iBio, Inc. Common Stock Wells Fargo 21st Annual Healthcare Conference

Yeah. I think we have a couple of other complex chronic diseases we can take as a playbook for obesity. We have seen this before in type 2 diabetes, in hypertension. We're likely looking at a hypersegmentation of the market. We're really not interested treating obesity like a cosmetic disease. We're really interested in actually treating the underlying pathologies that lead to cardiovascular disease, to metabolic disease, that are shortening health spans of people. To achieve that, I think it's fair to say that combination therapies will actually be the predominant way of doing this, as we've seen before in other diseases. I think the GLP-1s are, I should broaden this group. The weight loss drugs, like the amylins, the GLP-1s, the dual and triple Gs, they really solve the question of lowering the body weight.

We have not solved the question yet how we actually keep the body weight low. We also don't know about the durability of the beneficial effects on the cardiovascular side. If you're looking at the bariatric surgery field, that was the first time we could lower body weight. Again, very invasive with a scalpel. Even after bariatric surgery, where you cut out part of your stomach, you still actually, after years and years, you see the body weight regaining. So we really have not solved this long-term strategy, and I think there's a huge unmet medical need to do this. Obviously, what you're going to see as well is the improvement in the adverse effect profile. We know that a lot of patients on GLP-1 are going to have adverse effects, gastrointestinal adverse effects mainly.

I think the early amylin data that Eli Lilly and others have shown is there might actually be beneficial effects of an amylin over a GLP-1, but I think this is going to evolve over the next years just to kind of keep patients on drug longer without having actually these adverse effects. Then you mentioned the quality of the weight loss, right? I think this is something we're, at the moment, underestimating. It actually is not muscle or bone density that makes us sick. It is actually inflamed visceral fat, the fat around our inner organs, that actually makes us sick.

I feel like this is one of the areas where I think we're going to evolve in the obesity space very rapidly in can we actually prove, which the proof is outstanding, can we prove that a reduction in visceral fat is actually conveying all of these cardiovascular and metabolic beneficial effects, or is it really overall weight loss that is doing this? Obviously, we strongly believe it is driven by a loss in inflamed adipose tissue, but this quality of weight loss, might it be preserving muscle to have a healthier aging population that can still actually walk up some stairs, and the reduction of visceral fat to kind of protect against cardiovascular and metabolic disease, I think that's going to be an important piece of the future.

Activin E is a really interesting target because it has a very strong genetic validation.

The last one that we saw with equally strong validation was PCSK9.

Not only the gene that makes Activin E is correlated if you suppress this, that you have protection against cardiovascular disease and metabolic disease. Also, its receptor, which is called ALK7, shows the same beneficial effects. This whole pathway really is related to metabolic and cardiometabolic disease protection. That is what makes this target so interesting. When we got into this space 2 and a half years ago, we were quite surprised that nobody had made an antibody.

Naive as we were, stumbled into that space and said, "We are just going to make one.