demonstrated what we believe to be best-in-class data. The metabolic disease programs are highlighted by our VK2735 molecule. It's a dual agonist of the GLP-1 and GIP receptors. It's currently in a Phase III program we call the VANQUISH Phase III program for obesity, and there's two trials underway there. We have an oral formulation of the same compound that has recently completed a Phase II study, successfully achieved primary and secondary endpoints in that study. And then finally, we have an amylin agonist, a novel amylin agonist that we plan to move into the clinic late this year or early next year following the filing of the IND. We have additional programs that are focused on the thyroid beta receptor. VK2809 is a thyroid beta receptor agonist that completed Phase IIb in NASH. And then we have a separate molecule, VK0214, that's completed a study in X-linked adrenoleukodystrophy. And both of those are in-house available for licensing, but not something we'll focus on in the near term. This slide shows the pipeline where we stand today, the VK2735 subcutaneous formulation in Phase III, the oral formulation just completed the Phase IIa study, and then the amylin agonist heading into the clinic later this year. So a little bit of the background on the peptide hormone program. We initiated this program back in 2019. And we looked at all of the agonist, the mono GLP-1 agonist, the dual agonist where you add the GIP activity on top and then the triple agonist with the glucagon agonist on top of the dual. And we selected the dual agonist really because the triples didn't look any better to us, and duals just seem to be very attractive. So we stuck with those. VK2735 was the lead that we selected based on the initial profile, and it has completed now a Phase I SAD/MAD study that we reported in the first half of '23, a Phase II study reported last year, and the Phase III studies are underway with the VANQUISH registration program. With the oral formulation, we completed the SAD/MAD work last year, and then a Phase II study just recently read out in the third quarter. This just shows some of the early data. All of our compounds are very potent at the GLP-1 and GIP receptors. Robust weight loss has been observed in multiple species. And this slide just shows the weight loss over 14 days, generally up to about 30% weight loss relative to vehicle. Pretty clean PK, 2- to 7-day half-life in primates. This shows a compound we call VK2745. And just an example of how tight the PK profiles are, very consistent, well-behaved PK profiles. So we had selected VK2735 as the compound to bring further into development. And we just reported some data in August from the oral tablet formulation. So I'll walk through the tablet first, and then the subcu formulation after that. These are the Phase I data from the oral tablet. This is a 28-day study, daily dosing for 28 days. And in this study, we did see a dose-dependent reduction in body weight across all of the arms leading up to around 8% from baseline at the 100-milligram dose, about 7% placebo-adjusted. But overall, I think, an attractive dose response here in a 28-day study. When we look at the trajectories from this study, really nice, again, dose response and a consistent progressive effect through the 28-day window. And one thing that was interesting when we looked at the follow-up data from this study was this period following 28 days out to day 57. You can see, it's most obvious here with the 100 milligram, really a durable effect. This was 8.2% from baseline at 28 days, 8.3% from baseline at 57 days. So a very nice maintenance effect reflects, we think, the long half-life. And I think it suggests that maintenance might be feasible at lower doses than the induction window. The takeaways from the Phase I study, up to 8.2% reduction in body weight after 28 days. Progressive effect across all doses suggests that you should see an extension of that efficacy with longer treatment. Majority of the weight loss in every arm was maintained 4 weeks after the final dose, and very good tolerability in the Phase I study. 99% of the adverse events were mild to moderate, very minimal GI adverse events with low rates of the common GI adverse events, nausea, vomiting and so forth. We did include an exploratory cohort in this study that looked to transition from 80 mgs daily to 80 mgs every other day. And we think those data looked very promising. Weren't in this deck, but they're in our poster from ObesityWeek, suggests a feasibility of a lower dose for maintenance, providing a good maintenance effect. And so the Phase I data supported advancing into Phase II. So we designed this study, we call it the VENTURE oral dosing study, 13-week study, multiple dosing arms. Lowest dose was 15 milligrams flat for 13 weeks. Second dose, 30 milligrams flat for 13 weeks. And then 60 milligrams, 90 milligrams and 120 milligrams, each of these titrated starting at 30 milligrams for 2 weeks and then to the next dose for 2 weeks and the next dose in 30-milligram increment. So the 120, for example, started at 30 for 2 weeks, went to 60 for 2 weeks, 90 for 2 weeks and then 120. We have at the bottom here, an exploratory cohort that we thought was really interesting. These subjects were titrated very rapidly to 90 milligrams. So 30 mgs per week, 60 mgs per week and then 90 mgs for 4 weeks and then transitioned back down to 30 milligrams daily for 7 weeks, and that was to further explore the potential for a low-dose maintenance regimen. Here are the data that we reported in August. This shows the percent change in body weight at 13 weeks. And again, just like what we had shown previously with the subcu formulation, a really nice dose response here, leading up to 12% from baseline at the top 120-milligram dose. Progressive and dose-dependent across all of the treatment arms would suggest that an enhancement of the effect should occur with longer dosing. And when we look now as we head forward, we'll probably be focusing on these doses in the 20- to 75-milligram range. And so that's why I circled this range here, 30 -- 15 to 90, really attractive and competitive weight loss here, 7% to 8.7% with the 60-milligram dose. Here's the data from the maintenance cohort. So this again was the cohort that rapidly titrated up to 90 milligrams and then brought people back down to 30. And so this is in comparison. This line here is the cohort that titrated up to 90 and held at 90. And there, you see 11.1% weight loss from baseline. The green line shows the cohort that titrated very quickly up to 90 and then at week 6, transitioned to 30 milligrams daily. And you can see after 6 weeks, 4 weeks of which were at 90, you see 8% weight loss, transition people to 30 and hold them there for 7 weeks, and we saw another 1.1%. So it clearly supports this transition phenomenon where you can go to a lower dose, and here not only suggest maintenance, but actually a continued improvement in body weight. This shows a secondary endpoint, the proportion of patients achieving at least a 5% weight loss. Again, nice dose dependency, up to 97% at the 120-milligram dose. But even at the low dose, you're about 3x what the placebo rate was. So very positive on the secondary endpoint there. A bit delayed on the buttons here. Maybe the battery died. Okay. Okay. Proportion of patients, another secondary endpoint proportion with a 10% weight loss. And again, a nice dose response, 7.5%. Not significant there, but moving up to around 80%, experiencing 10% weight loss at 13 weeks, with the trajectory suggesting that all of these bars should improve over time with longer-term dosing. When we look at discontinuation rates in this study, here, we can see the proportion who discontinued treatment early that's stopping taking the medication. And you do see 18% in placebo trending up a little bit higher in the higher doses and discontinuation of the study really pretty flat across here, maybe a little uptick at the highest dose here, but pretty flat. Overall treatment emergent adverse events also reasonably consistent across the treatment arms. Drug-related, maybe a slight uptick when you get to the higher doses, but that would be expected from the GI adverse events. And then the drug-related treatment of emergent adverse events leading to discontinuation, really no signal related to placebo. So the majority of the treatment of emergent adverse events were mild to moderate here. And when we look then at the doses that we'll likely be bringing forward, that 20- to 75-milligram range, again, really not a significant difference relative to placebo on discontinuations or overall treatment emergent adverse events or those types of things. When we look at GI tolerability, what everybody likes to look at with the GLP-1 mechanism, we do see, as you go across doses, an uptick in overall nausea at the higher doses. These middle doses really didn't separate too much from placebo. Placebo had a pretty high rate of nausea. Vomiting slightly higher in the treated arms, likely addressable with slower titration rate. And then the other adverse events, really not much of a signal at all. So again, when we look at our likely future doses here between that 20-milligram and 75-milligram range, compared to placebo, really not a significant delta at all on any endpoint. So we're very satisfied with the AE profile, given this rapid titration compared to placebo as being highly competitive. This slide is really interesting because it shows the time course of adverse events over the course of the study. And so you can see here, by far, the majority of the nausea and other GI events happened in that first week of treatment. So that's the initial exposure to the mechanism. Following that first week, you see a substantial drop off. It ticks up a little bit here at week 3, and that's your first up titration. But following that first up titration, really drops to pretty much 0 across the rest of the treatment window. So the lesson here and from the prior tables is you want to start low and you want to go slow. And you will probably this pull in quite a bit, and these probably remain pretty flat. This is all doses combined. We don't yet have the individual cohort data. But overall, this graph looks very similar to what the subcu data showed, and that was initial exposure gives you a little bit of nausea. Following that, it never comes back, really. So the VENTURE Phase II oral study takeaways, up to 12% reduction in body weight after 13 weeks of oral dosing. We see a progressive dose-dependent effect across all of the treatment groups. The maintenance cohort, very exciting for us as we successfully demonstrated the proof of concept from high dose to low dose, maintaining body weight, really promising tolerability profile with a vast majority of adverse events, mild to moderate. In particular, the majority of the GI adverse events were mild to moderate and transient, and we expect those to improve with the optimized titration that we would pursue in a subsequent study, which would probably have 4-week treatment windows or titration windows. And then next steps here with the oral would be to initiate a subcu to oral maintenance study, which we've talked about in the past, and that will begin late this quarter or early next quarter. Now I'll quickly review the other formulation. This is a subcu formulation, a weekly dose. This was data we reported last year from the Phase II, we call it the VENTURE, the other one is VENTURE oral, this is VENTURE, they're pretty much the same study design. This went from 2.5 mgs to 15 milligrams, a parallel cohort with a 3-week titration blocks for the 5-, 10- and 15-milligram doses. This study achieved its primary endpoint, a significant reduction in body weight observed after 13 weeks. This is the dose response from 2.5 up to 15 milligrams. Beautiful dose response, approximately 15% from baseline after 13 weekly doses, and progressive with no sign of moderation through the treatment window. This is the trajectory for weight loss from the weekly injection study. Again, we see a nice dose response and a very rapid effect throughout the 13 weeks. All doses statistically significant starting at week 1 and remaining that way through the course of the study. This summarizes the GI tolerability in the subcu study. So pretty modest GI effects, what you would expect to see. You see a dose-dependent uptick again in the higher doses here, 15 milligrams and 10 milligrams. But overall -- and same with a little bit of an uptick in vomiting as well. But overall, nothing that you wouldn't expect from this mechanism. And again, the majority of these are mild to moderate. This shows the time course of adverse events for the 2 higher doses. This is the 10-milligram cohort, this is the 15-milligram cohort. And I show these because it dramatically illustrates the effect of titration. So the 10-milligram cohort, blue here, is nausea. And you can see a 15%, 16% rate of nausea, and that first dose drops off a cliff and then comes back at your first titration step and then pretty much goes to 0 after that. So this cohort started at 2.5 milligrams. This is the 15-milligram cohort. Big difference with the 15 is these guys started at 5 milligrams. So you can see this massive change in nausea that's brought way down by just starting at a lower dose. So following that first week, then you see a rapid drop in GI adverse events. You see a little bit of a tick up here, and this was when you went from 10 milligrams to 15 milligrams. So it just further illustrates that mantra, start low and go slow. This guy started twice as high and did twice as high a step here out late. So you just want to be steady through the treatment window to minimize GI adverse events. And I think these 2 cohorts really show that nicely. So the study takeaways from the subcu study, up to nearly 15% weight loss after 13 weeks of treatment. A very encouraging tolerability, over 90% of the drug-related treatment emergent adverse events were mild to moderate. GI-related adverse events generally occurred early and then resolved quickly. When we look at durability here, we saw that more than 90% of the efficacy that was observed at week 13 was retained at week 17, so a very attractive durability signal. And we think the PK profile from this study suggests that a monthly regimen would be feasible, particularly in the maintenance setting. So the current status of the subcu formulation. We've got two studies ongoing, VANQUISH-1 is our study in obese patients. That's about 4,500 people. VANQUISH-2 is in patients with diabetes and obesity, that's a little over 1,100 people. Both studies include an extension to assess long-term safety and efficacy, and we initiated these in the second quarter of this year. Something that's upcoming for the subcu formulation is this monthly dosing study, and this is designed to evaluate a monthly regimen in the setting of maintenance. So you titrate people up to a high weekly dose and then transition them to a monthly regimen. Second element of that study is a low-dose oral regimen. So we'll bring people from a high weekly dose to a low-dose oral or to a monthly regimen. And this will look at PK tolerability and weight maintenance. So I'll wrap up with the balance sheet here. We ended the second quarter with over $800 million in cash, and that's, we think, provides a runway to finish the Phase III trials, very fortunate to have the runway that we have and to support the programs to develop them aggressively. Bringing us back to the first slide. So pipeline is focused on metabolic and endocrine diseases. The VK2735 compound for obesity is the lead program, the subcu formulation in Phase III, the oral formulation just completing a successful Phase II, and then the earlier program is an amylin agonist that we hope to move into the clinic towards the end of the year or early next year. And that's all I have, and thanks for your attention, and I'll open up to questions. Thanks.

Fantastic. Thank you so much for walking us through there. And obviously, the recent Phase II data for the oral has been kind of the source of a lot of investor focus, a lot of investor questions. And maybe just to talk through the next steps off the back of that. I think you've highlighted that there is the oral maintenance study that you anticipate to get up and running in the back part of this year. The next question is kind of the oral weight loss study and kind of the potential path to achieving that. What do you need to see? What do you need to explore? What do you need to validate on your oral [ asset ] before you are in a position to initiate that Phase III?

Yes, we hope to have in the fourth quarter, an end of Phase II meeting with the FDA to review all of the data, the animal data, the human data and then understand what might -- what additional work might be required prior to Phase III. And so we're hoping to schedule that in the fourth quarter and then decide on the next steps from there. In the interim, yes, we will be starting near term, the -- that study I just mentioned where we transition people from a high weekly dose to a variety of oral maintenance. We have 2 cohorts that will be a low-dose oral daily, and then 1 cohort that will be a weekly oral dose as well, just to explore the maintenance effect. So that would be the nearest term with the oral. But the end of Phase II, I think, will be very valuable in mapping the path forward there.

Fantastic. And as you think about kind of the endpoints that exist in these trials today and the labels that we see for some of the GLP-1s and GLP-1 GIPs that are out there, they tend to be based on weight loss rather than necessarily weight maintenance. As you think about the path for the oral coming to market, do you need to have in your mind, individual studies that generate weight loss evidence for that oral? Or is there a path that you can foresee kind of purely in that maintenance setting?

Yes, there isn't a maintenance approval path right now. So every cohort that you would look at in a Phase III oral study would be designed for weight change from beginning to end. And it would be up to the commercializing party to position it in maintenance or an induction, which is one of the reasons we're exploring these maintenance to see where is that dose for the maintenance effect. But it's true, there's not a regulatory path for maintenance. So every drug that's approved today anyway is approved for weight loss.

Fantastic. And perhaps as I look at kind of some of the Phase IIIs that you've got up and running, the VANQUISH-1 study, you've made the decision to have a BMI cutoff at 30. You contrast that with some of the other studies that we see out there tend to go down to 27 with kind of patients that have comorbidities. You've decided to kind of keep it a little higher. Can you talk about kind of that particular decision, why that feels like the right decision for you? Is that a trade-off of kind of expense of the trial, getting the right patients in, delivering the evidence versus where the product might be used in the market?

Well, both studies allow -- both studies -- it's 30 and above or 27 and above with the comorbidity. So they are kind of in that traditional bucket. It turns out that the vast majority are always above 30, but we did drop it. If you've got a weight-related comorbidity, we drop to 27 as the standard.

Great. That's super, super helpful. One other thing that I think is really important as we look at development of drugs in this space is -- and this was certainly a large part of the conversation at EASD last week on the ground with physicians -- is the idea of placebo-controlled trials and whether they still make sense. And this really comes down to kind of two parts of the puzzle, one on the patient side, kind of how are you going to kind of ethically, in some instances, offer a placebo to a patient who needs weight loss. And then the second side of it is kind of for the company itself, how do you entice enough patients to come into a trial so you can recruit appropriately, but also maintain enough patients in your trial over your 60-, 70- or 80-week long trial that they may be in for that Phase III. As you look at kind of your position in the market, entering a market that's rapidly maturing, how are you making those trade-offs at the moment? Because it obviously impacts cost of trials, it impacts speed of trials. It impacts a lot of different factors that I'm sure you're weighing up.

Yes. The retention of placebo -- right now, the registration path is it requires placebo-controlled studies. Active comparators could be an important component in the future, but the registration trials are placebo-controlled, according to guidance. But yes, the question is, how do you keep those guys in. It's a really huge challenge for anybody working in the space. If you've got a person enrolled in the study who's not losing any weight and doesn't feel any GI adverse events, they sometimes feel like maybe they're on placebo. Everybody faces the challenge. I think one thing that really helps with retention, probably the best thing to help with retention is to guarantee access to active therapy upon completion of the primary endpoint date. And that -- as long as people are sure they're going to get active therapy and they're getting it for free and they're receiving active medical care, that really does make a difference in retention. But it's always there, and I think everybody needs to try to navigate that. It's always a challenge.

Absolutely. Yes, it was a much louder part of the conversation, I think, over the last week at this conference than it has been in the past. I want to talk a little bit about Viking as a company as well. We've been deep in kind of the drugs, the trial design, kind of where you're going. As a company, as you think about the next 3, 5 years, we're going to be going through some of these Phase III clinical trials, beginning to get to kind of some of the data cards turning over at the end. What does success look like for you at Viking? And you made a comment kind of on your last couple of slides, you've got about $800 million of cash sitting there to fund kind of the position that you're in right now. What degrees of freedom does that enable you? And kind of what are the pathways will you be wanting to explore to ensure that you've got all the choices that you might need to have so that you can have viable commercial products that are really competitive entering the market and Viking sitting in the best place that it can?

Yes. We're pretty lean. We've always run pretty lean. We have just over 50 employees today, and that will probably grow over the next couple of years as the Phase III trials mature as we prepare for commercialization. But we've always, I think, gotten a lot done with limited resources. And all of our expenses are -- or most of them are to external execution-related vendors. And I think what's really unique about the obesity market, which probably wasn't in existence before the obesity market started to expand so rapidly, is the direct to patient is a really effective means. And when you look at the successes of these compounding pharmacies and the compounders, they don't have any sales infrastructure. And our estimate is that over $10 billion in revenue right now is going to that channel. So it's a very unique market, the way obesity is maturing. And it, I think, fits nicely with a company like Viking that's always been very lean on infrastructure and has had a pretty low expense burden for infrastructure. So I think the market here is set up very nicely for a company like Viking to be really successful. We just don't have that underlying infrastructure expense that a larger entity might have.

Super, super useful. And as I think about some of the big choices you have to make ahead of you, one of those is something that you reiterated, I think, a couple of times in the session was that -- the presentation, which is that notion of go low, go slow, which we hear repeated as a mantra from so many physicians. And I think the most extreme version of this that I hear from some physicians today is, oh, I don't even get any AEs in my patients at all these days because they are going much lower and much slower than what the labels tell me for the products that are out there. And so this is a growing appreciation, I think, in this market that you can really tolerize these patients with time and you can manage their adverse events. But it's a trade-off on kind of being able to deliver efficacy, a kind of weight loss demonstration or health outcome demonstration over an efficient length of trial. And so as you look forward and kind of making that deployment of cash against some of these future clinical trials, how are you thinking about that particular trade-off?

Yes. Well, for the Phase III trials, we did slow down the titration rate just to make sure there are 4-week blocks and ease people into the dose escalation. But for all of the studies for registration, you've got to be at 52 weeks from the post titration dose to the endpoint. And so ours is 78 weeks. I think if you titrate faster, you can compress that a little bit, but the tolerability profile will suffer as a result. And in the real world, people titrate to tolerability, really. And so I think for us, it's just the way our titration works is it's going to get us through 78 weeks before we get to the endpoint. But in the real world, we would expect it to be used kind of custom -- just like we see right now with the current weight loss agency, people dose up to whatever they can tolerate. What's interesting, we've heard anecdotally from some investigators is we've heard about patients coming into their clinician and asking to be up titrated because they're not feeling any more GI adverse events. And they feel like, oh, it's not working anymore so I'm not seeing -- so it's kind of a backwards way to think. They shouldn't think that way, but I -- it tells you that some people are really looking for that. And we think we probably saw a little bit of that in our -- in the oral Phase II study with the higher-than-expected rate of nausea in placebo. It's just that everybody knows somebody who's on a GLP-1, and they all -- everybody talks about the GI profile.

Absolutely. And certainly, on that point, I think -- two things that came to mind in your comment there. In my old life back in industry, kind of I do think there is this idea, it's almost a bimodal distribution of patients, patients that want to treat a disease as hard and fast as they possibly can, and the other patients that want to forget that they have the disease and want to make sure that, that drug is kind of unrecognizable in kind of the course of their lifestyle. And so I do think kind of there are different shapes to the way that this kind of shows up. Perhaps just as we kind of get into our last 5 minutes or so of this conversation, I do want to open up to kind of the market evolution. Because as we think about the GLP-1 space -- and you made the comments about the direct-to-consumer platform, which I think is a really important one. What other fundamental parameters of the GLP-1 market or the obesity market that are critical to framing the opportunity that you think you have? How do you see the market evolving? And kind of do you see Viking and your assets as they come to market joining a growing market or disrupting a growing market?

Yes, it's a good question. We think the #1 fundamental that both patients and clinicians want is efficacy. Everybody wants the most effective weight-loss drug. And so you have to expect that and really be able to compete on that. And that's why I think our study, with the doses we selected and the profile we've seen with the drug so far, should be highly competitive on efficacy. I think second then, tolerability becomes more important following efficacy, and then learning how to properly titrate somebody is an important element of that. And how we see us entering the market, I think the 2735 molecule will be very competitive based on the profile we've seen thus far. And as we look to the future and we expect efficacy to always be the attractive -- most attractive characteristic for most people. When we think of our amylin program, we think an opportunity to combine the amylin with the dual agonist would, we think, possibly provide a weight loss effect that's above and beyond anything we've seen thus far in the pipeline. So that's where we see sort of the next step, just like we've seen with the GLP-1 and then GLP amylin, GLP GIP, GLP GIP glucagon. Adding different mechanisms on top of that GLP-1 backbone will likely continue to incrementally improve efficacy. And I think if the amylin program matures and the way we hope it does, it should allow us to be really, really competitive.

Fantastic. And one of the other things I want to ask, you mentioned as you kind of we're talking about the Phase III clinical program that you've been a very lean organization over time and the roles and capabilities will kind of need to evolve that you lean into. As you look at different ways of doing that, kind of doing that fully in-house versus partnering versus collaborating, how do you think about kind of those decisions and ensuring that you're taking on the right risk within your own entity versus sharing risk with other players that might want a piece of the opportunity as well?

Yes. Well, we have to be receptive to ideas. And we've always felt that the programs could be most effectively developed with the help of a larger party, so we're certainly open to collaborating with larger companies. But we also have to be able to map out the future if that doesn't materialize, and that's what we've been focused on a lot. So whether you build in-house or contract and the contracting is a little bit more expensive, but it is more a variable cost, so it's easier to terminate than an in-house sales force. We're actually looking at all of those options right now, what's the best path. Our feeling is that if you build carefully and thoughtfully, in-house is probably a better model than the rent a sales force, any of these more external models when it comes to commercialization. When you're in development, it's much, much more effective to outsource things, and that's the model we pursued this far -- thus far.

Absolutely. And then our last couple of minutes, if you were thinking about Viking in 5 to 10 years in the future, what does success look like? And what are the challenges where you pinpoint and say, these are the biggest decisions I've had to make that's enabled this success?

Well, I think where we would see the company is hopefully having more than one product on the market and an international footprint. A lot of work to do there, but I think with the sort of direct-to-patient model, that can be utilized in the U.S. and utilized in Europe. It can be utilized globally. And I think that's -- it allows us to remain lean. Building appropriately where we need to, but it would allow us to remain lean and also competitive. But I think at the end of the day, it's the products. The products need to be the most effective or compelling to patients because, again, when you look at the compounders, these products sell themselves. People are going to compounders and health spas and asking for products that they're not -- doctors aren't getting detailed in those places. So it's just a unique opportunity that I think is suited really nicely for a company like Viking.

Absolutely. Absolutely. Well, I think we're sitting here on the precipice of lots of exciting decisions ahead for Viking and lots of exciting data cards to continue turning over as well. So thank you so much for taking the time with us today. It's been a pleasure to have this conversation with you. And I hope everyone who's listened in has had the chance to understand the story a little bit more and see the catalysts that are on the horizon for Viking.

Thanks, Courtney. Thanks.