... everyone, I'm Sam Semenkow. I'm one of the biotech analysts here at Citi, and it is my pleasure to be hosting BioAge for a fireside chat. I'm joined today by CEO Kristen Fortney and CFO Dov Goldstein. Kristen, Dov, thank you so much for being here. Yeah, thanks for having us. Thank you. Yeah. So why don't we jump right in it then? Why don't you share a little bit of high-level overview of BioAge? Tell us about your proprietary platform, you know, how that's led you to identify a number of interesting targets that could address like a range of diseases in the metabolic space. Yeah, for sure, so broadly, BioAge is focused on understanding mechanisms of aging and metabolic aging from large human populations. Our special sauce is in our platform. We partner with biobanks that have longitudinal human data collected over several decades of aging. We have access to, you know, thousands of individual samples and follow-up records from people around the world, and what we do is we use that data to find pathways and targets that are implicated in healthier aging and healthier metabolism. We really like to see that a target that looks promising preclinically also has a really nice signal in human data that makes us more confident internally about its potential for translation. It was that data set that led us to NLRP3, as well as to APJ, some of the targets that we focus on, and we also have a couple of collaborations, on our platform around target discovery and drug development with Novartis and Lilly. Got it. Helpful overview. So why don't we start with the NLRP3 program? You're developing BGE-102. It's oral, it's CNS-penetrant, and I think obesity is your lead indication. So maybe we just start with what makes your molecule unique. There's a couple other NLRP3s in the clinic, and yours just entered the clinic. Congrats on that. So maybe we start there. Yeah, sure. Happy to. So our molecule, just to focus on the molecule first, what distinguishes it are a few different features. We think it has potential best-in-class properties for a brain-penetrant molecule. The Kp,uu is 1, so you basically achieve similar levels in the brain as in the periphery. And it's also the most potent in terms of inhibiting IL-1β in cells. So we think that profile is really exciting. Scientifically, it's also distinct. We actually just published a paper yesterday with our collaborators in the Journal of Experimental Medicine. We have a novel binding site to NLRP3, which has led us to novel chemistry as well. Can you say a little bit more about that publication? Like, how did you find that novel binding site? You know, was that a part of your proprietary platform? Sure. So our platform led us to the target. And NLRP3, as you mentioned, we're going to pursue initially in obesity for a number of reasons, which we can go into, but it's one of these targets that has potential in multiple different indications. And what we saw in our human data sets was that middle-aged humans with higher NLRP3 levels at midlife were more likely to live shorter lives, and specifically have accelerated cognitive decline, which is why we focused from the initial get-go on molecules that would penetrate to the brain. We started off with a DNA-encoded library approach to get to novel chemical matter, and then working with Matthias Geyer, who's a structural biology expert on NLRP3, we showed that the compounds that we discovered were binding a novel site on NLRP3, and we've continued to characterize those. Got it. Okay, perfect. So then, you know, let's go ahead and talk about the mechanism a little bit and what makes it ideal for obesity. And I'd love also to hear a little bit on some of the other indications that this mechanism could be effective in. Yeah, for sure. So as you mentioned, there's a couple other, two other, brain-penetrant NLRP3 molecules that are going to be evaluated for obesity, Ventyx and NodThera. And it was initially NodThera's preclinical data set from a year and a half ago now, where they showed that if you have an NLRP3 inhibitor that gets to the brain, but not just the periphery, then you could have this very nice monotherapy effect in the DIO mouse model, where you see weight loss on par with semaglutide. And on top of that, you could have additivity on top of an incretin therapy. So it's something that you could, you know, add on top of an incretin drug. And what's particularly exciting to us is that this is an oral small molecule, right? With, you know, GLP-1 in a pill is not going to give you tirzepatide-like weight loss. That's been very clear. So the search is still very much on for combination mechanisms that can give you increased weight loss in a pill. But beyond the weight loss itself, NLRP3, you know, doesn't seem to have any GI side effects so far in the data sets that have been released. So there are advantages to the mechanisms beyond the weight loss itself, as well as the anti-inflammatory effects, which have effects which, you know, could have potential beyond obesity and are relevant to several comorbidities. For example, cardiovascular disease, OA, et cetera. Do we know, what about the inflammatory inhibition, specifically in the CNS, is driving the weight loss component of this mechanism? Yeah, so this data isn't our own, but the theory that's out there and the data, this is mostly from NodThera's work, shows that inflammation in the brain can dysregulate appetite. So this is a mechanism, unlike APJ, for example. It's not an energy expenditure mechanism. When you inhibit NLRP3 in obese, but not in lean animals, you suppress the appetite, and they eat less food. So it's driven by neuroinflammation, and it's related to appetite suppression. Got it. Interesting. So, maybe let's recap what you've shown preclinically, because you have some preclinical mouse data, I believe, for the asset, monotherapy and in combination. Yeah. So we've shown that when you take the standard, diet-induced obesity mouse model, and you treat with this drug as a monotherapy, you do get weight loss on par with semaglutide, so a very potent monotherapy effect in a preclinical model, which historically translates very nicely to the clinic. And additionally, we see very nice additivity on top of an incretin background. So if you add this drug on top of semaglutide in the mice, you do see a doubling of weight loss. So we're pretty excited about the potential there to amplify the weight loss you see with an incretin. And the doubling is in the context of less muscle loss for the NLRP3 specific mechanism? So, I guess, can you characterize a little bit on what that means when you're having maybe less muscle loss for that mechanism versus, you know, a typical GLP-1? Yeah, this mechanism, I would say the jury's still out as to whether it's going to be muscle preserving. I mean, one of our other targets, APJ, that's very clearly related to the mechanism. This is more of an appetite suppressant, so I don't know how differentiated it'll be in terms of the muscle loss, but it does lead to additional weight loss, again, driven by, you know, appetite suppression. Got it. Okay. And then, I guess how does it compare so far on a preclinical basis versus the Ventyx molecule and the NodThera molecule? So pretty similar to what NodThera saw in their original paper, like large monotherapy effect, large combination effect. The Ventyx effect that they published last year was more muted in combination. Okay. But you've said that you're most potent on IL-1β inhibition. Is that known to translate through to humans? Or do you think that you could have a more pronounced effect on weight loss? Yeah, so what we showed preclinically, too, was that the extent of brain penetration was very relevant to the weight loss effect. So the more the compound you got in the brain, the more exposure you got in the brain, the more weight loss there was. So really consistent with the idea that the brain exposure is key. So that's what we've done preclinically. Right, and your ratio of brain to systemic was quite high, yes? Yes, that's right, and the important thing to keep in mind, too, is that the potency translates directly to dose. Mm-hmm. From what we can predict, what we've done preclinically, and we've done the IL-1β, inhibition in primates as well as in mice, we predict a once-daily, below 50 mg dose. Got it. Okay. And so then, you know, you recently started a phase I healthy volunteer study, and we're looking forward to that SAD data, I believe, by the end of this year. Can you walk us through a little bit of that design and maybe talk about what doses we're looking at in the SAD portion? Yeah, sure. It's a standard phase I SAD/MAD design. I don't think we released the particular doses, so I won't mention those, except that, of course, they'll span what we think is the predicted dose in humans. And the important difference from a standard SAD/MAD is that when you're looking at an NLRP3 drug, you can do this very nice whole blood IL-1β, inhibition assay, which lets you choose your dose. So we'll already have that information coming out of our phase I, which dose of this drug inhibits IL-1β at 90%, and that'll let us select the dose that we take forward into our obesity trial next year. Got it. Okay. So then, I guess when we see the data at the end of this year for the SAD portion, what are the key - obviously, safety. Yeah IL-1β, inhibition. What else is there to look for? Those are the big ones: safety and the dose that achieves the 90% inhibition of the target. And you think you can see 90% inhibition with just a single dose? We do. We saw that in primates already. Yeah. Got it. Okay. So then, you know, that'll be the end of this year. So then we'll give you a lot of information and help you inform what you're thinking about for the obesity study, but we also have MAD data in the first half of next year. Is this just more confirmatory in terms of safety, and again, IL-1β, inhibition? That's right. It's mostly confirmatory. It won't be really different in kind. Got it. Okay. So then, tell us about what the design for an obesity study is looking like right now with the, you know, understanding you might be shifting some things based on the clinical data you generate in the next coming quarters. What are you thinking? Yeah, for sure. So this is really a new target for obesity. We think the most important thing to de-risk is the monotherapy potential for obesity. So right after our MAD reads out, we'll go immediately into a three-month monotherapy study, powered to look for a semaglutide-like effect. So we're gonna be initiating the study next year, and it'll read out by the end of next year. So by the end of 2026, we'll have data for, you know, a 50 versus 50 patient design, looking for a semaglutide-like effect. So it's three months of treatment with the dose we'll select from our phase I, with weight loss as the primary endpoint, but looking at inflammatory biomarkers, et cetera, as well. Do you think it's important to test more than one dose in obesity patients? Not necessarily for the target, right? Because the goal here is just to inhibit the target by a certain amount, so that we're planning to take one dose forward. Got it. Okay. I guess, what is the bar for weight loss then, from this, from this obesity study? Yeah, I mean, keeping in mind that we see the biggest value here is something that is additive on top of a semaglutide or, I mean, I shouldn't say semaglutide, an oral GLP therapy, basically, right? So even something smaller could be interesting. But that said, we're really looking for a semaglutide-type effect, like the same type of weight loss you would see with semaglutide at three months. Okay. And how should we... I know this is far off, but when you envision a combination, an all-oral combination, I assume a fixed dose, you know, combination is possible. You know, what is the weight loss goal that you're targeting? Is it tirzepatide-like at the end of the day? Yeah, we think there's a lot of interest in having... And also, this is a, you know, a real goal, too, right? If you could have tirzepatide-like weight loss with a pill, that would be really exciting. Because right now, these are, you know, therapies like orforglipron are likely to be more maintenance therapies as opposed to, you know, your first treatment that really drives that substantial weight loss in year one. But tirzepatide, of course, is multi-mechanism, right? So right now, we're looking at mechanisms like NLRP3, like APJ, that could have tirzepatide-like weight loss together. And I don't want to discount the other benefits as well. I mean, it could be exciting as a monotherapy for maintenance, et cetera. It could be exciting, too, just from the improvements to tolerability, if you can crank up the weight loss while maintaining the tolerability profile. Right, of course. And so what do you think we should be paying attention to the third-party readouts from the other NLRP3 inhibitors in obesity? Yeah, no, we're excited to see the Ventyx monotherapy readout, which should be coming in October. So that'll be, you know, really interesting. And the NodThera readout will be coming towards the middle of next year. And so, you know, outside of the in-class assets as competitors, there are several mechanisms, you know, several other orals. The obesity space is quite, you know, rich with mechanisms and assets. How do you think about competing in that space? I mean, the way that we think about it is that the oral space is still wide open. You know, with injectables, we already achieve very substantial weight loss. There's next generation drugs like amylin, et cetera, coming down. But within the oral space, we still haven't solved that first need, which is the weight loss itself, so we think there's a lot of room for novel mechanisms. Most of them fall into two categories, right? They either inhibit your appetite to suppress your appetite, or they increase your energy expenditure, and there's a few novel mechanisms in both categories that will be going through their clinical paces in the next couple of years. Can I ask you about the safety tolerability? So what would you say, you know, would be a competitive, you know, profile there? I think with orforglipron, that's around 10% discontinuation rates, but that's probably the best, you know, we've seen. There's been a ton that's been in the, you know, 30 +, which almost seems like a non-starter. That's right. Now, these are very much usually a function of, like, sort of tolerability profile for the weight loss, right? So the goal would be to, you know, either have the same extent of weight loss with substantially reduced tolerability, but the 10% isn't that bad. But ideally, the ideal profile would be to amplify the weight loss while maintaining the tolerability profile. Right. And then just given your mechanism, I think Lilly's only gone after, uh, hypertension as beyond diabetes and obesity, maybe other indications, but given the oral convenience, there could be a ton more. Would you be quicker to go after, you know, maybe neuropsych indications or inflammation or a bunch of- there's a bunch of other things that this category can kind of touch. For this target, you mean? Yeah. Yeah, yeah. No, the target has potential in a lot of different indications, so we're going to be following the readouts pretty closely. Novartis will have an osteoarthritis readout, for example, by the end of the year, which we think is a really interesting population because the majority of patients are obese, so there could be additional benefits to a brain-penetrant compound there. Also several comorbidities of obesity, right? So cardiovascular disease, et cetera, is another one that pharma have some interest in for this mechanism. So- Have you done a lot of work preclinically using, you know, looking at non-diabetic or obese populations just to try to tease out maybe an effect? Yeah, we've done some preclinical work, but not shared it yet. Oh, okay. Yeah. Yeah. Sorry about that. I've lost my train of thought. Is there a specific patient segment that you think within the obesity space where, you know, an NLRP3 inhibitor, CNS penetrant, as a monotherapy or in combination, would be best suited? You mentioned maintenance, but are there others? Yeah, I mean, you know, if it's a combo pill, that's really for everybody, you know? But I think what's exciting too is just the benefits beyond the weight loss, right? Weight loss drives inflammation, which drives some of these comorbidities we just talked about, whether it's cardiovascular disease, et cetera. So in those patient segments, the anti-inflammatory effects of the drug may have additional benefits, right? Yeah. At what point do you think it would be helpful, or do you plan to partner this asset? Like, let's say that you see pretty exciting results from the three-month obesity study. Do you need a partner to come in to help you develop it from there, or is this something that you could take through registration? I'm just curious in your thoughts on when you would need somebody to maybe help commercialize. Sure. I mean, that's always a hard question to answer. Sure. Commercialization, certainly you need a partner, right? Ahead of that, you don't necessarily, but there can be advantages to going earlier as well. Yeah. But you could presumably take it into a phase III for obesity. Sure - on your own. We could. Okay. Yeah. But when we think about some of the questions that Jeff was asking about additional indications within obesity, comorbidities, but even outside of that, in some of the neuroinflammatory ones, we have some Parkinson's data for NLRP3. Is there a point where you need some help developing it, or is this something that you're going to take pretty far on your own? Yeah, it's too early to say, and it's certainly going to be indication dependent. Certainly, if we were taking it into phase III for obesity ourselves, you need that three thousand patient database- Mm-hmm ... and there's an opportunity to look into other, you know, related, comorbidities as well. Got it. I think in the past, we've talked about you have some backup molecules in the NLRP3 space. I'm wondering if they are better suited for any indications that maybe not obesity, but maybe others? Yeah, we haven't shared any details on those, but part of the intent is that we do believe this is a target that's going to be efficacious in multiple indications, and we want to have molecules that could address them. Got it. Okay. Anything else that we didn't touch on for NLRP3? I think that's the big stuff. Anything, Dov? No. Yeah. We've been quite thorough, so I'd love to take some time then to speak on your APJ program as well. You are working on a couple alternative oral small molecules, structurally distinct from azelaprag, but you also in-licensed, I believe, a nanobody towards APJ. That's right. Can you just talk through, you know, where you are with that particular target? What's this overall strategy? Yeah, for sure. I mean, the overall strategy is that we believe this mechanism is very complementary to incretins and its ability to amplify weight loss as well as preserve muscle. And as we think about the future of obesity therapy and what that looks like, we're very bullish on orals, and also there's a lot of interest in long-acting injectables. So this strategy really lets us serve both those markets with an APJ agonist. And as you mentioned, we recently announced that we've made good progress with our novel oral small molecules. The goal is to file IND next year. And we also in-licensed a nanobody agonist, which we're pretty excited about too. It was originally developed by Dr. Fei Liu, who first published the crystal structure of APJ, so she's a structural biology expert. And it's a, you know, very highly potent antibody agonist. And for the long-acting piece, would that be for the antibody function, or, or would that be something that you could take the small molecule and make a long-acting small molecule? Oh, that would be for the antibody, yeah. That would be for the antibody. That's right. How long do you think that you could go? I mean, it's so early, I don't want to pin you down- It's super early. ... but like, hypothetically, for a nanobody, like, what are the bounds of what you could do? Yeah, I mean, you know, once a month is reasonable, right? Right. You know. Okay, once a month. Perfect. So then, you know, I guess where does this fit into the obesity landscape? We talked a lot about NLRP3. How do you balance that versus your APJ program? Yeah, so it's another complementary mechanism with a different set of potential benefits, right? So with APJ, we've shown preclinically as well as clinically in an older patient cohort, that the mechanism can preserve muscle, which we think is really exciting in the general population, but especially in the older population, taking weight loss drugs. I think physicians are starting to think more about this too, is that you see people cycle on and off these drugs, which might accelerate the loss of muscle. So we think that's really interesting. I should point out, too, that, you know, we published last year that APJ was additive to weight loss on top of several different mechanisms that suppress appetite. NLRP3 suppresses appetite, so this is also a potential combination we have within the company today. But then there are two, right? There are going to be different comorbidities where APJ is especially high potential, including cardiovascular disease. How large is the elderly obese population? I'm just curious on that patient segment. Yeah. I'm trying to remember because I'm a bit out of date. I think it was something like 20% above 60. Is that right? Yeah. Okay. Yeah. Yeah. It's in that neighborhood. Reasonably sized population. A reasonable segment. Yeah. Okay. And obviously, you know, the older population is also more likely to have some of these comorbidities, particularly with cardiovascular, potentially. That's right. And in older patients, you know, it's not specific to incretins. When they lose weight for any reason, even if they just go on a diet, they tend to lose relatively more muscle, and then when they gain weight, they tend to, you know, gain more fat, right? So these sort of cycles of going on and off drug can have especially, you know, devastating consequences there. Right. And so apelin, though, is well, the mechanism preserves muscle- Yes ... we've seen that in humans. Yeah. You have a human study for that. Are there other mechanisms for the elderly population that you think could do a similar thing that you could be competing against, or is apelin quite unique in what it does? Yeah, not in the oral space, right? There's sort of bimagrumab and myostatin in the injectable space, very nice data sets there. And especially for, you know, older adults at risk of mobility disability, you know, if they don't have a lot of muscle on board, that could be a promising therapeutic direction. But apelin is very differentiated in that it's oral and that it seems to be, you know, the tolerability profile is very different as well. Okay. And when you're looking at the different scaffolds for the APJ agonist, you know, what gives you confidence that these ones aren't going to run into perhaps a similar safety signal that we saw with the azelaprag? Sure. I mean, anytime you do small molecule drug discovery, you can be surprised with liver tox. That's kind of the nature, as opposed to antibody drug discovery. Mm-hmm. But the liver tox that we saw was structure related, so that's why we're focusing on compounds that have no structural similarity, so they won't be failing for the same reason. Okay. And when you said IND for the oral compound next year- Yes ... I guess should we also expect that you could potentially initiate a phase I healthy volunteer study? Would that be the next step from IND filing? Yeah. Following IND filing, we would go into healthy volunteers. Okay. That's right. Would it look very similar to what you're doing now for the NLRP3 asset? Yes, but without the benefit of the ex vivo blood assay. Yeah. Right. No, of course, 'cause that's unnecessary here. Yeah. Okay. And then, you know, I guess as you progress the nanobody, how far away from the clinic is that asset? Yeah, the goal there, too, is also to file IND next year. So they could both be, you know, have some data in the near term. Got it. So you could have three clinical assets, next year? That's what we'd like. Yeah. Okay. Perfect. So things would really start to get exciting then from a data perspective, from the clinic. Okay. So yeah, I guess, you know, what else can you do with your platform? Like, 'cause you have the ability to nominate more targets. I'm sure you already have targets in mind. You know, you're advancing these with three potentially next year in the clinic. When is the right time to start introducing additional mechanisms and assets into your pipeline? Yeah, that's a great question, and we do do a lot of early work, including with partners, so I won't comment on specific targets or timelines given their early stage. But we have a partnership ongoing with Novartis. They're very interested in finding other targets like apelin that can help the exercise mimetics, those that have potential for, you know, metabolic disease, but also for neuro, for example, right? So that's like a collaboration where we're investing in data science to find novel targets from our human data sets. And then we also have a collaboration with Lilly, which is different in kind, where we've selected a couple of targets from our platform that we're really excited about, and they're helping us build molecules. So we do have early work ongoing, and we would disclose that once those molecules or programs got to later stages. It is unique that you have a renewable resource, right, to continue to mine and generate- That's right. That's right. Yeah. No, there's a lot of different targets emerging from the data that we're excited about. Is there like an out-licensing opportunity? I mean, would you take a molecule into preclinical and maybe send out before you...? 'Cause there's been so many deals on Chinese assets for a ton of money. They have some human clinical data, but not a lot, right? Yeah. No, that's right. No, that's interesting, right? It identifies both targets and also potential assets that are out there already, as well as targets that we can work on to develop ourselves. So the benefit of both of these collaborations has been that it really increases our bandwidth, you know, to find promising targets and to build assets, and then there's different strategies we can use to take those forward. It's also not trivial in terms of expense and resources. You have to file IP, tie it up all in a bow before you out-license it, you know? Yeah. I mean, you know, like relative to a clinical trial, the sort of like pre-IND work is not like too large an investment, right? So you want to have some of those in parallel. Yeah. Yeah, makes sense. What is your capacity to do additional partnerships with pharma or even expand the current ones that you have, if that were to be of interest? Yeah, that's something we're always exploring. So yeah, we- we'd be interested in doing that. Okay. So then, you know, I guess we've talked a lot about the future because a lot of your... we've already just gone through the end of 2026. But when you think about BioAge, when you think about into the future, say, five years from now, how do you envision the company looking at that time? Yeah, so as we mentioned, you know, we'll have a meaningful readout for NLRP3 next year in a patient population. We shouldn't be too far behind with having multiple assets in the clinic, and the goal is really to advance, you know, a portfolio of differentiated complementary mechanisms, you know, into phase I, into phase II, that check the boxes, that have a very compelling signal, you know, in our platform. And that are these. I I kind of think of it as the weight loss plus category, right? So, like, there's all these different mechanisms that you can combine with an incretin to do basic things like improve weight loss or improve tolerability, but also to have additional benefits to the particular patient populations, because obesity usually comes with many comorbidities. So we really want to identify and advance multiple different assets. Do you also anticipate, you know, building out things like, you know, manufacturing capabilities? A lot of the maybe supply chain rate limiting things that today, you know, we're playing out in the metabolic space does take some capital to do, but that's sort of anticipating, you know, moving from mid to late-stage clinical trials. Yeah, that's a great question. That's not really our focus right now. We do with the oral focus, it's a little bit simpler than if you have, you know, peptides, but certainly with antibodies, that can get, yeah, expensive. Yeah. Yeah. I think orforglipron is something like 25-30... That's a complicated small molecule. Sure. Yeah. That's a bit unique. Yeah. Yeah, yeah, yeah. Yeah. But you're right- Yeah ... biologics are a little different. Yeah. Yeah. But both your, APJ and your NLRP3 small molecules, they're of the simpler sort from a manufacturing perspective? Yeah. APJ, too early to say, but NLRP3 will not be like, orforglipron. Yeah. Got it. That's fairly unique. Yeah. Okay. I've left you alone, Dov. Maybe I can give you a question. Can you just talk about the financial outlook from the company, a bit about your cash runway, and, you know, how you're thinking about capital allocation over the next several years? Yeah, so the guidance we've provided at the end of the June quarter, we had around $313 million. That provides runway of 3+ years, assuming all the milestones we've taken you through, that runway will come in as we'd go into phase II trials with the assets we've talked about. And so, you know, we're very fortunately capitalized to execute on these three exciting programs that we have, and also be opportunistic if other ones come about, we're interested in. Is the- I know pharma or biotech partnerships are kind of one source of capital and collaboration, but there's also royalty deals. There are some unique, you know, attributes to this market. What's your view of kind of all these, you know, sort of funding sources, assuming that you have some success and you'll have, you know, we have to spend some capital in the next, you know, year to two, to get into mid-stage development? Yeah, I mean, from my seat in the company, it's really about bringing opportunities to the Board to lower the cost of capital for the organization. So, you know, I think of royalty deals traditionally as later stage deals- Yeah ... at least phase II completed. And further, I know those folks quite well. So but that's something we'd definitely you know think about as an option for the company. And like Kristen mentioned, your question about capital allocation for manufacturing, that's not something that we currently think about just 'cause we have simple small molecule solutions to these problems. But you know, in certain political environments, you know, onshoring manufacturing may make sense. Is there a lot of, say, CapEx or capital needed to support the underlying platform and the data and things? Is that investment, you know, pretty much been made, and there's not a lot of maintenance CapEx with it? So that investment has been made, so there is a data set that's in place. As part of the Novartis collaboration, we're making some additional investments in that to increase the number of data points in the data set that we... So, the answer is yes, it's been made, but we're making some additional investments as we speak. But it's incremental, though. I think overall to the... Yeah. Yeah. Yeah, but that's also how we see the pharma collaboration as a source of capital for platform. Yep. Yeah. Yeah, of course. We've been efficient with our time. Kristen, I want to give you the opportunity, though, to just give a quick overview of what you think the investor pitch should be for BioAge. You have a lot of things executing right now. I would love your thoughts on, like, what, you know, why investors should be, you know, interested in you, with you right now versus, you know, maybe a little bit closer to some of these data readouts. Yeah, for sure. I mean, we've captured all the highlights, and I think investors are usually focused on data, right? The near-term data readouts. So we know we're very bullish on NLRP3. We think we have potentially the best brain-penetrant molecule, and there will be a lot of key data readouts, not ours, you know, but key data readouts before the end of the year, as well as de-risking data for ours in terms of the dose and the IL-1β inhibition. So that's not too far away. And the patient data, too, you know, our obesity study is end of next year, so that's sort of been the near-term thing. With APJ-2, I want to say that we still have, you know, the opportunity to be the leader there. It's still very much a novel target. With both of these modalities, we can be in the clinic fairly soon. You've spurred one more question for me. For NLRP3, when we see some of those data sets ahead of yours, and we're thinking about the potential of the mechanism, what should we keep in mind about your molecule, that might not be translated in those data sets in terms of efficacy? What we think about is that, you know, the data set that Ventyx released pre-clinically was not as robust as what, you know, we or NodThera saw, so that's the key difference with the Ventyx program. With the NodThera program, it's really one of dosing. They may need to dose twice a day to achieve efficacy, and this is a once-a-day drug. Got it. Okay. All right. Well, thank you so much, Kristen and Dov. Really appreciate it. This has been a wonderful conversation. Thank you. Thank you both.