BioAge Labs, Inc. Common Stock Citigroup’s Biopharma Back to School Summit 2026

Thanks, Sam. Great to be here.

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

Good. Do I need that for the webcast?

Yeah. Okay, cool. Yeah. When we started the year, we were in the middle of phase I 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. Then we started two different trials, one in an obese inflamed population, a phase II, and as we announced just yesterday, a phase II in a diabetic macular edema trial. 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.

Or, well, it's not a setback for the target, but the IL-6 setback and the way that people are thinking about cardiovascular outcomes trial in particular for this target is, of course, a riskier proposition. There's still a lot of potential that we're excited about. By the end of the year too, we're still on track to file IND for apelin as well. It's a good year for us.

For sure. Of course, the ZEUS news from Novo Nordisk just over a month ago, a huge disappointment. Really unfortunate to see that, especially for patients. As you mentioned, Novo Nordisk 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. That's really unfortunate. There's still two potential explanations for what's going on, and those won't be resolved really until we have additional data.

There's, of course, hopefully more data from Novo Nordisk 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 drove very profound reductions in MACE. As a function of CRP, the biomarker that you mentioned. Amongst those people who normalized their CRP, they saw a 25% MACE benefit, which is super meaningful to patients.

It was really disappointing to see a hazard ratio of basically one with IL-6. The two things to be aware of that I think are being discussed right now is, one, that the ZEUS trial population was a lot sicker than the CANTOS patient population, so these people have profound kidney disease. There could be a lot of events that are not related to cardiovascular inflammation that could make it challenging for this mechanism to shine. 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. But the second explanation is that this might be the wrong target. 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.