And we’re not going to do that. So we think we’re going about the right way. We think it’s the prudent, but a prudent, but also ensuring that we ensure fast to market, and we’re confident that we’re on the right track right now.
Unidentified Analyst : Great, thank you so much. And then on the ARVO data?
Nancy Lurker: Jay, do you want to take that ARVO data?
Jay Duker: Yes. So the model that was used was a retinal detachment model in animals. After retinal detachment is created, the photoreceptors will degenerate because they’re no longer in contact with the retinal pigment epithelium. And what you’ll see from our data is that eyes that were treated with Vorolanib had much less damage to their photoreceptors and their subsequent visual acuity than the control eyes that were not treated. This is a model for neuro protection. Retinal detachment technically is subretinal fluid and you may be aware that subretinal fluid is also a feature of wet macular degeneration, and diabetic macular edema. So, while this is a general model for neuro protection, we think they will possibly and likely be read through to the diseases that we’re currently treating with EYP-1901.
Unidentified Analyst : Great, thank you so much.
Operator: Thank you. One moment for our next question. And that will come from the line of Georgi Yordanov with Cowen. Your line is open.
Georgi Yordanov: Hi, everyone and congratulations on all the progress. Thank you for taking our questions. So maybe starting with the Rallybio partnership, we didn’t notice they have two C5 assets based on the antibody platform. Maybe can you talk about the requirements of putting a large protein into the Durasert, maybe talk about why some previous attempts to develop long acting Eylea have not been successful and in general what gives you confidence that you’ll be able to formulate it with one of Rallybio assets? And then we do have a follow-up on the DAVIO trial.
Nancy Lurker: Yeah, let me just — let me make one quick comment and I will let Jay take it from there. First of all, let me make a statement on this, the Rallybio C5 is alpha body, it’s a smaller — it’s smaller than the large ligand blockers, like Eylea that are on the market today. So I want to make that clear, it is not as big as an antibody. So that’s a key point. Second of all, I’m not going to claim this is going to be easy, it’s not, but we do have a stellar scientific team. And they’re already going to quickly begin working on this. So we’re — we’ll see what happens. But I think this team is very, very well versed in how to deal with this and hopefully, we can be successful. Jay, you want to go ahead.
Jay Duker: Yeah, so in order to get a drug to work in Durasert, there’s a lot of different factors. The size of the molecule is really what helps to determine the payload. Obviously, bigger molecules, you’re not going to be able to get as many into an insert. So that’s one factor. Proteins in general tend to degrade at body temperature and that’s why small molecules have been preferable. Our team is optimistic about our ability to deliver this alpha body in a sustained release fashion. But until we really have some data to share, I would say that, again, we are optimistic but as Nancy said, this is — it has a difficult path, others have tried and with large molecules and they have not been able to achieve it. But we’re optimistic.
Georgi Yordanov: And do we have any idea of — have you disclosed when you could potentially hear an update on the progress of this program?
Nancy Lurker: No, we’re not going to get that right now. It’s way too early for that.
