Here in New York, yeah, here in New York, so it's good to be back here looking at the summer. We're close to mid-year 2025, and at Kodiak, we have been very busy, and we have a number of activities in progress and a number of activities in preparation. It's an exciting time for Kodiak. It's an exciting time, I think, for people to look at us and to think about what our potential is as a company. We, of course, have always tried to be science-driven and to think about the design of our molecules and the designs of our clinical studies. I think we've learned a lot, and we've put all of those insights around the science and the design of our medicines and now the designs of our clinical trials. The third element is sort of the design of Kodiak's portfolio. So what does Kodiak look like? You know, what are we going to look like, and how fast is all of that going to come together? It's a fun moment to ask those questions because, actually, the many years of preparation have really brought us to this moment. We have the tarcocimab, our lead, the antibody conjugate in retina for wet AMD and diabetic retinopathy as well, and also retinal vein occlusion, so 3 very big indications. We have that in the GLO2 study that's been fully enrolled now for some time, and we'll have top-line data from that in February of next year. We also have tarcocimab together with KSI-501, our VEGF IL-6 bispecific conjugate, together with tarcocimab in the DAYBREAK study in wet AMD. That's enrolling well. We are working hard to have enrollment near completion at the R&D Analyst Day, which is scheduled for mid-July. We are working hard to achieve that. In any case, what we will have is a clear update about the enrollment of DAYBREAK, in my own mind, targeting, you know, the end of the second quarter or, let's say, the end of June of next year for top-line data. Okay. For our ABC medicines, the conjugates, the antibody conjugates in retina, we have tarcocimab in the GLO2 study reading out in February of next year, and we have both tarcocimab and KSI-501 reading out in and around, let's say, June of 2026. Those reflect the new formulations both for tarcocimab and 501. That is really the science kind of update or the scientific insights that we had looking at our prior studies and looking at the design of the molecule. The objective, of course, has been durability, improved durability in retina, but it is important that durability should also come with efficacy. It should also come with immediacy of activity. Ideally, it comes in the form of a biologic. That is what Kodiak built with our ABC platform and the new insights of the enhanced formulations. How do we tweak what we have, not just to deliver the world's best durability as a biologic, because we've really proved definitively that we have that? We have the aqueous tap data, might that we shared when we took samples from the eyes of 50 patients over more than 6 months and showed that we do have the world's best durability as a biologic in the retina with a mean of 20 days and a range of 5-50 day half-life in the patients, compared to the other biologics, the marketed biologics that have, say, a range of 6, 7, 8 days. We have the world's best durability with our platform as a biologic. What we looked at was, in some patients, our immediacy was weaker, perhaps given the large size of the conjugates that we make. We were able to make a straightforward modification, I think a thoughtful scientific modification to the platform, to tarcocimab and also to 501, to have now a mixture of unconjugated protein and the conjugated, to have sort of a co-formulation approach to drive that immediacy of that smaller antibody at a full pharmacologic dose, together with the majority of that being the conjugated form. Having applied that both to tarcocimab and also to KSI-501, having put tarcocimab back into diabetic retinopathy as a GLO2 repeat study in DR, which, by the way, is really an amazing indication opportunity for us and for patients with many millions of potential patients. We have some amazing images we want to share at the R&D day where you can really see the angry eyes of these diabetic retinopathy patients with hemorrhages all over. In the context of the GLO1 data, where we move to twice-a-year dosing with tarcocimab in those eyes to just show total clearance in an amazing, beautiful-looking eye in the patient. A real opportunity with the twice-a-year safe biologic medicine, even in DR, which is really a forgotten, unknown indication in retina, to massively open that up with a new kind of biologic with tarcocimab. Of course, that is not even talking about RVO, which is, you know, 10-15% of the massive anti-VEGF market, plus the opportunity that we are showing in DAYBREAK to really solve the problem finally in durability and, I would say, the combination of efficacy/immediacy and durability in wet AMD with a biologic, which is what tarcocimab can offer. The DAYBREAK study will allow us, I think, to definitively show what can our technology, what can our science, what can our products do in wet AMD against aflibercept. As I said, we have both tarcocimab and KSI-501 in that study, which is a nice, innovative design. It is efficient and smart. We are very excited about the 501 with the combination of the VEGF and the IL-6 in wet AMD as a conjugate with the enhanced formulation. A smart study design in DAYBREAK allows tarcocimab to go out to every month dosing all the way out to every 6-month dosing. Then 501, we are going more narrowly every four and every eight weeks versus Eylea's 3. Let me summarize that the lead program, tarcocimab, your VEGF antibody, that I agree has shown the longest durability in a randomized controlled study. I would have to quote the exact number, but I think it's almost 50% of people went out to 5 months, somewhere around that, right, Victor? Yes. That's the greatest durability that has been seen, although the primary endpoint had been missed in that phase III study due to an aggressive study design. Therefore, we are going back to redo that phase III. That phase three III will read out, as you said, potentially in the summer of 2026. Hopefully, we've got that completion of enrollment announced at this Analyst Day. We'll see in a month. We, meaning you, have a package for tarcocimab where you have at least one or two positive phase III studies from a couple of years ago, and you're trying to revisit one or two phase III studies. One is DR, which I think you just said should be an easy win. I want to be careful with that word because nothing is so easy in biotech. That DR study reads out in Q1 of next year. I think you said February. That's right. That should be very high probability success to hit because it's essentially identical to the one a couple of years ago. You agree? Yeah, that's a BLA package for DR and RVO right there. We believe the DAYBREAK study's process. Then this AMD study coming back, if you take a look at it, I would encourage investors to take a look at this because the durability's all there. It was just an aggressive study design, and you did not allow for people to offer the opportunity to get monthly dosing. Now it is a more straightforward design, more traditional design where you allow monthly and all the way up to 5 months? 6 months. It's up to 6 months. Yeah. All right. Therefore, we're going to see a good breakdown where people are going to hit the primary endpoint, but also people have the ability to see that you're going to have, on average, up to probably 4, 5, 6 months of durability. That should be pretty high probability success too. You agree? I think so. The study's progressing very well. It's a study design where we lean away from the risk because we've put more science into the molecule. It's our third wet AMD study. Don't forget we have the monthly wet AMD study with tarcocimab DAYLIGHT that we ran. There is already one positive phase III study as well. Let me be clear about this. Appreciating we need to execute and we need to get to next year. In the minds of Wall Street, you know, sometimes that's a little bit far away. We got to get there. You're planning to file multiple positive phase III studies to the FDA next year. I'll hold you. It's a, you know, after sometime after that results. You should be at the FDA with a complete package. What would you be asking for? You'd be asking for an AMD, DR, RVO label? That's correct. You believe then, so therefore, what is the value proposition if this occurs versus high-dose Eylea, which is on the market? I think Regeneron was around here somewhere. You have got high-dose Eylea. You have got Faricimab. You know, there are some huge multi-billion-dollar drugs out there that are on the market. How are you differentiating on that product? You are appreciating your layers to market. I think the commercial, the continued commercial success of the Eylea franchise and the new, perhaps surprising commercial success of the Vabysmo franchise give us a lot of confidence that our products, tarcocimab, and then, say, following behind it, the KSI-501, as biologics can have tremendous commercial success because everybody has been sort of skating to where they're trying to get to, which is immediacy, efficacy, and durability. Really, only tarcocimab and, say, 501, our platform and our products have the potential because nobody has actually arrived at that kind of promised land yet. Eylea HD gives you a powerful immediacy, let's say, and the Vabysmo gives you some combination. I think what the KOLs, they call them generation 1.5 agents. They really have their leg still in the past. What we are trying to do is to have our dominant leg really in the one place that nobody's been able to get to yet with biologic. Okay. It's pretty exciting. I think we have a tremendous opportunity. What we need to do is clinch it with a strong win in DAYBREAK. Okay. I think based on the new scientific design and the design of the study and how the study's prosecuting so far, we really have an amazing chance to be that winner. If you go back and people feel comfortable that the efficacy of the program will be resolved because of the trial design here in the AMD study, and that seems reasonable because you just kind of walk through the, we fixed the study design to work now. Safety was also a head-scratcher a couple of years ago. Maybe just talk about, in my opinion, in Wall Street's opinion, numerically higher inflammation, but also some additional side effects that you think may be improved on with the design of the new molecule and why you think that won't be an issue because, as I recall, I think that was in DME, to be fair. Yeah. Maybe that won't be an issue. Can you just talk to the safety components of this and why you feel comfortable? We always push back a little bit on the criticism of the IOI and the intraocular inflammation. I think our blended rates of intraocular inflammation, I think we've given over 13,000, maybe approaching 14,000 injections of our ABCs into patients at this point. I liked at the R&D day we had in September where we had David Brown and Charlie Wyckoff, who are top KOLs, and I believe they've both in their sites each dosed more than 100 patients with our medicines. Yes. They said they have 0 concerns of safety with Kodiak's platform. I mean, look, I'm the analyst. I was there. Like David Brown and the second one was. Charlie Wyckoff. Charlie Wyckoff, 2 of the most renowned folks in the space. I thought it was interesting. They both came up and said, "We are definitely not getting paid. There's no way." You know, those are tough guys, but David Brown is a well-known tough guy. They basically were up there in support of the programs and involved in the studies and said there was differentiation. Yeah. They are well known as tough guys. Yeah. On the IOI, just to say, our blended rates of inflammation are the same or even maybe even better than Vabysmo. Okay. It's not as though we have an overhang in that regard. Okay. All right. So going back to the issue in the diabetic DME patients, how you fixed that? Right. In the DME studies, GLEAM and GLIMMER that we ran, what happened is we had an imbalance in cataracts versus Eylea. Let's say Eylea had, as our comparator, 10% adverse event and we had 20%. That difference led to impact on the vision, and that destroyed the studies. The first thing is to say that in our DAYLIGHT study, which was in wet AMD with the same molecule where we dosed once a month for a year and Eylea was every other month, tarcocimab had fewer cataract adverse event rate than Eylea. It is not something that related to the indications in the BLA. Repeat that again. I didn't catch that. Compare it. In DAYLIGHT, we have fewer cataracts than Eylea, even though we dose monthly for a year. In AMD? In AMD. Okay. Yeah. I think that's important, number one. Number two, in the small number of the DME patients, let's say they had very serious, like sugar crises, and their lens was very swollen. Okay. In those patients, the older formulation of tarkosamab was fairly viscous, so it was more like a honey. When that was dosed, it took, say, eight to ten seconds to dose. That's really having the needle in there too long in these very fragile lens eyes. As part of the new formulation, it wasn't just designed to drive the immediacy, which it does, but part of the redesign or the modification of the design was to make the manufacturing easier, to make it more like a liquid. At the same time. Less viscous. Yes. To make the injection, you know, two to three seconds as opposed to eight to ten seconds. By the way, there's a good video of that. The injection is, you said, was eight seconds versus Eylea, which is pretty quick. Yeah, it's about one. Yeah. Maybe that had an effect from a physical standpoint that could have caused the cataracts. Yeah. You get like these kind of concept of these microtraumas in and around the lens capsule. Right. Where they're Right. Where they're injected. You can get that in a number of different ways. Now the material is much more dispersive in its material. Now, would that affect the durability in the drug if you were doing less of the conjugated form versus the unconjugated, which is giving you the immediacy because it's the naked antibody versus the conjugated, which is giving you the durability? Was there any trade-off there? We don't think so. Okay. We've, you know, done different modeling and different animal work at different concentrations and such, and we see a consistent exit rate that's not driven by our viscosity. For the audience, what did you change? Previously it would have been 100% conjugated ventricular antibodies. What is the ratio now? For tarcocimab, it's now 80% conjugated. I call it the one plus four. So we've maintained 5 milligrams as the dose. It is 4 milligrams. Now it's 4 megs of conjugated and 1 megs of unconjugated. And then for the 501, it's a 1.5 plus 3.5. In any case, you're not running DME, so do you feel that there shouldn't be an issue in this because it's DR and AMD? That's correct. Yeah. I mean, I do think. In the population. Yeah, I do think there's, you know, views that we could run DME in the future and how we would want to go about that. Right now we have a portfolio of three molecules, so we don't need any one molecule to achieve every disease. All right. So bottom line, because I want to move to the second part, is that you are executing on the lead program in phase III. I still think this is obviously critically important before I get to the second part. Yeah. You feel that the probability of success should be pretty high. We got to execute and get to that data next year, but that should be positive. The efficacy should be positive. The safety should be better and improved. Yes. You should be able to file with the FDA. Yeah. We have our own commercial facility. We're manufacturing at commercial scale. We're continuing all of the BLA-facing manufacturing activities for tarcocimab. It's basically almost finished. Yep. If we can replicate some of that durability of effect that we saw in AMD, which we are going to get in this DAYBREAK study. Right. That is definitely differentiated, and it's a huge market. Yes. There is an opportunity there. Okay. Yeah. Let's get an update on the status of that, but I would hope that you're going to be completion of enrollment. It'll be close. By the analyst day. Okay. Let's get to the second part because this is very interesting. Over the last year or so, you had introduced the IL-6 VEGF bispecific. Without getting too complicated here, one's a biopolymer conjugate again. I'm quite interested in just the naked bispecific. Yes. The reason is because you are looking at this for MESI, macular edema secondary to inflammation, this indication. People have been learning about this indication. We are getting more information because Roche has an IL-6, not bispecific, just an IL-6. They have been dosing people. They have had some data. They are in a phase III for a different macular inflammation. They actually quite talked about it a lot here at the Jeffries Conference, actually. Perfect. Now, their phase III for their IL-6 UME indication is later this year. They haven't had a whole lot of data, but they're bullish on it, and we're going to see it. My question to you is, describe what MESI is, macular edema secondary to inflammation, and how is your IL-6 going to treat this? Is it better than the Roche one? Yeah. I think it will be better. That's what we think we're seeing. It's very exciting. It's nice to have the dual mechanisms of action. Right. You're a dual. Okay. Bispecific. Yeah. Yeah. Talk about the indication and what you're trying to do. Yeah. MESI is a nice way to understand macular edema secondary to inflammation. Macular edema is something you can see very easily on the OCT machine. It's just fluid under the retina in different areas. What happens is you can have a breakdown of the barrier between the body, the systemic, and the eye, as a result of different types of immune attack. When that barrier breaks down, you get fluid there. That can be a medical emergency. I mean, if you have macular edema and you have inflammation in the eye, that's a medical emergency. There are many causes, and some of them are idiopathic. They're not known why somebody would have that. In other cases, maybe a third, you have a systemic autoimmune disease. Even there's, you know, recent work that was at the ARVO meeting where people who have tattoos, a certain percentage of them, the body attacks the tattoo. At the same time, it attacks the eye, and you get macular edema secondary to inflammation. You get MESI. You see it's many different causes, okay, that have often, it's an immune element, obviously, and it's attacking the eye. In many cases, you're having an attack at the same time somewhere else, but you may never know where your primary attack is. You got a tattoo, then boom, you get, you know, your vision goes down and you have fluid under the retina, and this is a chronic condition now for you. It's kind of scary. Kids get it from having juvenile idiopathic arthritis. Adults get it by having, you know, autoimmune disease. You may not know what your primary is and you get it. The number of people in the United States, for example, who have non-infectious uveitis, which is another pathway, that's really a feeder. You have uveitis as an inflammation in the eye, and it's not infectious. You have that. Maybe that is around, say, 750,000 people in the United States have that. Okay. It is fairly large. And then what percentage of people have a more severe form of that that progresses? The barrier is degraded sufficiently that they get the macular edema. Okay. That depends on, you know, how you want to think about it. Is it a third of patients the way Roche may indicate? It's probably less than a third of those patients. There is quite a large number of people. This is very serious. A lot of it, I think, is it the fourth leading cause of blindness in the developed world? Okay. It's a mixture of inflammation, but it's not just inflammation, but it's an immune-mediated thing. And because it relates to fluid, right, macular edema is the fluid under the eye, it's helpful to have the anti-VEGF component because, of course, in wet AMD, which is also about fluid, you want to have anti-VEGF to get rid of the wet. Here, people know that anti-VEGF alone is helpful in some patients with MESI, but not everybody. The combination of the IL-6 that can rapidly decrease your inflammation and can get rid of the fluid, as Roche showed. In our case, we see a synergistic combination of the anti-VEGF to kind of squeeze additional fluid or to help in the speed of getting rid of the fluid. Yeah. When you look at some of the Roche data in phase I and phase II, it's promising. Yes. You believe that your, and by the way, with that, you know, it's a little bit, did they have some side effects and tolerability issues or antibody? Really great on getting all the details here, but they did push forward into phase III. Yeah. Your molecule you think will be better because it's a bispecific hitting two targets. You have put out some data. I think that was back at the beginning of this year in January. You're going to have some more data. How does your data look compared to their data? We're going to show it. We're excited about it. I think the point is, will our data help people to feel comfortable that there's actually a key differentiation against their molecule? We saw a few patients in January, to be fair, and that showed significant improvements in BCVA, right? I think I recall that. Yeah. A small number of patients, but some early big drops on BCVA. Yeah. You feel pretty good about what you're seeing there. What we need to, you know, it was a tough time in the market too, but we need to see more data, more patients, and more follow-up. Yeah. What we want to talk about at the analyst day is to have a nice focus and highlight on the KSI-101 program. Okay. That's this program. Introduce the molecule, talk a little bit about that. Talk about the data. You know, we'll show more data from the APEX study. I think we had only three patients in January, but we'll have north of 20 patients' worth of data. Okay. Across the dose levels. Okay. Okay. We'll be able to take a look at its immediacy and its power, okay, in this, you know, diseased population. And we'll be able to put that in context of what we think we understand about the Roche molecule. And more than that, we'll have time to talk about what is MESI, right? What is the disease? Right. You know, what's the commercial opportunity for the molecule? And we'll also be able to tell you that we'll already be live enrolling in the two phase III studies, at least one of the two. Wait. Repeat that again. You're already pushing this forward into phase III? That's right. The phase III will be live at the R&D day. Wow. Okay. It's actually somewhat new to me. Yeah. That's exciting. That's a very exciting program. If you think about Kodiak, and we believe it depends a little bit on the speed of enrollment for the PEAK and PINNACLE studies for 101, but we believe that it's possible that we could have top-line data for PEAK study in 2026 at the end of the year. Wow. If you think about Kodiak, we have three different assets. They'll all be in phase III. Each of them is interesting in different ways. Right. They're all science-driven. Right. They are all in phase III studies. Those phase III studies can have readouts across 2026. Let me ask you a question because this event is coming later this year, calendar 2025. Is that, I'm having a hard time kind of handicapping the Roche readout. And to be honest, because again, Wall Street is trying to figure out this indication. Do you anticipate, is your base case that Roche's phase III probably will work? Yeah, I think so. Okay. I think the challenge for them with the endpoint of three-line gainers. Three-line gainers. Okay. Is that these are very sick eyes. Okay. What percent of patients will, even though they're going to have a powerful response? Okay. Maybe the Roche molecule is slower in its power than ours. Okay. I think that will likely be true. It's an important medicine for a very sick unmet need population. Their medicine's probably slower than ours. Okay. They went out into phase III first, so it was more unknown. We have a lot more information. Okay. Their endpoint with three-line gainers, I think where they may be at risk is what% of patients can actually achieve. Why did they pick that indication versus say just change in BCVA or whatever, you know, what would your endpoint be? Yeah. What's your endpoint? Just to say, and so the issue is maybe more what their placebo 15-line gain rate is because it's a superiority study. In other words, like it's more of a sample size question for them. Wow. Do they have enough patients to get the delta between, you know, active versus sham to meet, you know, to meet the superiority? They have two, their two lowest doses went into their study. Okay. So they went to the lower doses. I'm just saying, why would a sham injection have three-line gainers? I mean, it's. Heterogeneous? Yeah. It's a complicated, you know, are they in a flare? Are they not in a flare, right, at baseline, et cetera? I think their medicine works probably well. Okay. The question is on there. Did they power it enough? Do they have enough people? You know, let's wait and see. The point is, like I said, there's some uncertainty about it. Yeah. If it's positive and looks good. Directionally for us, you know, it'll be very favorable. Yeah. I think. Also, we'll have a chance because our studies won't be finished. We'll be able to take a lot of learnings that we can see. If needed, we can modify or do. Victor, in the last minute, how much cash do you have? What is the formal guidance as to where that takes you? Because I'm hearing you've got multiple phase III studies reading out and an R&D day. Right. Certainly, we have well north of $100 million in cash. And we're burning a little north of, say, $30 million a quarter. We recognize that we have a financing kind of overhang on the company. Yeah. I think our objective has been to focus operationally to get us to this sort of snapshot of having the three phase III programs in phase III. Yeah. With good prosecution of those. Our attention will turn to the financing overhang. We're looking at a range of different options. There's a lot of inbound interest, tremendous inbound interest. We could raise capital overnight if we wanted. We're just thinking about when is the right time and in the right move. Makes sense. Okay. Victor, thank you very much for the update. Love it. We will see you at the analyst event and looking forward to continued execution. Thanks a lot.