Pleasure to be here with Aardvark Therapeutics, for another panel. We have Tien Lee, the CEO, and Tim Kieffer, CSO. Thanks both for joining. I know there's a lot going on, so I appreciate you guys being here. Maybe we can just start with a quick overview, Tien, of kind of, you know, ARD-101, where things stand, and then we can jump into some Q&A.
Great, great. Yeah. We have, ARD-101 is our lead program. It's an oral small molecule drug. It's gut-restricted, which is normally not a characteristic you're looking for in a small molecule drug, but it's hitting gut receptors to convey gut-brain signaling to turn off hunger, as well as mediate eating behavior, and with a lot of other metabolic benefits. Our lead program is in Prader-Willi syndrome, a pediatric rare disease, defined by hyperphagia. We had very encouraging phase II data earlier with 18 subjects completing that phase II, and we're in the middle of our phase III HERO trial, Hunger Elimination or Reduction Objective, with anticipated top-line readout in Q3 of 2026.
Awesome. So yeah, maybe diving into some of the, like, specifics here on, like, the scientific side and the mechanism side, it's a really interesting approach and unique, and I think you, you know, you kind of alluded to it specifically addressing hunger. It'd be great to maybe just kind of expand a little bit more on this idea of, like, hunger versus appetite, kind of the panel of gut peptide hormones that you're impacting, and just kind of, like, why this mechanism is kind of, you know, well-suited for, for specifically hyperphagia and Prader-Willi.
Great. I'll start off, and I'll just turn it over to our CSO, Tim, to kind of give more color. Basically, hunger and appetite are normally not thought of as really different. We think of appetite; sometimes you call it hedonic eating. It's a reward-giving drive, right? If you like ice cream, for instance, appetite's compelling you to eat it. We think the existing medications, including GLP-1s, are good at abrogating appetite, but they don't address hunger so much. Hunger is a feeling you get with prolonged fasting. Your brain will want to eat something, and then food quality becomes less important, and that's a kind of, like, it's a separate driver. They're both simultaneously regulated, and when you eat food, a panel of gut incretins helps give a feedback loop.
A lot of this regulation is related to gut-brain vagal signaling. I'll just turn it over to Tim for further color.
Sure. Maybe I'll just add, coming back to Prader-Willi, we know for certain it's hunger-driven. Those patients aren't eating garbage because it's appetizing. It's hunger-driven. The unique thing about the Aardvark approach is that it's stimulating this panel of, as you said, gut hormones that act synergistically, and they're released at the right place, which is in the gut. That's important because the way they typically work is through that gut-brain signaling, through activation of the vagal path specifically that Tien was talking about. The other evidence for Prader-Willi being hunger-driven and not appetite is the GLP-1 class of drugs doesn't work very well in those patients, so we know those specifically dampen the appetite but not the hunger. When you take ARD-101, it stays in the gut. It activates TAS2R receptors on the enteroendocrine cells lining the gut.
They release these hormones that work synergistically to not only bring down appetite but hunger. That's really unique to the Aardvark approach.
Yeah. Yeah. That makes sense. I know, you know, you've talked a lot about CCK specifically. Obviously, there's other ones like GLP-1, Ghrelin. Maybe talk about in a little bit more detail, just, like, some of the, like, CCK versus some of these other ones, if one's more important than the other, and just, like, any of the key highlights of, like, why these things, you know, may actually be impaired in, in Prader-Willi.
Sure. First of all, the evidence that CCK can reduce hunger is really strong in patients. If you give individuals CCK during a meal, they will report less hunger and reduce their meal size. There is no question CCK's activating, you know, that hunger path. There is also evidence in individuals who have hypothalamic obesity, specific damage to the hypothalamic centers that regulate hunger, that CCK will do the same thing. It will re-reduce hunger. That is kind of the hallmark of Prader-Willi. I guess the most compelling evidence is we give ARD-101 to patients with either obesity or Prader-Willi, and there is a diminishment of hunger. You know, that is a clinical reading. I think, you know, that is pretty compelling evidence.
Yep. Yep. Makes sense. And I guess what's the right way to think about, like, how much we need to produce sort of in the gut? Like, is it just about kind of hitting these systems, or is there a certain magnitude we need to kind of restore that signaling pathway?
Yeah, that's a good question to think about. I would say it's not like the system's broken per se, and it's just on or off. It's a very dynamic process. Like, when we consume food, the way our brain measures that or assesses it and dampens, you know, appetite and hunger is by the signals that it's getting, which are generally in proportion to the amount of food. You have these enteroendocrine cells literally throughout the 20 feet of intestine. You can imagine taking that ARD-101, and it's traveling through the gut. It's going to be activating all the way through its path. It's going to be activating those enteroendocrine cells to be tonically turning up their signaling, which ultimately, you know, dampens hunger.
Yep. Yep. That makes sense. I think, you know, one of the other sort of interesting biological questions, well, actually, I guess first, you know, kind of in the context of that, maybe it'd be helpful to understand kind of how you selected your dose, this 800 mg b.i.d., and, you know, kind of why you think that's, that's, you know, sufficiently hitting the, the target.
Yeah. Yeah. We're actually pretty confident 200 mg was an effective dose, but we noted that some of the patients in our first cohort in our phase II, the ones that took the medication between meals had a slightly better response than the ones that took them with the meals. And, you know, the variability of volume in your gut can quite vary quite a bit. We think that, just to abrogate the effect of meal size, going up to 800 mg could ameliorate some of that variability with food. But, you know, we're pretty confident that the dose range that we've selected should be sufficient.
Mm-hmm. Yeah. Kind of sufficiently saturating the, the target. Okay. Great. You know, again, I think one of the other interesting sort of biological questions here is, you know, obviously in Prader-Willi, it's a very complex disease. We don't necessarily, like, fully understand the biology as maybe, like, a right way to sort of summarize it, but how do we know that these pathways are still functioning in Prader-Willi patients so that even if you kind of hit them, it's actually going to relay something to the brain, the hypothalamus, etc., and drive a clinical effect?
True.
I would come back to that clinical data. You know, that's the ultimate proof. There is no good animal model of Prader-Willi. I'm trained as a physiologist, and my whole career has been in doing preclinical studies. And for obesity, fortunately, we have the high-fat-fed mouse, which is really predictive. You know, I was just this summer at the International Prader-Willi Conference, and everybody was kind of scratching their heads, like, what mouse model do we do? As you kind of articulated, it's a very complex disease. It's not just one gene or, you know, one path. It's, you know, people are now imaging the hypothalamus in patients with Prader-Willi and saying it's probably underdeveloped. It's actually smaller, right? That doesn't mean the pathways are broken. They can still respond.
That requires clinical data because, as I said, there's no preclinical model to show it. For me, the most compelling is you give it to patients, and their hunger goes down.
One more thing I would add to it. There's a lot of inferential data that suggests that they, Prader-Willi patients, have a deficiency of sufficient gut-brain signaling. One of the reasons why we selected Prader-Willi as a clinical target, knowing what our drug was doing, was because the panoply of clinical syndromes of Prader-Willi manifests similar to what you would expect if you didn't have a sufficient gut-brain signal. In-including hyperphagia, which is a predominant quality of life impairment, but also this hyperanxiety behaviorally that you see, systemic inflammation, and very, very delayed gut transit times, with gut transit times of five days being not atypical in Prader-Willi, and also high body fat percentage, gallstones at an early age. Everything I listed previously is congruent to a syndrome where you have insufficient gut-brain signaling. Amplifying that would seem to be clinically relevant.
Yep. Yep. That makes sense. I think Brian's talked about too, just this idea that as patients age, they kind of get better at sort of controlling their disease and hyperphagia, and that obviously would suggest that the system's still functioning. I think that's another interesting point, but makes sense on the clinical data itself. Yeah. Maybe, you know, jumping to the phase II data, maybe we can kind of just, like, level set with, you know, some of the key highlights and, you know, anything specifically you wanted to highlight from the phase II data.
Sure. I think one of the consistent observations is, it was open-label data. It was not placebo-controlled, but I think the strength and consistency and directionality of the benefit was extremely compelling. We saw, on HQCT9 measured patients, you know, over like a minus eight, reduction in a very short period of time. One thing to really highlight is that the really compressed period of time in which they saw benefit. At the time, we all could only dose patients for 28 days, and in that small window of time, we saw this really dramatic reduction in HQCT. Importantly, we saw benefits anecdotally beyond just HQCT, including the anxiety and signs of clinical improvements of inflammation. Those are all formal secondary endpoints in our phase III.
I think the rapidity in which that, the improvement was noted and the degree of benefit, the anecdotes are also incredibly compelling to us. Patients leaving food on plates or forgetting about meal times, those are things that are hard to expect in the context of a Prader-Willi individual.
Yep. Yep. That makes sense. Yeah, I mean, I guess, like, what's the best way to sort of put it in context with, like, Soleno's phase II data or Acadia? Like, you know, there's a lot of data sets out there. Some have worked, some others haven't. Like, what's the best way to sort of kind of compare, you know, your data versus some of these others?
Trying to be a good scientist, it's, it's not the same study, so it's hard to kind of directly correlate. I would say the general experience is that within a 28-day period, a minus two HQCT from placebo or treatment effect has been what's been generally seen. The fact that we have a minus eight, you know, in a short time period is especially helpful, we think. Also, we had not curated the patient population with especially high HQCT scores. We have a higher cutoff for inclusion in our phase III, so our starting baseline will be higher as well. I think the general expectation is to have even a more robust benefit. If you cross-compare, you know, minus two over a total of 28 days is something that you would generally see often.
We see the minus eight off of a lower baseline. I think that actually is indicative of something that's, you know, superseding expectation.
Yep. Yep. Yeah. Kind of like along those lines, you know, what's a typical placebo response? Obviously, hyperphagia, at least to some degree, is subjective. You know, just curious kind of what we typically see over this time course on placebo and what kind of gives you the confidence that the signal's, you know, real, I guess you could say.
Sure. Again, we'll see in the phase III, but I think generally speaking, within the first 28 days, placebo was maybe like a minus two or maybe at three months, it's closer to minus four. I think the general expectation is that because the way the HQCT is measured and because of the behavioral perseverance of Prader-Willi individuals, it's expected that a three-month treatment assessment will manifest as a deeper response than the one month as well too. I think based on the meta-analyses of previous studies, we have, you know, pretty good confidence that the level of benefit that we saw, even with open label, is really indicative of an effective agent.
Yep. Yep. Makes sense. You kind of touched on some of the secondary data or, you know, other benefits beyond just hyperphagia you've seen. Yeah. Is there, like, any more color on, like, key secondaries that kind of, like, reinforce your confidence?
I'd love to. You know, CGI score, we think, you know, that's truly, you know, what you want to aim for, for patient outcomes. We think that'll be a benefit because of all the secondary features that we think we might be addressing. We have PADQ, which will be a formal assessment of the anxiousness of those Prader-Willi individuals, which is a very close second in terms of the main quality of life impairment. We'll have pro-inflammatory cytokines, metabolic biomarkers. We'll have DEXA scans. One of the things that we shared previously was that in our 28-day treatment period, we saw a 1.5% reduction in body fat percentage and 2% lean body mass gain without diet and exercise in our phase II, and we would expect to see that consistency in signal in our phase III.
We looked for this because our preclinical model suggested this would be in effect.
Can I just add one of the important metabolic biomarkers is glucose. These are patients that are prone to getting hyperglycemia. Based on our mechanism of action, stimulating GIP, GLP-1, we expect glucose will go down.
Mm-hmm. Okay. Great. And I know you've shown some of that in your preclinical data as well, which in obesity, which we can definitely get to. Maybe it'd be good to jump to the phase III now. And I know you, you kind of touched on it a little bit before. There's, like, some design elements that you're, you know, versus the phase II that you've made, in terms of, like, enriching for severe patients, etc. Maybe just, like, talk through some of the key ones and, and kind of, you know, why you designed the trial the way you did to, to kind of, like, optimize POS.
Sure. We'll have an inclusion cutoff HQCT, congruent to what others in the space have done. I just want to be very notable that we don't have fasting as a requirement, which helps with patient recruitment. We don't have renal sufficiency as an exclusion criteria. Hyperglycemia, even type 2 diabetes, it's not an exclusion criteria. We also have a way to account for what we believe in. I think KOLs believe to be a main contributor of placebo response, which is kind of like an implied motivation for over-reporting to qualify for trials. I mean, it's very understandable if there's a cutoff of HQCT minimum. As a parent, you know, I could understand there's a pressure to over-report HQCT.
Once on trial, that natural, more objectivity leads to a drop that contributes to the placebo response. We're accounting for that by having the same screening criteria in terms of the cutoff as what is typical in the space. Within 28 days, there will be a second baseline. At that point, the patients will already be randomized, and they will have, you know, assurance that they will be on the trial. The probability of getting placebo or treatment is the same, but it's almost like a prompt for a more objective HQCT measurement, and that's the baseline that we'll be measuring from.
Yep. Has anyone done something similar to that in, in Prader-Willi or other disease areas? Like, just curious if there's some data kind of supporting that it, it kind of can tampon down some of the placebo response.
Yeah. No, we don't, I mean, I don't think in Prader-Willi, I'm not aware of that, there's that. I think it's a particular driver in Prader-Willi because of that component, but I don't know. I don't have any,
I would just say our KOLs and FDA kind of applaud us for doing this, right?
Mm-hmm.
Yeah.
Yeah. It makes sense intuitively, for sure. Okay. In terms of the size and empowering, maybe it'd be helpful to kind of just walk through some of those details and what kind of underlie those assumptions.
Sure. So I think a lot of folks would look at our study and say, you know, 90 patients, that's sufficient, right? If you look at the statistical analysis, if we presume that our drug has a six-point benefit better than placebo, which we actually think is a low-end estimate based on factors I could enumerate, that implies we only need 23 patients per arm to have 90% confidence, even with a standard deviation assumption of six points, which we think is quite generous. If we, and right now, we're powered to have 90% confidence for effect size of four better than placebo, right? I think implied within our design is optionality to also do a randomized withdrawal study, should we need to do that. We actually are very confident that we'll be able to hit on the primary endpoint.
Okay. Okay. That's interesting. I know you guys have talked about how you have, a sample, like an interim sample size re-estimation. Maybe just, like, talk a little bit about that, when that may be triggered and, you know, what the outcome scenarios really are there.
Sure. There's not a traditional fertility analysis. It's mostly for sample size re-estimation. That'll be completed when 45 patients have completed 12 weeks of treatment. There'll be an unblinded third party that will actually assess, and we have the flexibility to expand up to 135 subjects enrolled.
Okay. Okay. Is that something you'll, like, announce to the, to investors, you think, or still TBD when?
The TBD. We haven't given guidance on whether we're giving, like, granularity on that. We have confidence that we can deliver on the Q3 top-line readout. I think enrollment is going very strong, and we have very active engagement with the sites and the patient advocacy groups.
Yep. Yep. Makes sense. That was gonna be one of my other questions, just, you know, how enrollment's going. Obviously, Vycat's out there, but it sounds like it's going well.
Yeah. Yeah. No. I mean, it's, it's fortunate that, there's an option for patients, right, but that we think there's a, a lot of room for further therapeutics. We had actually originally anticipated Vycat's approval, which is why a lot of our sites were XUS. I think even in the United States, we're seeing a lot of engagement and interest for enrollment in our trial.
Mm-hmm. Are patients allowed to be on background Vycat, or do they have to have discontinued it previously?
Yeah. For the precision of our study, we are excluding.
Yes.
Contemporaneous Vycat, but in the future, there wouldn't be any mechanistic capability.
Yeah. Yeah.
Yeah.
They can come in if they've been on it after a couple month washout.
Yep. Yep. Yep. Makes sense. And then XUS you mentioned, like, do we have a sense of how, from Soleno's data or others, how efficacy is tracked across geographies? Like, has it been consistent across U.S., XUS?
Yeah. I think there's, like, the different outcomes, you know, for different regions in, I think, in the previous studies in the literature. I think what we are being very careful and precise in terms of is normalizing the, you know, what each of the questions, answers of HQCT mean. There's a lot of precision in the conduct of our phase III. I think we're not worried about the variability of interpretation of HQCT because each of the sites utilized have familiarity with using the scale. I think there'll be a normalization of conduct.
Yep. Yep. Okay. Makes sense. Great. And then, what was I gonna say? It was one other question that came to mind for the trial. I guess, like, you know, data 3Q next year, this whole idea of potentially, you know, having the optionality around randomized withdrawal, is that, like, what would that look like in terms of would the data have to be kind of close and then you could just confirm it in, like, an open label extension? Like, just curious how you guys think about that optionality. Were there to be, you know, maybe the trial just misses or something?
Yeah. I think there's a lot of different permutations.
Yep.
From this, but we, based on our conversations with the agency, we think this trial right now as designed is potentially re-registrational and pivotal. We are very optimistic that we can hit on the primary endpoint given our confidence. There are various factors that give us a lot of optimism that even the phase II suggestion of signal is actually an underestimate of what we think we could be driving in terms of a larger phase III data result.
Mm-hmm. Yep. Okay. Makes sense. I remember the question I was gonna ask. Last one on sort of like the trial and phase III. Obviously, Acadia failed recently. We haven't really seen detailed data yet, or at least I haven't seen it. Is there anything specifically you're looking for in those data to help inform sort of or confirm your kind of powering assumptions with placebo or anything like that? Or is there really nothing to kind of learn from that study?
I mean, I would never say there's nothing to learn from something 'cause, you know, we wanna be good scientists. There's always something to learn about it, but we don't have the new information to judge. I think, you know, unless something's really surprising, I think the contribution to placebo and the dynamics of recruitment, it will kind of recapitulate the previous experiences, we're assuming.
Mm-hmm.
As data become available, you know, we would obviously assess, but we think there's plenty of data in the literature and in the experience to kind of inform how we're conducting our trial currently.
Yep. Yep. Makes sense. And then I just, I guess just, you know, commercially, I mean, I think everyone appreciates that Prader-Willi is a really big market. These drugs could be used orthogonally with, with Vycat. That drug's not gonna be for everyone. But maybe just, like, be great to get your perspectives on how you think about sort of the opportunity here, positioning versus Vycat, and maybe also, like, in this commercial context, like, what IP looks like for 101.
Okay. Sure. I'll try to make sure—let me know if I haven't addressed every single one of those. But, you know, the way we see it is if Vycat were the only drug to be approved for Prader-Willi, there's still approximately 50% of patients with Prader-Willi that may not be able to chronically continue taking Vycat, either because of, you know, insufficient responses or intolerance of the drug, or exclusion based on renal insufficiency, which is an exclusion criteria.
Mm-hmm.
We think that, of course, again, it's not, there's no direct in-interest study comparison, but we have optimism that we have benefits across a variety of domains beyond hyperphagia. The degree of hyperphagia improvement is also particularly robust for our drug. Again, we think that the tolerability profile is very unique in the fact that it's gut restricted. I think there's a lot of perspective advantages there. As far as IP, we have composition of matter IP until 2038 or orphan drug designation. Even though it's sunsetting officially, we have PRV status. You know, we have good confidence around the IP position. There's actually eight families of patents between 101 and 201, and that's just the first one.
Mm-hmm.
That we think will expire.
Okay. Great. Any other questions on Prader-Willi? 'Cause I did wanna jump to obesity as well. Great. So yeah, I mean, you mentioned 201. You guys had an event last week, shared some data on your obesity efforts. It'd be great to just kind of like set the stage on kind of what 201 is and then, you know, some of the trials that you're ramping up now.
Tim's always better at describing things, though.
I don't know about that.
201 is a combination of ARD-101 and sitagliptin. Sitagliptin's a DPP-4 inhibitor. The concept here is we take ARD-101 to activate enteroendocrine cells to release hormones. Dipeptidyl peptidase 4 rapidly inactivates them. GIP, GLP-1 have a half-life of around one and a half, two minutes due to that enzymatic cleavage. If you take the DPP-4 inhibitor, we're not only stimulating the release, but we're boosting the duration of their biological activity. That's kind of the concept with 201. Sitagliptin, this is Merck's Januvia. It's been in millions of patients. It's used to treat diabetes, very well tolerated, so it can be an oral combination. Yes, last week we had Obesity Week. We had a late-breaking abstract presentation on ARD-201, preclinical. We used the high-fat-fed mice, put them on a high-fat diet. It's highly translational, particularly for the incretin field.
Even the relative potency of tirzepatide versus SEMA is reflected in that animal. And just can I give some soundbites?
Yeah.
Snapshots of the highlights. With ARD-201 in that model, we got 19% weight loss at 30 days. To benchmark that, high-dose tirzepatide gave 20.5%. We're almost on par with that injectable with this fully oral combination that we expect should be really well tolerated, as I mentioned, given the mechanism of action. We then did a study where we had two phases. First phase, we induced weight loss with high-dose tirzepatide, and then we transitioned some of those to the ARD-201, and we had equivalent weight maintenance. There was no difference of staying on high-dose tirzepatide or switching to the oral ARD-201. We're gonna test that clinically in the POWER trial. Can we offer an off-ramp to patients who are on a GLP-1 but maybe aren't tolerating them?
Lastly, we included a group where we had ARD-201 with a micro-dose of GLP-1 receptor agonist, tirzepatide, one-tenth the dose, which should be very well tolerated. There we got 30% weight loss at 30 days. Just, you know, really a fantastic finding. New data we released is the glucose homeostasis. The animals on 201 had glucose homeostasis just as good as high-dose tirzepatide. The ones on the micro-dose combo were even better. They were maintained on a high-fat diet, but their glucose homeostasis was as good as animals maintained on a regular chow. That was pretty fantastic. Lastly, body composition data. Tirzepatide animals lost both fat and muscle. 201 was fat only, which is just remarkable. The combination lost even more fat.
Mm-hmm.
All in all, very well received at Obesity Week.
Yeah. Yeah. That's a really good, really good summary. Yeah, you kind of sort of answered one of my questions, but was, you know, these obesity models, sounds like they've historically been very translatable and even on like a quantitative basis. Just like if you could just expand on that a little bit more in terms of kind of like how strong these kind of animal models have been predictably.
Yeah. It is kind of accepted as the gold standard. We used to use genetic models, like mutations in leptin or the leptin receptor, and then we realized that really reflects a very small portion of the population. The high-fat-fed model, particularly for Incretin type studies, has been very predictive of kind of human outcomes. Of course, it is a mouse, and we recognize we're gonna need to replicate these findings in the clinic.
Yep. Yep. You know, you mentioned too, you had some obesity data with 101. I know that trial wasn't specifically designed around weight loss, but maybe kind of just talk about some of those data and how it kind of fits into this broader picture here of the obesity efforts.
Yeah. Thanks for that. That was a 28-day study, a short, you know, relatively short period in obese individuals. Average BMI was between 34 and 35. This was just the 101, which, going back to that mouse model that we talked about being predictive, the 101 in that mouse model was fairly weight neutral. It prevented weight gain on the high-fat diet, but did not really cause weight loss. That is more an appetite-driven model compared to the hunger-driven phenotype of Prader-Willi. We saw essentially the same thing in the clinical trial. It did dampen weight gain. At the end of 28 days, there was a 0.8 kilogram difference. We had a follow-up for about 16 days. At the end of study, a 1.3 kilogram difference between placebo and ARD-101.
Doesn't sound like a lot, but to benchmark that, if you look at the STEP trial with 2.4 milligrams of semaglutide, it was 1.6 kilograms. In our study, again, it was just the 101. We didn't have the DPP-4 inhibitor, and there was no diet and exercise guidance. You know, I think overall it's supportive of the thesis, and we're really excited to see that combo, which we'll do in the POWER trial.
Yep. Yep. Makes sense. Yeah, I guess just on the last minute here, those data, they'll be coming second half next year, right? The, the POWER data.
Yes.
Maybe just like what's, what does the win look like? You know, like what are you kind of, you know, hoping to see?
I'll give it to Tim again. Yeah.
Cool.
Okay. The second half, 2026, we'll have data from the, they think the natural history of weight, weight bound is actually quite well established when patients have established weight loss and they go off of the injectable GLP-1s. You're getting 70% weight regain in a year, and more than half of that is the first 12 weeks. Even at 12 weeks, we'll be able to see a really stark difference. If it actually has meaningful benefit like we expect based on our preclinical models, I think it wouldn't take that many patients to really show a substantial benefit. That's what we're actually looking forward to. We're looking at body composition and metabolic biomarkers as well.
Yeah. Okay. Maybe just last in the 30 seconds here, obviously there's a lot of strategic interest in, in obesity. Like, is this something you guys plan to bring forward yourselves, partner out? Like, what, what can you kind of say about how any of those conversations or, you know, your strategic options have kind of evolved?
We're entering conversations now with multiple, you know, the usual suspects. I think, we, I think with demonstration of benefit, we definitely are looking to partner that asset out. We're not looking to run like two phase III trials, you know, in the base population and market it ourselves. Prader-Willi, we still think we can, you know, take that forward. I know we're out of time.
Yeah. No, that's perfect. Great. Thanks both for being here, and thanks everyone for joining.