And welcome to the Jeffreys Global Healthcare Conference. My name is Camden Sisler with the Healthcare Banking Group. It's my pleasure to introduce Kristen Urema, CEO of Imagine Bio.
All right. Thanks, everybody. Thanks very much to the conference organizers for having us here. I'm Kristen, CEO of Imagine Bio, and I'm delighted to have the opportunity to talk about our company and our program with you here today.
So we've got the usual forward-looking statements.
So ImagineBio is still a relatively new company. We were only formed at the end of July 2025 through a reverse merger between a private company, Imogene, and a public company, Ikena. We also had a concurrent financing with that. So we are now nine months into our journey as a new public company. We are well-funded with a really strong investor group and a cash runway that takes us into the first quarter of 2028. So that gets us through our important data readout. We've come all the way from the West Coast. We're headquartered in San Diego, California. And we think about our company as being very focused. We're going to try to do a couple of things and do them really well. We are anchored on program IMG007. This is a differentiated next-generation anti-Ox40 monoclonal antibody. And it is in Phase 2B for atopic dermatitis. Many of you are aware that's probably the most common form of eczema. And we are also moving into a Phase 2 study with an indication expansion in alopecia areata. And that study will commence later this year. This is our crown jewel, and we have worldwide commercialization rights to this program. So overall, what we are trying to do is find a very different, unique, new way of targeting the immune system to develop a potential best-in-class anti-oxicority treatment with differentiation in the features that are really going to matter both to patients and their prescribing physicians. So here's a quick look at our pipeline. As you see, we've got the atopic dermatitis indication in confirmatory development in phase 2b. We have guided top-line data for Q4 of 2027. And then, as I mentioned, we are moving forward in alopecia areata. We have a proof-of-concept study and data in that area as well that I will share with you later. And we will initiate this phase 2 study later this year with data projected in 2028. So we're often running in two different medical dermatology indications. That's a really good place to start because of how the mechanism OX40 is implicated in those diseases. And also, it's a closely related group of prescribing physicians. So there's nice synergies both in clinical development as well as ultimately commercialization by starting in medical dermatology. That said, the OX40 mechanism is actually implicated across a wide range of autoimmune and inflammatory diseases So we really do have pipeline in a product potential here. You see across the bottom of the slide, you'll see autoimmune diseases or inflammatory conditions spanning respiratory, rheumatology. You've got neurology in there with multiple sclerosis and also GI with IVD and celiac disease. So, again, we're starting where we're starting, but the downstream potential for indication expansion with this product and this mechanism, we believe, is vast. So what is OX40 anyway, and why is OX40 signaling important? Well, when we think about these autoimmune and inflammatory diseases, we generally think about them as what component of the immune system is really root cause at fault. So you can have B-cell driven diseases, you can have T-cell driven diseases, and atopic dermatitis is squarely in the T-cell disease driven camp. Okay, that's great. But what kind of medications and therapies do we have to treat AD today? They tend to be all very downstream in the signaling cascade, starting from activated T-cells. And they focus really, for the most part, on a single cytokine or a single group of T cells out of the many that can be implicated. So if you're familiar at all with atopic dermatitis, you've heard about Th2. And most of what we have today are Th2-directed therapies. But if you look at this cartoon up here on the slide, you can see it's actually a very complicated picture. and if you talk to any dermatologist, the first thing they will tell you is that atopic dermatitis is a very heterogeneous disease. Patients have Th2 involved, for sure, but they also have all this other stuff, all of these other cytokine-producing T cells, as well as T-memory cells, which are believed to be responsible for the chronic nature of atopic dermatitis, And you also have downregulation of your Treg cells, which are kind of responsible for keeping the whole thing properly regulated and in check. So if you take as a premise that AD is a T-cell-driven disease, maybe you want to think about a therapeutic approach that goes straight to the activated T-cell and works broadly enough that you have the ability to potentially correct many different pathways or many different groups of signaling cells and their cytokines that might be aberrant in the patient with atopic dermatitis. And that's really what we're trying to do here. So where does IMG007 fit? Well, this is a next-generation anti-ox40 monoclonal antibody. The whole class is not that old. There have only been a couple programs ahead of us. And yet we would say that this molecule is so different that we would really consider it to be next generation. And we have engineered it with three, we call it a trifecta, of important angles of differentiation. So the first is that we target the receptor, not the ligand. So this is always a choice when doing drug development for these kinds of receptor-ligand interactions. In this case, we think targeting the receptor is the path to stronger efficacy. Why? Well, it's the receptor that's present on the activated T cells, which are in circulation. the ligand is actually on cells that are in the tissue and in the skin. So if you want to cover your target and inhibit the pathway quickly and completely, we think that a better way to do that is to target the receptor in this case. Very importantly, this molecule is also T cell preserving. So it does not deplete or kill T-cells. There have been other programs looking at this kind of pathway that took a T-cell depleting approach, and that concerns us both in terms of the overall safety profile and adverse event profile, but also in terms of your therapeutic window and therapeutic index. You know, if you're generating a lot of adverse events and tolerability problems because you're killing T cells and releasing various cytokines and so forth, you can't really do proper dose escalation and really explore the therapeutic index of this molecule. So our molecule has been engineered with FC silencing, and it is T cell sparing, and we have generated the data to show that. So think T cell preserving, path to better efficacy, path to better safety. And then finally, this molecule has an extended half-life. It's about five weeks, about 35 days, and we really think that that's a sweet spot. So with that kind of half-life, that really opens up the opportunity for very patient and physician-friendly dosing intervals. So we believe that that could be at least every few months, possibly more. We'll take a look at our study design in a few slides, and you'll see we're looking at monthly as well as quarterly dosing, just in the first phase of our clinical development, when you think about maintenance therapy, what's very intriguing about this mechanism is, you know, could you go to much longer dosing intervals or even potentially stop giving the therapy altogether if the patient has reached a level of low disease activity or some kind of remittive state. So if you kind of step back and think about what would be the cluster of attributes you would really want to put into an OX40 molecule, it lines up really, really nicely with IMG007. All right, so let's now talk about atopic dermatitis. You've got a lot of, you know, numbers on this slide and facts. What I think we all have to appreciate is atopic dermatitis is one of the largest autoimmune disease states where we have a really under-penetrated patient population and simply not enough effective therapies. So take a look at this number on the bottom right, 49 million, almost 50 million adult patients. That doesn't even count the pediatric population, which is considerable. 50 million adult patients worldwide with moderate to severe atopic dermatitis that ought to be candidates for a biologic therapy. And yet, Even though this market is already 15 billion and growing year over year, only, look at the bottom, only one in eight patients, 15%, ever even get a biologic today. And of those, 30 to 40% don't get an adequate response. Let's remember that this entire biologic and JAK inhibitor market in atopic dermatitis is under 10 years old. So there are so many patients and so few categories of drugs that the growth potential is truly vast, and there's great room for a novel mechanism like Oxford. All right, so just a few points to really, I think, amplify here. Remember how I said that atopic dermatitis is considered a heterogeneous disease? If you look at the signatures of the cytokines in patients with atopic dermatitis, you can very clearly see that different patients may have different signaling pathways active. They probably all have some Th2, but this patient might have Th2 and Th1. This one might have Th2 and Th17 and Th22. To really address the needs of all patients with confidence, it's really appealing to think about a mechanism that might have impact on all of those different pathways, such as OX40. and we believe that if you can do that if you can bring the immune system back into homeostasis without killing the t-cells that really opens up the potential for deep unprecedented long-term durable responses and a lot of people with this mechanism talk about the potential for a true disease modifying effect potentially remission or a low disease activity state that could persist for you know many months we haven't really started to see all of that data yet with this mechanism but I think we will in the very near future what have we started to see well this is really the reason to believe so what you're looking at right now is data from the first generation OX40 agents. There are two of them. The one on the left is the Rocatinlimab program that has been discontinued from development. That is a receptor-targeted antibody. The one on the right is from Amlitellimab. That's a Sanofi program directed against the ligand, where they've announced an intention to file for regulatory approval later this year. So why are we showing this data and why is it remarkable? Let's start with the rocket data on the left. Take a look at these two graphs that look very similar. Those are different measures of nearly total clearance of atopic dermatitis. So the one on the left is using an investigator global assessment measure of clear or almost clear, but with a very high bar. And EZ90 means 90% or greater clearance of atopic dermatitis. So these patients have been treated continuously for a year. They were treated monthly. And what you see is that one year, over 60% were 90% or more clear. And you don't even see a plateau in the efficacy. So this data has been, I would say, really inexplicably overlooked, but it's really compelling. We think we have a molecule that can be even more efficacious as well as much more safe, and so this data is exciting. And then if you look at the right side, the amlitellumab data, it's similar. It's hard to make a direct comparison. That's directed against the ligand. Again, we think the receptor is intrinsically the more efficacious approach. so this is some of the data that we have in mind when we think about target product profile and what kind of efficacy we expect to see you know when our trial data is mature and by the way this kind of response has not been seen with any other mechanism with any on-market medication or anything that we've seen in development for atopic dermatitis so let's talk a little bit about our data in our trial. So we ran a proof of concept study in atopic dermatitis. It was admittedly small. It was 13 patients. It was open label. What we did was we gave three doses, just three doses in one month, week zero to four. And then the patients were followed out to 24 weeks. So what's exciting about this data and why I joined the company, frankly, is you see a really quite rapid decrease in this measure of eczema, the EZ score, and that then persists very nicely even though the patient is off drug. And if we think about this in terms of responders, EZ75, 75% or more clearance, 90% or more clearance at EZ90. It's 16 weeks. That's the same time point that dupilumab uses, the IL-13s use. 54% of patients were at EZ75, and almost a third reached EZ90. So those are very, very competitive numbers and really motivate us to be excited about where we are now in phase two. Let's talk a little bit about safety. So there's a really favorable emerging safety profile that we have seen. So we saw no serious adverse events, no treatment-related AEs, infusion-related reactions, no pyrexia, chills, apthos ulcers, malignancies, including Kaposi's sarcoma, really very, very benign. And I would also add that as we've continued development, we've started providing blinded safety reviews across all of our studies that have been incredibly consistent. So, you know, we think that what we expected to see with this molecule in terms of its safety is what we are continuing to see. We talked about all those different pathways and the ability of OX40 to address them. Well, here's some biomarker data that takes a look at that. So these are serum proteins that would be associated with Th1, Th2, or Th17 pathway signaling in cytokines. And what you see is across all of these pathways, at baseline, patients were out of normal range. And with anti-ox4D treatment, with IMG007, they were brought into the normal range. So we really do feel that we have evidence for this pan-pathway effect. So where are we now? We are squarely in phase 2b with the adaptive study. This is a schematic of its design that you see right here. And we have designed this study to be really robust and definitive to fully support our transition into phase 3 development upon its conclusion with selection of the right dose. so you see four active arms and a placebo arm with a crossover at 24 weeks which is the primary endpoint but the overall design is that we are treating patients for a totality of 48 weeks or their last dose is at 48 weeks so it's continuous treatment and we will get a really good view as to what continuous treatment with IMG007 is capable of. You also see that we have a triple low dose. So we were very excited by what we saw in the proof of concept study with those three doses and then no treatment. And we know in derm diseases, it can be important to deliver a lot of drug to the skin early on. So we have leaned quite heavily and in a way that programs ahead of us did not do into the idea of a loading dose regimen. So we're going to, I think, see if we can get both quite rapid and deep onset of action through this loading dose approach and then continue to build upon that through the course of the study. We're looking at two different doses, 300 and 600 milligrams, and we're looking at two different dose intervals, Q12 weekly and Q4 weekly. So we have a really nice overall range of exposures, and we're also looking at varying that loading dose regimen as well. So this really covers the space for dose finding, and we have a high degree of confidence that this will give us exactly what we need to move forward to phase three upon its completion. I also talked about alopecia areata. We're very excited about alopecia areata. We have a proof-of-concept study there as well. This is a newer area. We have no approved biologics for alopecia areata at all. There's only JAK inhibitors approved at a relatively high dose. And they are not very popular as treatments for alopecia areata. So there's a great need for a biologic that is durably efficacious and safe. And OX40 is quite heavily implicated in alopecia areata as well. So it's a very nice complementary indication for us. And it's not small. So just in the U.S. alone, you've got 300,000 people living with moderate to severe alopecia areata, just to give you some context. Here's the data from the proof-of-concept study. It was a similar design to what we did in atopic dermatitis. So in this study, we actually did run two doses, 300 and 600 milligrams IV. But same principle, three doses at week 0 to 4. And then the patients were just followed out to, in this case, 36 weeks. And you see the 300 milligram didn't really do all that much. That's not really a surprise in alopecia areata. Alopecia areata is considered tougher to treat. And, for example, we see higher doses of Jax used. So the expectation is you probably have to give a little bit more drug. But we do see a very nice response with the 600-milligram dose in 23 patients there for a mean change in baseline salt, which is a percentage of hair that's missing, up to 33% by week 30 and durable. And in this disease in particular, you know, nothing really says it like photographs. So these are three patients from our study, and you can see their progression over time. And again, this was in no way optimized therapy. We just gave three doses and followed the progress. So now as we move into a more well-structured approach into phase two, we're quite excited to see what continuous treatment and, you know, again, exploration of maybe some different exposures of the therapy can really deliver in alopecia areata. But if you've been following the space at all, and I'll just go maybe back one slide. You know, if you've been following the alopecia areata space at all, which is still pretty new, but, you know, is getting more and more attention, again, the magnitude of this drug effect that we saw in our proof-of-concept study I think stacks up very favorably compared to other emerging agents. And again, we didn't do any optimization at all. So we're really looking forward to initiating the phase two study later this year and continuing with that. Let's touch on the safety profile that we saw for alopecia areata as well. It was entirely consistent with what we have seen for atopic dermatitis. So, again, really nothing of note. And we've included the alopecia areata patients in our comprehensive safety review as well. So maybe just to close, we think we are in a fantastic spot to execute. I'm saying we're in execution mode at this point. Our study is on the rails. It's recruiting very well. It's currently active in the U.S. and Canada, and we will be bringing Europe and some other countries online over the next coming months. um we feel we are really putting a lot of attention into the execution uh execution excellence of that study and again being really focused on this we have the ability to really you know sweat those small details which can be extremely important in clinical development for both atopic dermatitis and alopecia areata um you know we do not believe that we will face the same challenges others have faced with, for example, placebo rates, but we've been very thoughtful in our study design and in our execution to manage some of those potential risks. So for this year, our focus is continuing to enroll and push forward the AD study and get the AA study started. Once again, top-line data is anticipated from the Phase IIb study in AD before the end of the year in 2027 and the AA data in 2028. We are fully funded to execute that, our runways into Q1 2028, with $145 million in pro forma cash. So thanks very much for listening to this overview, and I'm happy to take any questions if there are any questions okay well thank you very much and best wishes to everyone for the rest of the conference