That body of evidence makes it a compelling pathway. The recent readout from Sanofi that we mentioned looks completely in line with that. So it looks to be safe. It looks to be effective. And what was interesting in that study is that the effects seem to get better over time, which is what you’d expect if you were able to reset the immune system. So for all those reasons, we think the pathway is very exciting and has broad potential in a growing space in atopic dermatitis and also in other conditions. ABCL575, as I said, we believe, is one of the first behind it. Now you don’t know what people have inside their pipeline that they haven’t disclosed. But based on disclosures, we think this one has the potential to be one of the first to come behind it.
And we have engineered it in a way that we think provides the combination of potency and developability and formulation and half-life that would give an advantage in dosing. So that’s why we’re excited about that particular one. As it compares, I think you mentioned Regeneron and Dupixent. Dupixent is obviously an amazing drug. Our view is that in inflammation, not every patient responds to the therapies that are available, and there is a lot of interest in finding alternatives and perhaps even combining therapies in the future. So we don’t see that as a negative at all, but rather as an example of the huge opportunity that exists in this space.
Robyn Karnauskas: And just as a follow-up, do you think you can improve upon — I mean, their view is that the current ones they have are just not going to — or current ones that are on the market are too dirty, I would use that word like they’re too broad? Like what AbCellera technology can you use to understand to make a better Ox40 because that is a hot target right now. So, maybe you can show up what the technology as well, and then I’m getting back in the queue.
Carl Hansen: So to be clear, so we have an antibody that is going to get Ox40 ligand, not Ox40. There is, of course, an Ox40 antibody that is being developed by Amgen. That antibody is a depleting antibody. So it’s an antibody that binds Ox40, which is presented on T cells and that causes the ablation of those T cells. There’s some evidence that, that may cause problems. I mean I don’t want to speculate too much. The antibody that we have engaged an Ox40 ligand, which is not presented on T cells, but rather on antigen presenting cells. And our antibody has been engineered to be non-ablating. So it has Fc Function that does not result in the killing of the antigen presenting cells, very similar to amlitelimab, which I mentioned, which is being developed by Sanofi.
So we don’t see a problem with it being dirty. We don’t see a big problem with toxicity. And of course, we’re getting that information from the disclosure that Sanofi has made and they’ve got the most advanced molecules. So to our knowledge, this looks like a quite clean profile and one that’s effective and one that has a lot of potential in inflammation and other conditions.
Operator: The next question will be from the line of Andrea Tan with Goldman Sachs.
Andrea Tan: Carl, maybe one more question for you on 575 here. Strategically, can you speak to the decision to pursue atopic derm as the initial indication. Just curious given how crowded that landscape is. If there are other indications where mechanistically, it might make sense to also bring this asset forward but one where you could have an advantage of being first-in-class.
Carl Hansen: That’s a great question. I mean atopic dermatitis is the most obvious place because there is the data out already showing efficacy. It’s also — in derm is one of the easier places to get early clinical data that shows efficacy, let’s say, in a Phase I or IIa trial. So that’s probably the main reason. We feel based on the pathway and what we’ve seen in the clinic from other molecules that this has a very high likelihood of working, not just in atopic dermatitis, but in other conditions. That’s our sense right now. But this is a competitive space, as you mentioned. So right now, what’s most important is that we not delay in getting this molecule through to the start of clinical development and through the early trials.
