Hello, welcome to Oppenheimer's 36th Annual Life Science Conference. I'm Jay Olson, one of the biotech analysts here at Oppenheimer, it's a pleasure to welcome you to our discussion with BioAge. It's an honor to introduce Kristen Fortney, Co-Founder and CEO of BioAge. Thank you so much for joining us here today, Kristen. I'll turn it over to you. Yeah, thanks, Jay. We're thrilled to be here. We have a few other team members. I don't know if they're all visible, but joining, we have BJ Sullivan, Dov Goldstein from the BioAge side, and I'll be happy to start and take you through our presentation. Briefly, at BioAge, we're really focused on harnessing the biology of human aging to develop new therapies for metabolic disease. All of our insights around those targets we believe will be translational, come from the BioAge Discovery Platform, which takes us basically from human data to novel therapeutics for metabolic aging. Our platform is validated by ongoing partnerships we have with Novartis and Lilly to discover drugs as well as drug targets. What it consists of is over 150 million molecular data points. It's really one of the world's largest collections of longitudinal human aging data and functional outcomes. It's basically, you know, molecular information collected over decades of individuals' lives and tied to long-term outcomes like longevity itself, but also, you know, chronic diseases, cardiovascular disease, metabolic disease, et cetera. Our platform forms the basis for our collaborations, but it also forms the basis for those targets that we bet on and develop internally, including our lead program, targeting NLRP3. That'll really be the focus of today's discussion, giving some of the exciting recent clinical data we've had. BGE-102 is an internally developed oral brain-penetrant NLRP3 inhibitor, and broadly, you can think of this mechanism as a potential pipeline in a pill, targeting efficacy in line with injectable anti-inflammatories across multiple different indications. A lot of the focus and the best evidence is around cardiovascular risk. There's a potential here in an oral format to have, you know, really profound CRP reduction, which translate to improved MACE outcomes, and we'll know more about that, of course, with the Novo trial readout later this year. From a CRP reduction perspective, our molecule shows potential best-in-class profile. The figure I'll highlight is that basically, when we announced an initial data set for our ongoing phase I trial in January, showing that people who are obese with elevated CRP at baseline were able to normalize 93% of them back to healthy CRP levels, meaning CRP below two. That's basically best-in-class performance here and compares very well with others. That corresponds to, you know, percent-wise, about an 86% reduction hs-CRP from baseline. Cardiovascular risk is a really important, probably the most important, development direction for this molecule. We recently announced another indication space we're really excited about as well, 'cause again, this is a molecule and a pathway really implicated in many different aging-related diseases, and that's really the ophthalmology space and retinal diseases driven by inflammation. You know, this is there's two different indications that we think are particularly promising here, but we'll walk you through our initial plans to go into DME. We also think this is also promising for geographic atrophy as well. The advantage with DME is that IL-6 has also shown a benefit. It's very much de-risked by some human data, and we can think we can get some exciting clinical data pretty quickly there. This is going to be a catalyst-rich year for BioAge. We're going to have our full phase I data set reading out by the first half of this year. Pretty imminently. That'll consist of additional cohorts that we expose to drug at different doses for a couple of weeks to look at CRP reductions, to really learn basically how IL-1β inhibition translates into CRP. That'll let us pick our dose for the study we run in the second half of this year, which will be a three-month monotherapy exposure to BGE-102 in a larger number of patients, to look at CRP reductions and their durability over time, to get longer-term safety, and also to look at a really rich set of metabolic and inflammatory biomarkers and how they change after longer-term exposure to our drug. We're also initiating our DME trial towards the middle of this year, and that'll read out in the middle of next year. That's our lead program. We have other programs as well at BioAge, we'll touch briefly on APJ agonism, which is another mechanism we're very excited about, that has the potential to be an exercise mimetic for obesity. The company has both oral and injectable programs we're working on here at the preclinical stage, targeting IND later this year, so they'll be clinical before too long. The potential here is for these therapies is to increase weight loss and restore healthy body composition in obese populations when combined with incretins or other appetite-suppressing mechanisms. As I mentioned, the near-term catalyst there is IND submission later this year. This is a longer than 25-minute presentation, so I'll go lightly through some of the initial slides here. Just briefly, right, our whole thesis at BioAge and our platform is focused on understanding what makes some people age a lot better than others, right? There are individuals like the man on the right who live to really healthy old ages, so we know that it's possible in the human context. We know that there are different pathways and different targets that promote health, NLRP3 and APLN being examples. As I mentioned, we have ongoing partnerships with Lilly and with Novartis on the platform, and always, you know, interested in building more there as well. We've got a great and experienced board of directors, as well as an experienced management team driving our progress here. I'm going to dive and spend a lot of time now on NLRP3. Just, you know, overall, I think NLRP3 is known to be related to many different diseases, and also specifically in our human cohort data, it predicts poor human longevity. If you're middle-aged and, you know, not already sick, but you have elevated NLRP3 relative to other people your age, you are predicted to have a shorter lifespan. That was one of the signals that got us really interested in NLRP3 to begin with, and there's very strong human genetic evidence as well from a Mendelian randomization, for example, linked to heart failure with this target. Our program is really differentiated versus the other ones out there. As we mentioned, we think we have a potential, you know, best-in-class profile to address diseases driven by inflammation in both the CNS as well as the periphery. This just highlights some of the key properties of our molecule. We have potential best-in-class potency based on our ongoing phase I trial with an 1.8 nM IC90 in the human Ex Vivo whole blood stimulation assay. We've shown that we can get 24-hour IC90 coverage at 60 mg once a day in humans, where we're suppressing IL-1β over 90%. Again, the real headliner is that we were able to normalize nearly everybody back to healthy CRP levels after a couple of weeks on drug. Our drug is very highly CNS penetrant, the most highly penetrant shown to date in human populations with a 0.7 Kp,uu CSF, has an attractive safety and tolerability profile. All AEs observed to date are mild to moderate, self-limited, with no dose dependency. Coming out of our one-month tox, we have great margins, safety margins of 40-90 fold at the 60 mg dose. Importantly, too, in that initial study, the NOAEL was the highest dose we tested, meaning we have so far in that study observed no dose-limiting toxicity. Importantly, too, we have a very strong IP position. I'll go into this in the next slide, but we have 2045 composition of matter, and in our granted patents, we also have claims for other molecules that bind to our binding site. We've described a novel binding site to NLRP3 with that should have certain advantages and also really enabled our chemistry as well. Just briefly, we've shown that we have a novel binding site to NLRP3 with our molecules and a novel mechanism as well. We were the first to describe this binding site, and we published the crystal structure last summer. If you look on the bottom right of this page, there's actually three papers that we put out over the last year and a half or so on our chemicals, our mechanism, and our crystal structure. If you look on the left here, you see basically a cartoon showing where the other molecules bind in that purple site versus where our molecules bind in that green site to NLRP3. There's a few important differences between our site and the other one, but one of the ones I'll highlight now is that there's, you know, different forms of NLRP3. There's an active form as well as an inactive form. The purple binding site, where other molecules bind, is only available in the inactive confirmation of NLRP3, whereas our binding site is always available, which could translate into efficacy benefits. Jumping now into the phase I update. We kicked off this study a few months ago, right in the middle of it right now. This is sort of showing you the study as a whole, the design, single ascending dose in healthy volunteer and obese, multiple ascending dose in healthy volunteer and obese. Where we are today, right in the middle of multiple ascending dose in obese cohorts with elevated CRP at baseline. We've completed already, you know, several single doses in people. We announced our initial data set in December, which basically consisted of the healthy portion of the trial. Right now, we're going to be doing three cohorts at three different doses, where we're giving our drug to people who have elevated CRP at baseline. One of the really exciting data points from the Ventyx readout back in October, was how quickly CRP could change in this population, right? When we saw that, we really went back and redesigned our trial because we thought we can basically do dose ranging right in the phase I and see how dose translates into CRP reduction in the patient population immediately. The highlights so far, it's got a great profile to date. From a safety perspective, very well tolerated, with all mild and moderate self-limited AEs. From a PK perspective, nice dose, proportional exposure, once-a-day dosing. From a PD perspective, as we mentioned as well, very potent suppression of IL-1β. In fact, at the 120 mg once-a-day dose, we can fully suppress IL-1β, which is a differentiating feature of our compound versus others. We can also achieve drug levels in the CSF exceeding the IC90. Finally, from an efficacy perspective, potential best-in-class profile here as well. I'll take you briefly through the healthy results. Again, nice dose proportionality in our SAD cohorts here as we go from 10 to 30 to 61 up to 120 mg. Here, if you look at 14-day dosing, you can see that both the 60 mg dose once a day, that's the purple line, as well as the 120 mg dose once a day, when given over 14 days, you know, well exceed the IC90 for the target for IL-1β in the whole blood stimulation assay. That's the dotted line here at the bottom. This is looking in the periphery. If we look now in the CSF as well, we can see that that's also true in the CSF. We're just over the IC90, 60 mg dose once a day, and several fold over it at the 120 mg dose once a day in the CSF. In an NLRP3 trial, it's great because you can also look at PD with this Ex Vivo whole blood assay. Like, these are healthy individuals, but you can take a blood sample, you can give it an inflammatory stimulus, and then see how much you can knock down IL-1β. As you can see here, the 60 mg dose once a day is already knocking down IL-1β 90%. This is looking at day 14 trough. At the 120 mg dose, we're basically completely turning it off. It's 98% knockdown, consistent with, you know, full lockdown, basically, of IL-1β. We don't know if that's necessary for therapeutic efficacy, but we know that we have the flexibility to go there, and also to be safe from what we've seen so far. This is just showing you that, you know, that last figure was at trough. You actually are knocking down the target over a full 24-hour period by day 14. If you look here, we're looking at, you know, every few hours, and you can see that IL-1β is basically fully turned off. I'll go now into the obese MAD cohort, the first of the three that we'll be reporting on. Again, the design here is very simple. The goal was to really get to a patient population very similar to the one that Ventyx used in their three-month trial that read out a few months ago, and where they saw some very nice results. Here, these are individuals who, at baseline, are obese with a BMI above 32, CRP above three, and no incretin treatment for 90 days, and they received our drug once a day for a couple of weeks. This is the most, meaningful result right here. Like, basically, as a brief reminder, you know, in the CANTOS trial, with IL-1β inhibition, where they saw these really profound MACE benefits, the critical threshold was you had to get patients below CRP levels of two, and then you see a 25% sort of MACE improvement, right? If that's sort of the critical threshold for patients, we're asking how many people who have elevated CRP can we correct to a CRP level below two? That's basically shown here in the light blue. By day 14, nearly everybody, 93% of individuals out of 13 or 14 treated patients, are restored. Most of those changes already happened by week one. As you can see here, it's 86% of patients were already there by week one. If you look at the dark blue lines, here we're looking at how many patients actually had their CRP corrected to below one. CRP below two means, you know, normal. CRP below one means you're actually protected, you know, from cardiovascular outcomes. As you can see, a majority of patients are, you know, actually in that protected bucket. We're really excited by these data. On a raw percentage basis, this corresponds to basically an 86% reduction in CRP versus baseline. At, you know, at baseline, basically in our cohort, the median CRP was around five. It's basically 4.85, and we're knocking it down by 86% already in a couple of weeks. Consistent with what others have shown with this mechanism, we see about a 50% reduction in IL-6 and a 30% reduction in fibrinogen at day 14 as well. This is an important figure, too. Our drug is brain penetrant, right? We're really hoping to see some brain PD. These individuals in our study didn't necessarily have inflammation in the brain, but we were fortunate when we looked into the, you know, the 14 people enrolled in this experiment, to see that two of them had elevated IL-6 in the CSF. The threshold there is they have to have their baseline IL-6 above seven. As you can see, these individuals, there's sort of two of them right there. Really interestingly, we actually reduced the IL-6 levels in the CSF by 84% in those individuals. Really profound reduction. We believe this is really driven by brain IL-6, not peripheral IL-6, because if you look on the right, those same individuals had much lower IL-6 levels in the plasma. It's not like the plasma leaking through to the brain, this local brain IL-6 that's being impacted by the mechanism. Finally, here, too, we looked at trough, IL-1β suppression, and again, you're turning that down by 93%. Really potent suppression of IL-1β in these patients. There's a number of therapeutic areas you can take this forward to, right? A lot of the focus right now is around cardiovascular. You know, there's a lot of related areas, too. People are looking at, like, MASH and insulin resistance. You know, our focus internally on development will really be focused on cardiovascular, but also ocular, and we'll speak a little bit more to that. Actually, given the time, I won't tell you too much about the cardiovascular side, 'cause I think most people are familiar with that, except to sort of mention, again, right, like CRP is a really meaningful biomarker for cardiovascular risk reduction. In fact, it's more predictive of MACE outcomes than LDL or Lp(a). There's really a lot of potential here. That's shown here on the left. Again, on the right, you know, just to get across the point that normalizing CRP, getting it below two, that is the sort of critical threshold that translates into a 25% reduction in MACE. That is, you know, a really meaningful for patients, that we can get most of our, you know, nearly everybody, back below that threshold. Yeah. The goal here, of course, right, is that everyone is very excited right now about IL-6 injectables for cardiovascular disease, and we're gonna have some, you know, imminent readouts there. Of course, the promise here is that this could be, you know, similar efficacy, potentially better efficacy, but in an oral format. I'm just gonna skip beyond some of this right here. Briefly, of course, there's a number of advantages to orals, right? Like, one of the ones I want to emphasize is there is the potential for fixed-dose combinations with other cardiovascular risk mechanisms, whether it's -1, whether it's PCSK9, right? there are independent contributors to cardiovascular risk, to MACE outcomes. what's exciting about having a, you know, a multi pill or a poly pill that addresses several of those at once. this is the trial that we're gonna be kicking off soon, that will read out by the end of the year. It's really, you know, quite similar in design to the Ventyx one that read out in October, where we're giving our drug to, you know, 50 patients on BGE-102 at a particular dose. what we're doing right now is just picking that dose empirically, you know, in our CRP experiments, versus 50 patients on placebo. That again, will be obese with elevated CRP at baseline. the primary endpoint, of course, will be CRP, existing reductions in CRP over time, learn about safety. We're also gonna have a much richer set of biomarkers and endpoints from an inflammatory and metabolic perspective, not everything changes as rapidly as does CRP. We'll look at additional CV risk factors like Lp(a), fibrinogen, IL-6. We'll look at MRI imaging of the liver, specifically metabolic parameters, et cetera, and we'll have this full, rich data set by the end of the year. That's the major focus for the cardiovascular area. You know, BJ will really speak to the opportunity in the eye here. Again, this is a molecule and a mechanism with multiple different indications, and we were really excited to pick a second one that took advantage that basically satisfied a few criteria. We wanted to take advantage of the fact that our drug is not just peripherally restricted, it also gets into the brain, gets into the eye. There's a lot of potential, so it's a unique feature of our molecule we want to take advantage of. There's a lot of indications there, too, that have been de-risked by IL-6 already, so it's a really compelling thesis there. Yeah, BJ will speak to that. All right. Thanks, Kristen. Just to start, I want to frame the retinal opportunity for BGE-102. First and foremost, it's very exciting, the prospect of having another mechanism to address retinal diseases. A lot of the indications that we're looking at, they're really dominated by therapies that are going after a single target. They're very saturated, you know, around a single mechanism of action, we think it's really meaningful to be able to bring forward, you know, an anti-inflammatory, you know, for a variety of these retinal indications. The second key feature here is really lowering the patient burden. The prospect of having an oral is really meaningful for patients, where, you know, right now, the standard of care is, you know, up to monthly injections, sometimes in both eyes. You know, that leads to non-compliance and real-world treatment outcomes that really lag what we see in clinical trials. Really meaningful for patients to have an oral option, you know, and part and parcel of that is the ability to treat, you know, bilateral disease simultaneously. You know, you take a pill, you know, you're treating both the systemic risk factors as well as both eyes. You know, in the case of geographic atrophy, patients have to come in typically on separate visits, to inject either eye. If your both eyes are affected, you know, you're going in up to twice a month, you know, for therapy, and so you can imagine the burden this puts on patients, right? Lastly, you know, we don't think of the oral as just a convenient way to access the retina. You know, we think, you know, in all of the indications that we're looking at, there are also systemic benefits of therapy. In thinking about DME, where hyperglycemia is the key risk factor, there's strong data to support NLRP3 inhibition, improving insulin resistance. Similarly, in geographic atrophy, systemic inflammation is a key risk factor and prognostic marker, and I think we've demonstrated here we have the ability to address that key systemic risk factor. That's a value proposition that I think is really resonates with physicians and it's important for patients as well. Of course, BGE-102 is shown therapeutic retinal exposures across a range of preclinical species, you know, including primates. We can walk through some of the preclinical data that really supports this ability to get really strong efficacy in the retina with oral administration. Next slide. NLRP3 really sits at the, you know, the crux of the nexus of the disease biology in both DME and GA. The triggers are different in either case. In DME, it's really hyperglycemia and oxidative stress that trigger inflammasome activation. In geographic atrophy, you can think of it almost like a, one of the neurodegenerative diseases, where you get an accumulation of cellular debris, like drusen and lipofuscin and these Alu RNA, this toxic RNA, they build up and trigger the inflammasome. You know, regardless, NLRP3 is activated in both cases. In DME, what you have is a release of secreted factors like cytokines, like IL-6, VEGF, both contribute to vascular leakage and vision loss. You also have pyroptosis, so this inflammatory cell death that happens in endothelial cells that also contributes to that, you know, disease process. Like Kristen mentioned, we were excited about the, you know, the efficacy signals that have been observed with programs targeting both VEGF and IL-6 as sort of a motivation here and, you know, broadly de-risking the concept of using an anti-inflammatory approach in DME. What I would point out is IL-6 is only one part of the potential benefits of NLRP3 inhibition. You know, again, we think of it as a motivation, but not necessarily the benchmark for what we would ultimately hope to see in terms of, you know, clinical performance. Next slide. I will go through this quickly, but just to say that DME and GA are both highly prevalent, you know, diseases. They're again, really dominated by one modality. In DME, it's VEGF, in geographic atrophy, it's complement inhibitors. The unmet needs, you know, for DME are reduced injection burden. Again, real-world treatment outcomes lag, you know, what we see in trials because of non-compliance. I mean, which makes sense if you're having to go in every month for eye injections, it's both a burden and unpleasant. That's a major unmet need, and there's a significant refractory population of over 40% of patients who are either non-responders or suboptimal responders to VEGF. On the geographic atrophy side, really, there's a great need for new therapies, right? Complement inhibitors are approved, but they have pretty modest efficacy, just a new therapy, regardless of MOA, is really meaningful. That's really reflected here, some of the key statistics in terms of, you know, quantifying and capturing, you know, the unmet needs across these two indications. Next slide. To talk about our motivation here, you know, there are several IL-6 programs, you know, conjugating with VEGF to, you know, to improve treatment outcomes in DME specifically. These programs have shown improvements in both BCVA, so best-corrected visual acuity, as well as CST in a short period of time. What this enables for us is the ability to demonstrate proof of principle for really retinal exposure and pharmacodynamics, as well as sort of a proof of concept in DME in a short period of time, right? This sort of tees up the study we'll be introducing in just a few slides. This is the sort of our key preclinical data in DME. This is a streptozotocin mouse model, which has profound hyperglycemia, and this shows the BGE-102 delivered orally as a monotherapy. If you look at the left-hand side, this is really the macro picture of retinal vascular permeability. You can see this is fluorescein angiography, and you get this white haze in the streptozotocin mouse there, and that just reflects leakage of the dye into the eye, right? You see really nice dose-dependent correction back to healthy controls with one or two monotherapy. If you zoom in on the right, this is looking at the integrity of the microvasculature in the retina. What we're staining for here is claudin-5, an endothelial cell tight junction marker, which is significantly reduced in the streptozotocin mice and corrected with 102 monotherapy. If you look at the big picture, as well as sort of the microvascular integrity, you're seeing a, you know, a really nice, you know, monotherapy efficacy for 102. Next slide. And this is, these are results from actually a diet-induced obese mouse model, so not streptozotocin, showing an improvement in HOMA-IR, so insulin resistance, with 102 monotherapy that is in line with semaglutide. This is, again, to support the idea that, you know, we can treat both the retinal inflammation as well as, you know, the critical systemic risk factor. This is totally in line with NLRP3 knockout mice and which show a similar phenotype. Just, you know, and here to introduce our proof of concept trial that we'll be initiating in the middle of this year and reading out in the middle of next year. It's going to be three arms. With the first two arms, you can think of this as essentially, looking at the same, the same setup as some of the IL-6 VEGF bispecific assets, looking at VEGF with placebo and VEGF and 102. We'll be, again, looking at VEGF and the anti-inflammatory to look for those, you know, acute changes. We'll also be looking at a sham 102 arm to see, you know, whether one or two has monotherapy efficacy, you know, as we've seen in some of our preclinical models. The key goal here is to demonstrate a pharmacodynamic effect in the eye. We'll be doing aqueous taps and looking at inflammatory biomarkers like IL-6. That's the primary objective of the study. We will also be looking at, you know, BCVA, CST, and, you know, and other measurements on an exploratory basis, and certainly looking for directional changes that are consistent with the biomarkers that we're looking at. That's the trial, and, you know, again, we'll be initiating that in the middle of this year. I'll turn it back to Kristen in just our last minute to maybe recap the upcoming catalysts and, you know, give a portfolio highlights. Yeah, thanks, BJ. Yeah, the focus, of course, today was all about NLRP3. We have four things going on as well, and this final slide really summarizes the whole pipeline overview and the milestones coming up. As a brief reminder, we have really a lot of exciting milestones for 102 coming up. Our full phase I data release will be in the first half of this year, including the sort of the CRP readouts at multiple doses in obese and inflamed cohorts, so that's coming soon. By the end of the year, we'll already have our three-month monotherapy look at BGE-102 in a patient population, how it impacts CRP, but also other critical biomarkers. Then, in the first half of next year, towards the middle of next year, we'll have this DME readout that we're really excited about. It'll enable development, as BJ mentioned, in DME, but also in geographic atrophy, once we've confirmed the drug gets into the eye and has efficacy there when it's on its pathway. APJ, we didn't touch on today with time restrictions, but we are really excited about this target as well and are on track to file IND for both an oral and injectable program for this year by the end of the year. As we mentioned as well, at earlier stages, we have from our platform collaborations with Lilly and with Novartis on multiple novel targets that have potential, you know, a signal for human aging and potential to address metabolic disease. That's together with a strong cash balance as well, and we'll end there. Yeah. Thank you. All right. Well, thank you, Kristen and BJ, for bringing us up to speed on the impressive work that you're doing at BioAge. Hopefully, we have time for a couple quick questions. Congrats on the really impressive hs-CRP data that you've shared. Really, really nice outcome. I guess as investors look ahead to the full phase I data, this half, how would you want to frame expectations for the full data, especially since you have longer follow-up and you've got patients at higher doses? I guess, how do you want to set expectations for investors looking forward to that data? Yeah, for sure. The phase I now is really around dose selection, right? We'll sort of see which dose we want to carry forward into that three-month experience, and then we'll learn about really the durability of the CRP response, which we would expect to persist. That's what we've seen with other, you know, in other hands with similar mechanisms. What you see at week one generally you know, continues on to month three, but you do want to de-risk that. It's important and informative, too, from a safety perspective. Also, there's a lot of, you know, very interesting biomarkers that change that are relevant to cardiovascular disease and more broadly, that do take longer to change than does CRP, so they'll really only emerge after a three-month trial. Like we thought the liver inflammation signal, for example, that came out of the Ventyx data was really interesting, so MRI imaging is an important part of what we're looking at, as well as just sort of like a longer set of cardiovascular-relevant biomarkers. This, you know, NLRP3 is upstream of IL-6, but also IL-18, right? Like, there's all this, which is an independent risk factor for cardiovascular disease, so there's really a lot that we can learn from the three-month trial as well. Good. Great, thank you for that, and maybe just one last really quick question. A lot of investors ask us about potential read-across from Novo's ZEUS outcomes data for its IL-6 program. I guess, how are you guys thinking about that, especially in terms of potentially, streamlining future registrational studies for the NLRP3 class? Do you think hs-CRP could eventually be, utilized as a surrogate biomarker for accelerated approval? That would be great. I mean, I think we'll certainly learn a lot more about how CRP translates into MACE outcomes. Like, we've already seen that for CANTOS, right? You know, so with the IL-1β mechanism, which is really directly downstream of NLRP3, so that's kind of, you know, already de-risked very much by CANTOS. This will be, like, more, you know, separate evidence for another related pathway, that those CRP reductions really do translate into outcomes benefits. That'll be, you know, very meaningful for us and for the field, and we're looking forward to that readout. Okay. All right, well, we'll look forward to that, and we'll wrap things up there. Thank you all so much, Kristen, BJ, Dov. Really appreciate your sharing your time with us today, and also, it's great timing, coming on the heels of our initiation. In case anyone out there missed it, we just initiated coverage with an outperform rating and $60 price target for BioAge. Super excited about all the progress you're making in NLRP3, and thank you again for joining us here today. Thanks very much, Jay. Thank you for having us. Our pleasure. Thanks, everybody.