BioAge Labs, Inc. (BIOA) September 9, 2026 Conference Transcript

Good morning. I'm Sam Semico, one of the senior biotech analysts here at Citi, and it is my pleasure to be hosting BioAge at Citi's 2026 Biopharma Back to School Summit. I'm joined by Kristen Fortney, CEO, and Dove Goldstein, CFO of BioAge. Kristen and Dove, thank you so much for being here and welcome.

Thank you.

So why don't we just start off? It's been an eventful year for BioAge. I think we started off, you know, with a lot of highs for NLRP3 and recently we've had some news. So why don't we just stop broadly, like level setting on the NLRP landscape and also where BioAge sits today?

Yeah, for sure. No, as you said, it's been a super eventful year for us and for the target. So, you know, when the year started in January, we were in the middle of our phase one. We published the full. Oh, am I not on?

Do I need that for the webcast? Yeah, I'm on.

Is that better? Yeah. Okay, cool. Yeah, when we started the year, we were in the middle of phase one with BGE-102, our lead program. In April, we released the full data set showing we have a potential best-in-class inhibitor with, again, potential best-in-class brain penetration, full suppression of IL-1 beta, and also CRP results, which is relevant to multiple different indications. Um, and then we started two different trials, um, one in an obese inflamed population of phase two. And as we announced just yesterday, a phase two in a diabetic macular edema trial. So we've got two parallel indications going on. So we're really excited about that. Of course, for the target, there was the setback a month ago, and I'm sure we'll talk about that. Uh, well, it's not, it's not a setback for the target, but the, the IL-6 setback and the, the way that people are, you know, thinking about, um, cardiovascular, uh, outcomes trial in particular for this target is of course a riskier proposition. Um, but there's still a lot of potential that we're excited about.

Yeah.

And by the end of the year too, we're, we're still on track to, to file IND for, for April and as well. So it's a good year for us.

Yeah. So we're going to dive into all of that. So maybe we do start with the ASCVT, ASCVD opportunity, um, and just maybe just help us frame how we should be thinking about NLRP3 going forward, given the IL-6 failure from Zeus and then the two other studies that were halted for that particular asset as well. And I think, you know, one of the major questions is we thought that the translatability of maybe CRP reduction and IL-6 reduction would translate to reduction in cardiovascular risk factors, and that didn't seem to be the case. So when we think about the landscape for NLRP3, where does that leave us, and how confident are we that this can be a target in ASCBD?

Yeah, for sure. So of course, the Zeus news from Novo just over a month ago, a huge disappointment, right? Really, really unfortunate to see that, especially for patients. And as you mentioned, right, that Novo did indicate that they saw CRP reductions on par with what they were expecting. So we're assuming somewhere in the 80% range, but that failed to translate into MACE outcomes, at least in this patient population, right? So that's really unfortunate. And there's still two potential explanations for what's going on, you know, and those won't be resolved really until we have additional data. There's, of course, hopefully more data from NOVO coming in November, and then the other trial that they have next year, the Artemis trial will read out in the first half of next year. But the two explanations, as people are aware, is that is it a target problem or is it a patient population problem? because, of course, the inflammation hypothesis is partly anchored by some very robust data in the Cantos trial, where an IL-1 beta antibody drew very profound reductions in MACE. And as a function of CRP, the biomarker that you mentioned, right? So amongst those people who normalized their CRP, they saw a 25% MACE benefit, which is super meaningful to patients. So it was really disappointing to see a hazard ratio of basically one with IL-6, right? And the two things to be aware of, um, that I think, you know, are being discussed right now is one that the Zeus trial population was a lot sicker, uh, than the Cantos patient population. So these people have, you know, profound kidney disease. There could be a lot of events that are not related to cardiovascular inflammation that could make, you know, make it challenging for this mechanism to shine. And that's why everyone is still looking to the Artemis trial reading out in the first half of next year, which is IL-6, but taken to a very Cantos-like patient population. Um, but the second explanation is that this might be the wrong target, right? We don't really know yet. Because again, what worked before was IL-1 beta. IL-6, while it reduces CRP, does not affect IL-1 beta at all, right? Of course, that's different for NLRP3, right? So IL-1 beta is already validated in this population. And the entire target engagement biomarker for NLRP3 is IL-1 beta. And we showed in our phase one that doses of our drug could fully inhibit IL-1 beta. So there's still, so it's really like a quite a different proposition. But, you know, the unfortunate thing, right, is that CRP didn't mean what it used to. Before, we were hoping even, no one ever thought it was a causal biomarker, right? But we were hoping that across patient populations, lower CRP would mean improved MACE outcomes. And that's not true. It's not enough by itself. It might depend on the, be a combination of the biomarker with the patient population or with a particular target like IL-1 beta, but it's just more uncertain.

And you mentioned that you can get that full IL-1 beta with your drug. You've seen that in, I think, your phase one healthy volunteers and your obese patients so far that you have data for. I mean, how should we think, so you're already reaching the max that you need to be cantos-like, but your gut better safety on, you know, infection risk, you know, how do you reconcile that?

Yeah. So there's different pathways that can turn on IL-1 beta and what you want in your ideal profile is you want to turn off the bad constant background, you know, inflammation that's turned up too high, which we believe is through NLRP3, but you still want to, if an infection comes along, be responsive, you know, to that infection. Because of course, CRP, you know, the inflammatory response can be very useful too. It's not universally a bad actor. So what's nice about NLRP3 is that you're turning off the NLRP3 dependent IL-1 beta, but the rest of your, there are parallel inflammasomes that should be responsive to infection. So there's a potential for a safety advantage over an IL-1 beta.

Right. Okay. And so then, I mean, we have the canto's data we know that there was a stat sig mace reduction with an nrp3 doing the same thing like you know how where's your confidence then that nrp3 could still work in ascbd and how do we move forward to get confident enough to run a large study that would be required to show it yeah no that's a great question right and part of the challenge here is just that it's it's large and long like uniquely large and long right it's not one of those phase twos that you can run in a year for 20 million, it's 500 million of spend, five, six year massive outcomes trial.

So I think strategics are openly still bullish on NLRP3, right? Novo, AstraZeneca, they say, oh, we might have to go upstream. NLRP3 is promising. But, you know, it's a big bet to make, especially for biotech, right? But I mean, that really relates to the rest of the story and for our focus at BioAge, because the focus, of course, has been on ASCVD for a few months. Because of this Zeus-Rito we were all so excited about, but this is not a target that is relevant to only one narrow disease indication, right? Like there are a whole number of different indications that are de-risked with human, either IL-1 beta or IL-6, depending on the indications. There's a lot of other places to take it. And I think that that, you know, for us as a smaller company, we want to have, we want to be ready, right? In case Artemis reads positive, in case things shift in our favor for ASCVD to like move quickly, but, but that's really, you know, upside now, right? Like we really want to focus on these opportunities that we as a small biotech can move forward that are also really big and exciting.

Right. And we're, we're definitely going to dive into the ophthalmology piece and beyond as well, but just, just really quickly before we go there for the Quell CV study that's ongoing, we're going to have data before the end of the year. You know, what can we take from that? What should we be looking for in that? Because, you know, it seems like more external factors are driving some of the next steps there, but mechanistically, I think there's probably something we can learn from this study. So what should we be looking for when the data reads out?

Yeah, for sure. So a quality CV study, and we announced as part of our oracular press release yesterday that that one's fully enrolled on track for top line by end of year. So as a reminder, that's actually not in a cardiovascular disease population. That's a lot broader than that. So it's really closer to our phase one obese inflamed cohort. So these are people who are overweight, who have elevated CRP. And that means that they're really helpful to look at a host of different markers that are relevant in a variety of different contexts, right? Like for example, we're looking at liver inflammation with MRI because Ventix saw some really promising data there, right? Like there's a whole host of other markers and diseases that are relevant in these patients. NLRP3 has relevance in other metabolic indications beyond the cardiovascular one. So I think we're going to learn about frankly, all of those from the biomarkers that we look at in this patient population that's at risk for numerous different metabolic diseases. Cardiovascular is one of them and a big one, but not the only one. And importantly, too, it's going to be relevant for dose selection for really any peripheral indication we take forward. Right. So as a brief reminder, in QAL-CV, we're looking at three different doses of our drug, 30, 60 or 90 megs once a day. And we're looking at, you know, every biomarker you can think of, which is you know um cardio of course but but it's a lot broader than that um but but and as a reminder too right in our the reason why we're doing these three dose levels is because in our phase one data we couldn't really distinguish between the two top doses like 60 milligrams once a day might already sort of max out all the inflammatory biomarkers and we're going to learn that from this study and it'll really let us um bring us you know select a single dose that will then carry forward into our other indications, other peripheral indications that we're excited about.

Got it. Okay. Well, looking forward to that and maybe some additional indications from that data set in the future. So, okay. Maybe we spend a good bit of time then next on ophthalmology. As you said, you initiated or you announced that you dosed the first patient in the Quell DME trial. Just maybe level set for us. You're the only one that I'm aware of going into ophthalmology with NLRB3, just what is the rationale here for this mechanism to work?

Yeah, for sure. So this is a unique feature of our molecule too, which is that as an oral agent, it penetrates the eye really well, right? Which is, you know, can come along with brain penetration, the blood brain barrier and the blood retina barrier are not dissimilar. But we, you know, we don't know if others are even positioned to go there, should they choose to. But we're really exciting indication is that there is already human de-risking data with IL-6. So unlike in cardiovascular disease, IL-6 significantly improves what is the approvable endpoint in that indication, like it improves BCVA. And Roche and Kodiak have bispecific programs with VEGF and with IL-6 that they're taking forward. And we really see as IL-6 as more of a potential floor when you think about all the things that NLRP3 is doing. It has the potential additionally to suppress pyroptosis, you know, to have other additions. There's even like a VEGF drying effect preclinically. So we can see full correction basically of the DME deficits and preclinical models. So we're really excited to bring that to patients. And of course, that's even ignoring the fact that this is a pill, right? Like typically these patients, it's an injection into your eye. So they don't even start treatment until they're quite severe because patients don't want an injection into their eye. So there's that whole sort of early patient population that isn't addressed at all. There's a number of them that aren't VEGF responders as well, right, where another mechanism can make sense. So we're really excited about the potential there. And as a final point too, I'll mention that DME happens in the context of diabetes, right? And pre-clinically, there's evidence that NLRP3 inhibitors can have numerous benefits in diabetic animals. We're waiting for more data from Noddera to see what they saw in patients as well. But so the body is not just like a convenient way to get to your eyes. There could be benefits there as well in the diabetes that is really driving the DME.

Are you looking for that in the study, the more systemic effects? Look at peripheral biomarkers as well. Yes. And does that include, I guess, you know, glucose tolerance and things like those?

No, well, all the usual, just biomarkers, not like specific sort of challenge tests, but biomarkers. Yeah.

Okay. Okay. So you'll get a, I guess, early feel for potentially what impact you could have in a broad diabetic population.

Yeah. Additional benefits that could be relevant to the eye. Yeah. As well. Yeah.

And then, you know, going back to IL-6 in the eye, when you talked about the validation that we've seen from there, when you think about the IL-6 reduction you get from BGE-102, is that on par with the dedicated agents or is it like a little bit less of an IL-6 reduction plus some other, you know, benefits of like, how do you delineate like the IL-6 specific effects of 102 versus some of the other effects that it's possibly having?

Yeah, for sure. So basically our NLB3 inhibitor, like others, reduces IL-6 by about 50% peripherally. We would expect a similar amount in the eye. That's about, you know, comparable to what we saw in the brain as well when you looked in the CSF. Um, so it's not like a full ablation of IL-6, but again, this is one of many inflammatory cytokines that are relevant in NLRP, uh, in DME. So we think it's important to go upstream and hit all of those, um, as opposed to like IL-6 being a special cytokine there.

And we've seen, you know, some difficulty in some of these trials with agents in combo with VEGFs trying to improve upon VEGF monotherapy. I guess, how do you think about, you know, of that dynamic? And what gives you confidence that NLRP3 inhibition and combo can perform better than VEGF monotherapy? I think we've all recognized that VEGF is a very effective target.

No, part of that is the data we've already discussed, right? Like there already is a significant improvement when you add IL-6 on top of VEGF. And then of course, there's also this huge patient segment that doesn't get VEGF because they're not ready for eye injections yet, right? Where a monotherapy oral that has a significant effect would be very meaningful. So both of those are exciting opportunities for us.

Is the study designed to test both combo and monotherapy for 102? Maybe just walk us a little bit through the design.

Yeah, for sure. So this is, as we announced, you know, when we've been, the last time we spoke about this, we were probably thinking about it as a biomarker trial, right? So it's a true efficacy phase two now, about 180 patients. There's patients who are getting our drug alone. There are patients who are getting VEGF alone, and then those patients getting the combination. So we're going to basically be able to learn about all of those in the same study. And the primary endpoint is BCVA, where we have good power to see a clinically meaningful difference.

And is this population on the more severe side, more typical DMA population, not the earlier stage that you were alluding to as that's a potential future population?

Yeah, it's a typical phase two DMA design. So it'll include both naive patients as well as ones who've had, you know, experience with VEGF and who have washed out. Yeah. Okay.

Um, and so then, yeah, so I guess, what do you need to see just, you know, improvement on PCBA? I'm sure that there's a statistical and remind me what, how many, how many letters do you generally have to gain to make it clinically?

Yeah. And that's, what's been shown with the IL-6 as well.

Yeah. Okay. Got it. So if you have that in any of your, you know, monotherapy and or combo arms, that's enough for you to want to move this forward.

That's right. No, that'd be really exciting. So that data is going to come before the end of next year. We could potentially go into a pivotal trial after that, right? This is the clinically relevant endpoint. So that's going to be a really meaningful readout for us. And as a reminder too, right, we see this as really the first ocular indication for 102. We're really excited as well about geographic atrophy. We went for DME first because we could see proof of concept faster, but we're also going to be looking at target engagement biomarkers in the eye. And, you know, some exciting data there could support broadening to look at, you know, not just DME, but also GA, also messy, right? There's a number of opportunities where inflammation plays a really important role in the disease.

And of course it'll be like totality of data as you're making those decisions, but let's call it one line on BCBA, plus you were saying some biomarkers. Are there any specific to GA that you are particularly watching that would give you confidence to move forward in GA?

It's a different disease, right? So the confidence for GA really comes around this, the sort of the separate data package. So, I mean, preclinically, there's some very nice evidence like NLRP-throw and knockout animals are protected. We actually developed in-house, and this is in our corporate presentation, like a natural model. Like I should And say, too, there's already like there's all the usual models of GA where you give the animal some toxin, they get some junk accumulated in the eye and you can improve that with a drug. But what we also really like is that if you just take really old mice, just like really old people, they accumulate junk in the eye and it's a not, you know, it's a more natural model of the disease. And we also see a very profound effect there. So we're excited about that already. There's also been some recent data. There was an update over the summer from a small company called Inflammazome Therapeutics. they have an implant that goes in your eye so it's not it's not competitive modality perspective but it's it's a it's an inflammasome inhibitor and they've seen some really um promising early data you know strongly outperforming the complement inhibitors there so there's pretty good rationale yeah and how does what mechanistically how does it work how does nrlp3 inhibition clear out the junk in the eye as you called called it um or you know stop the progression of of the geographic attribute i mean when you remove the inflammation does that just allow the body to do the natural healing that it normally would be cleared on its own right but these the various junk in the eye whether it's turzen or lipofuscin right like that activates nlrp3 which you know further like weakens things opens up the barrier allows it to accumulate more right so it can sort of stop the things getting worse and also as you mentioned help things clear on their own and potentially even improve. Yeah. Got it. Okay.

And then just from a commercial standpoint, this is an oral therapy. We know that ophthalmology is used to injections or eye drops. This would be new, right? Like I can't think of an oral therapy for the eye. I don't know if you have examples, but just how do you think like the patients and physicians will respond to this? Like I'm wondering if you've done any market research here.

Yeah, no, there's a lot of interest because eye injections are not appealing to patients, right? There's really a lot of demand for something like this.

And you want to take that one, though?

Can you hear me?

Yes.

Great.

Okay. Yeah. Oh, no, we cannot hear you.

Does that work?

I've turned it on. There you go. I think we got it.

So Kristen alluded to this earlier. If you look at the distribution of the markets, about 40% of the market doesn't get injections. So this is the watchful waiting group. So the physician, it's generally a little bit of edema without vision loss. And the physician and patient decide together to not give injections and just wait. So that's an optimal group you mentioned earlier. That's a different treatment group, clinical group that we'd have to address later. there's a group of patients with VEGF who it doesn't work anymore so they're refractory to VEGF therapy and that's another group that's optimal so this could come in and replace what is basically no option at that point so no doctor wants to give injections of drugs that aren't working for patients and you'll see that over a serial progression so those are the two optimal groups as we talk to people and talk to physicians um and then just the the general desire to treat

earlier in the in the paradigm that watchful waiting group is is there for sure and there's nothing in the development pipeline landscape that sort of you know fits that exact mold beyond your uh molecule right now right everything else is injectable so it wouldn't really work for that watch and wait population. That's the big take home. And everything else is comboed with VEGF. So if you don't respond to a VEGF, you have potential to respond to a combo, but your combo could also be quite effective.

That's right. No, we think it's a big opportunity here for sure. Okay.

Well, when you look at the overall competition in the space, obviously there are the IL-6 inhibitors that are probably the most direct competition that we can make for NRLP3s. There's probably other mechanisms out there as well. How do you think about competing versus them and is one line enough in the context of some of these other mechanisms that maybe could achieve a similar level of efficacy but you know perhaps maybe not quite as safe.

Yeah it's mostly the point that I've mentioned right is that there's these kind of wide open patient segments that are really only going to be addressed by an oral especially the sort of early watch and wait so it's there's not a lot of competitive intensity there.

Yeah got it okay anything else you really want to highlight on ophthalmology before I switch topics.

The changes we announced this morning are important also for the timeline of the entire program. This is a true phase two study, a full phase two study in as much as the primary endpoint is a primary endpoint for approval. So that will allow us to go immediately into a phase three study, therefore accelerating the program as compared to having to go into a subsequent phase two study. So that's a very important point as well.

Yeah, that seems prudent. And is top line data still expected next year?

Yeah, second half of next year.

Second half of next year. Wonderful. So, well, looking forward to that. Before I leave NLRP3, I just want to ask again about other opportunities that you could bring forward. You know, you mentioned in the beginning, Kristen, that there's just a lot of opportunities for this mechanism. How are you thinking about prioritizing and how are you thinking about capital allocation in particular for any additional indications or disease spaces that you would want to enter?

Yeah, I know we're well financed with cash on hand and that includes the potential to support one or two additional indications with NLRP3. And it is our intent to communicate another one, at least one other one by the end of this year. But, you know, I don't have too much more to say about that, you know, beyond what I just said, TBD, you know, but, but there, you know, again, like inflammation is important in so many different diseases. And there are a lot of indications where there are even approved therapies, right? Where it might be an injectable anti-inflammatory, either IL-1 or IL-6. And even just the oral prospect is very appealing. So there's a lot of very attractive opportunities in this space.

We look forward to hearing more there. Okay. Let's spend a little bit of time then on just your APJ portfolio. You mentioned that you're still on track for IND later this year. These are next-gen APG agonists for obesity. Any update that you could share beyond IND still on track on where these programs stand or where do you think we'll hear more information on, on next steps?

Yeah, for sure. No, we like to share all our additional data, you know, when we do the IND, when we get to that stage. So, so more coming soon by end of year, but briefly, um, these are, you know, incredibly potent, um, orals and biologics that have the potential to enhance weight loss, but also increase body composition. And now that I think we've seen some of these oral incretions on the market, right. If anything, there's even more need for enhanced weight loss, right so like that's that that's a very exciting proposition that was uh true for our earlier program as well that you could have a combination pill that achieves injectable like weight loss that would be really exciting with you know an orfo or with some of the other drugs that are being advanced here and then in the injectable space too i mean i think we are going to see more focus on quality of weight loss and muscle retention um which is where the injectable program has this the chance to shine yeah got it so we will look forward to all of that i'm curious you You know, do you think that NILRP3 still has a path forward in obesity? We kind of crossed it off last October with the Ventix data. I mean, you can't rule it out. I think we'll know for sure by the end of this year. I'm assuming Nodthera didn't see that in their diabetes trial either. We might have heard about that. But, you know, as a reminder, right, like our QL-CV trial right now, it's an obese inflamed population. So if something's happening, we'll have the power to see it. Um, but given that, uh, you know, that's, that's sort of purely in the upside category for us, given that Ventex with their brain penetrant molecule, um, really just didn't see anything there.

Yeah, fair enough. I want to go, um, a little bit into the broader business as well. You know, the foundation of the company is the proprietary longitudinal healthspin database that you have. It's, uh, you know, something that you've leveraged through partnerships as well as your own drug discovery. When we think about where BioAge could be in, say, the next five years, you know, how should we be envisioning, you know, additional assets coming out of that pipeline? And how should we think about the internal pipeline perspective of growth as well as partnership?

Yeah, no, happy to speak to that. So BioAge really started off by us creating data sets that we thought would be useful for target selection and ultimately drug discovery. It was the signals in those human aging data sets that gave us initial conviction around NLRP3 and also around Apolin and formed our, you know, our drug programs there. And it's those same data sets that have driven our partnerships and collaborations with Novartis and Lilly, right? And what's unique about our data, it's in a sense very much like DECODE or UK Biobank, where it's a large population cohorts, but with one key difference, which is that it's the same individuals longitudinally profiled over five to six decades. So over most of their life, over the whole period of aging. And what, you know, we have a big collaboration with Novartis and what excited them about our data was that, you know, you really want to go and see what's different about people before they get sick. you know, like what changes precede cardiovascular disease or Alzheimer's by a decade, right? Like what are the earliest drivers that you can modify as opposed to those changes that only happen after you're very sick, right? When intervention, frankly, might be too late. So, and separately, right, you might be able to learn from those particular humans who age really well. Like there are people in our cohorts who make it to 100, 105 and still relatively good health, right? So what's what's different about those people that can teach the rest of us so with Novartis we have an ongoing target discovery collaboration and the focus there is on completely novel targets that no one's ever worked on before that they want to take forward and that's a collaboration where they you know provided an upfront and are supporting our platform it's great non-dilutive funding for our science to keep that part of the company humming along and with Lily it's a couple of promising targets that we've selected where they're helping us build drugs that we can potentially carry forward. But to your question, yes, like both through collaboration and also internally, we're always working on additional programs. And like Apolin, like NLRP3, we will over time advance other molecules to the clinic with the same kind of similar kind of data package, right? Cardiometabolic potential, really nice grounded human data signal as well.

And is BioAge leveraging AI within the business, particularly within this part of the business at all? I'm just curious how it might be used in your business.

Yeah, for sure. The everyone question. Yeah. I mean, you know, we were a data play from day one, right? We have these huge data sets and we've leveraging AI to find promising targets and to integrate the universe of data has always been sort of really a core of what we do, actually. What's been exciting about, the most exciting thing about the past year actually is probably using LLMs to help with their regulatory docs, all this like stacks of paper. Yeah. But, but we love it for the data science too. And that's, that's a core part of our, our business. Yeah.

And then just a question on, you know, how to think about translating genetic data into a drug, you know, you have a patient, a person who has, you know, a variant and has a lifetime of exposure to that variant and it's driving, deriving benefit from it. But when you create a drug, it's a shorter term exposure. So when you were picking new targets just across the board for yourselves, for your Novartis, you know, whoever, you know, how do you think about, you know, balancing the short-term versus, you know, the actual, you know, variant? Like, how do you make that distinction on what's a real drug target?

Well, that's a great question. It's something we worry about, right? Because human genetic data is great, of course, right? People have published papers showing it more than doubles your chance of success in the clinic, but those are still poor odds, right? Like double a very small thing is still a very small thing. So I think for us, we like to, you know, we insist on having that human signal to know that it's relevant in the human, to know that there is that potential to achieve a benefit with a human, but then we do rely on, like, that's what animal studies can be good for, right? Like if I actually intervene in a model and in our preference, like a natural aging model, as opposed to some very artificial disease construct, like, can you fix it in a short amount of time? And that's also very, where there's like precedent to, to help us, right? Like what's very nice about our lead program and LRP3 is that the anti-inflammatory class has been in a lot of human diseases and you can make a list of things where it does work in the near term and where it doesn't. And that lets us focus our development efforts.

Excellent. Okay. So I think we're coming up on time. So I'm just going to turn it back to you, Kristen, and perhaps to just give any closing remarks, remind us of the cash runway. And I think that there is plenty that we can look forward to over the next 12 months from you as well.

Yeah, for sure. No. So yeah, it's going to be exciting next year for us with our cardiovascular Quell-CV and, you know, metabolic trial results coming out end of this year. We're looking forward to hearing more, more news from Zeus in November as well. Right. And then in the next year, in the second half of next year, we'll have again on NLRP3, this, this really meaningful phase two efficacy readout for our ocular program. And then of course, by end of year, the APJ IND filing, right.

And then we'll have some clinical data for that next year so so a lot's going on and do you want to summarize the the cash and plans yeah so um at the end of the second quarter we had 381 million dollars we've guided to that being cash through 2029 um that as chris mentioned earlier is um sufficient funding for us to do one or two additional nlrp3 indications the runway will come in a little bit but not a huge amount to do that um yeah and that's the cash guidance and all the activities that chris had mentioned for apj and nlrp3 are all covered in that guidance

wonderful okay well thank you so much this has been great i really appreciate the time thank you thank you