Hi, everyone. My name is Maury Ray croft. I'm one of the biotech analysts at Jefferies. It's with great pleasure that I'd like to welcome Victor Perlroth, the CEO of Kodiak Sciences. Victor's going to do a presentation, and then at the end, we'll do some Q&A. Thanks so much for joining us today, Victor. Okay. Thank you, Maury. Thanks, everybody. We're pleased to be here again at the Jefferies Conference. Please be aware I might make some forward-looking statements, so refer to our SEC filings for risk factors, please. We're going to run through a good amount of content. If you're interested, you should download the slide deck and read it at a more leisurely pace. This is a wonderful time for Kodiak. We're pre-commercial retina-focused biotech. We have a lot of investor attention on the KSI-101 asset, which we're developing in an indication of what we call MESI, or Macular Edema Secondary to Inflammation. And we'll talk a lot more about that. There is a lot of investor interest in KSI-101, and that's a strong reason to believe in Kodiak as an investment opportunity. We also have our conjugates, the tarcocimab and KSI-501, that are being developed. We have very interesting phase III readouts in the first quarter and the third quarter for tarcocimab and 501. They're what we consider to be very interesting options in the $15 billion+ anti-VEGF market. On top of that, we have, I think, a fascinating science-based pipeline that's really emerging with some good momentum. We have very interesting activities in digital health, which we haven't spoken much about, but which have made tremendous progress inside the company. We have a commercial manufacturing capability. When you think about Kodiak as a retina-focused company, it's quite exciting. We have three phase III programs. On the left side, bookended KSI-101, an anti-IL-6, anti-VEGF trap bispecific protein being developed in MESI, which is a rare disease with, let's say, north of 150,000 initial addressable patients. On the right side of the bookend, we have our tarcocimab and KSI-501 conjugates in the retinal vascular diseases, obviously, with quite a lot of patients. In the middle, we have very interesting pipeline development and pipeline leadership. We have KSI-102 and 103 as pre-IND-based bispecific proteins in retinal inflammation. We have very interesting new science duets, we call them, preclinically for geographic atrophy as a bispecific and also in glaucoma, interestingly, as bispecifics. Very interesting retina-focused, and I would say leading pipeline company with bookends on the three phase III programs and four phase III studies and evolving earlier programs. What about a quick spotlight on these phase III programs? We have tarcocimab as an anti-VEGF conjugate, our ABC, trying to build medicines with strong immediacy and an industry-leading durability, looking to file a BLA mid-next year in three retinal diseases with data in Q1 and Q3. Our KSI-501, it's an anti-IL-6, anti-VEGF bispecific trap conjugate, again, looking at the retinal vascular diseases with phase III data in the third quarter of next year. Then we have our new KSI-101 molecule as a high-strength IL-6 VEGF bispecific protein. And there's quite a lot of investor interest in that opportunity. We have, for tarcocimab, three phase III studies that have read out with positive phase III data, the BEACON, GLOW1, and DAYLIGHT studies. We have the GLOW2 study that's in progress. We'll have last visit in January of 2026 and expecting top-line data announcement early March of 2026 for GLOW2. We have the DAYBREAK wet AMD study. Last visit is in August, and we're expecting to be able to announce top-line data mid-September for the tarcocimab in the DAYBREAK, and also the KSI-501 will also be having top-line data in the same DAYBREAK study mid-September. The KSI-101 program, where we're actively enrolling the PEAK and PINNACLE phase III studies, those are enrolling quite quickly, and we feel good about top-line data for the PEAK study in the fourth quarter of 2026, so let's say 12 or 13 months from today. That'll be quite exciting. We're looking towards a BLA filing based on positive top-line data from GLOW2 and DAYBREAK for tarcocimab mid-next year. When you think about Kodiak and you think about us as a retina company with these bookends of these three late-phase or phase III programs, we can begin to think of ourselves today as a pre-commercial company looking at early tarcocimab revenues based on approval in mid-2027. As we begin to look into 2028 and later, we begin to see revenue potential from three different late-phase retinal programs. We'll talk briefly about tarcocimab and 501 and try to leave some time to walk through some data analysis on the new KSI-101 program. Tarcocimab and 501, like we talked about, are being developed in the retinal vascular disease market. I think what's really important is this sort of four-quadrant framework that we think about. On the left Y-axis, we look at the efficacy of the anti-VEGFs, and on the X-axis, we look at the durability of the products. We know that Eylea and Lucentis and the biosimilars now are the Gen 1 agents, and they have shown over the last 20 years to have very high immediacy and very high efficacy. Immediacy meaning when you give the dose, you see the activity within essentially right away. The new agents of Eylea HD and Vabysmo, following in the footsteps of Eylea and Lucentis, really have not achieved maybe what people had hoped. The data cards are on the table. The medicines are being sold commercially. Vabysmo may be moderately better, maybe than Eylea or Lucentis, maybe a little bit better durability, incrementally so. For Eylea HD, similar. I think in the industry, they have really been termed Gen 1.5 agents. On the bottom right, you might have new technologies that are being explored for durability, but they do not have a lot of immediacy or very strong efficacy, but they are meant to be there to provide some continuous small stimulus of anti-VEGF activity. In the upper right quadrant, as a continuation of these biologics, the mainstay biologics, as you move to the right in the context of high immediacy and high durability in the same product at the same time. Over a 20-year period, nobody has developed and been able to successfully demonstrate a product that fits an unmet need in this upper right quadrant. That is what we are playing for with our conjugates. Even incremental therapies, like, say, these Gen 1.5 agents, are selling really well in the marketplace, which is funny and surprising given that there is such continued interest in branded agents. That is because there remains a very strong unmet need, even for very incremental therapies. What if you had a more disruptive therapy? What could be achieved? There is an open opportunity for a biologic that provides high immediacy and high durability at the same time and in the same therapy. That is what we are trying to develop with our conjugates. We have been developing them now for some time. I think we have designed them well. They are very potent in vitro. We have shown very nice extended half-lives in animals, and we have shown very attractive extended half-lives in humans. Now, based on the new formulation designs, the enhanced formulations, we have redesigned them to have a very powerful bolus effect and to have the extended clinical durability through our new formulation design. What is it about our science and about our conjugate design? When you inject these biologics individually, when you have the free proteins that are smaller, the immediacy is driven based on the lower molecular weight, and durability increases as molecular weight increases. The concept for tarcocimab and 501 is to bring a little bit of the left side and a little bit of the right side into the same biologic. We bring immediacy with free protein, and we bring durability with our conjugated protein. For tarcocimab, our redesigned formulation, I call it the 1 plus 4, 1 mg of free protein, which is a full pharmacologic dose, plus 4 mg of the conjugate. For the 501, we have 1.5 mg of the free bispecific protein and 3.5 mg of the conjugate. We showed that tarcocimab, as an example of our conjugate in patients, has a mean ocular half-life in humans of 20 days, which is three times longer than faricimab. You see quite the spread, both for faricimab, but obviously more narrow, and for tarcocimab broadly in the population. We showed that we have that similar 20-day half-life across all three of the major retinal vascular diseases: wet AMD, DME, and RVO. Our view for tarcocimab and 501 as ABC-enabled mainstay biologics, tarcocimab driving for strong immediacy and an industry-leading durability, and 501 really trying to build based on the bispecific of the anti-IL-6 on top of the VEGF trap conjugate to drive for better efficacy with strong immediacy and an industry-leading durability. We have a number of studies completed. We have a number of studies in progress. We're looking towards top-line data in diabetic retinopathy on the GLOW2 study in the first quarter and top-line data, as I mentioned, for DAYBREAK for both tarcocimab and for KSI-501 in September of next year. As you know, the design of the DAYBREAK study in wet AMD, enrollment is complete. Approximately 690 subjects have been enrolled. They're moving monthly through the study. The study design is attractive. It's a conservative study design for loading doses for tarcocimab once a month and 501 once a month versus Eylea on its label out through 48 weeks. Historically, we've shown very successful data for tarcocimab in diabetic retinopathy in the GLOW1 study with all patients on every six-month dosing and showed very strong treatment effect and also very strong prevention of disease progression, prevention of sight-threatening complications. I mean, a picture speaks a thousand words. If I were a patient with severe or moderately severe diabetic retinopathy like this patient from the GLOW1 study at baseline on the left, when you see all those hemorrhages in the eyeball, and then you see the same patient after treatment with tarcocimab on every six-month dosing, I think the diabetic retinopathy market is underappreciated. We look forward to hopefully very successful data from the GLOW2 study in the first quarter next year. Historically, also, tarcocimab showed very strong data in retinal vein occlusion, which is a large part of today's anti-VEGF market. In the first six months of the BEACON study, we showed very strong non-inferiority against Eylea with a doubling of the treatment interval. In the second six months, we had a matched phase head-to-head dosing against Eylea and showed the same vision and OCT pattern with 75% of patients on a six-month regimen in the second half of the study. Revisiting the core unmet need based on the science of high immediacy and high durability, we believe tarcocimab and 501 are poised to fill what we call the golden quadrant. Let's be very objective about it, and let's turn the data cards in Q1 of Q3 next year. Let's turn our attention to a really exciting third asset in Kodiak's pipeline, KSI-101, in Macular Edema Secondary to Inflammation. First of all, what is MESI, as we call it? Fundamentally, it's a physical thing. It's just a physical sign. You don't see it with your eye, but you see it on the OCT machine, and you see this fluid, this macular edema in the retina. It is a common clinical presentation of a wide spectrum of diseases. On the right, it can be caused by the traditional VEGF-driven diseases like wet AMD or retinal vein occlusion or DME. On the left side, it can also be caused by inflammation or by autoimmune attack. What is it? Like I said, a common pathophysiology, like an immune disruption of the barrier. This is a barrier biology disease leading to inflammation and angiogenesis causing this physical finding, the macular edema in the retina. The question is whether KSI-101, our new bispecific that inhibits VEGF with the trap, anti-VEGF, and IL-6 as an antibody, whether it can be a unifying therapy in this new disease. It is a heterogeneous group of diseases. It has a common identifiable presentation, right? The macular edema. What's interesting is our drug seems to work irrespective of the location of the inflammation: anterior, intermediate, posterior, panuveitis, and also independent of the specific etiology because many different types of autoimmune insult are causing the macular edema in the retina, as you can see down below. Macular edema is the leading cause of vision loss among patients with ocular inflammation. What causes it? Like I said, it's really a three-step thing. You have some sort of autoimmune trigger. It could be a systemic autoimmune disease, or it could be an autoimmune disease in the eyeball. That breaks down the barrier, right? The blood-retinal barrier. It's really a barrier biology. That breakdown of the barrier leads the leaky stuff to get into the eyeball, and then that leads to sort of an amplification pathway. Okay? Together, IL-6 and VEGF compound the damage to the barrier. There is a core unmet need in MESI. Again, here, it is for a high-efficacy medicine that is safe, okay? Targeting, in this case, both IL-6 and VEGF. There is a potential by restoring the barrier for it to be disease-modifying. A high-strength drug, a potent drug, a minimally invasive intravitreal injection, and strong safety that is highly differentiated from steroids. What has the community and what has Kodiak learned about MESI? We can learn a lot from the Roche studies, the Dovetail Study testing Roche's Vamikibart anti-IL-6 monotherapy. They tested it in the Dovetail Study given once a month three times. What we learned is that anti-IL-6 monotherapy can provide vision and anatomical improvement in patients with inflammatory macular edema. On the left, strong vision gains, and on the right, very useful improvements in fluid. A clear dose response was seen with IL-6 anti-IL-6 monotherapy in patients with inflammatory macular edema. While intravitreal IL-6 monotherapy with Vamikibart was helpful, 50% of patients had persistent intraretinal fluid on the left side down there, which is similar to the overall failure rate of, say, other drugs like systemic Humira, leaving room for a more potent and/or broader spectrum biologic therapy. More recently, and importantly, the IL-6 pathway was further validated with Roche's Vamikibart in recent pivotal study readouts at American Academy of Ophthalmology. It really showed that IL-6 is a key target for inhibition in inflammatory macular edema. On the left, the two pivotal dose levels showing improvement in OCT in both the MEERKAT and the SANDCAT studies. Clear anatomical improvement was seen. On the right, very nice visual acuity gains, in particular in the MEERKAT study with almost 13 letters gained on both the 0.25 mg dose and the 1 mg dose. Okay? Nicely, a low rate of intraocular inflammation was observed. No on-target adverse events were identified in the pivotal studies, really saying that anti-IL-6 inhibition is safe in the eyeball in these patients. At the same time, the Vamikibart study also showed that although it did decrease intravitreal or aqueous IL-6, it had no impact on aqueous humor VEGF, which is an important mediator. How can the opportunity in MESI or in inflammatory macular edema be addressed, in particular by Kodiak's KSI-101? It's a potent bispecific protein inhibiting, as I said, VEGF and IL-6 with a modified FC formulated to 100 mg/mL strength. It is designed to address the core unmet needs: dual inhibition as a bispecific, the potential for it to be disease-modifying, and we have nice preclinical data to support that, a powerful high-strength formulation administered locally, and hopefully a safety profile in line with the community's experience with intravitreal biologic therapy. Recently, we presented the week 20 extended follow-up data from the phase I APEX study. We gave four doses once a month at three different dose levels. We enrolled a fairly sick population with relatively low vision, pretty thick on the OCT, 460, 490, 530 in terms of baseline OCT. What we showed was with monthly 0, 4, 8, and 12-week injection, we showed very nice gains at all three dose levels and a nice dose response. With the top two dose levels achieving very meaningful vision gains of more than 10 letters already by week four, and then continuing to improve even from week 12, week 16, and even coming out of week 12 dosing, from week 16 to week 20, we see further strengthening of the vision and achieving actually 20/25 vision by week 20, and with continued strengthening of the visual acuity and looking both at the observed visions as well as the mean change. We are very proud and impressed to see this nice and continued strengthening of the vision. At the same time, more than half of the patients achieved a greater than three-line gain with additional benefit observed at the top dose levels, with 54% and 62% of patients achieving the three-line gain. At the same time, we showed very meaningful improvements on the OCT, reaching less than 325 microns as early as week four, further deepening over time. More than 90% of patients in the top two dose levels achieved and maintained an absence of both IRF and SRF, the intraretinal and subretinal fluid through the study. That is very impressive data. It was very well tolerated, consistent with, I guess, the experience of Roche in the same disease population. How does 101 fit into the emerging landscape? While Dovetail showed Vamikibart and even the SANDCAT and MEERKAT that intravitreal IL-6 monotherapy is helpful, 50% of the patients still had persistent intraretinal fluid, whereas we are bringing nearly 100% of patients to have absence of fluid. Here's a quick analysis that we thought was illustrative. Obviously, it's a comparative kind of analysis between studies, and it should be interpreted with caution. On the left, we have the baseline CSTs in our APEX study at the three dose levels. On the right, we included the three dose levels in Dovetail and then the two dose levels in the MEERKAT and SANDCAT pivotals. What happens is you can see the impact of a single dose in terms of drying the retina. On the left, you can see that at week one, the effect of a single dose at 2.5 mg, 5 mg, or 10 mg of KSI-101 brings you a very significant improvement in OCT. With the Vamikibart, if you look at Dovetail, MEERKAT, and SANDCAT, they sort of reinforce each other. You have fairly weak onset of action with Vamikibart. Now, if you look at what is the effect at week four of that single dose, we continue to see some nice improvement with KSI-101 and APEX on the left. On the right, you see some modest improvement through week four with Vamikibart in those three studies. If you continue on the right, what is the effect of a second dose through week eight? You still are seeing some marginal improvement. What about the effect of the third dose at week 12? Not a lot of further improvement. Maybe by week 16, you have marginal further improvement, whereas a single dose of KSI-101 seems to provide a deeper drying effect than actually four doses of the anti-IL-6 monotherapy. As we continue to look at the effect on the left at week eight of the second dose, some further improvement, some modest further improvement, again, with the effect of three doses. Dual inhibition, therefore, of IL-6 and VEGF with KSI-101 seems to provide a very synergistic drying effect that is very strong, takes you more quickly and more deeply to where you want to go, which is a healthy, dry retina. We are currently enrolling the PEAK and PINNACLE phase III programs. They are enrolling well, perhaps slightly ahead of our expectation. We're not going to speed up the readouts of the studies, but I think the learning maybe from the Roche studies is we'll use the same time points to enroll nominally more patients inside of the primary endpoints to increase power and increase overall probability of success in the programs. PEAK and PINNACLE are being enrolled under, I think, a fairly innovative master protocol design in the same sites globally. Kodiak is a pre-commercial retina-focused biotech. We're on the move. We've had a very exciting 2025, and we're looking forward into 2026 with our three late-phase assets and three to four phase III readouts across both the very large retinal vascular disease market with very interesting scientific leadership there and some nice clinical trial designs. Now with our new KSI-101 asset, we're excited to see the continued enrollment in the PEAK and PINNACLE studies and then the eventual readout of the PEAK study before the end of next year. Thanks a lot. Thanks, Victor. I'll start off with questions. I'm glad you mentioned the Roche data, which definitely helps de-risk your program and potentially sets a bar that seems achievable for your program. One of the common questions we get is just around the different patient populations with Roche and UME and your studies in MESI. Maybe talk a little bit about that. One of the questions we have is just whether all inflammation that leads to macular edema, if that's encompassed by MESI, or are there some exceptions to that? Yeah, we see a lot of overlap between what's traditionally called the UME population and the MESI population. By analogy, the population that was enrolled by Roche in their Dovetail and then their SANDCAT and MEERKAT studies and the population that we've enrolled in APEX and that we're currently enrolling in PEAK and PINNACLE. I guess you could consider MESI a little bit of a UME plus, but by and large, it appears that more than 50% of the Roche population was more of an idiopathic UME, and more than, say, 50% of our population is also sort of an idiopathic MESI. In both cases, you might just consider them inflammatory macular edema. We have slightly broader inclusion criteria just because with the addition of the VEGF, we don't need to exclude certain populations that Roche excluded because they didn't have any scientific hypothesis that their drug would work. For example, when patients have long-standing retinal inflammation, then the eye can become hypoxic, and then they can get angiogenic vessel growth. They exclude that population, but we include that population. In some way, I think it's maybe different words to say similar population. We're just more inclusive, and that's supported really by, for example, the 39 subjects that we've enrolled into the APEX Study where, irrespective of whether the cause is anterior or posterior, we're treating those patients well. Irrespective of whether the name of whether it's an idiopathic population or the physicians don't know what the trigger for that MESI or for the macular edema or the inflammation is, we're treating them well. Irrespective of whether they're in a more traditional UME, which means they're HLA-B27 or they have juvenile idiopathic arthritis, all of those patients are responding well to KSI-101 in our studies. Got it. For the types of patients that you're enrolling into both PEAK and PINNACLE, from my understanding, the design is that for both of those studies, the design is identical, but you've got slightly different patient populations in both studies. That's right. Maybe talk more about that and whether those patients are more similar to MEERKAT or SANDCAT from Roche. The PEAK study enrolls a slightly more severe population than our APEX and slightly more severe than the SANDCAT and MEERKAT. It's patients who have their OCT CST north of 400 microns and maybe a vision that's a little bit lower than what we allow in PINNACLE. It's a bit of a sicker population. If you look at the APEX data we've presented before, that PEAK equivalent population, say, has a higher three-line gainer percentage. Okay? It's a bit enriched for more severe patients, even versus SANDCAT and MEERKAT. Our PINNACLE population, let's say, is a more similar population to SANDCAT and MEERKAT, and it reflects less than 400 microns on the OCT. We've done an analysis that also looked at the APEX patients that have the PINNACLE profile. They're both very attractive populations for our phase III designs, in our opinion. Got it. When you report the PEAK data first, I guess, what should investors be looking for there? How should we compare and contrast versus Roche data? How are you setting expectations for that? Yeah, I think we're very excited for the PEAK population and for the PEAK data. That's enrolling maybe like a three to two now coming out of the master protocol of patients into PEAK versus patients into PINNACLE. We're seeing a little bit more rapid enrollment into PEAK. That's why we also think it's a bit of a more severe population, so we'll have a little bit more power. I think we're going to let that float a little bit longer to increase the N above the 50 per group, one to one to one that we had originally thought, because it's enrolling more quickly. We'll have more power in a more severe population, and we're excited to present that data first. For the PINNACLE, we're also excited about that. We'll probably increase the sample size a bit more. Clearly, the mechanism is solid, and these are very sick patients, but we'll probably increase the power a little bit more relative to the PEAK study, if that makes sense. Yeah, it makes sense. Maybe one other question. Just Roche has shown promising data combining IL-6 inhibition with anti-VEGF in DME patients. Given you have two assets with this mechanism, do you plan to expand it to DME? And if so, would that be with your 101 program or with the 501 program? Yeah. That's a really good question, Maury. Obviously, we're ahead. There's always been this search for another powerful mechanism in retina beyond just anti-VEGF. I think that race is still open. I think IL-6 now, based on our data and the data that Roche shared, combining Lucentis with their Vamikibart, IL-6 is a very credible candidate to be this powerful second mechanism in retina. They showed the potential or the promise that perhaps the dual inhibition of IL-6 and VEGF may be able to provide curve separation or superiority in vision in DME. Obviously, that's very attractive. The question is, should that be developed with our 101 asset as a protein, or should that be developed within our KSI-501 asset, where we have the equivalent of, say, 1.5 mg of the KSI-101 unconjugated protein and then 3.5 mg of the conjugated? We haven't made a decision. We certainly have the capability to run DME studies and to run one or more pivotals and to do that where we include 101 and 501 together, kind of like what we did in DAYBREAK, or whether we keep 101 separate and focused on this new commercial population of MESI and think a little bit more about DME in context of KSI-501. I think as we move to complete the unmasking, right, and to get to primary endpoint and top-line data for the 501, that would certainly educate us. If we see nice data on 501, that would allow us to really accelerate into DME with 501. Alternatively, we might want to start some pivotals earlier than that. We certainly have the capability to do that, and we have not made a final determination. I think overall, it is a bit of an embarrassment of riches to decide which of these two amazing molecules should be developed in DME with the potential to show superiority would be really amazing. That is just a decision we have to make. Okay. I look forward to that decision. Thanks so much for joining us today. Thanks, Victor. Thanks a lot.