BioAge Labs, Inc. (BIOA) June 2026 Conference Transcript

All right. Welcome, everyone, to Jeffrey's 2026 Global Healthcare Conference. My name is Roger Song, senior in this cover of Simica Biotech. It is my pleasure to have the five-side chat with BioAge Labs. And then we have CBO, BJ, and the CFO, Dov, here. Welcome, gentlemen.

Thank you for having us.

Maybe, BJ or Dov, you want to give a couple minutes overview of BioAge. It's a very exciting time, so you have a lot going on coming, and then give us some state of art, and then we'll have a conversation.

Sure. So, we are BioAge Labs. We're a clinical stage biotech company founded on just the thesis that, you know, we can interrogate human aging to identify drug targets for cardiometabolic disease in particular. So, our lead program is BG102, which I'm sure we'll speak about at length today. It's a, you know, potential best-in-class NLRP3 inhibitor that we're developing for cardiovascular disease as well as ophthalmology. We recently reported our Phase 1 results a few months ago. We are going to be reporting results from our cardiovascular risk Phase 2 dose-ranging study end of this year, and we'll also be initiating a POC trial in DME in the middle of this year, which we'll read out in the middle of next year. In addition to our lead program, we're developing both oral and parenteral APJ agonists, which we view as a complement to incretin therapy, so both oral and parenteral. So thank you, Roger, for having us.

Yes, you have an agent discovery platform, and then you have a couple pipelines coming out of that platform. I believe today we're going to mostly talk about NRP3, maybe in our CV and in the ophthalmology disease as well. So, but we just want to emphasize the, you do have the other pipeline as well, right? Okay. So, for MNRP3, I think the field has been involved kind of over the past couple of months. So, what happened there? So, MNRP3 from a multi-target or multi-deleased area target become, it's more prominent in the CV space. And then how BioAge is going to capitalize this?

Yes, there's been a lot of growing excitement in the NLRP3 space. I think, you know, one of the exciting catalysts last year was Ventix reporting results from their three-month trial showing efficacy that was approaching that, that we see with the biologic injectable modalities. So that catalyzed a lot of interest. Obviously, they were acquired by um Lily shortly thereafter um Zeus um the the Novo IL-6 program has their ASCVD readout in the third quarter of this year so a lot of eyes are on that um on that catalyst as well and so yes so we're we're very aggressively pursuing um ASCVD so we reported our um phase one results at the a few months ago and in as part of that we included two um cohorts of obese participants who had elevated CRP at baseline, so very similar patients to those that VENTIC studied in their trial. And in those patients, so 60 milligrams we treated for three weeks, 120 milligrams QT we treated for two weeks. And there we observed, you know, what we believe to be best in class efficacy in terms of biomarker reduction. So we saw an 86% reduction in HSCRP in both cohorts. And importantly also, so we saw a normalization rate of CRP to below 2 mg per liter of 87% in the 60 mg cohort and 93% in the 120 mg cohort. And this is really important because, you know, what we learned from the Cantos trial of canakinumab in ASCVD is, you know, the headline MACE reduction in that trial was 15%. But if you actually look at, you know, responders, those patients who achieved HSCRP below that 2 mg per liter threshold actually had a 25 percent benefit, whereas those that didn't had, you know, essentially no benefit. And so in terms of thinking about how these early Phase I results connect to, you know, long-term potential cardiovascular outcomes, we were really buoyed by that data. So in addition to that, you know, looking at these, you know, HSCRP was supported by concordant changes in IL-6 and fibrinogen, as well as sort of what we believe to be an exceptional tolerability profile, which is critical for this indication. And furthermore, I think as we think about the NLRP3 landscape, there's efficacy, there's tolerability, and then there's also dosing and administration. And so we're now looking at, you know, an oral once daily dose range of, you know, 30 to 90 milligrams, which is, you know, commercially, I think, you know, important to have a, you know, once daily dose and certainly provides flexibility and potential, you know, co-formulation, thinking long-term, lifecycle management strategy. So, across all those dimensions, we're feeling, you know, really, really great about our program following these phase one results.

Now, so, NRP3 is a high interest target for some time, and then with this, the recent acquisition and then also the CVR data HCRP reduction, probably the interest level will even go higher. So maybe tell us how unique and or differentiated from the BGA102 and then in terms of, you know, how you design the molecule and then what's the property to make you feel the best-in-class signal you're seeing is real.

Yeah. So in addition to the phase one results, You know, this is, we can sort of bring you back in time, so we discovered this program internally. It's a homegrown program. We originally identified the HIT through a DNA encoded library, and so we were looking. We blocked the sort of the binding site that, to our knowledge, all other programs target, which is the ATPase pocket. And so we were looking for a novel binding site, and so we found this HIT. We've sort of optimized the molecule over several years, but I think, you know, in our detailed characterization of the structural biology, this binding site is actually accessible in all conformation, so both the inactive form as well as the active inflammasome. And so, you know, that may help explain, you know, both the rapid onset of action, you know, we're seeing, you know, HSCRP reductions, you know, profound by day seven of treatment, as well as the magnitude of the depth of the biomarker reductions that we're observing. you know, in our clinical trial.

Got it. Okay. So you give us, you know, phase one data. Now you are running the phase two and then try to give it a bit longer term data and then across different doses. So what is the base case here? Because we see pretty rapid reduction for the HCRP along with many other biomarkers. So you're already pretty deep and then we don't expect you need to be even further. But, you know, durability wise, is that, you know, kind of a base case you will be sustained kind of reduction to that end?

Yeah, so that's our expectation. You know, I think what was really interesting about the Ventix data, again, is that they showed essentially their maximum biomarker reduction within the first couple weeks of treatment. And so that's actually why we added those obese inflamed cohorts to our Phase I trial, because we thought that we could actually get a lot of the answer early, you know, and that it would be sustained, you know, with chronic treatment. And so we were initiating this dose-ranging Phase II trial. that will read out by the end of the year, this is going to be three months of treatment. And one of the goals, I mean, the key goal is to show, you know, a stable reduction in these inflammatory biomarkers and sort of extending the results from the phase one trial, you know, both in terms of biomarkers, safety tolerability, and, of course, we'll be adding incremental assessments, you know, that are, you know, are only feasible with this longer treatment duration. So, for example, we'll be looking at MRI imaging of the liver, liver fat content, liver inflammation. This is another area where Ventix saw, you know, a meaningful signal in their three-month trial. And so we'll be hoping to recapitulate the same.

Okay, good. So we're going to see a little bit more kind of efficacy endpoints.

Yeah, and maybe an important point, too. So the dose ranging here, we're exploring three doses. So we're looking at 30, 60, and 90 mg QD. 90 milligrams essentially gives us, you know, what we expect to be about 98% inhibition of the target. So that's, you know, if you need complete inhibition of NLRP3 to get your maximal biomarker response, we think we can deliver that. You know, and then we'll be exploring 60 and 30 megs as well. You know, based on our modeling, we expect 30 will give us a suboptimal biomarker response. And so this is really important because, you know, time is such an important value driver for this program, and so we want to, you know, end the year with, you know, confident in dose selection for a potential phase three trial, you know, starting next year. So as we think about, you know, the profile we have in hand given the phase one results, you know, we want to do these enabling activities. We expanded the study to do dose ranging. We've initiated CMC to support, you know, a phase three start next year. We want to be, you know, addressing some of these long lead time items and making sure that we're doing all of the enabling work.

Got it. Okay, good. And then in terms of the safety side or tolerability side, we learn from the old days from IL-1, so you see some, you know, infection risk there. That's why they haven't really gone to, you know, forward or move forward into the cardiovascular space. And then IL-6 so far is fine. So at least from the, you know, normal, they are doing the IL-6, and then, you know, they're running a large kind of main study. So how are you confident about the NRP3 safety, you know, database, and then what are the key evidence to support the long-term safety for NRP3 target?

Yeah, it's a great question. And so there was a small but significant increase in infections in the Cantos trials. So this is with an IL-1 beta neutralizing antibody. And so this is something we'll be looking at, of course, in the Zeus trial. But I think, you know, inflammasome inhibition is fundamentally different from cytokine neutralization. If you think about NLRP3 being sort of the key sensor of sterile inflammation and triggering the cytokine, you know, cascade of IL-1 beta, IL-6, ultimately CRP. you know, when you block, when you neutralize a cytokine like IL-1 beta or IL-6, you do have the potential of just knocking out that node in the inflammatory, you know, pathway. Whereas, you know, with inflammasomes, there are redundant inflammasomes. So NLRP3 is the predominant sensor of sort of sterile inflammation triggers. But there are a number of other inflammasomes that are not targeted by our drug and by selective NLRP3 inhibitors. And so in the context of a pathogen response can certainly, you know, help mount an infection and you have all of the downstream machinery still in place. And so there are certainly, you know, strong theoretical reasons why this sort of different strategy may be, you know, advantageous in that context.

From a clinical perspective, how much NRP3 inhibition we have known for the long-term safety? I know you haven't done that. Many of the other NRP3 companies haven't done that. Any like those long-term safety, we should give the people a little bit more kind of comfort?

Yeah, so, I mean, I think Ventix to date has the largest safety database with their three-month trial, right, where there didn't seem to be any, you know, on-target safety or tolerability issues. You know, Nodthera will have two readouts this year as well that'll build on that. So we'll be looking for evolution in this space. I mean, thinking about our molecule in the Phase I results that, you know, we had an exceptional tolerability profile, with, you know, and certainly, you know, AEs as well as, you know, looking carefully at clinical chemistries and just saw no adverse changes of any kind. So, you know, when we think about that, when we think about the 50 to 100x safety margin we have based on our, you know, three-month, you know, GLP talks to date, we feel really good about the, you know, the safety tolerability profile of the molecule.

Got it. Okay. And then one of the components of your compound is that brain penetrant. So understand this is not CNS indication, but how much it will help the overall profile, you know, even you're going after the cardiovascular disease?

Yeah. So the one of the differentiators of BG-102 is it does have, you know, exceptional CNS penetration. So we showed a KPU-UCSF of 0.7 in our phase one trial. So what that enables is us to address the broad range of diseases driven by NLRP3. But there may be benefits even if you're talking about things, indications that appear on the surface to be peripheral. So for example, you know, ASCVD, neuroinflammation is thought to be the result of even psychological cognitive stress, right? And that triggers a beta adrenergic response, you know, that promotes peripheral inflammation. So even in something that, you know, appears peripheral on the surface, having CNS exposure may actually, you know, even when you're solving for the peripheral sort of inflammatory biomarker may actually be advantageous.

Okay, that's interesting. Okay, good. All right, so I think all eyes is on the Zeus, you know, particularly related to the RNP3, IL-1, IL-6. So we know we have quite a few acquisitions happen in the RNP3 and then also IL-6. So what is your base case for So, you know, what would the MACE reduction consider to be validating, very good for the space, and then what would be, you know, you think it's, you know, either worse or, you know, more bullish case?

Yeah, no, all eyes on that trial, for sure. I think we remain cautiously optimistic about that. The, you know, any significant MACE reduction, I think, is going to be really exciting for us, and I think validates the overall thesis that you can target this inflammatory axis and, you know, have that result in meaningful MACE benefits. I think, you know, we'll be looking at the headline number as well as, you know, what's the relationship between inflammatory biomarkers, you know, and those patients that, you know, benefit the most. So I think, you know, Canto certainly provided rich substrate for subgroup analyses and really understanding those relationships. And so, you know, we'll be looking to Zeus for, you know, for the same.

By the way, Zeus is IL-6. It's not necessarily direct kind of to our P3. and then you just mentioned you have a few other biomarkers also, you know, beneficial, right? So when we look at, let's say, MACE 15%, that seems to be the bar usually for the cardiovascular benefit. And if they get to 15%, that's certainly validating this class. And then would you say, obviously, with, you know, slightly different kind of approach, maybe you can get higher MACE reduction?

You know, there's certainly that possibility. So I think, you know, the way we look at it, what excites us about this program is, you know, in our phase one, we're achieving reductions in CRP that are essentially on par with what the Zilcovecimag dose showed, the dose that was carried into the Zeus trial. So on that just sort of raw anti-inflammatory horsepower on that central axis, we feel like, you know, it's quite comparable. There are also aspects of NLRP3 biology that are not captured by IL-6 that are independent. So, for example, NLRP3 also regulates the cytokine IL-18, and that in Cantos was shown to, you know, independently predict, you know, MACE in that trial, baseline levels, and there are Mendelian randomization or human genetic signals that support, you know, a causal role in ASCVD, and, you know, there's the sort of pyreptotic inflammatory cell death that NLRP3 regulates that's, you know, there's work to support that, you know, that may contribute to plaque destabilization as well. well. So there's a lot of NLRP3 biology that overlaps with IL-6, but by going upstream, we're able to address incremental biology as well.

Okay. Very good. All right. We just like you said, if the top line hits, great. So we can go into the details later. But if the top line, for some reason, didn't get to the level people want to see, still you have a chance to look at the details and then see, okay, how this will translate to NRP3. That's a little bit more nuanced, but I think that's probably the scenario you also want to do.

Yeah, yeah, no, of course, we're going to be looking far beyond the headline number. Yeah.

Okay. All right. And then, okay, so in terms of your clinical strategy, you are running phase two, so that's a 12 weeks, three months trial, and then you're going to read out, you know, maybe after this, so it will be very interesting. So, I mean, by the way, what's the timing of that? And then when that data read out, along with Zeus, I think the timing should be pretty close. And then what's next?

Yeah, so we were, you know, anticipating and guiding to results from the phase two dose ranging trial by the end of this year. So, we're expecting Zeus results in the third quarter of this year. So, I think, you know, our position will be, you know, materially advanced, hopefully, by, by end of year, um, given these internal and external catalysts, um, but what comes next? So, we are, um, you know, I think, and, and, and a phase two meeting, you know, and, and really getting, revving the, revving the engines for, um, you know, a, you know, a phase three trial, um, we're, we're targeting enablement for a, and a start next year, um, so, so it would be sort of, um, full speed ahead on, on AICVD, and we're also working on ophthalmology, of course. So, we have a, you know, a POC trial in DME that we're initiating in the middle of this year, and we're guiding to data for that in the middle of next year. And so, that's a, you know, a totally sort of orthogonal, you know, an indication area that we're really excited about.

Yeah. No, we will touch on the ophthalmology or DME for sure. And then, in terms of ASCVD, obviously, you're open for any kind of a partnership or any, you know, potential BD situation. And if that's, you know, in parallel, you're also committed to do it on your own, and then, you know, what will be the next kind of trial look like if you go by yourself, like a mace or a certain subpopulation, and how do you think about this as of now?

Yeah, I mean, I think from, in terms of, you know, a trial perspective, the base case would be a mace trial, right? I mean, this is an enormous clinical opportunity. We think, you know, an oral, well-tolerated once a day, you know, anti-inflammatory could be, you know, the next statin. This is a major risk factor that's sort of currently unaddressed. And so to unlock that opportunity, you know, requires an outcomes trial. You know, what that could look like, it could look more like the Zeus trial on one end. It could look more like the, you know, New Amsterdam Prevail trial where, you know, you're looking broadly at the secondary prevention setting with elevated CRP as sort of the key eligibility criteria, you know, as a biomarker. So, you know, we're looking at the full range of possibilities at this point. But, Dov, I don't know if you want to speak to add anything there.

Yeah. You know, one of the questions that was raised by investors this week was go it alone or go it with a partner.

Yeah.

So, which is obviously an important question. And the short answer there, Roger, is we have to be prepared to go it alone and go fast. So we're already making investments in things like CMC for the May study today. Those are longer lead time items, not huge capital commitments, but gets us in a position to start that trial at the end of 2027. because and then as well as financial resources were very well funded to date about 385 million dollars at the end of the first quarter which gets us a long way there in funding a potential may study this will eventually go to a big company in a commercial setting and quite frankly it may be advantageous if the right deal is struck for it to go in the clinical stage and for them to run the MACE study. But we need to be prepared to do it on our own, we feel.

Yeah, yeah. No, honestly, you have to run the company, not just be for sale. But on the other side, it makes a lot of sense for, you know, big partner to take on this kind of massive MACE, particularly if they have the capital to run multiple trials in parallel. That's always maximize the value here, right? But on the other side, you do have the DME. So, and then ophthalmology, I think that's a very smart strategy because we know NRP3 or HCRP or L6, so should, you know, work in many other different indications. And this DME ophthalmology, is that something you think, you know, BioAge as a, you know, biotech company potentially can take this a little bit further and then maybe even towards that approval if you launch it?

Yeah, no, we're very excited about ophthalmology, and I think it takes advantage of, again, the ability of the molecule to access these privileged compartments, so we get really nice CSF exposure in our trial. You know, we see therapeutic retinol exposures across preclinical species, so rodents, rabbits, NHPs. I think the ability to target, you know, the inflammasome specifically and inflammatory drivers generally with an oral is a huge opportunity across a range of indications. You know, we're prioritizing DME as our POC for a variety of reasons. So, one, you know, the IL-6 drugs have shown a benefit here. So, I think specifically, you know, Vamikebart recently released monotherapy data at Arvo. They saw a nice monotherapy effect. They've previously shown incremental benefit on top of VEGF. So, at a high level, it shows that selective anti-inflammatory strategies can be efficacious in this setting. They also show the maximum efficacy at around two months of treatment, and so this enables us to sort of, within a relatively short treatment period, ideally demonstrate, you know, proof of concept. And so, the trial that we're running is going to be three arms. So it's going to be BG-102 monotherapy, VEGF monotherapy, and then VEGF plus 102. And so we'll be able to look at sort of the pharmacodynamic effects in both of those treatments settings. And so the goal of this study is really to show a clear PD in the eye. We want to show that the drug gets there and hits its target in the eye as sort of a way to stage gate further work in ophthalmology. So our primary endpoint is intraocular IL-6. We'll be doing aqueous taps on these patients, so removing the aqueous humor. We can look at biomarkers there as sort of the primary outcome of the trial. But we'll be doing, you know, a variety of functional assessments like BCVA, we'll be doing OCT imaging, so we'll be able to look at CST and other anatomical endpoints. And so, we'll be looking at the totality of the data here to show, you know, a clear pharmacodynamic effect and ideally, you know, trends at least in some of these clinical and anatomical endpoints that are concordant with, you know, biomarker reductions. And so, that's the setup of that trial. I think, you know, we do think IL-6, that data is at a high level de-risking, but the biology, it's not one for one. I think thinking of this as an oral IL-6 is simplistic, you know, especially in this context where going upstream also enables you to capture biology that's of IL-1 beta, for example, that's independent of IL-6, so that directly induces VEGF. And activation of NLRP3 in endothelial cells actually causes degradation of the microvasculature in the retina, and so there are aspects of of NLRP3 biology that are not captured by IL-6 that we think are really exciting here.

Makes sense. And then one thing I want to, you know, emphasize is your brain penetrant is the best among all the NLP3, and then the retinal penetration is, you know, nearly one to one, and so which means you also is the highest penetration into the retina. That's why the ophthalmology may make you also best in class among the NLP3.

Yeah, yeah. So we're really excited about our sort of differentiation here and ability to, you know, address a range of indications that are, you know, where NLRP3, we think, you know, plays a major role, and that includes DME. Another indication of high priority for us is geographic atrophy. Those are the terminal stage of dry AMD where there are, you know, the disease is sort of characterized by the accumulation of the cellular debris that is highly pro-inflammatory. And And there's, you know, a lot of nice preclinical work and some supportive clinical work showing that if you block NLRP3, you may have a very meaningful impact in slowing the growth of lesions that cause central blindness.

Got it. And then your benchmark, obviously, you have the standard of care, but also a couple, you know, IL-6 drugs is in the indication that's also you want to, you know, make sure you're at least comparable, if not better than the IL-6.

Yeah, so IL-6 is being developed in DME, so especially like IL-6, VEGF, bispecifics. You know, we see a really interesting, a few interesting segments, you know, where BG-102 could play really well here. So there's the 40% of patients who are in the watch and wait category where they have edema, but they don't have sufficient compromise of visual acuity to initiate intravitreal therapy. So if you can treat those patients and delay that, I mean, these intravitreal therapies are a huge patient burden, you know, and as a result, there's a major disconnect between what's shown in trials and what's shown in the real world in terms of disease control. So that's one, you know, highly, highly addressable patient segment where you're really not competing with VEGFs. You're trying to delay initiation, you know, and then on the sort of the opposite side of the, you know, the sort of the patient, you know, journey here, patients who are on VEGFs but are refractory, you know, have imperfect sort of disease control with VEGF alone. This is another group where, you know, initiating BG-102 on top of VEGF could be, you know, highly effective. So, those are sort of the priority segments and positioning for us right now.

Excellent. Okay. I think we went through quite a lot of things here and then touch both STVD and then the ophthalmology. Anything else you want to discuss, you know, highlight to people before we wrap up?

Yeah, so I would just touch on our, you know, we are developing, again, we have two APJ agonist programs, so an oral small molecule and a sub-Q. You know, this is a target that, you know, we're really excited about in our sort of, in our platform. It's one of the, it's a target that is among the most highly associated with not only longevity, but preservation of physical function. You know, it's a target where we've previously shown, you know, really, really nice preservation of muscle size and quality in a bed rest situation. And we think that there's a lot of potential for, you know, interesting incretin combinations in obesity to increase both the quantity and the quality of weight loss. So, you know, we're guiding to filing our first IND here by end of year.

Now I have one more question for you, maybe the last one. So your NRP3 initially is also just like Vintex thinking about the obesity space as well. So in pre-clinical, you're probably the only one showed the weight loss compared to other NRP3. I know this is a two-week study. You're not supposed to show anything. We're going to see your poster at ADA. I don't expect that you will see the weight loss there. But when the 12-week study, you know, with some enrichment on the HCRP, how likely we're going to see some weight loss signal there? That would be the huge upside if you can show this.

Yeah, it would be a surprise upside. The, you know, our view is that the likelihood is low and that there was a translational gap here, you know, given Ventix, you know, showed nothing on that front. You know, the three-month study will be, you know, powered for that, and it will be a sufficient duration of therapy. So, you know, if for whatever reason there was something idiosyncratic about that molecule, you know, we'll have our data there by end of year.

Well, what's the BMI cutoff for the phase two?

So it'll be patients with BMIs between 32 and 42.

So it's potential. Thank you so much, BJ and then Dave, and thank you, everyone.

Thanks, Roger. Thank you for having us.