Thank you for joining. My name is Samantha Semenkow. I'm one of the biotech analysts here at Citi, and it's my pleasure to be hosting BioAge at Citi's Global Healthcare Conference in Miami. With me today, I have Kristen Fortney, CEO and co-founder of BioAge, and Dov Goldstein, CFO. Kristen, Dov, thank you so much for being here.
Thanks for inviting us. It's great to be here.
All right, so maybe we can just set the stage for everyone, just a high-level overview of BioAge. Tell us about your proprietary platform, how that has led you to identify a number of interesting targets that it can address a range of metabolic diseases?
Yeah, for sure. So BioAge is really focused on the idea that by understanding some of the drivers of human aging, we can find important new targets for metabolic disease, and we like to look at large human data sets for a couple of reasons. One, it can help us narrow down which targets are translational, are actually going to be relevant in the human context, and two, it can give us some signal of whether targets can be safe as well, if they're elevated, for example, in humans for several decades and only associate with positive outcomes, so what's unique about our platform at BioAge is that we've partnered with biobanks, so resources like, for example, UK Biobank or deCODE, or some of the ones you may have heard of. Our biobanks are similar with one key difference, which is really the length of follow-up.
These biobanks often have samples collected as long as 50 years ago initially. The initial sample set was collected decades ago when people were middle-aged and healthy. And then there's sort of follow-up samples and longitudinal health records tracking future health outcomes. And what we do with the company is we go into these samples, these fairly unique samples, and we profile them with today's technologies, metabolomics, and proteomics, and ask what's different about those individuals who are functional and have better outcomes in the long term. And it was that type of analysis that initially led us to apelin signaling, the target of our lead asset azelaprag, as well as to NLRP3, which we're also targeting with a drug where we're filing IND next year, as well as to the two earlier platform targets that are at earlier stages of development.
Got it. So a lot to dig into there. So maybe we just start with apelin. So you identified apelin in the platform, as you said, as an attractive target, and you were able to in-license azelaprag from Amgen. I mean, there's a number of things that I could list that makes it attractive, but perhaps you could just speak to some of them. I know you have a lot of safety data. It's an oral small molecule. What made a azelaprag for you a really good business decision to in-license?
Yeah, for sure. So first of all, it's really interesting from a biology perspective. So apelin is described in literature as an exerkine. It seems to be one of the mediators of the benefits of especially endurance exercise. And if you increase apelin levels either genetically or through an intervention, you can recapitulate several benefits of exercise. So we're really excited about that pathway. And as you mentioned, we saw in our human data sets that people who at middle age had higher levels of apelin, they were physically functional for a longer period of time, and they were also living longer lives. So that was sort of the initial biological data set that got us excited about this pathway in general. And as you mentioned, we were able to identify an asset developed by Amgen that already had phase 1 data.
That gave us a couple of other key advantages here. Azelaprag, initially developed by Amgen, has been in over 200 people in phase 1 studies, very clean from a monotherapy tolerability perspective in the data to date. When you combine azelaprag together with an incretin drug or potentially an appetite-suppressing mechanism in the context of obesity generally, there's the prospect for enhanced weight loss and improved body composition with a favorable tolerability profile.
Excellent. And then so what really drives that synergy, do you think, mechanistically? Maybe we could take it separately with the weight loss and the body composition piece. And I know you have a lot of preclinical data that you've generated to support this, but I'm just curious, mechanistically, what is driving that?
Yeah, for sure. So we like to think of the whole weight loss landscape as really divided into two buckets. There's kind of only a couple of ways to lose weight. You can either eat less food, so less energy in, or you can burn more calories and have more energy expenditure. And azelaprag, an apelin receptor agonist, seems to be in the energy expenditure side of the equation. It's in that bucket of mechanisms.
Specifically, why you see synergy on top of an incretin drug or potentially that whole class of appetite-suppressing drugs is because when you are obese and you go on a diet, which happens in a situation where you calorie restrict or go with no drug intervention, or where you take an incretin drug or a CB1 drug, for example, when you're obese and you calorie restrict, that reduces your apelin levels and reduces your energy expenditure. And if you were to restore apelin levels and energy expenditure, that would lead to a lot of additional calories being burned and weight being lost, which is what we see preclinically. And as you mentioned, we also have a clinical data set. This is not an obese data set.
When our first clinical experiment, we were focused on physical function in older individuals, and that goes to the muscle that you mentioned earlier. We also saw, so Citi, basically, for those of you who aren't familiar with the paradigm, we did a very focused experiment in older individuals, which is called a bed rest model. So the intervention is you have a bunch of older people come to a phase one unit where they sit in bed for a 10-day period. And this is an intervention where you very reproducibly get suppressed metabolism and also a reduction in muscle size. And we saw a very nice monotherapy rescue with azelaprag. And while this is an obesity, it's a very different indication from obesity, there are aspects of that that should translate to the obesity context because bed rest, like caloric reduction, suppresses energy expenditure, suppresses muscle protein synthesis.
We saw very nice rescue of those in the clinic.
Right, exactly. And so you are running a phase 2 study now. So we don't have data in obesity patients yet, as you mentioned, but we have a phase 2 running, and you have another one or two planned. So maybe just can you walk us through that trial design? This is the one, the STRIDES trial combining with tirzepatide. And what are we hoping to see in the readout for top-line data in the third quarter of 2025?
Yeah, so we're doing three different phase 2 trials with this drug, with azelaprag, over the next couple of years. And the one that's well underway now, our first readout, which will be at the end of Q3 next year, is the STRIDES trial where we're collaborating with Lilly. And we're evaluating whether azelaprag, together with tirzepatide, can amplify weight loss. And just to give you the broader sort of strategic positioning here, what's very exciting about azelaprag is that this is an oral small molecule that when you combine it together with an incretin can amplify weight loss. And this is especially compelling as a value proposition for today's oral obesity medicines. Oral GLP-1 agonism alone is not going to get you to injectable-like performance, 20%, 25% weight loss at one year.
Pharma companies are very actively looking for complementary mechanisms to plug together, potentially in an oral FDC type of pill, to achieve injectable-like weight loss. Our phase 2 trial with Lilly is designed to really evaluate exactly that question. In that trial, we're comparing ourselves to tirzepatide alone at the low dose. The 5-milligram dose of tirzepatide shows similar weight loss efficacy to today's oral small molecule incretin drugs, meaning that they achieve about 50% weight loss at one year on this dose. We're comparing that tirzepatide alone at this low dose, tirzepatide plus different doses of azelaprag. We have 90% power to show a weight loss increment that would be very exciting.
So this is a six-month trial, and we have 90% power to show a weight loss increment of 3.3% at six months versus tirzepatide alone, which corresponds to a weight loss increment of more than 5% at one year. And the 5% figure is relevant for a couple of reasons. One, it's the regulatory hurdle for approval. FDA wants to see an incremental 5% weight loss for approval, but it also happens to be the difference in performance between today's oral drugs and today's injectable drugs. And if we could really get an oral molecule with a profile, oral combo, rather, with a profile of the weight loss profile of an injectable drug, that would be really exciting.
Yeah, so a couple of questions on that. One of the ones I get from investors is you're running the study with an injectable, but long term, you're looking at all oral combination. I guess how do you make that step? Obviously, the first step is to get data from the study, but what is the, or how do you make that transition to an all oral down the line clinically?
Yeah, great question. So we're currently using injectable drugs, tirzepatide, for the ongoing trial. We're also going to do a semaglutide trial next year because these are the approved drugs. So there are no approved well-performing orals right now for obesity. It would have required a lot of additional work before being able to do the trial. So it lets us move faster. And as I mentioned, we very deliberately selected the dose of the injectable that seems to behave like an oral, but it's, of course, not an oral medicine. Preclinically, we recently presented at Obesity Week. We have looked at oral incretins along with injectable incretins, and the performance is very similar. Orfo from Lilly is likely to be the first approved oral, and we would incorporate that into phase three if that were the case.
Got it. That makes sense. So then just going back to STRIDES, STRIDES is actually in the older population. And when you move into the phase two with semaglutide, that's going to be an all-comers adult. So I guess what are the advantages of running your first obesity study in that older population?
Yeah, so as you said, STRIDES is basically a run-of-the-mill obesity trial with one key distinction. We are initially targeting an older population, people 55 plus years of age. The primary rationale is because that's the population where we already have very nice mechanistic human data. Our phase 1b was an older cohort at bed rest. That's where we saw this very nice monotherapy efficacy. So we wanted to look there first. So that's the primary reason. But to your point, there are additional benefits to look at in an older population, especially around body composition. So older people, when they lose weight for pretty much any reason, whether it's gastric bypass surgery or just going on a diet, they do lose more muscle than do younger people.
So if there's a body composition benefit, which we have reason to believe from the mechanism, we'll have a better chance of seeing that there. But of course, from a weight loss perspective, mechanistically, we would expect this to work just as well in young people as in old people because when you're obese and you calorie restrict, whether you're old or young, that suppresses your apelin, and that suppresses your energy expenditure. And preclinically, we've seen the same weight loss benefit in young and old animals. And that's why our semaglutide trial will incorporate more of an all-comers design.
Got it. Maybe we can talk about the body composition piece for a little bit. So when you think about from a potential commercial perspective, of course, you need to show that synergy and improvement on weight loss. I think that's well understood. But the body composition piece, there are a lot of mechanisms right now that are under investigation to help improve this and make the ratio more favorable by sparing lean muscle mass. So I guess, how do you think about what you need to show there and how important do you think it is to be commercially successful that you do actually achieve that body composition improvement piece?
For sure. No, that's basically in the upside category. Dov, do you want to take this one?
Yeah. So the real value proposition here when we talk to pharmaceutical partners and physicians is the weight loss. So that's really the key focus. We think it's a very attractive commercial product if we have weight loss alone. The DEXA scans and other functional endpoints are all exploratory endpoints. So it's not something that we're guiding investors to expect a readout there. And as Kristen mentioned, that would really be in the upside category.
I mean, are we looking for trends out of STRIDES of improvement? Maybe perhaps it's not powered statistically for such a thing, but that data would inform a future study that might be powered for such a thing. Is that the right way to think about it?
Yeah, we mark them in the exploratory category, these endpoints, because we don't really know how much power we have. There's not enough data in this population. Of course, we'd love to see a difference, and of course, we'll also learn how to properly power future trials to see something here. As Dov mentioned, it's really not part of what regulators consider now, but that could change with time, especially for certain subsets of the population, like older individuals where muscle loss is more of an issue.
Yeah. And so, how, I mean, and you mentioned this, we're early. We don't really know what the right endpoints are quite yet. How are you thinking that might evolve as we get more data, both from yourselves and just as a field?
You mean muscle endpoints?
Muscle endpoints specifically for body composition.
Yeah, that's hard to say because there's very clear guidance from FDA for obesity in terms of what they want to see from a weight loss perspective. I think that the conversations are evolving right now. As you know, there are muscle agents in phase 2, including with large pharma sponsors. And I think that they will go to FDA with data in hand to have those discussions, and we'll see that evolve.
Okay. And then maybe we could just go back a bit and touch on the collaboration you have with Lilly. They're providing tirzepatide and also some clinical trial support. How impactful has that been so far for the execution of STRIDES?
Yeah, that's been a huge help for the company. I mean, this was the first time we've done a trial in obesity, so it was really good to have their help both in the design and the execution of the trial. We were able to power our trial using Lilly's tirzepatide response data in our age cut of the population. And then from an execution standpoint, we're working with sites that have delivered quality data for Lilly. That's been a huge help the whole way through.
Got it. Okay. And would you expect in a future study, if it were to involve tirzepatide or if a GLP-1 brand, is that collaboration expected to evolve as you advance azelaprag?
We're planning to do other trials on our own. This is sort of our first obesity trial where, again, Lilly supplied the tirzepatide, which is a big help, as well as helping us with design and execution. And in exchange for that, they have a soft right-of-first negotiation, like really a first look at the data. And so for future trials, now that we've learned the trials and how to get these done, we're planning to go it alone.
Got it.
One of the exciting things about Orfo is that as a small molecule, it'll be readily available in the marketplace. So part of the strategy with Lilly was just getting access to tirzepatide, which is difficult to do when we established the collaboration. So in a phase 3 program, as an approved agent, it's something we could just readily buy and do a phase 3 study with.
Semaglutide too, right? Like the supply was tighter for everything last year. Yeah. But as Dov mentioned, for small molecules for Orfo, that should be less of an issue.
I was going to make my question. So semaglutide, you're sourcing on your own?
Correct.
Perfect. Okay. So then let's talk about that semaglutide study and also the insulin resistance study in type 2 diabetes that you're planning. Those both are initiating in the new year?
In the first half of next year, correct.
I guess it's a monotherapy study, I believe, for the insulin resistance. Is there anything you can share there, or is that something we can look forward to closer to initiation?
Yeah, we'll share a little bit more detail on that in the future. We have shared at this point that it's a phase 2 in a diabetic population. And as you think about obesity, which is a lot of different people, a lot of different comorbidities, there's a couple of different patient subsets that we're really excited about the potential of azelaprag because of its mechanism. And one of those is diabetes. The other one is heart failure. And in diabetes, there's a very nice set of evidence, including genetics, like apelin, knockout animals, for example, have a lot more visceral fat, worsened insulin resistance. There's even a small clinical experience in a glucose clamp study that showed positive results with infused apelin peptide.
So we're particularly excited about taking potentially the azelaprag incretin combination to a diabetic obesity population where the weight loss has been more challenging and where you can also, beyond the weight loss itself, there might be azelaprag specific benefits. So we're going to have an early look at the behavior of this drug in that population.
Got it. Looking forward to more details there. And then you touched on this as well, but preclinically, you have a bunch of data with several mechanisms, multiple incretins. We've also recently seen CB1 data combination, all showing very synergistic effects in mice, at least. How broad do you think the combination potential is for azelaprag across the many different mechanisms that we know are being developed in this space?
Yeah, we'd expect it from the mechanism to be additive to appetite suppressants. Because it's in an appetite suppression context, again, even if you just go on a diet where you see the suppressed apelin levels and also the suppressed energy expenditure, I mean, that might not be true for every appetite suppressant. Maybe there's some mechanism where they maintain energy expenditure, but that's certainly been true for the ones we've looked at so far. So that's exciting, as you say, because we've already shown it can be additive with incretins, oral or injectable. We've now shown it can also be additive with CB1 agonists, but we would also expect amylin to be additive. We haven't generated those data, but there's reason to believe that would be additive as well. And NLRP3 is another one, right?
So that's an emerging target where we have one of our programs as well, which looks like another appetite suppressant. So there's certainly novel appetite suppressants coming down the line, and we could potentially be a partner to each of those.
Got it. That's exciting. And so for azelaprag, you've started co-formulation work. So it's an easy small molecule. It's oral. One of your scenarios for what this could look like commercially is a co-formulation single pill combination. I guess maybe, Dov, you touched on this a bit, but maybe we could go through it in a little bit more detail. How should we think about where azelaprag gets used commercially? What are a couple of those scenarios?
Yeah, so azelaprag, we really think about it in two different ways. One is an incretin agnostic label, where that's our go-it-alone strategy as BioAge. So we would do the phase three program ourselves, and we would do it likely with at least the three agents available, so tirzepatide, semaglutide, and Orfo. And the label would be analogous to the PCSK9 labels that have use with statins in general. So that's the standalone strategy. And then there's a partnership strategy or acquisition strategy where a larger partner that has their own tirzepatide agent wants to combine it with us, most likely an oral GLP-1. It gets put into a fixed dose combination, and the phase three program is all that. Sorry. Okay. I thought it was too loud.
In that latter scenario, is it likely that that's an exclusive partnership where that partner would be the only one making that fixed dose oral, or could you retain some rights to do an additional?
I mean, there are more complicated commercial strategies where you do multiple relationships, but most likely someone's going to want to be the dominant player in the marketplace, and this allows them to get from 15% to potentially 20% plus weight loss with an oral.
Yeah, that makes sense. And then I think that's maybe a good segue just to talk about some of the competition in the space. I mean, I think azelaprag is a bit of a unique mechanism given the ability for it to be broadly combined, potentially with a lot of different appetite-sparing mechanisms. But I guess how do you become the mechanism of choice? Because there's a couple that could be combined, particularly with incretins. What separates azelaprag, and what data do you need to generate to really have that commercially be successful down the road?
Yeah, that's a great question. And as we mentioned earlier, we kind of divide the universe of obesity therapies into the appetite suppressants and the energy expenditure mechanisms. And it's probably only so far you want to suppress appetite, right? I mean, that's going to be limited. And we really think of that energy expenditure category broadly as being complementary. So that's sort of like the relevant competitive set for us. And it's an important point that there's really only a small handful of mechanisms in that bucket that are at our clinical stage, right? So there are some other very interesting biologies being looked at, like mitochondrial uncoupling, AMPK, et cetera. One of the key points of differentiation for azelaprag is the monotherapy tolerability profile to date. So there have been to date no issues of overlap with the incretins, no GI tolerability issues.
In contrast, some of the other mechanisms may have overlapping issues, which is a concern if you want to ultimately combine them. I think that's an important... If you're another company with another even oral GLP-1, there's sort of a large universe of competitors right now. When you think of those of us in the energy expenditure bucket, there's really a large universe of potential partners, even those companies that haven't made a bet yet on an incretin, and that might be getting into the space some other way.
Yeah. That also sort of the question asks questions around whether the market's going to be monolithic or fragments. And we're sort of believers that the market will fragment. And so the initial GLP-1 treatment injectables serve people well with large weight loss needs for six to 12 months, but sort of chronic therapy and maintenance therapy and oral agent is ideally suited to play there. There are other places we've talked a little bit about lean muscle if that plays out, then they're elderly patients. So we're sort of believers that the market will fragment. And it's obesity, so the market's so large, each of those individual fragments is very valuable by themselves.
That's a really important point, and just to briefly elaborate, we're especially excited about azelaprag being part of the regimen that helps you keep the weight off. There's very nice genetic data and monotherapy data to support that, that it can help you keep weight off, and for the weight that you do gain, it can be healthier quality, a better ratio of muscle to fat, and that people are not going to want to be on these medicines with side effects for a decade, for two decades. These are chronic medicines, so as we look to the future of obesity therapy, we see it as moving more oral and more maintenance-oriented.
Yeah, I think that that's a big question in the field. How long do you need to treat with, let's call it, induction therapy versus maintenance therapy? And you, again, are well positioned in terms of the maintenance, just given your really very clean safety profile and easily manufactured oral therapy. And you bring up a good point about patient segmenting, which is, you call it fragmenting, but I've heard people refer to it as patient segmenting too. So maintenance makes sense, potential for lean muscle mass improvement. But are there other indications that azelaprag could be well suited for? Or conversely, is there one that's maybe it's less well suited for?
I mean, azelaprag as a standalone therapy is interesting for people who can't tolerate the medications and have to go to lower doses and need more weight loss so that can go on top of it. People plateau before they hit their weight loss goals. That could be an add-on for those people. We've talked previously about segments of elderly patients who are particularly susceptible to muscle loss. That's a segment where it's particularly attractive. I'm in the company. I'm very excited about what we do, so I don't really see any area that it's not interesting for, but those are three areas that are particularly of interest.
Yeah, I don't have one off the top of my head as well. I just thought that if they're... I thought it was prudent to ask just in case there is one that we can say you're not going into, but it doesn't sound like that's the case. Okay, so then I guess there's a lot to be excited about on the obesity space. I want to ask a little bit more about the other drugs in your pipeline, but I want to give you the opportunity. Is there anything we didn't discuss about azelaprag that you think is worth highlighting right now?
No.
We're very thorough today. Great. So then you have your second drug. It's also an oral small molecule, and it targets NLRP3 for obesity potentially, but also for neuroinflammatory conditions. So I guess maybe let's just go through what makes that molecule unique.
Yeah, sure. So again, this is a target the company has been excited about for several years because it's a strong association to outcomes in our human longevity data. It's the opposite of apelin, right? People with more mid-life apelin have better outcomes, and then the opposite is true with NLRP3 activity. Even in people who are otherwise healthy, more activity predicts accelerated cognitive aging and also shorter lifespan. So the things to know about our program is that we, from the beginning, wanted to build something that was highly brain penetrant. So our molecules have close to parity in CNS and periphery, and they're very highly potent. We're distinguished by we have a potential best-in-class potency profile. So as you look at the other molecules out there, that's one of the unique features of ours. And that's really enabled by the fact that we have a different binding site.
We've been collaborating with Matthias Geyer, who's the structural expert on NLRP3 biology. We've characterized that binding site, and knowledge of it has really directly enabled our chemistry. So we are an order of magnitude more potent than the competition. So we're really excited about bringing that forward. As you mentioned, it's a really important neuroinflammatory pathway, also implicated in obesity. So our plan right now, we've given guidance that we'll file IND in the second half of next year. After that, moved into a phase 1 SAD/MAD as well as monotherapy obesity cohort. The other thing to keep in mind is that from the other data we've seen so far, this looks to also be an appetite suppressant mechanism.
So we're particularly excited about that because it might mean that we have an interesting combination within the company if we also see a similar amplification with the azelaprag on an NLRP3 background.
Right, okay. And so maybe we can dive a little bit deeper into the mechanism. How exactly does targeting NLRP3 lead to appetite suppression? And then additionally, then the neuroinflammatory conditions, how can it do both?
Yeah, no, I think that's a great question. I think that's frankly still being worked out. I think some of the initial paper from NodThera came out earlier this year. I think it surprised us, that's for sure. But we've seen that data in the hands of a few independent groups now. It looks quite compelling. What's clear is that you need to have the brain penetration to have the anti-obesity effects, and it seems to be specifically neuroinflammatory mediated. I think we're still working out exactly what's going on beyond that.
Got it, okay. And so for that asset, when I think about neuroinflammatory conditions, are there any that stand out as obvious ones where this mechanism could work? I don't want to put you on the spot to commit to any indications, but if you could just speak broadly about what types of indications this could work for outside obesity.
For sure. So I mean, again, we saw this link with accelerated cognitive aging. So cognitive decline, what measured via sort of standard scores. So that points to a number of different indications and if you look at what the other companies are doing, there are ongoing trials in things like Parkinson's. There will be data readouts that are relevant to how we think about our development. So we are behind a couple. There are two more advanced programs than ours, but we also will learn a lot from their experiments.
How do you make the decision internally? Or maybe you don't have to prioritize, but if you had to choose obesity versus something like Parkinson's, which is also quite a large opportunity, how do you make the decision on which to prioritize first?
I mean, from a development perspective, obesity is very appealing. Parkinson's trials can be very challenging. Obesity weight on a scale is a very easy. It's interesting too, right? Because in some ways, our first drug, azelaprag, is relevant to physical function and to muscle, and if you look at drugs like bimagrumab, those functional endpoints are actually very challenging, but now with a weight loss endpoint, it's a very different development path, so it's just a much cleaner readout. It's very easier to see a signal, definitive signal, early and quickly in an obesity context. Of course, the mechanism is very different, likely in those two different indications, and we're very interested in the brain applications too, but those are just fundamentally more challenging trials.
It isn't a binary question there because we have a pipeline of compounds. So we have both multiple CNS penetrant and multiple peripherally restricted compounds. So there is a lead that we're advancing in GLP-tox studies. But behind that, we could take it ourselves in obesity and then partner it out for neurodegenerative diseases, some other compounds as well.
Yeah, so it could turn into a bit of a pipeline and a product or in a suite of molecules with the same target optimized for.
It's probably important. Yeah.
Yeah, optimized for each of those particular indications.
Yeah.
I'm looking forward to seeing more about that as we move forward. You also mentioned at the very beginning, Kristen, that you have a couple of undisclosed assets in your discovery pipeline. I guess when we're looking forward to the company news disclosures, is there a time period when we can maybe think to learn more about this or?
Yeah, sure. No, it's too early to give specific guidance, but except for the general point that we do continue to advance novel targets from the platform. And we did share that there were two where we're in the molecule building phase. And the targets really share the same key criteria as azelaprag and our NLRP3 asset. So the targets are linked to long-term functional outcomes in large human data sets, right? That's the box that we'd like to check in terms of safety and efficacy. And they will also have applications and metabolic indications because that's what we decided to focus on as a company.
How do you think about leveraging your platform for potential collaborations for companies that maybe want to take a look or if they're interested in a certain type of indication? Is there a way that you could identify a target there rather than going target first? Could you do indication, then do target? I'm just curious on how ubiquitous this could be.
No, that's a really great question because aging is just what we're looking at. That's what our data sets are powered for, for basically lifespan outcomes. And age is a huge risk factor, not for many different diseases, including brain diseases, including diseases that have nothing to do with metabolism. So those discussions are always of interest to us. Of course, we'd like to focus on metabolism at the company because that's already a very broad space. We like to have our expertise and our models in one particular area. But you could certainly orient our platform to particular disease areas and work with a potential partner to bring those targets forward. And that's of interest to the company as well.
Excellent. So maybe to close, we could just recap upcoming catalysts, what we're looking forward to, your cash runway, and just any other closing remarks you really want to highlight on the stage here.
Yeah, for sure. I want to summarize catalysts.
Yeah, so the STRIDES 2 readout is on target for the third quarter of 2025. We've told people we'll start, sorry, STRIDES, STRIDES 2 will start in the first half of 2025 and run through the second half of 2026. That's the semaglutide study. And then the diabetes study will start in 2025 and end in 2025. That's our guidance. We'll also file an IND for the NLRP3 program in the second half of 2025. So that's the key guidance. At the end, for the last Q on a pro forma basis, including the execution of the green shoe, we had $360 million of cash. And that runway guidance is through 2029.
2029.
Yep.
That's quite a healthy runway. Okay, well, thank you so much for being here. I think this was great. We covered a lot, very efficient, and I really appreciate having you both here. Thank you.
Great.
Thank you.
Thank you so much.