BioAge Labs, Inc. Common Stock 12th Annual Cantor Fitzgerald Global Healthcare Conference

Yeah, thanks for having me today.

Yeah, for sure. At BioAge, basically, we have a platform that helps us identify promising targets for metabolic health and longevity. Our lead program is BGE-102. It is a potential best-in-class NLRP3 inhibitor. We showed earlier this year in our full phase I data set that we have potential best-in-class brain penetration, IL-1β suppression, as well as CRP reduction. That drug is currently in 2 different phase II trials. A trial focused on cardiovascular results, which we will speak to later with the ZEUS results and everything and what that means for us. We also announced earlier this week that we have also advanced that same drug into a phase II trial for diabetic macular edema with a phase II efficacy readout coming in the second half of next year. It is a really exciting area for these therapies.

We also have an apelin agonist program and are on track for our first IND filing at the end of this year. Those are the closest milestones.

Yeah, no. For us and for everybody else, especially for patients, it was really disappointing to see that IL-6 failed to move MACE outcomes in the ZEUS trial, right? That initially was an important area of focus for us. We were getting ready to go, potentially, into a phase III ASCVD trial as early as next year. That is really on pause for us now. That was a challenging indication for a small biotech, even if ZEUS had been wildly successful, right? Mostly because it is capital intensive. Frankly, if it were not that capital intensive, if it were a $20 million or $50 million bet, we would still go for it because the biology is different and we can get to that.

As for ZEUS itself, there are still two different potential explanations that we are waiting for more data to learn which of those it was, whether it is a patient population question or a target question, right? Because the history of this field, there is precedent with IL-1β in the CANTOS trial, where that led to very robust MACE benefits, 15% in the whole population, up to 25% if you look at patients with low CRP. That just failed to translate entirely, right? That was a milder patient population. The ZEUS population, as people have discussed, include patients with quite severe kidney disease. Potentially, we will know more when we learn, hopefully, at AHA, potentially there were a lot of events in that trial not related to heart inflammation, right?

The good news there is the one trial Novo hasn't stopped yet is ARTEMIS, which is a post-MI population. We will get a look at what this mechanism does in that population as well. But the other potential explanation is that this is the wrong target, that we need to look further upstream. What we know is that IL-1β seems to work, and IL-6, of course, doesn't impact IL-1β. NLRP3 does. It's the canonical marker. In phase I, you look for IL-1 suppression to see how your NLRP3 drug is doing. So it might be too downstream to have the effects that you need in cardiovascular disease.

Okay. Oh, I will mention briefly, there's even a couple of strategics are very open about that.

Novo themselves have said so, that NLRP3 specifically is a very promising mechanism here, and IL-6 could be too far downstream.

Yeah. The most interesting information of that trial, I am going to guess, is going to be related to different patient subsets, whether they can separate the severe from the less severe and see anything different. That said, given the hazard ratio was so close to one, we are not holding out a ton of hope, but we would love to see anything they find there.