Hey, everybody. My name is Hardik Parikh. I'm an equity research analyst at J.P. Morgan covering pharmaceuticals. Delighted to have here today Brian Lian, CEO of Viking Therapeutics. I'll turn the stage over to him for a brief presentation before we go into a Q&A. Thank you.
Thanks, Hardik. Thanks to J.P. Morgan for the invitation. It's great to be here. We've got a great schedule, so really appreciate it. I'll be making some forward-looking statements today. I would refer anybody hearing this presentation to the Securities and Exchange Commission website for the most current information on Viking Therapeutics. So we're based in San Diego. We're focused on a portfolio of novel therapeutics for metabolic and endocrine diseases. We're going to spend most of the time today on our metabolic disease programs. That's highlighted by a peptide called VK2735, which is a dual agonist of the GLP-1 and GIP receptors, currently in a phase III program called the VANQUISH program. We have an oral formulation of the same molecule that has just completed the phase II study last summer, late last summer.
And we are submitting those data for the European Conference on Obesity in the second quarter of this year. Then we have an amylin program as well. Hope to file an IND with that program later this quarter. We have a couple of earlier stage or additional programs we're not actively developing on the thyroid receptor space. So VK2809 is a thyroid receptor beta agonist for MASH, completed a successful phase IIB study. And VK0214, another thyroid beta receptor for X-linked adrenoleukodystrophy , that's been through a successful phase IB study. This is just kind of a graphical representation of the pipeline here. VK2735 in the registration program, two phase III trials in progress. We also have a phase I maintenance study that we just announced last week has fully enrolled. Expect to read out those data around the middle of the year, third quarter.
With the oral program, phase IIA is complete, and then with the amylin agonist moving into an IND later this quarter. So moving more into the peptide hormone program, we started working on these compounds back in 2019. We looked at the GLP-1 monoagonists, and we have, I think, a good family of potent monoagonists. We also have the dual agonists, which I'll talk about today. And we also spent time on the triple agonist where glucagon was added. And the glucagon didn't necessarily present any additional incremental efficacy, so we really prioritized the dual GLP-1 and GIP agonists. VK2735 was selected as the lead compound. We have two follow-ons, IND ready with the 2735 compound. We completed and read out data from a phase I SAD/MAD study in the first half of 2023.
Followed that with a phase II study in the first half of 2024, and then started the phase III program last summer, VANQUISH registration program. With the oral formulation, we've completed the phase I SAD/MAD study and then read out data from a phase II obesity study third quarter of last year, so a couple of new slides. We've talked about this stuff in the past. We haven't really presented slides on it before, but when we look at the thing that made us really excited about VK2735 is the PK profile in monkeys looked really differentiated versus other compounds in development. This is a plot of comparison, head-to-head study against tirzepatide and single-dose study in primates, and what you can see in these curves is the Tmax a little bit later relative to tirzepatide, Cmax clearly higher, half-life quite a bit longer than tirzepatide.
And over time, that results in a significant improvement in AUC. When we look at over time how that delta manifests, the right-hand graph shows the effect after eight weeks of dosing in obese primates. Again, head-to-head study. And you can see a significant difference in the overall exposures of VK2735. And you would hope that this would translate to some benefit in how the efficacy profile manifests. And so this is head-to-head in obese monkeys. Here's the body weight changes in that study. We saw significant and progressive weight reduction over eight weeks, about a 40% improvement over the comparator. And so it does align with the profile that you would expect to see from the PK profile. And it certainly supports the delta and exposures that we see. I'll talk about the tablet first since there's the most recent data in the tablet formulation.
This is some of the early work we did, a 28-day phase I study where we dosed from 2.5 mg per day up to 100 mg per day. And in this study, we saw nice dose-dependent reduction in body weight up to a little over 8% from baseline after 28 days. And I think a really nice progression in weight loss as well. And this shows the trajectory of weight loss in that study. Something that really struck us when we were looking at these data is most pronounced in the bottom three lines, but really easier to see in the red line. This was looking at day 1 through 28. That's the steep part of the curve there. And then we had several follow-up visits out to day 57, so another four weeks after the last dose.
And when you look at the efficacy, we saw 8.2% at 28 days and then 8.3% at 57 days. So it really speaks to this interesting durability in body weight reduction. And we think that is sort of in line with what you might expect from the long half-life that we see with the compound. When we look at the phase I data from GI tolerability. Really remarkably well tolerated in this study. You see a little bit of an uptick in nausea as you go across to the 100 mg arm, but really mild nausea. Vomiting as well, pretty much a non-issue. But overall, the tolerability profile is really excellent in this first study. So the study takeaways from the phase I study: up to 8.2% reduction in body weight after 28 days of dosing. Progressive effect, we think, is suggested. Obviously, dose longer, you'll see better weight loss.
Majority of the effect maintained four weeks after the last dose. Really excellent tolerability with the majority of the AEs, mild to moderate. Low rates of vomiting, diarrhea, and constipation. And then we had an exploratory cohort as well that transitioned people from 80 mg daily to 80 mg every other day. Don't have that slide in this deck, but really showed minimal differences between those two. And it suggested once you get some inertia to the weight loss, maybe you could transition to a lower dose. And it was the first kind of hint that maintenance dosing would be really interesting with the oral. This was the phase II study that we then conducted, a multi-arm study, 13 weeks. Went from 15 mg to 120 mg.
The green line there at the bottom is an exploratory cohort where we dosed people up to 90 mg and then for the final seven weeks brought them back down to 30 mg. Just another exploratory effort on understanding a maintenance effect. This slide shows the weight change at 13 weeks. We saw a beautiful dose-dependent reduction in body weight up to a little over 12% at the 120 mg dose. Really no plateau and highly significant in every cohort except for the lowest dose, and we're going to focus more in the future on this 20-75 mg dose range where we think you see a really nice efficacy effect and really great tolerability. This slide shows the trajectory in all of the cohorts here.
So a really nice progressive effect across the board here up to 12% in that 120 mg arm and statistically significant at all time points other than the 15 mg at all time points starting with week 1. We also looked at maintenance durability here in this study, and we saw a really encouraging signal here. So looking at the 30 mg, 60 mg, and 90 mg cohorts here, and that's kind of the sweet spot we think for further development. When we look at the body weight change at 13 weeks, the range was 7%-11%. And you look at 3 weeks after that last dose, largely maintained effect, 6.7%-10.3%. So the majority of that weight loss is maintained, that additional 3 weeks. And that, again, further data on a durability signal. This is a really interesting slide that shows that exploratory maintenance cohort that I talked about.
So the gold line is the cohort that was titrated up to the 90 mg final dose and just held at 90 through the study. The green line is a cohort that was titrated up to 90 and then at week six transitioned back down to 30. And this was to explore once you get some inertia, what happens if you drop the dose. And what was interesting here is that when we drop that dose, you see more than just a flat line. You see a sort of a continued, more gradual, but a continued reduction in body weight up to 9.2%. So it suggests maybe maintenance dosing could be achieved at doses below 30 mg. So really encouraging cohort there.
When we look at discontinuation rates and treatment emergent adverse events from the study, we did see, if you look on the, as you go to the far right side of the table, dose-dependent increase in discontinuations and overall treatment emergent adverse events. Drug-related treatment emergent adverse events also maybe an uptick at the higher doses. But really, when we look at the drug-related treatment emergent adverse events leading to discontinuation, really no difference from placebo. Vast majority mild to moderate. I think some of this is probably related to the titration rate that we used here. We did two-week blocks in this study. I think in the future studies, we'd want to use four-week blocks to ease into that exposure a little bit better, and the most common treatment emergent adverse events leading to discontinuation were the expected GI-related adverse events.
When we look at the cohorts where we would really be looking at the sweet spot going forward, pretty minimal delta from placebo in that 20 - 75 mg range. So that's what makes that range very exciting. Looking at the GI tolerability profile from this study, you again, pretty flat across the board until you get to the far right of the table. Then you see an uptick in nausea, a little bit of an uptick in vomiting. But when we look at the anticipated future dose range compared to placebo, there really is no difference. So that's what makes us really excited. Thinking starting low and going slow would be the best approach here. This is the GI adverse event frequency over time through the course of the study. This is all cohorts combined. Constipation in green, diarrhea in aqua, nausea in blue, and vomiting in gold.
And you can see the up-titration steps there. So accelerated titration here every two weeks. We thought we could get away with that because the phase I study was so well tolerated. But when you look at these adverse events over time, you can see obviously the first week is by far the greatest incidence of adverse events. And nausea, mild nausea is by far the most common. The next most common occurs in that first step up in titration at week three. So it suggests that if you were to start lower, we started at 30 mg in this study. If you started around 10 and stepped over four weeks, you'd probably mitigate a lot of these GI-related adverse events. So the oral study takeaways, up to 12% body weight after 13 weeks of dosing. Progressive effect, dose-dependent across all of the treatment arms.
We thought the maintenance cohort was particularly exciting because it did demonstrate that proof of concept. You can drop the dose, not necessarily see a rebound. Good tolerability. Most of the treatment emergent adverse events were mild to moderate. The majority of the GI-related adverse events also mild to moderate and transient. As I said, I think we can optimize that quite a bit with a different titration scheme. And we're also, I'll show a slide later, conducting now a sub-Q to oral maintenance study. Then we hope to have the data later this year. I'll now move into the sub-Q formulation. We've done a SAD-MAD, a phase II study, and now we're in phase III. In the SAD study, we saw data consistent with what we saw in primates. Later Tmax, pretty gradual onset, 72 hours, half-life up to a little over 10 days.
We think that's amenable to weekly dosing. In the MAD study, we saw dose-dependent improvement of up to around 8% from baseline after four weeks. Durable weight loss 21 days after the last dose. We also looked at MRI-PDFF in this study and saw really, I won't have a slide here, but we did see a nice reduction in liver fat up to 50% in the 28-day study. And then excellent exposures from weekly dosing suggesting that a monthly regimen might be a possibility. And then finally, really good tolerability. Following the phase I, we conducted the phase II study we called the VENTURE study. This was a multi-arm phase II study, 2.5 mg to 15 mg. 2.5 was a flat dose, 2.5 mg a week for 13 weeks to 5. Started at 2.5 for three weeks and then went to 5 for the remaining 10 weeks.
10 started at 2.5 and stepped up in 2.5 mg increments. The 15 was a different titration schedule. The 15, two things different. It started at 5 and then went to 7.5 and 10, and then it jumped from 10 - 15. So I'll show why that's important when we get to the tolerability slide. But really, a lot of great information came out of this study. When we look at the primary endpoint here, body weight change after 13 weeks, we saw a significant reduction. Really, at all doses, up to about 15%, 14.7% after 13 weeks, highly significant in every cohort. When we look at the trajectory of weight loss in this study as well, no plateau at all. And again, 9%-14.7% weight loss. So we would anticipate a longer dosing window leading to a further improvement in body weight.
When we look at GI tolerability, the majority of the expected GI-specific treatment emergent adverse events were mild to moderate. You can see the nausea ticking up a little bit as you go up to the higher doses, but still a reasonable rate of nausea. Vomiting also slightly higher at the higher doses. But overall, nothing surprising in the adverse event profile. It's a GI tolerability profile. This slide is another histogram like I showed with the oral. And it's really interesting because when you look at the left-hand graph, this is the 10 mg cohort. So these guys started at 10, and then at week, after three weeks, they went up to 5 mg and then 7.5 and then 10. And you can see, just like with the oral, same color scheme, constipation, diarrhea, nausea, and vomiting. You see a higher rate of nausea in that first exposure.
Then the second highest rate is in your first step up in titration. And after that, pretty much non-issue at all. But when you look at the right-hand graph, very interesting. And the two things that are different about this cohort are clearly evident. These guys started at five mg. So you can see that rate of nausea is quite a bit higher because you're starting at twice the dose as the 10 mg started. Similarly, when you get out to that week 10 time point, they went from 10 - 15 mg there. So a larger jump. And you can see that led to a commensurately higher rate of nausea even though you've been exposed to the drug for some time. So it's a great clinical example of that mantra, start low and go slow.
So, the study takeaways from the phase II trial, up to 14.7% weight loss after 13 weeks. Most of the drug-related treatment emergent adverse events were mild to moderate. Most of them occur early and then resolve. Didn't show it in this deck, but when we look four weeks after the last dose, more than 90% of the weight loss efficacy was maintained for a month after the dose. We think the durability and PK profile suggest that a monthly regimen would be worth exploring, and that's what we are exploring, and the results from this study were just published in Obesity last Friday, and what we're doing now with the sub-Q formulation is conducting the phase III VANQUISH program. This is two studies. We initiated them last June. VANQUISH I is enrolling patients with obesity, and VANQUISH II is enrolling patients with obesity and type 2 diabetes.
Both studies will include a one-year extension to look at long-term safety and efficacy. And we announced last year that VANQUISH I had completed enrollment and we're on track to complete enrollment in VANQUISH II in the first quarter. This is the study design for the VANQUISH trial. So four arms, placebo, 7.5, 12.5, and 17.5. All of these will go with a 2.5 mg uptick in titration, but they will all also start at 1.25 mg. So two weeks at 1.25 and then four weeks at 2.5, four weeks at 5, and so on up to 17.5. And when you get to 17.5, that's when the 52-week stable dose window starts. Primary endpoint is change in body weight, and then secondary and exploratory endpoints will look at proportion with certain thresholds of body weight reduction met as well as changes in function and other metrics.
I also mentioned earlier maintenance study, so this is an outline, a very complicated slide, but an outline of the maintenance study. The top half of the slide above that blue bar is the sub-Q portion of this study, so we are randomizing people into a variety of arms. You dose up on a weekly basis all the way up to 22.5 mg, and then after 19 weeks, people are then transitioned to a range of different monthly doses, 22.5 - 17.5 as you go down that slide, and then we have a 7.5 mg every other week cohort. We have a control arm that stays on 17.5 through the duration, 31 weeks.
And then we've got a 17.5 mg arm that transitioned to placebo at week 19 to look at the delta from someone who comes off therapy completely to someone who goes to monthly, to somebody who goes to every other week. In the same study, if you go to the bottom half of the slide, we have an oral portion. So in this part of the study, everybody's titrated up to 17.5 mg weekly. And then after 19 weeks, one cohort is re-randomized to a 17.5 mg daily dose. Another cohort explores 27.5 mg daily. And then we have a weekly cohort where people are dosed with 110 mg weekly. So a lot of moving parts in this study, but it should give us a really, really interesting data set. And we expect that mid-year.
We announced it was completed enrollment last week and hope to have data around mid-year or third quarter. Quick snapshot of the financials. We were really fortunate to have a strong balance sheet, over $700 million in cash as of the end of the third quarter. And this brings us back to the first slide. So overall focused on novel therapeutics for metabolic and endocrine diseases. Metabolic disease program highlighted by VK2735 in two phase III trials for obesity, the VANQUISH program. The oral program just completed phase II study, read out data last fall. And then an amylin program I didn't talk about, but that's moving into phase I trial first half of the year that IND has planned for the first quarter. So that was the last slide. I can stop here.
Thanks very much for your attention.
Thanks, Brian. Appreciate it. We'll just move on to the Q&A. So you mentioned you said there's two VANQUISH trials going on. The first one in just pure obesity has already finished enrollment. And you said you had commented previously that it had kind of the pace of enrollment was faster than you expected. How's the pace coming along for this VANQUISH II relative to your expectations?
Yeah. Yeah. The first one enrolled probably faster. We over-enrolled it because we had so much demand. So it enrolled to larger N and more quickly. The second one is, it's slower because that was so abnormally fast. It's really kind of going along what we expected to be the enrollment schedule. So that one's just according to plan.
Okay, and when do you expect readouts for those two trials?
Right. They're 18 months from last patient's first visit. So you could probably expect data in the 2027 timeframe.
Got it. What do you think good data here looks like? There's obviously a lot of competition, and the bar seems to be changing quite a bit. So what do you think? What's your?
Yeah. Very, very fluid. Well, I would hope that the weight loss is competitive with other incretin axis agonists. I think tolerability is becoming a more important metric for people. But it's hard to project. I mean, obviously, we'd certainly anticipate the data would be better than the phase II data by a good margin, but hard to know what the actual 78-week efficacy signal will look like.
Okay. And then you, in the slides, you were talking about how the highest dose in the VANQUISH trial is a little bit higher than what you had tested before.
Yeah.
How did you kind of walk me through kind of that risk-benefit rationale there?
Yeah. It was higher than what we'd explored in the phase II study. We thought that the safety and tolerability profile looked really encouraging. So we thought that you could probably come up maybe a little bit in dose. It's always a question whether or not the FDA will be okay with it moving up in dose. And they didn't have a problem with it, provided that we had more randomized to those higher dose arms than the lower dose arms. And there was no problem. So we decided to proceed there.
Less N in those?
Just the low, the 7.5 is a little bit smaller than the 12.5 and the 17.5.
Okay. I think audience question.
Sure. Unni Westermark , Copenhagen, Denmark. Thank you for the nice presentation. So I'm curious about the 2809 for MASH that you had positive readout in 2024. What is the plan forward for that program?
Yeah. That's open for licensing. We probably aren't going to pursue that, at least near term, by ourselves. And I'd say a fair amount of interest in that program these days.
So I just want to move on. The FDA had come out with some developments in December. One of them was the FDA Commissioner saying that they would require only kind of one phase III trial. I wanted to see, does that impact any of your programs specifically in terms of what you would have to kind of do and timelines?
No. It was interesting. We had gone kind of back and forth internally on the oral. If, suppose we went into an oral phase III, would we do one study or two studies? And I think you could do either, but we had decided to do two if we were going to go forward. One in, just like the VANQUISH, one in a dedicated obesity population and then a smaller one in the type II population. You could put them in the same study, but it just gets a little bit more complicated on the data analysis. So the suggestion from FDA didn't change any of our plans. We were planning to do two.
Okay. And then we've also seen a couple of these GLP-1 therapies recently received the FDA BTD designation, basically cutting down the review timeline to one to two months. Do you think that that's like a, do you think going forward that's going to be applied to the class broadly, like whenever a new GLP-1 comes to the FDA's desk, or do you think it's more of a drug-by-drug basis? And the second part of the question is, is that something you guys have thought about for your drugs?
To answer that, yes, it is something we've thought about. It's unclear if it's going to be something that's really likely to be available to subsequent compounds, but certainly something that we would be. I mean, it'd be in everybody's best interest to ask about it.
What are some of the positives and negatives you like about that program?
The quicker review time is the big positive. I don't know that there would be an obvious negative. It's just, is the agency going to allow multiple examples of a particular mechanism or something like that to proceed under that really accelerated path?
Okay. And then you mentioned, I think in the past you said the FDA end of phase II review for the oral was in December. I don't know if you can comment on how those talks have progressed and when you would hear from the FDA about potentially moving directly into phase III for the oral?
Yeah. We did have that meeting in December, and we have not yet received the minutes yet. So it's hard to comment on what the next steps are. Until you really get the minutes, you wouldn't want to say something that you'd have to correct later.
But you're still fairly confident that you don't see any reason why it wouldn't be able to move forward?
Nothing obvious to us, but we got to get the minutes.
Gotcha. And I think you had kind of tailored down the next kind of doses and future programs for the oral therapy. And I was just wondering, in those specific dose ranges, what do you see the role of that oral formulation in the market?
Yeah. We've always thought the oral is best utilized in a maintenance setting, so if you start with the injectable, the injectables just work well. Everybody's comfortable with them. Once you get to some target weight range, then transitioning to a low-dose oral, that's the way we've thought about it. Everybody thinks about this differently, but that's kind of the way we thought about it, and so one advantage with the molecule is since we have two formulations, if you lose weight with the injectable and then you're thinking about transitioning, we have our potential monthly dose for the injectable or a potential low-dose oral to keep your weight maintained at that target range, and having the same molecule, we think probably mitigates the risk of new or unexpected side effects after that transition.
And I'll get to the maintenance study in just a bit, but I was wondering, I think you had said in the past that you would start this next phase of the oral program at a lower dose. I don't know if you've commented on specific dose you would start at?
No, we haven't.
Or did you think about it?
No, we haven't commented on that. We started in that phase II just because the phase I was just pristine, really, really clean. So when that was even starting at 80 mg in that top 100 mg cohort in the phase I, started at 80 for two weeks and then went to 100, or 80 for a week and then went to 100. And there was no tolerability signal. Now that we've got more experience and we've seen the aggressive titration rate led to a little bit higher incidence of GI side effects, if we could start at, I don't know, 10, 15 mg or something like that, and then keep people there for four weeks in just kind of the standard four-week cadence that is more common, I'm confident that that would really, really produce a nice adverse event profile.
Got it. And then in that phase IIA trial for the oral, you talked about that little arm that you did where you went from 90 mg for six weeks, and then I think you transitioned people into 70, right?
30.
30 or seven weeks. Do you think the fact that they lost on average one percentage point, how consistent was that in the overall patient group? I don't know if you have that idea. And then two, do you think that was due to really kind of the residual tail effect of the 90 mg? Or do you think it was?
Yeah. I mean, it's a good question. There could be some contribution there, but you would think that the half-life is around eight, nine days. You'd think that after seven weeks, you'd probably see something, and it was a pretty consistent. It's a little bumpy, but a pretty consistent negative slope there. Yeah. Is it driven by a couple of people? I don't think so, but I can't remember off the top of my head. No, it's not really an outlier that's pulling that down.
Okay. But so it was generally consistent throughout the population?
Yeah. Yeah. Yeah.
Throughout the population. Okay. And then Eli Lilly, at the end of last year, also put out its ATTAIN Maintain trial for orforglipron, showing basically people who switch from both semaglutide to orfo and then tirzepatide to orfo. What were your main takeaways in terms of what are the read-throughs to your maintain trial?
Yeah. So for the injectable portion of our maintenance study, not a lot to read through. It's just different. We're keeping with the same Sub-Q formulation. With the Sub-Q to oral, I don't know. I mean, we're looking at multiple doses. We're also looking at that weekly. And we're looking at the same compound. There's a big difference there if you switch from a GLP-1 focused peptide and a dual agonist focused peptide to a small molecule. So I don't know how translatable those data would be or predictive for us. It's the same compound, and we're giving it at exposures that should produce some pharmacologic effect. So it was interesting. You did see a little more rebound in the tirzepatide to orforglipron, not a lot, but a little bit more of a rebound there than in the semaglutide to orforglipron.
But I don't know that you can mix and match our study to that study.
Yeah. Yeah. Obviously, you guys are keeping with the same underlying molecule.
Yeah. Right.
Let's say you fast forward into the commercial stage. What's just your gut feeling that you think potentially oral VK2735 could be a better maintenance therapy than orforglipron for people transitioning off of tirzepatide specifically because of the same GLP-1?
Oh, I don't know. Yeah. You'd have to do the study to really answer that intelligently. But I just think it might resonate more with people if they know they're not switching molecules or staying in the same molecule, just a different formulation. And when you switch to the oral, the exposures are lower. So that should reduce the risk of any new side effect occurring.
Okay. I know you didn't get a chance to talk about the amylin much, but I know, so correct me if I'm wrong, the timeline is you will file an IND in the first quarter, go into trial first half. Could you talk about just how you think that this molecule is differentiated? Obviously, there's a lot of amylin now coming out. How do you think it's differentiated from a chemistry perspective or an oral profile perspective?
Yeah. Well, it seems to be potent. That's the thing that stands out to us is in obese monkeys, it has a pretty powerful effect on body weight reduction, more than the 2735 compound. So we think that that is an interesting standalone. We think maybe it'd be an interesting compound to layer on top of 2735. But these are sort of future studies. The first one will be a SAD study, just like the early 2735, do a single ascending dose study and then follow it with a 28-day multiple ascending dose study. And then what we have in the back, combination studies kind of progressing along.
What do you kind of see? It's still up for debate what the role of amylin is. What do you kind of think? If you fast forward five, ten years?
Yeah. It's kind of a roller coaster of sentiment on the mechanism. We originally thought that amylin would probably be best as a combo agent on top of a GLP-1 or a dual agonist. But you see pretty good efficacy with the amylin. So maybe for someone whose BMI is 32 to 35, not 45, maybe amylin would be interesting for that population. Another group might be somebody who can't tolerate a GLP-1. amylin might be a suitable candidate. But I think the single agent and the combos are pretty interesting with that mechanism.
Okay. And then the last two questions is just, we talked about the combinability. Do you think you could do some sort of a one pill combination or one solution combination?
Yeah. Yeah. Very complicated, but encouraging, I think, what we've seen so far. But too early to say. If you're looking at oral, single dose combo versus two tablets, two tablets, one single compound in each tablet might be just logistically easier. But we've spent a fair amount of time on both of those.
Okay. And then the last question is just, can you just talk about the breadth of kind of strategic interest you're seeing in here in this space as pharma companies try to enter where you are?
Yeah. It's been pretty steady over the last couple of years. I think the interest probably is broader than is visible. I think that there are more parties sort of circling, I guess, the space and very intrigued, but trying to understand what is the how do we commit to obesity? Do we pursue a brand new mechanism? Do we pursue something that's proven? Do we go really early at a low price point? Do we a little more expensive at a later price point? I don't know. All those things feel like are kind of under consideration, but I'd say what we're happy about is as we continue to develop our program, it should get more valuable, and we think there is a fair amount of interest out there across the industry.
Got it. Brian, thank you. I appreciate you taking the time. I hope to see you again next year.
Thanks.