ImageneBio, Inc. (IMA) September 2026 Conference Transcript

Good afternoon, everyone, and my name is Arthur Hur, a senior biotech analyst at H.C. Wainwright. Thanks for joining us today. We have a conversation with Dr. Christine Yarema, CEO of ImagineBio. Christine, thanks for coming down.

Thank you so much, Arthur. It's great to be here.

So maybe, Christine, for people meeting Imagine for the first time, Could you give us a quick overview about the company and what is the leading asset and what did you try to do with that?

Absolutely. So Imagine Bio, we're headquartered out of San Diego, and our lead program is Olivaprovart. It used to be known as IMG007, but now we have an INN name, so it's Oliva. And this is our next-generation receptor-directed monoclonal antibody targeting OX40. we believe it is truly next generation and highly differentiated i'm sure we're going to talk about that um but that's that's what we're doing and we're pursuing oliva in both moderate to severe atopic dermatitis as well as alopecia areata sure thanks christy so i guess is uh for ox 40 since the beginning of the year it's been a quiet journey um so and two of the program has accident in a topic program and so I guess a lot of people kind of reasonable question if the ox 40 is still a validated target I guess your answer is no but then why is that a wrong rate yeah so look I'll be the first to say that the ox 40 space has played out rather more dramatically than I think anyone anticipated but our thesis from the beginning before anything happened was that the first two programs in the space rocatinlimab and amlitellimab were very unlikely to uncork the full efficacy potential of of this pathway and of ox40 blockade and there are different reasons for that on each side, but the whole reason that I joined ImagineBio and came in to help drive this program to become a medicine for patients and create value is because we thought there was a tremendous opportunity for a differentiated molecule with the right features and attributes to show a lot more efficacy than either ROCA or AMLE with a favorable safety profile. And we engineered in those features into this molecule from the beginning. Now we're studying them in phase 2B, which is our adaptive study, which is ongoing. Sure.

So, you speak of the differentiator of the Oliver, and could you elaborate that and also kind of give us more kind of why those kind of special features of Oliver is important in the clinical?

Yes, absolutely. So, I said we're headquartered in San Diego. We're technically headquartered in a suburb of San Diego called Del Mar. Del Mar is famous because it has a big horse racing racetrack. And so I like to think of the features that are in our antibody as a kind of a trifecta of important attributes. So there are really three things that we hone in on that we think are critically important. The first is that the antibody is raised against the receptor, not the target. Now, rocotinlumab was also against the receptor, but it was a depleting antibody. Ours is not, and we're going to talk a whole lot about that in just a second. But we always thought that targeting the receptor would be the approach that would be more amenable to maximum efficacy through oxfordi blockade, because the receptor is expressed on activated T cells. And so if you want to get complete coverage of your target as quickly as possible and maintain that coverage, we think targeting the receptor is the way to go. The other molecule, amlitellumab, that targeted the ligand. And I think we saw in the data that it was, you know, less efficacious overall than rocotinlimab. So we feel we can go even, you know, to a much higher level but we were encouraged by by the evidence in the field the second feature is that as i said our antibody is non-t cell depleting so it it carries a mutation that silences the adcc function in contrast the discontinued rocatinlimab had an enhanced it was engineered for enhanced ADCC activity, and they published in Lancet, you know, very, very clear depletion, deep depletion of the T cell population. So it didn't just block the signaling, it killed the T cells. In contrast, what we do is just attenuate the signal, but maintain the T cell population and the other important functions of T cells. So that's important for two reasons. It's important for efficacy because rocotinlimab showed a lot of side effects. I think we're going to talk about Kaposi's sarcoma, but they also saw quite high rates of treatment emergent fever, pyrexia, chills, apthys ulcers, headache, a constellation of adverse events that has been associated with ADCC and T cell depletion. We haven't seen any of those. We've been doing ongoing blinded safety reviews across our entire program, and we've reported publicly that we have, you know, we have seen zero rates of any of those things. So we think one reason that you never saw much efficacy with rocotinlimab is they probably could not give a sufficient exposure. You couldn't really dose range that molecule because of the acute adverse events. But T cell preservation is also important from a safety point of view so we should be able to appropriately dose range oliva for more efficacy but we're not depleting the t-cells and so maintaining their function and then the third feature that has been engineered into oliva that's very attractive is it has a long half-life it's about 35 days so we think that that opens up the opportunity for you know very patient friendly dosing intervals. In our ongoing 2B study, we're looking at monthly as well as quarterly dosing, and that's just the starting point. It may be possible over time for us to go to even wider dosing intervals.

I see. So I guess you mentioned about Kaposi's sarcoma. Obviously, that's the kind of elephant in the room. But I want to see what you're thinking about the real issue for that risk for the Ox40 access and the reason or how you guys can mitigate those risks for Oliver.

Yeah, no, I appreciate the question, Arthur. So for anybody who's following this that may have, you know, missed the memo. So across the two programs that were ahead of us and were discontinued in atopic derm, there were four confirmed cases of Kaposi's sarcoma out of about, you know, a number of thousands, you know, maybe 7,000, 8,000 total patients across the programs. The cases all seem to have been in a particular sort of clinical phenotype, so elderly men, you know, potentially men with a history of sexual relations with other men. And it has also been circulating out in the community that those cases of KS went away upon removal of the study drug. So what has been seen in these programs ahead of us is definitely a signal, you know, worthy of attention and to take note of. We don't know if this will be something that we have to deal with with our program or not. We have not seen any cases of Kaposi's sarcoma, nor even anything, you know, suspicious or remotely, you know, resembling that. And we do think that our molecule could have the potential to be safer not only than rocotinlimab, as I mentioned, but also it may, you know, has the potential for favorability toward amlitellumab, again, because of that receptor targeting. The ligand that amlitellumab targets is expressed on cells that are the known reservoir of HHV8, the virus that causes Kaposi's sarcoma. So we like our molecule. We do want to keep an eye on this issue. And I think we're very favorably positioned to do so, Arthur, Because, you know, when you know the type of clinical phenotype that these cases have emerged in, and again, you know, the view is that it's been a quite consistent clinical phenotype, you can take measures to really ensure that appropriate patients are enrolled in the study and that appropriate physician-patient dialogue can take place. And we've incorporated some of that into our study. So we've looked very carefully at inclusion and exclusion criteria. We have done a lot of training, which our investigators have really appreciated on the whole topic of KS. And we have really instructed and counseled people how to properly monitor, observe, and have appropriate conversations between patients and physicians. We also remain very interested in the prospect for assaying for HHV-8. If you're not very familiar with HHV-8, this is one of the family of human herpes viruses, latent herpes viruses. And it's not very prevalent overall in Western populations. We think it's only somewhere, you know, a few percent, somewhere between 3% and 5% overall in Western markets. And that prevalence is inclusive of a much higher prevalence in certain subpopulations, such as MSM or elderly men of Mediterranean descent. descent. So if one had an assay, one could, you know, potentially screen for patients to see whether they were even, whether they even were positive for HHV8 at all. And if you don't have HHV8, you are certainly not going to get Kaposi's sarcoma. So I think we see, you know, as the dust has settled on this topic somewhat, that the view in the community is, it certainly is something to watch. We're very vigilant in our program, but that overall it should be manageable. And the real place to keep the eye on the ball is around the amount of efficacy that Oliva might deliver. So when we think about, you know, how can value be created? What is the profile of a drug that can be commercially successful? You really have to have definitive efficacy. You have to have market segments that you can target. And you have to have safety that rides along with that. So let's just put the efficacy need into a little bit more perspective. Atopic dermatitis is a very heterogeneous disease. And today, we basically have 50 million moderate to severe AD patients worldwide, only about one in eight maximum, somewhere between one in 10 and one in eight of those patients will ever even receive a biologic therapy. And of those, 30 to 40 percent are not going to get the kind of response that they want from that therapy. And at the same time, we really have, in the U.S. at least, only three real classes of approved advanced therapies. We've got dupilumab and the IL-13s, kind of IL-4, IL-13 class. We have nemolizumab, works on IL-31, doesn't really, you know, address disease symptoms other than itch. And then we have JAK inhibitors that work but carry, you know, their own significant safety liabilities. So we really need different mechanisms that can add to what we have with the potential to treat atopic dermatitis effectively, and I want to emphasize effectively, in a different way. And in particular, mechanisms that can treat disease more broadly than just focusing on Th2-driven disease, which is where, you know, DUPI, IL-13, emerging STAT-6 inhibitors would all fit. So our thesis and what we're looking for with this phase 2b dose ranging study is to show that with Oliva, we finally have the right molecule, you know, targeting this pathway with the right cluster of features. And by appropriately giving enough exposure and having the right molecule to begin with, we can see levels of efficacy that, frankly, we're never seeing with either rocotilumab or amlitellumab.

Thanks, Christine. That's a lot of very information there. And I guess you touched a little bit on the adaptive trial. I guess you guys guided for the readout at 4Score next year. So maybe you can set up some expectation for what we should expect for that readout.

Yeah, absolutely. So that's our guidance. The study is ongoing. It has been up and running for a little over a year at this point. We've been very happy with our recruitment and things are going well with the study. study. And we've been very intentional about this study. So, in fact, we amended it once to even further improve the design based upon some of the learnings that were coming out of the Amlitellumab program to really make sure that we were fully dose-ranging it and that we were going to come out of this study with, you know, clarity, absolute clarity on what would be the dose to carry forward into phase three. So we're looking at two different doses, two different dosing intervals. And unlike previous programs in this space, we're also really, you know, working with and studying very closely a loading regimen. We've seen loading regimens be quite impactful with some other drugs for other medical dermatology conditions. And we think with Oliva, in addition to it just being a, you know, putting regimen to get a high concentration of drug to the skin early, that we may see faster and deeper responses that really outpace anything we've seen with this class. and were encouraged from our proof of concept study data where we saw at 16 weeks over half the patients, 54%, had a mean easy drop of 87%. They maintained that. 54% reached easy 75 and almost a third reached easy 90, which is, you know, a difficult benchmark to reach. And that was with only three doses at week zero, two, and four. So in our adaptive study, of course, we're dosing continually. Our primary endpoint is at 24 weeks, but the study itself is actually looking at treatment for 48 weeks. And this will really be the first study, I believe, where we will see the impact of continual dosing beyond 24 weeks.

We certainly really haven't seen that data from the programs that were ahead of us I see so let's shift the gear a little bit so I believe in the alopecia area Oliver also kind of was it just the three doses they are keeping the hair growth until I think after a week of 36 that's right so I given dad I guess my question is I know you guys are looking to initiate the phase two study in alopecia as well so what could be a phase two data if you're going to call it a good outcome for for that study yeah so so you

know what you're referring to Arthur is that we have a second positive proof of concept study in alopecia areata and no one else has shown that kind of data with this mechanism ever but again it was unoptimized it was just three doses at week zero to four and then following the patients out to 36 weeks and we saw a mean decrease of about you know salt 30 for the patients that were enrolled in the word with phase two development in alopecia areata and we have guided that we will have some data for that in phase two in 2028 okay uh and so for that study initiate what's the gating factor now before the study getting well there's no gating factor uh so we're you know we're capitalized to you know through our phase 2b readout in atopic dermatitis and to uh you know to get the AA study going. So, you know, we're thrilled we were able to do that on the back of a modest pipe earlier this year. And, you know, so as you mentioned, our intention is that that study is up and going this year.

Good. And for, I think you mentioned the, you guys well capitalized. So what's the runway for the current cash in hand?

Right. So at our last earnings, we reported $136 million in cash. That carries us into Q1 of 2028. So it's inclusive of the top line readout for the phase 2B adaptive study. It doesn't carry us all the way through all of the data for alopecia areata, but it gets us with that study well in progress as well.

I see. Last question is, you guys are going to have two posters at the upcoming EADV, so anything you want to remind us to pay attention at the conference?

Yeah, so, I mean, one of the two posters really does, it's, you know, it's going to showcase the PK and why we've designed the adaptive study the way that we have. You know, you'll see, you know, with real numbers, which you don't always get with PK data, you know, how we're looking at a twofold range of CMAX, a fourfold range of total exposures. So, you know, the adaptive study is meant to be really robust and definitive and has been, you know, carefully designed to do that. So, you know, again, others ahead of us have definitely had their problems with this pathway, but we don't think they had the right molecule, and I'm not sure they had the right study design either. So, you know, take a look at that, and we will also be continuing to really invest in and build out underpinning science, so a scientific story and more of a research and translational medicine program to really elucidate a lot of Oxford E biology that we think has been overlooked and not yet sufficiently developed.

Awesome. Thanks, Christy. Thanks for coming.

Thanks, Arthur.