Good morning, everyone. Thank you for joining us on day two of the Jefferies Global Healthcare Conference. I am Michael Yee, one of the biotechnology analysts, and I'm really happy to introduce this morning the CEO of Kodiak Sciences, Victor Perlroth. Victor, a exciting and developing pipeline. Things are moving along. I know Wall Street has been a bit confused about some of the different things, so you're here this morning to run through it. Tell us about what's going on, and tell us about how excited you are about the progress at Kodiak. Good. Thanks, Mike. Thanks for the introduction. Good to be here again at the meeting. As you mentioned, it's a good time for Kodiak to be telling its story. Yeah. Please be aware of forward-looking statements. Please review the risk factors in the Form 10-K and the 10-Q. The deck that I'm gonna walk through now is posted on our website. There's a lot of information in it, and so I encourage you to skim that. As you know, Kodiak's focused on retina, ophthalmology and retina in particular. And as you know, Kodiak's medicines, two out of the three clinical programs, are built on our ABC platform, which is designed to enable multi-mechanism therapies for durability. And the concept around our conjugates, our antibody conjugates that we make, is to combine the best durability with the right efficacy, and it's the foundation both for tarcocimab and also for KSI-501, two of our ABC medicines in late-phase clinical development. Importantly, they have an antibody that brings the activity, and it has the conjugate or the biopolymer that brings the durability, and we'll talk more about both of those pieces. In addition, we haven't spent too much time talking about the earlier science around our ABC platform for multi-specific, what we call high DAR or high drug antibody ratio medicines. But over the next few months and through the end of this year, we've had tremendous progress in the pipeline. It's powerful, in particular for ophthalmology medicines, but also for more than that, and we'll begin over time to talk a bit more about this unique extension of our ABC platform. This is slide 6, and it's a really important slide because I think it represents a kickoff or a new foundation for Kodiak and for our science. So we have a bit of an embarrassment of riches in a way, where we have a portfolio now of three clinical programs that are designed to address key limitations of today's therapies across a broad spectrum of retinal disease. So as you know, we have the ABC platform-derived biologics, tarcocimab, and KSI-501. And what's important is that with the conjugate platform that we have, we want to be able to bring the best durability of any biologic, and importantly, we have to figure out how to also bring the right efficacy for the patients. And for both tarcocimab and 501, it's about high-prevalence retinal vascular disease. So for tarcocimab, which is our anti-VEGF ABC, I think one of the important questions in the marketplace is, is the battle for the best, you know, for the appropriate next-generation anti-VEGF therapy, has that battle been won with the introduction of Roche's Vabysmo and Regeneron's Eylea HD into the market? And I think definitively, our view, and I believe our view in conversations with retina specialists in the market, is that, no, the battle has not been won yet. Vabysmo and Eylea HD don't bring a science of durability to their design, and rather they're more incremental improvements to existing therapies. So what we want with tarcocimab is to bring a compelling first-line durability profile and to figure out how to do that without compromising on the efficacy, with the objective for it to be the longest-acting anti-VEGF biologic, a six-month predominant medicine, while also, in our label, preserving the flexibility to dose monthly, which we have from our DAYLIGHT study. It has an enhanced 50 mg per ml formulation. Now, for KSI-501, which is our bispecific anti-IL-6, anti-VEGF ABC, the objective is to bring first-line efficacy, right? Bringing the two bispecific mechanisms to bring a higher level of efficacy to patients and also to bring the best durability. It's a first in class, and it's designed to address retinal inflammation and vascular permeability simultaneously. And the 501 program brings all of the learnings of the 10 years of work on tarcocimab. It also includes an enhanced 50 mg per ml formulation. Importantly, Mike, and we'll be talking a lot more about these bottom two elements, what we call these two science updates for the platform, over the next, you know, between now and eternity, through the end of the year in particular. The first is, from a science standpoint, that our platform, the ABC platform, is supported by a true science of durability. We have the design of the conjugate with the biopolymer to create the large size that drives the long residence time in the eye. We have the best animal ocular, you know, half-life data in model systems, and now we've begun to test also the human clinical ocular half-life data from some of our earlier studies, and we're continuing to see the same multiple of our conjugates versus unconjugated proteins. For example, predicated anti-VEGF, such as Lucentis, Vabysmo, and Eylea. So a true science of durability that gives us, based on the design, a multiple of the ocular half-life. That's the first component. But when you make something larger, like we do, to bring the durability, then what we've learned in our studies is that that doesn't come without a cost. Right? Large gives you the half-life, but does it give you the immediacy and the clinical efficacy, let's say, on the early doses that physicians want? Because they don't want to sacrifice immediacy and efficacy for durability. So is that a solvable problem, right? Is that something that we can learn and then make course corrections? And the answer is yes. So we've built an enhanced formulation for tarcocimab and also applied that logic and science into the KSI-501 program, that combines conjugated form and unconjugated forms and balances towards durability, so that we have the six-month predominant medicine in the majority of patients, but also doesn't compromise on the immediacy. So these two elements of science are new, they're powerful, and they're gonna allow us to take both tarcocimab and 501 to a next level of efficacy and durability. Now, in addition, we've added a third molecule to our pipeline, which is KSI-101, which is raw power as a bispecific with two important mechanisms of action, and we're bringing that into patients with important and serious inflammation in the eye, macular edema secondary to inflammation, for which no approved intravitreal biologic exists today. So it's designed to be a first-in-class bispecific protein to address retinal inflammation and the vascular permeability simultaneously, and that's at a high 100 mg per ml formulation strength. So let's talk quickly again about tarcocimab. Our objective is to bring a first-line durability profile without compromising the immediacy for patients with high prevalence retinal vascular disease. We have three completed phase 3 studies that have met the primary endpoint, DAYLIGHT, BEACON, and GLOW-1. And for the approval package, we're running the GLOW-2 study, which is a repeat of GLOW-1, that also provides a bit of additional flexibility to the physicians and the patients with the third loading dose. It's actively enrolling. We hope to complete enrollment by the end of this year. And then in addition, we're very close to starting the DAYBREAK study, which will bring tarcocimab as well as 501 against aflibercept. It's designed to showcase the durability, and also the improvements of the enhanced formulation very clearly, and also to allow KSI-501 to have a successful, BLA-facing wet AMD study of its own, and to allow us to showcase the power of the anti-IL-6 mechanism for KSI-501 versus aflibercept and also versus tarcocimab. The new GLOW-1I study design on Slide nine is an attractive study design. We believe it has a very high probability of success because it's essentially a repeat of the GLOW-1 study against sham. The DAYBREAK study design here on Slide 10 is an attractive design. It brings all of our knowledge from the six prior pivotal studies that we've run. Importantly, we're looking back. We've had over 55,000 patient visits across the portfolio of Kodiak's Phase III studies. We bring all of the knowledge into the design of these next set of pivotals for tarcocimab, 501, and 101. Our product vision, I think for tarcocimab, Mike, which really brings together the learnings that we've had from some of the stumbles that we've had in our phase III studies. But as an innovator that's really trying to bring a first-line medicine to the table, it's important to learn the lessons and to be able to make the course corrections needed so that when we come out, we can be a winner. So what we've heard from retina specialists in a variety of ways, and now that we've begun to tell the story of our new science, we hear something here that's quite interesting. My experience with tarcocimab-treated patients in your trials is that you have the durability, but you didn't dry as well in the loading phase. But with the formulation of conjugated and unconjugated antibody, then you fix that, and you have a drug that primes itself and then takes patients longer. Together with monthly reimbursement from our DAYLIGHT study, where needed, I don't know why you wouldn't be a contender for first line after step therapy from Avastin. That's where we look for tarcocimab. Now, KSI-501 brings all of that and more. It's designed to address the opportunity for improved efficacy with the extended durability in the high prevalence diseases. And I think what's important is we've dosed, say, over a thousand patients with aflibercept as comparator across our pivotal studies. And when we look deeply into that data, we see profoundly the need and the opportunity for improved efficacy. An anti-IL-6 on top of the anti-VEGF, together with our ABC platform design, with the conjugate and the mixture of the conjugated and unconjugated with our enhanced formulations, is designed to be the best player in the field. It's designed for picomolar binding, both to VEGF, two hands on the ball, like they say at Regeneron, as well as picomolar anti-IL-6 as part of a conjugate. In addition, the enhanced formulation brings 10 years of learnings to maximize each individual patient's efficacy as well as durability. IL-6 is an important mediator of inflammation implicated in retinal disease. Patients with higher IL-6 have poor, less good vision gains over time. So we bring the anti-IL-6 together with the anti-VEGF trap in the context of our conjugate, in the context of having a mixture of conjugated and unconjugated. In addition, what's exciting also about anti-IL-6 and anti-VEGF together is that we've seen a synergy, and it drives superior normalization of the tight junctions, okay? Separating the eye from the systemic circulation, the barrier biology driven by the tight junctions, and the synergy with KSI-501 of inhibiting both... to a greater extent than either monotherapy alone. And with the synergistic effect, we believe KSI-501 has the potential to be a new disease-modifying therapy, which retina hasn't seen. We do more symptomatic relief. The phase I study, as you know, has been reported. It was a multiple ascending dose in each patient across four different dose levels, and with half treatment naive and half previously treated, showed very nice data in terms of the power, the efficacy of the medicine, and the durability through 24 weeks. Now, KSI-501 is being developed from the phase I multiple dose study. We're moving it into the DAYBREAK study, which is a pivotal BLA-facing phase III study in wet AMD, using the new enhanced formulation concepts that are part of our ABC platform. KSI-101 is the third, but shouldn't be forgotten. It's a powerful and important part of Kodiak's portfolio strategy. Two medicines with the ABC platform, one medicine without it. In this case, KSI-101 shares the same protein as 501, but it's formulated at 100 mg per ml without the polymer. Therefore, you should think of it as, as a medicine with the raw power to uniquely solve the problem for patients who have angry inflammation in the eye. That's our starting point, and from there, the label can broaden. Macular edema is a leading cause of vision loss among patients with inflammation, and IL-6 mediated pro-inflammatory signaling is a key driver. So when you have a lot of macular edema in the retina, with the fluid there, you can't see, and when you give the anti-IL-6, you get rid of the fluid. And on top of that, the anti-VEGF part is important because anti-VEGF is an anti-permeability agent. It's an anti-fluid agent. So you bring anti-fluid from the VEGF, and you bring the anti-inflammation and anti-fluid from the IL-6 together into a very powerful package for the patients. So there is no, there is no good treatment today, for local treatment for macular edema secondary to inflammation. It's a high unmet need area. And studies show that IL-6 and VEGF play key roles in the retinal inflammatory diseases. Our development plan for 101 is also, very cool, and we've had some very positive interactions recently with regulators. So we're moving the KSI-101 into the APEX study within the next several weeks. APEX will have both a DME portion, but importantly, it will have the same macular edema secondary to inflammation cohort group that we plan to have in our pivotals. So it'll evaluate three dose levels of 101 in patients with macular edema secondary to inflammation, with, let's say, 10 patients or so per dose level. So that will be a little bit like the dovetail studies that Roche has run with their anti-IL-6 medicine. And from this APEX study, we're gonna rapidly move into dual pivotals, called PEAK and PINNACLE, in macular edema secondary to inflammation. Those are BLA-facing studies. Down here on the top, you see or here on the bottom, part three, you see the APEX study design. For MESI, we call it macular edema secondary to inflammation. It's four loading doses once monthly, looking at week 16, and then end of study at week 24. But what's important about this study is it's the goal is really to look at to choose two different dose levels that are gonna go into these pivotals that we hope to start this year, PEAK and PINNACLE. These are matched pivotals that have been discussed with the agency for loading doses once a month, with the primary endpoint at week 16 against sham. So this is an important study for KSI-101, which is an important molecule as a part of our overall pipeline. Kodiak, with $246 million in cash and equivalents at the end of Q1, we're advancing three clinical programs into phase III BLA-facing studies this year, and we expect to have all three molecules in those pivotals this year. We're looking to achieve important inflection points within our current cash runway. Again, tarcocimab, 501, and KSI-101, at really critical junctures, and I would say, having rebuilt to a large degree from the foundation of science with our ABC platform for tarcocimab and 501, and then a separate molecule with the raw power for a very interesting high unmet need indication with KSI-101. Thanks a lot, Mike. Good. Thank you, Victor. So, maybe we could take some of those piece by piece. So starting with, tarcocimab, which has the most data, you have a plan to rerun another study. Can you just describe again or put up the slide, the design of that study, how you expect the progress of enrollment? And I presume it has a very high probability of success because you're basically redoing one of the successful studies. Is there anything that was changed in that, whether the formulation or different, as I recall, formulation of, of the drug to improve on the potential safety risk? Can you just describe any changes to this new study, or is it a total repeat, so you should be totally fine? Yeah, we're gonna run tarcocimab in two additional phase 3 studies. Okay, yeah. And we think that's gonna round out, the label and also the data, so everybody can see, tarcocimab fully. So the first study is the GLOW-2 study. Okay. It's a repeat of the GLOW-1 in diabetic retinopathy against sham. We generated very strong data in the GLOW-1 study. In GLOW-1, we just had a dose at 0 and week 8, and then at week 20, one quarter. So it was 8 weeks, then 12 weeks, and then 24 weeks. So every patient had what we called sort of a low, sort of like a slow on-ramp without a high level of dosing at the beginning. So it's sort of a gentle on-ramp, and then every patient was treated on a six-month interval in GLOW-1. In this study, we've just added an extra loading dose in the middle at the beginning. It's not that our efficacy was lacking, but we think from a label standpoint, it will be useful and important for physicians to have the flexibility to use three loading doses on patients where the physicians feel they may have more serious or more severe disease. So that's, and, you know, the important change between GLOW-1 and GLOW-2. We see very high probability of success of this study with a very similar design against sham, and this does use the, the new formulation, for tarcocimab, but it's not important for this indication. I would say more so- Yeah the DAYBREAK study is the second phase 3 study- Yeah that we wanna run with tarcocimab. In this case, of course, we're running tarcocimab with KSI-501 in the same study against aflibercept. But what's important for tarcocimab here is we are using the enhanced formulation. Okay, so traditionally, with more than 100% conjugate, you're really biasing towards the durability. And what we saw, let's say, in our wet AMD studies, is by biasing too much towards the durability, you can sacrifice on the loading phase immediacy. Physicians didn't like that. They were uncomfortable. They said: "I want to get to the promised land of the six-month durability that you uniquely deliver, but I have some anxiety because not all of my patients can get there if you don't have stronger immediacy." So by rebalancing in our formulation to have the conjugated and the unconjugated, this enhanced formulation will let us showcase that in this study. On top of that, we have Q4 to Q24-week dosing, and we hope that we'll be able to bring a majority of patients to the longest interval dosing that's been studied with the 40-week endpoint. So let me- GLOW 2 is already enrolling. Yeah. We hope to complete enrollment, if we're lucky, by the end of this year. DAYBREAK will be off the ground within, let's say, a few weeks or a month or two, and that enrollment will begin. We think there are not other compelling treatment-naive wet AMD studies that are enrolling today, and so will be a key study for everybody. And with the 40-week endpoint, we can have enrollment into Q1 of next year and still have last patient, last visit in 2025, along with GLOW 2. Yeah, let me take those piece by piece. GLOW 2, you said, could complete enrollment by the end of this year. The endpoint is how long? Forty-eight weeks. So it's about a year, and so there would be data around early 2026 or so. Yeah, that's our goal. Overtake. Mm-hmm. And then same with the second study, the AMD DAYBREAK. Same, same type of thing. It's starting up, could complete enrollment by early 2025, one year. So again, kind of a spring 2026. Yeah. Okay. It's a 40-week endpoint. Yeah. So. Okay, okay, 40 weeks. Okay, now, what I would love to clarify, and had some investor questions about this, is that in the DAYBREAK study, which is, I guess, a fifth study, you are using a different formulation, as you said, some unconjugated, conjugated, that may sort of... What, what did you say? Sort of reduce the friction or anything that could have been causing any of the glaucoma that you saw previously. And so how do I think about where many of the studies had been using the original formulation, and then one study of the five is using a slightly different formulation? How does that work from, like, a CMC FDA thing? Because that wasn't the exact formulation or drug mixture that was in all the other studies. Well How does that present? Well, there's been a shift in the formulation Yeah for tarcocimab, and also those changes and those concept have been applied into the KSI-501 program as well. Right. But within the tarcocimab program Yeah All new phase 3 studies are being run with the go-to-market material. Okay, so the So GLOW 2, as well as DAYBREAK. Okay, so two of the five That's right Are using that. Yeah, so we had multiple discussions with the agency- Yep To understand what's necessary. Also, these formulations for GLOW 2 and DAYBREAK with tarcocimab have been made in Kodiak's commercial manufacturing facility- Right At commercial scale. It's really part of the commercial scale-up concept for tarcocimab. The fact that there may be additional enhancements or additional benefits is nice, that it comes along with the manufacturing changes necessary to scale the drug to commercial scale. It has a number of additional enhancements or improvements in terms of the overall force needed for the injection, the overall time that the needle needs to be in the eye. Because by bringing a little bit more free protein and a little bit less conjugate and a little bit less polymer, there's less mass in the formulation, so it's more watery. There's actually many, a large number of benefits. Yeah. But luckily, we were able to do that. Yeah. We're now leaning into running 2 phase 3 studies. Yeah. One would have been enough to bridge the change, but we're actually leaning into- Two Two pivotal. So we feel very comfortable that will allow us to bring the best profile, you know, to both of the studies and broadly across the label. And that by bridging it with two, you know, pivotal phase 3 studies in- Yep Different diseases Yep That we have a very strong regulatory situation. So, so this to me, this DAYBREAK study is most interesting because here you have modified the design of the tarcocimab protocol. It's different than previous. Now, on one hand, it's interesting because it's now 4 induction doses versus aflibercept, which is traditionally 3, and also your prior studies used 3, and here you're using a fourth. Now, the fourth one is because of the change in the mixture. You wanna make sure that you're getting as deep of improvement early on, so that's why you're adding the fourth dose? And then you're doing a treat as needed after that. Is that how to interpret that? I, I guess so. Vabysmo, which is the- Yeah the marketed Roche bispecific, also has four loading doses. Okay. I think the concept is to have a balance, right? Yeah. Of balancing towards durability without sacrificing the early efficacy- Yeah Immediacy, and so we want to be able to showcase both. This study design, you know, it also sort of boosts a little bit the probability of showing that- Okay differentiation at both levels. Yeah. And then the 501, if you look here in the DAYBREAK study, because 501, although it benefits and is built on the ABC platform that can bring that enhanced durability, and with the mixture of the conjugated/unconjugated- Yeah Brings that early power. But here, the objective in DAYBREAK isn't to highlight around the durability. Okay? The objective with 501 and DAYBREAK is to really allow us to test and to explore the ability for the IL-6 together with the VEGF- Yeah to bring a higher level of efficacy if that's possible. So to finish off on tarcocimab, that arm should be a win. Yes. You should have four induction doses that should dry the eye, then you have a treat as needed. A proportion of different people will be at various three, four, and five-month dosing. Actually, we go one, two, three, four, five, and six. So we allow- You want all of that? Yeah, like the Vabysmo Okay Studies have done. And so you believe at the primary endpoint of 40 weeks, there'll be a proportion of people who only need this many, this many, this many, and it's a more traditional design, if I may say? That's correct. Okay. Yeah. That should be a win. On the 501 study, I would just say that's interesting because it's using these two investigational drugs- Yes In the same study. That's actually quite rare. I see that in cancer. But here we're using two different drugs, and that's to get the 501. You have a major study, so that should help the eventual 501 package. Right. And then together with the new 101 medicine that's outside the platform altogether- Yeah And goes against sham, into, disease with high unmet need- Agreed Where there's no therapy. Agreed. We think we have a, you know, a wonderful set of activities. Last question for you. When we do our model, we see you have $200-something million in cash, very solid. However, as you get through 2024 and 2025, which are execution periods, you're gonna be using up a lot of that cash just before you get to the phase 3 data in first half 2026. Can you comment on how we should think about that? Because you're coming up against some big data, but we're using up a lot of the cash in 2025. What would be the scenarios there? Right. We really think it's a question of what's the runway at the time that the data read out. What's important for us today is to get the studies operational- Yeah And begin to see enrollment rates. Okay. And then from that time point, we'll be able to project forward and understand what's our expected runway at the time that these core Phase IIIs read out. Okay. At that point, we'll be able to make whatever course corrections we want to in terms of capital. As it is right now, we see that we have sufficient capital to bring us through these phase III- Yes Inflections, and then it's just a question- Yes Of runway at that time. Certainly have the cash to finish the studies. That's important from a financial and ethical perspective, and certainly, we'll figure out the capital, as we get through 2025. Thank you very much, Victor. Appreciate it, and keep, keep up the progress. Thanks a lot, Mike. Thank you. Bye.