First Tracks Biotherapeutics, Inc. Ordinary Shares Wells Fargo 21st Annual Healthcare Conference

Yeah. We announced in September of last year our intention to create a new company, spinning out the R&D operations, and most importantly, I think the employees that go along with it for, what is 3 development stage assets in our preclinical engine, into what is now called First Tracks. Company was born April 20 of this year. We came out of the gate with a lot happening. A number of trials with our lead program, ANB033, which is a CD122 antagonist that are ongoing, one in celiac disease and another in eosinophilic esophagitis, as well as our 2 other clinical stage programs. We have the PD-1 depleter rosnilimab, and our BDCA2 depleter, which we have just recently completed a phase I-A for. A lot happening in the company. We are well-funded. We raised some money in April.

We have cash into the second quarter of 2028, and data coming soon in celiac disease.

Excellent. It has been busy.

Yeah. We are blocking a group of receptors, depending on the cell type, targeting CD122. There is two mechanisms embedded in blocking CD122. We are blocking IL-15 signaling as well as IL-2 signaling. It is not a bispecific, it is a straightforward antibody that does two different things. There has been really positive proof of concept data in multiple autoimmune disorders by only targeting IL-15, but then also blocking CD122. I think you could fast-forward here, the proof of concept is already there, both in GI disorders and derm disorders. IL-15 is an important protagonist to certain types of prolific CD8 cells that are present in disease. IELs, intraepithelial lymphocytes, are important in celiac disease. They get recruited in in response to epithelial damage. ILC2s, again, another type of immune cell that is present in disease, is densely expressing CD122 and trimeric receptor.

You are seeing specific cell types as well as CD8s and CD4s that are activated that express these receptors that show CD122. We think, and you have heard this in other places, we have the potential with a targeted agent here in what is called a pipeline and a product. There is dozens of diseases where we think this is important. We have taken a first stab with celiac and EoE. Across the landscape of the less than handful of us that are in clinical development, either targeting IL-15 or CD122, I think there is seven indications right now under development. There is a lot Yeah to potentially target here.

Yeah, no, exactly. I think the mechanism is spot on in this disease. There's nothing approved in celiac disease, no therapeutics approved. It's gluten-free diet or nothing.

There's so many of these patients who attempt to stick to a gluten-free diet, yet have mucosal injury. In many cases, severe mucosal injury when they think they're on a gluten-free diet or they're non-responsive to their diet. The reason to start in celiac, and again, there's lots of choice, is there was proof of concept with some of these other agents that are out there. There's nothing approved, it's a huge market, and there was clinical proof of concept. Then you layer on top of that, I think we have the most potent of the CD122s that are out there today. We think with the dual mechanism relative to IL-15, is there an ability here not only to be first to market or in the same timeline, but also have a very different effect over time, and be a leader in this disease.

That was the reason to start there.

When a patient with celiac disease is exposed to gluten, the down product that's broken down gliadin gets picked up and presented, and it activates CD4 cells. That happens very quickly. You just mentioned the IL-2 spike. That happens within an hour or two. It's measurable. That instigates the cascade that between the IL-2 and interferon gamma that it's expressed, it signals in the epithelial cells, the IL-15 expression on the IL-15 receptor. You see a breakdown in the epithelial cells, which recruits an IEL. So there are dual pathways here in this autoimmune disease.

We target both of those. So that's a little bit of how the mechanism works is what you're asking.