ImageneBio, Inc. Common Stock H.C. Wainwright 28th Annual Global Investment Conference

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

Absolutely. ImageneBio, we're headquartered out of San Diego, and our lead program is Olevaprubart. It used to be known as IMG-007, but now we have an INN name, so it's Oleva. 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. That's what we're doing, and we're pursuing Oleva in both moderate to severe atopic dermatitis, as well as alopecia areata.

Yeah. So look, I'll be the first to say that the OX40 space has played out rather more dramatically than I think anyone anticipated. Our thesis from the beginning, before anything happened, was that the first two programs in the space, rocatinlimab and amlitelimab, were very unlikely to uncork the full efficacy potential of this pathway and of OX40 blockade.

There are different reasons for that on each side. The whole reason that I joined ImageneBio 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 Roka or Amli with a favorable safety profile.

We engineered in those features into this molecule from the beginning. Now we're studying them in phase IIb, which is our adaptive study, which is ongoing.

Yes, absolutely. 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. I like to think of the features that are in our antibody as a kind of trifecta of important attributes. 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. Rocatinlimab 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. We always thought that targeting the receptor would be the approach that would be more amenable to maximum efficacy.

Through OX40 blockade. Because the receptor is expressed on activated T cells. 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, amlitelimab, that targeted the ligand, and I think we saw in the data that it was less efficacious overall than rocatinlimab. We feel we can go even to a much higher level.

I see. But we were encouraged by the evidence in the field.

The second feature is that, as I said, our antibody is non-T cell depleting. So 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 The Lancet, 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 rocatinlimab showed a lot of side effects. I think we're going to talk about Kaposi sarcoma. But they also saw quite high rates of treatment emergent fever, pyrexia, chills, aphthous 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 seen zero rates of any of those things. So we think one reason that you never saw much efficacy with rocatinlimab is they probably could not give a sufficient exposure. You couldn't really dose range that molecule because of the acute adverse events.