Summit 2026. My name is Yatin Suneja, one of the biotech analysts here at the firm. Our next company, or presenting company, is Surrozen, and I will be having a discussion with the Chief Executive Officer, Craig Parker. Craig, thank you so much for making time for us, always good to see you. Nice to see you. Why don't you make some opening comments, just to orient our investor on what we should be focusing on or what are the upcoming milestones, and then we go into the Q&A, if that's okay? You bet. So we're a combination of a Wnt biology company and an antibody engineering company. We've been that since the company was founded in 2016. We have a background in this really powerful biology called the Wnt pathway, that's really critical to development and to the function and structure and maintenance of function in a lot of tissues, including the eye. You know, we've pursued some other therapeutic areas and tissues because of the importance of Wnt biology, but we and others know that there's a particular receptor involved in Wnt signaling that's really critical during both embryonic development of the eye, as well as maintenance of normal retinal vessel and choroidal vessel function in the eye. So we're bringing this very powerful biology of the Wnt pathway, together with agonistic antibodies that are able to activate the pathway, focusing, in this case, particularly on a receptor that we know is intimately involved in retinal vessel function, called Fzd4. Mm. We know that's really important because there are some human diseases associated with loss of function of that pathway through the Fzd4 receptor. These are extremely rare diseases. We don't know that the drug would work actually where there are mutations present, so no one in this field is pursuing those very rare diseases. They're called Norrie Disease and FEVR, but they provide really important validation that this pathway needs to be functioning normally for there to be normal retinal vessel function. Where is that relevant? It's relevant in the really big retinal vascular diseases, like diabetic macular edema, wet AMD, probably retinal vein occlusion. And we're a bit behind now, but Merck has a molecule with similar pharmacology to one part of our molecule- Yeah ... and has shown really compelling phase I, II data. They're in a phase III trial right now, first of which we'll read out in September, that I think confirms that this pathway has a really important role in control of diseases like diabetic macular edema. And we think, and, Merck probably thinks as well, has an opportunity for, you know, really a truly disease modifying-type effect in the, in the disease because of some of the biological effects of Wnt signaling. Got it. Very good. Thank you for that sort of intro and helpful... I think if you can put in context, mechanistically- Yeah ... why it is relevant in these retinal vascular diseases. Are there particular type of retinal vascular disease, whether it's DME or AMD, where the rationale is more stronger? And then also talk about... Because historically, the pathway has been out there, right? But historically, it has been very challenging, mostly- Yeah ... on the safety. So why are we seeing sort of a change here right now, like what is driving that? A cell biology friend of mine's got a, I think, a great way to visualize, like, how important and difficult this pathway has been. He says, like, "Wnt is on the Mount Olympus of undruggable targets." The company was started because of the potential to overcome some of those limitations. I won't go into them. Yeah. There are certain ligand receptor- Yeah ... interactions that are fairly unique to the pathway. It's impossible, really, to make a recombinant protein that could be specific for the pathway. So one, that's, those are a couple of reasons why it's been undruggable. We have bispecific or multispecific, multivalent antibodies- Mm-hmm ... that are able to target to individual receptors in the pathway, so that's one way we've overcome- Yeah ... some of the limitations in the past. I think the safety, you know, this is a pathway that's really important physiologically in all of us. If we didn't have normal Wnt function, our intestine would not function normally, our bones would not function normally, our liver would not function normally, our eyes would not function normally, most epithelial tissues would not function normally. So it's a pathway that's active and physiologically relevant- Mm ... in all of us. So that's how I think about safety, is normal Wnt function is actually required for normal tissue function. Mm-hmm. I see. With regard to the relevance in vascular diseases- Yeah ... or retinal diseases. Yeah ... one versus the other. Yeah. So, as you all probably know, you know, the approved and very effective drugs in diabetic macular edema and wet AMD are blocking VEGF- Yeah ... and in one case, the Ang2, Tie2, activating that pathway. So, it's a very different biology to be inhibiting a pathologic factor like VEGF, where if it's present, it's contributing to the development of the disease. Yeah. What potentially Ang2, Tie2 are doing, that Wnt we know is doing, is restoring normal vessel architecture and function. So in DME, we know, and our experimental data supports this, and you can find this in the literature as well, that when you activate the Wnt pathway in the eye, you're upregulating what are called tight junction proteins- Mm ... which create the blood-retinal barrier in retinal endothelial cells. And so basically sort of sealing the leakage. So instead of inhibiting something that's causing leakage, we're actually directly reducing the leakage at the level of the cell-cell interaction. That's particularly relevant in retinal vascular endothelial cells and DME, because we actually see that tight junction protein increase, and then basically sealing up that leaking. Okay. There's a similar process in the vessels that are involved in wet AMD. It's not quite as direct, the biology, but we and others have shown that you can also prevent that leaky barrier function in the choroidal vessels as well. It's just really demonstrable and clear in diabetic macular edema. Got it. Is there a particular experiment you need to do in humans to prove that? How do you prove that in DME, that this disease-modifying effect- Mm-hmm ... is very, very unique to this mechanism? And what is the duration of those sort of experimental like? Yeah. We can use very typical imaging methods- Yeah ... to show better drying. So if you're normalizing the retinal vessels, you should see- Yeah ... a drier retina. We just use typical OCT- Yeah ... or even OCTA or wide-field angiography type of outcome measurements. These are what are used in, you know, across the board in the field. There are also some areas, in diabetic macular edema, that are called areas of retinal non-perfusion. And so these tend to be more peripheral, but VEGFs don't do anything in these areas. They do nothing to revascularize these areas. We see in mouse models that we can do that, and we'll be looking to that in our first clinical trials as evidence of this normal vascularization of areas of the retina, in addition to reducing vessel leakage. Got it. And then these things can be captured within a, let's say, 52-week studies? Oh, yeah, these. So if you look at other, but this is true for the Merck Wnt molecule as well as for anti-VEGFs. There's an almost immediate effect, so literally within probably days, but certainly within the time points of patient visits, which is four weeks, eight weeks, 12 weeks. You know, you see a pretty dramatic reduction in fluid- Yeah ... in the macula, and improvement in visual acuity within four weeks. Those are the- So these are really near-term, really near-term outcomes. Got it. So who are the players? So there is Merck there. Who are the players, and how are you situated within that sort of competitive landscape, and what is your offering? I think you have three programs, right? Yeah. One is with BI, two of your own. Just walk us through all of them. So the current market is, say, roughly split between Vabysmo, which is a Roche product that's VEGF and Ang2, and Eylea, both the 2-milligram and HD formulations. I think last time, last quarter, those were, you know, pretty close to half the market- Yeah ... each globally. You know, there are some smaller players, people without either without insurance who have to pay out of pocket, or certain payers require that compounded Avastin be used first, but that's a very, very small portion of the market currently. Lucentis, the first drug approved in this in 2006, very, very small portion of the market. So that's, that's the, the current market is really dominated by those two molecules- Within the Wnt ... franchises. I think my question was more on within the Wnt biology. Ah, okay. Who are the players, and how are you positioned? You know, the history of pursuing these kind of multi-specific antibodies, there were really just two players. There was Surrozen Mm-hmm ... and there was an academic at University of Toronto. That discovery is what became Restoret and now MK-3000. I see. So, that was spun out of a small company that he started in Canada. Merck acquired what was just that individual Fzd4 LRP5 molecule from EyeBio. The rest of that portfolio that, his name is Sachdev Sidhu, discovered was sold to Roche. I see. We think Roche has a Frizzled LRP that would be a direct competitor to Restoret, that would be a direct competitor to the BI molecule, our molecule that we licensed to BI. Those are just Wnt. Mm-hmm. Our lead molecule is Wnt plus VEGF inhibition. So even though we think there's all this powerful biology that I described in activating the Wnt pathway, we still think that inhibiting VEGF can contribute to better clinical outcomes. And I think there's just growing evidence that combinatorial approaches have additive benefit in these diseases. Got it. So let's maybe address your or talk about your program, 8141 and 8143 first, and then we'll come back to the Merck Brunello and Amarone readout. What are these molecules? Where are you on the development front? I think the IND is supposed to clear this year. When, like, what work needs to be done before you clear the IND? So maybe I'll start off with just the timing. Yeah. We'll update this, you know, with a little more specificity. We've just said 2026 IND. You know, we'll lay that out, the timing and the exact trial design and expectations for data from that study sometime soon. You know, the molecule itself is the Wnt business end of the molecule is pharmacologically really doing the same thing that- Yeah ... the BI molecule is doing, that the Merck molecule is doing. Okay. We think there are some important characteristics, biophysical characteristics or potency characteristics, that will differentiate the Wnt end of the molecule. We are the most potent Wnt agonist- Mm-hmm ... but we also have the VEGF inhibition- Yeah ... end of the molecule. So it's a bispecific. Yeah, so it gets a little confusing because, like, we started referring to this as multifunctional, because our molecule for the Wnt end is binding two of the same Frizzleds and two of the same LRPs. Got it. Formally, by antibody nomenclature, it's a bispecific tetravalent molecule. Got it. Merck binds two different epitopes, so they refer to theirs as trispecific. I see. It's the same pharmacology. Then when you add the VEGF, if you wanna actually use correct antibody nomenclature, it's trispecific tetravalent, and that all just becomes way too much of a mouthful. So- Molecule. Ours is WNT plus VEGF. Plus VEGF. 8141 is Wnt plus VEGF. The VEGF end of the molecule is behaving exactly the same as Eylea. Eylea. In fact, it's the same sequences, because they're publicly in the public domain now as Eylea. Got it. Where are you on the IND work? Maybe if you can just elaborate a little bit more on- Yeah, I mean, we're just, you know, completing some of the typical last stages of IND-enabling work, both on the CMC side and the tox side. And, you know, we haven't really given more details than that. Yeah ... but everything's going well. And then given that, you know, it's dual targeting, like, how should we think about the potency relative to Eylea? What about the volume, concentration of volume? Yeah. Where you are on the formulation work, all of that? Yeah, this is, you know, this is quite a large molecule. This is a 220 kilodalton molecule. So when we started out on this path, there were some risks associated with the complexity of the molecule. It's turned out to be actually extremely easy to manufacture and to concentrate. Mm-hmm. So I think we've disclosed, and Lonza has repeated this work. We have gotten to over 100 mg per ml concentrations with low viscosity, so acceptable viscosity for an intravitreal injection. That would allow you to give milligrams of drug, if you wanna do the quick calculation. And sorry, what was the second part of your question? Okay. The question was, like, what else...? Is the formulation ready, or you need to do more work to optimize it? Yeah, no, there, there's no more formulation work that's required. Okay. And then, hopefully you'll update the timelines on IND. Mm ... relatively soon. How far behind is 8143, the second molecule, and how differentiated it is? Mm-hmm ... what is the key feature of 43 versus 41? Yeah. Yeah, so we'll update timing, you know, for that molecule. It's months behind, it's not a year behind, 8141. So it's a similar molecule that adds IL-6 inhibition. So now you're talking about what we call trifunctional. Trifunctional. So Wnt activation, VEGF inhibition, IL-6 inhibition. You know, I think, people who follow the field know that, Roche and Kodiak and others- Uh-huh ... have shown that IL-6 is important, not just in UME, which is known to be a more inflammatory-driven macular edema, but in DME. Roche had some data with the combination of separate injections of an anti-VEGF plus an anti-IL-6 that showed clear incremental benefit in DME. So there could be an argument for 8143 to be the best molecule across the board in retinal vascular diseases, but I think initially we would see it as having a complementary positioning in the market, where 8141 is DME and wet AMD, and 8143 is UME, or what- Yes ... Kodiak calls MEIE. So these are inflammatory-driven macular edemas that are either because of background chronic inflammatory diseases or post-surgical inflammation. Got it. Got it. So now I wanna go back to the MK molecule, which, you know, is the Restoret molecule which they acquired from EyeBio. So I think they're running a few studies, but I think the two studies, the DME study is gonna read out this year. I think it's the phase IIb/III BRUNELLO study. What are your expectation? Could you just talk about- Mm ... you know, what are you expecting to hear or learn from them? So, they have two parallel Phase IIIs, same design. Yeah, one, they've said this now publicly, one reads out, first will read out in September, the second in March. Yeah. You know, everyone has their own definition or expectation for what top-line data means, so I'm not sure how much they'll disclose. I would guess it's gonna be best-corrected visual acuity data, which is the primary endpoint at 12 months, and perhaps retinal thickness, which is sort of total fluid in the retina. This is called CST. So, and I don't know, and perhaps safety, I don't know exactly what the totality of the data is gonna be. I think... So this is a study comparing Restoret alone with ranibizumab- Yeah ... Lucentis- Lucentis ... given monthly. What I think would be very supportive of this multifunctional, multi-target hypothesis is, you know, anything close to ranibizumab-like activity, of course, very good safety is a requirement in this field. I think would be very supportive of what we're doing. I don't think it has to even be at the level of ranibizumab- Mm ... to be supportive, that it's alone, has very good activity, and as I said, there's emerging evidence across the board that combinations can buy, can, can, create additive benefit. So, you know, if it looked like their Phase I, II data, you know, they'd have very, very good, you know, even Eylea-like, BCVA and- Yeah ... and drying effects. Got it. Got it. So it's dry, you know, visual acuity is a very tough. It's tough to be better than the best drugs today. But what we really look to, and we think the way products are really getting differentiated in the market, and where our mechanism suggests the opportunity for the most differentiation, is on the retinal anatomy, and that's measured through some of these drying endpoints, fluid endpoints. Got it. Very helpful. Then, you know, you also have a partnership with Boehringer Ingelheim, where they have one of your assets, SZN-413. Mm-hmm. What, what is that partnership? Are you doing anything for them? Do we have an update on when they might move that in the clinic, if they have not already? ... So this is a deal that we, I think, signed in 2022. We actually started negotiating it quite a ways before that. We worked on Frizzled-4 quite early, and then ended up partnering our first molecule. We've received, I think, $22.5 million total from the deal, which we thought was an attractive deal for a preclinical asset at the time. We had a very collaborative research phase, where we had normal, frequent, research team meetings. We exited that phase when they nominated it as a development candidate, so we just get infrequent updates from them. And so I'm hopeful they'll be in the clinic soon, but we won't know that until something shows up on clinical trials or we get paid our milestone for dosing patient. Okay. Okay. What about Roche? Do we know where they are? We have not heard anything from Roche. No. Yeah, I just know that they acquired that library of Frizzled and LRP binders that, again, were derived from University of Toronto work initially. Got it. Got it. So for you, I mean, obviously, two key things that we should be focusing on, right? One is obviously the MK data- Mm-hmm ... which provides the derivative read-through, and then obviously, the IND clearance of at least one of the molecules, which is, you know, 8141. Okay, I think that part is good then. Maybe just walk us through the IP estate, if you could, the scope and the strength of it, and then if you can also touch on the cash and the burn rate. So, I think as I alluded to, we discovered these molecules. These are wholly owned molecules. Our scientists are inventors on the patents. We've been, I think, pretty forward-leaning in building a broad patent estate around our discoveries. We have something like, not all of these have continued to be pursued, but 38 patent applications. Some of them have issued, including, quite a broad, what we think is a broad patent on, multivalent Frizzled and LRP5 or LRP6 binding antibodies. You know, we'll continue to try to strengthen our intellectual property as initial discoverers of these type of molecules to activate Wnt signaling and, you know, ultimately, if it gets to this, asserting what we think are the rights that go along with those patents. Got it, got it. How is the financial health, capital, and the burn rate? Yeah, so quite good. We did a PIPE in March of 2025. The total size of that was $175 million. Seventy-five million of that we received in March. We received a hundred million when our IND is open. There are some warrants associated with that. As of we haven't filed our K yet, but as of the third, end of the third quarter, we had $80 million in cash. Got it. Very good. Well, very good, Craig. Thank you so much. Thank you. That's all I have.