Evommune, Inc. Morgan Stanley 24th Annual Global Healthcare Conference
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Good afternoon, everyone. Welcome to this session of the Morgan Stanley Global Healthcare Conference. We are very excited to have Luis Peña from Evommune here with us. Let me just get through a quick disclosure, Luis, before we get started. For important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. With that, I am Judah Frommer, one of the senior biotech analysts. Like I said, very happy to have Evommune here. It has been an eventful year. You came public shortly after this conference last year. Maybe give the audience a quick intro to the company and how the team came together.
Well, thanks very much for the Morgan Stanley and Judah for having me here. My name is Luis Peña, President, CEO, founder of Evommune. The company has been around six years now. I founded it just after I was a co-founder of Dermira. We had sold that to Lilly, that had bought lebrikizumab, which is now Ebglyss and doing very well on the market in atopic dermatitis. The goal for us has been to be a serious player in chronic inflammation, and we have been very disciplined since the inception of the company of putting a brand new program into the clinic with a novel target every 18 to 24 months or so. Fast-forward six years later, we have four programs currently in the pipeline. There really are two co-leads. There is an oral MRGPRX2 inhibitor, which is currently in a Phase IIb study in migraine.
There is an IL-18 biologic that just showed very positive Phase IIa data earlier this year. We are scaling up the manufacturing and will be in a Phase IIb study in atopic dermatitis the middle of next year. We have just started talking about a very potent TLR7/8 inhibitor that we plan to put into the clinic in the first half of next year, and there has been some very interesting positive data recently with the TLR7/8, as well as previously. We also have a very deep STAT6 inhibitor degrader program that is preclinical, and we would file an IND towards the end of next year. So very busy and pretty excited about the current pipeline.
Great. So plenty to talk about. Maybe we will start with IL-18, EVO301. Maybe just tell us a bit about the design of this molecule, its potential differentiation amongst IL-18 targeted therapies, and a bit of a history on the asset.
Sure. We have a very talented medicinal chemistry team, and we do on our small molecule all the discovery work internal. We had a gap between two of our programs, and following that 18-24 month discipline, we had been scouring the world to in-license and fill the gap. We found a company in South Korea called AprilBio, and what they do is they take existing or new biologics or novel biologics, and they bind them to a fob that allows it to bind the albumin. That gives us two really cool properties. One is that it extends the half-life, so the naturally occurring binding protein, which we like a lot, it has been optimized for a long time by nature, but it is cleared very rapidly. From a therapeutic perspective, it is pretty tough.
The binding to the fob allowed it to increase the half-life to two weeks, which in the maintenance phase, for example, for atopic dermatitis, you could probably dose every two months or so. That is a distinct advantage. In addition, it also helps it penetrate inflamed tissue, so that was really a bonus that was thrown in, and that might actually add deposition effect over time in the right area as we dose these patients for longer. From that perspective, we really liked the background, the phenotype of, not the phenotype, but the makeup of the molecule.
It had already been through Phase I.
It was very well tolerated, and it continues to be so. Right after we got the molecule, we took it into a- Phase II-A study that had very exciting data.
Okay, great. You are investigating it in atopic dermatitis. Just taking a step back maybe, IL-18 is usually not the first target that comes to mind when thinking about atopic derm, but you have generated some very interesting data in the indication. Before we get to the data, maybe tell us about the rationale for evaluating IL-18 in this indication and why it was a specific target of interest.
Yeah. You are right. It has really been over the last 5 to 10 years that there has been a lot of different publications that have shown elevations of IL-18 levels in many different indications, but no one has really dug into one. GSK generated some data that really caught our eye, and the reason it did so is the following. They had done a single dose study with an IL-18 monoclonal, very similar in potency to our binding protein. After one dose, they showed really somewhat of a similar profile to what we showed in our Phase II-A. They had IGA 0/1 scores in the mid-20s.
Reasonable EASI 50, 75, 90 scores, although those are not dose optimized.
It looked exactly like the data that we had looked at when we in-licensed lebrikizumab from Genentech. Lebrikizumab had done also a single dose study with topical corticosteroids on top, which somewhat increases the efficacy, but it was okay. After a single dose, they showed IGA 0/1 scores in the mid-20s, percent EASI change similar to what we had. Once we saw that- that to us was pretty clear validation that they had a biologic here with relevance.
We very aggressively went after the molecule and then licenses it and put it in a phase IIa with an IV formulation.
Okay, so maybe a bit more on the phase IIa data that you reported earlier this year. You mentioned the EASI and IGA changes, but maybe just a broader high-level recap of the design of that study and the top-line results.
Yeah. We had a pretty good-sized study where we were looking at 2-to-1 randomization of the active versus the placebo. We were really looking at percent change in EASI. As it turned out for the study itself, the placebo rates were very low, and that's important these days. We've seen an uptick in placebo response rates in the atopic dermatitis study, a lot of that driven by really two things. One is the severity of the patient population you put in there. The less severe you have, the more spontaneous resolution and the higher the placebo effect. Secondly, sites that don't have experience. If you take a site that does generalized studies, doesn't understand really how to read these lesions and resolution, then you may have an uptick. We were very careful with that.
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