Good morning, everybody. Welcome to day three of Jefferies' London Healthcare Conference. My name is Kyle Yang. I'm a Research Associate on Michael Yee's biotechnology team. Today, joining us is Dr. Victor Perlroth, CEO of Kodiak Sciences. Victor, I'll hand over the mic to you. Why don't you tell us a little bit about Kodiak Sciences, your platform, your pipelines, and what's exciting for investors? All right, thanks. Thanks a lot, Kyle. Appreciate the introduction. Thanks for the invitation to be at the meeting. Good to see everybody in the room. We'll get started. Thank you very much. First, a quick note on our forward-looking statements, so this is an important time for Kodiak in our 15-year history, and we'll walk through where we are as a company and why I hope, as a set of investors, you can be excited about the future and why it's important to pay attention to us over the next six months and, let's say, the next 18 months, so we believe Kodiak's primed for near-term and long-term success. As a company, over the 15 years, we believe it's important to continue to maintain an agile mindset. We've run a large number of studies: six pivotals that we've completed, two additional pivotals in progress, have over 2,500 patient years of clinical experience and exposure, with an excellent safety record. In our clinical studies, we've dosed over 13,000 intravitreal injections of our products into patients, run more than 55,000 clinical study visits, and we've maintained technical leadership and ownership in-house at Kodiak. And we've built a diversified, at this point, late-stage pipeline. We have three important different product or investigational therapies: three shots on goal, each in a BLA-facing development plan with filing for Kodiak on the lead program as early as 2026, including the programs that we'll talk more about: tarcocimab, the KSI-501, and also KSI-101. And importantly, we've maintained our independence as a company to this date, with flexibility to make each right choice for the products and for Kodiak stakeholders. We own global commercial rights. We've built and completed a commercial manufacturing facility, Ursus, together with our partner, Lonza, and we have the freedom and the flexibility of how best to commercialize, and we have a cash runway that's expected to support operations into 2026, so we strive to be a learning organization. And through the journey, especially over the last five, six years, we've gathered important insights from our studies and from our molecules, and importantly, we've transformed those learnings into important actions, so positive findings include that tarcocimab and our platform are very well tolerated in patients. With the number of clinical studies that we've run and the science that supports it, the signature durability or the differentiated six-month durability is real for our conjugates and for our platform, and now that's supported by recent human ocular PK data, which supports the durability. The ABC Platform, with the safety and with the differentiated durability and the efficacy that we've shown, it's a real platform. At the same time, we identified some important issues through the clinical studies and the pivotals. Importantly, an immediacy deficit that we've shown on the efficacy in the wet AMD disease. We had an increased cataract adverse event rate specific to DME patients. We had overly aggressive study designs looking backwards. What were the actions? We'll talk more about those. An enhanced formulation to course-correct issues identified in wet AMD in terms of the immediacy and in DME in terms of the cataract adverse event rate. We have new study designs, new pivotals educated from the prior studies and anticipated to have very high probability of success in our estimation. We've diversified the portfolio now to include not just tarcocimab, but to include tarcocimab, KSI-501, and KSI-101. So let's talk more about this. Importantly, in the field for retina and intravitreal biologics, intravitreal medicines' durability, surprisingly, remains still a key unmet need, even with new products from Roche, Vabysmo, and new products from Regeneron, EYLEA HD. Interestingly, despite all the hoopla, I suppose, about improved durability with these new commercialized agents, the improved average dosing interval extension, say, in moving from EYLEA to faricimab is only an additional seven and a half days. So what we're trying to accomplish with tarcocimab and our KSI-501 programs is to put them in the context still of the mainstay biologics, right, starting with the Gen 1 of LUCENTIS and EYLEA, which now transition now into more Gen 1.5 agents, EYLEA HD and Vabysmo, that still show fairly incremental benefit. So those agents have high efficacy, but their durability is still fairly challenged. So there's an interesting opportunity still for a medicine that can have a high efficacy and can deliver a truly differentiated kind of durability as a biologic. If you look on the bottom right, you have new types of technologies or new types of drug delivery agents that are trying to push a high durability, but not in the context of high efficacy. So in those cases, in general, they'll start with different doses of the biologics, say, EYLEA or LUCENTIS, and then on the basis of establishing control of the disease in the patient, then they come in as sort of a maintenance-type therapy for durability. But what Kodiak's trying to achieve is to have biologics that really is the heir apparent to EYLEA or to LUCENTIS or to the mainstay biologics and to deliver a biologic for all patients that has high efficacy and high durability and can be used in every patient. And I think based on the learnings and the course corrections that we have and the platform and the science, we're on track and very close, I think, to demonstrating this type of a profile across the three successful pivotals that we've run and the two new pivotals which are in progress. So let's talk more about that. So where are we in terms of these clinical programs? What kind of timelines and what kind of catalysts are we talking about? So for both tarcocimab and the KSI-501 program, we have important catalysts, I would say, in the Q2 timeframe of 2025. And that's really the target enrollment complete for the new GLOW2 study in diabetic retinopathy for tarcocimab, and also the target enrollment complete date for the new pivotal DAYBREAK study in wet AMD, which includes both tarcocimab and KSI-501. Both of those studies have a 48-week primary endpoint. So based on enrollment complete in early 2025, we're looking at top-line data in early first half, Q1, Q2 of 2026. And on top of that, we have the KSI-101 program, which is the unconjugated bispecific, which we're developing in a different kind of indication set for inflammation with macular edema. And we're looking and are generating data right now in our phase I-B study, the APEX study. And we'll be using that data, hopefully, by mid-next year to determine the two dose levels to move forward into the two pivotal studies for KSI-101 called PEAK and PINNACLE. We're excited about this diversified portfolio and the data that's currently in progress, so with three clinical programs leveraging our 15 years of learning, I see Kodiak as at a decisive moment in representing an exciting investment opportunity with catalysts looking in Q2 2025, which is really a setup catalyst for execution, and then from there, on top of data from the KSI-101 program, which we expect to present in Q1, Q2 of 2025, we'll be set up with enrollment complete, last patients into the pivotals for tarcocimab and 501 by early to mid-2026, and then have the clock ticking towards top-line data in early 2026. Sorry, enrollment complete in early 2025 with top-line data in early 2026. Let's step back a little bit and talk about science. We're a science-driven company. We've been building this science for a long time. What do we understand and where are we? So first of all, everything starts with the conjugate design for Kodiak's ABC Medicines. And of course, the principle in intravitreal and biologics for ophthalmology is that the ocular half-life increases proportionally with the molecular size of the molecule. So where are we in terms of molecular size? Well, Kodiak's platform, the fundamentals are to build antibody conjugates as biologics. And we conjugate a novel and proprietary phosphorylcholine polymer that we conjugate into antibodies, monospecific or bispecific antibodies that we design. So where do we sit comparatively? Well, our molecules, as the retina KOLs like to say, are a bit of the sumo wrestlers in the field. So if you start with, say, LUCENTIS at about a 48,000 molecular weight or EYLEA at 115 or faricimab at 150, we're looking at molecules in our case that are closer to a million dalton molecular weight. So what kind of half-life or what kind of residence time does that deliver? So you can look in animals, and we did, and we had a nice profile in the animals. And the half-life multiple is about 3x to 4x that of LUCENTIS, EYLEA, and Vabysmo in the animal model. And the standard model is rabbit. Well, that's nice. But only recently did we really have the human data to prove that that animal data was representative and translates into what one would see in a human. So looking at data from aqueous taps, samples that we had taken from the human subjects, from the patients in our clinical trials, and looking at the phase I-B where we gave three loading doses once a month and then went out basically six months in the majority of patients, and we drew samples, what did we see? We presented very interesting data at Kodiak's Capital Markets Day on September 23rd of this year. This is some of the data. It's quite interesting with every patient having a unique journey in terms of the exit rate of the drug from the patient, from the eye. If you look at individual patients, you can see how within that individual journey of each individual patient, how actually linear and precise the data is in terms of the select patients and the half-life, ranging in this case here from six days all the way to 40 days. And if you actually look at each individual patient, which we did, and then you can plot that and overlay that with individual patient data that's been shared from Roche's faricimab molecule, you can see that faricimab had a mean half-life exit from the eye of seven and a half days in subjects, and our mean is 20 days. And they have a range of, let's say, three days to maybe 16 days, and we have a range of 5 - 50 days. So it was very impressive data and very interesting. On top of that, we looked across the three major retinal vascular diseases and saw that the mean was similar across the three diseases, which was nice to see. And importantly, in retinal vein occlusion or RVO, which is a very tough test of half-life given the very high VEGF load. We were very pleased with that data. So again, from the principle of the design, the conjugate and the molecular weight, to really showing a human durability that's very differentiated from existing biologics today. So we were very pleased with that. So what's the evidence this actually translates into a clinical durability? Well, you can look across our different pivotal studies in different ways. I think importantly, in our diabetic retinopathy study, the successful GLOW1 phase III study, we tested every six-month dosing in every patient and generated very strong data, very impressive data in diabetic retinopathy, both for prevention of worsening of disease, but also for treating disease. And in our BEACON retinal vein occlusion study, we met the endpoint at six months for non-inferiority, dosing every eight weeks instead of every four weeks, so doubling the interval. And then in the second half of the year, actually, 75% of the patients only needed zero or one dose of tarcocimab and achieving the same or similar efficacy parameters in terms of vision as EYLEA. And in other pivotals in DME and wet AMD, we had very impressive six-month durability statistics, over 50%. So some people quibble and say, how can you talk about pivotals such as GLEAM and GLIMMER in DME where you didn't meet the endpoint and talk about durability? I think that's a good point, right? We're looking at science and trying to look at the directions of the science. But we can look at the patients who didn't have a cataract adverse event or didn't have a cataract at all because they already had their cataracts fixed, these so-called pseudophakic patients in the GLEAM and GLIMMER studies. And when you do that, you can see we had a six-month durability of 55% of the patients, and we had vision overlapping with the aflibercept control and very strong fluid control. So an impressive result nonetheless. And in our DAZZLE study, the early wet AMD study where we needed to make some course corrections and are now doing that in our new DAYBREAK study, we had very strong vision gains and very strong fluid control in the 59% of patients that were on the longest allowed dosing interval, five months. And in the GLOW1 study, as I mentioned, we had very strong data in terms of primary endpoint having been met, both for the treatment of retinopathy and the prevention of future complications with every patient on six-month dosing. In retinal vein occlusion, as I mentioned, we did very well both in terms of efficacy endpoint as well as durability. It's a bit of closing the loop, closing the loop of that science of durability from the conjugate design all the way through the human in -vivo PK data and now human efficacy data as well and durability. Importantly, what's the learning, right? The durability, you know, does it come at a cost? What we found is it did come at a cost. Immediacy seems to be the cost. This is data from Kodiak's monthly study, the DAYLIGHT study in wet AMD patients. What you can see is that through the early loading phase against EYLEA, the drying effect is weaker than aflibercept. Later, the potency is comparable to aflibercept. What's important is that at Kodiak over the last year and a half, we've applied course corrections to our science to solve this challenge in immediacy. We call this our enhanced formulation. You can see in the photo here that we have a mixture now, not just of 100% conjugated antibody, but we've doped in or we include a fixed amount of the unconjugated antibody to drive that early immediacy and to have a bit of an enhancement or a co-formulation. We brought this enhanced formulation concept into both tarcocimab and to KSI-501. Before, we had a 5 mg dose of antibody. We still have that. Now we have 4 mg of conjugated antibody and 1 mg of unconjugated. I call that the 1 plus 4. It improves manufacturability. It improves ease of dosing, which drives safety. It maintains the dose and potency, maintains our signature durability. Importantly, it brings a powerful immediacy. Is it sufficient, and the point is that the 1 plus 4 with the 1 mg, the unconjugated portion of the enhanced formulation of tarcocimab contains a very high molar equivalent alone, just the unconjugated portion, to that of the approved intravitreal biologics. So for example, it's 0.7 mg of the 2 mg aflibercept dose, the EYLEA dose. Basically, 2/3 of the approved dose is the equivalent VEGF binding of R1 out of the 1 plus 4, or it's a superdose of LUCENTIS, 0.7 mg equivalent versus the marketed 0.5 mg or 0.3 mg doses of LUCENTIS. Can we look at that differently? If we're a 2/3 equivalent of 2 mg of EYLEA, so let's say 1.3 mg. Well, a 0.5 mg dose of EYLEA was tested against the 2 mg in their early pivotal studies for Regeneron, and the 0.5 mg dose was found to be similar. You can see that on the right in terms of drawing power. You can also do the same analysis here. If you wanted to say, how much does the 1 out of our 1 plus 4 compare against LUCENTIS? Like I said, it's 0.7 mg versus their 0.5 mg. What about faricimab? Our 1 plus 4, the 1 is equivalent to a 2 mg dose of faricimab with their marketed dose being 6 mg. Some of the early phase II studies with faricimab showed that their 1.5 mg dose was similar or the same to their marketed 6 mg dose here on the right in terms of vision and also drawing power on the bottom. What's important is the objective here with the enhanced formulations. A key objective was to close the immediacy gap while also providing improvements in manufacturability, dose administration, and patient safety. How will this concept of the new or the enhanced formulations, how will that translate into patients? What's important is, as I showed you, you know, the data we generated from individual patients, each patient has a unique journey. It's not predictable in advance. We're going into treatment-naive patients. The concept is to apply our drug for every patient. And what's important is in the population of patients in the clinics, like for example, you can have a patient that's a very rapid clearance patient, for example, here on the left or on the bottom left. And the point is that we'll have a similar exit of our unconjugated to, say, faricimab, but we'll also have the conjugate that will deliver the longer durability. So say a patient who's a monthly patient, well, maybe there'll be a six-week patient on tarcocimab. Or maybe you have a middle-of-the-road patient that was a seven-day half-life patient for faricimab and maybe a 20-day for ours. So that might have been an every 8 to every 10-week patient, but maybe it's going to be an every 12 to 16-week patient on tarcocimab. Or on the right, you maybe had a pretty attractive patient on faricimab every 12 weeks. But in our case, perhaps that can be an every 16, 20, or 24-week patient and maybe achieve the majority of the patients showing signature six-month durability. So the science fits together actually very nicely. And we've applied and extended this concept of our enhanced formulation into all of our ABC Medicines. With the KSI-501, it's a 1.5 plus 3.5, so 1.5 mg of free protein and 3.5 mg of conjugated antibody. So our clinical program overview, right, as I mentioned, we now include three programs in the pipeline, tarcocimab and KSI-501, our ABC Medicines, our conjugates, and the new KSI-101, the unconjugated going into a different kind of disease category. So as I mentioned, for tarcocimab, it's the only intravitreal biologic that's demonstrated consistent six-month predominant durability in the high prevalence retinal vascular diseases. We're developing it to be a mainstay biologic that can be used in all patients. That's why we're enrolling only treatment-naive patients in our pivotals. The enhanced formulation is designed to deliver both a pulse and the durability. With 90% of the clinical and manufacturing activities already completed, we're really only one successful study away from BLA submission, but we're running two, and they're going to be reading out in a similar timeframe. Based on the study designs, we anticipate a high probability of success for those studies. We're excited to execute those. Our BLA package for tarcocimab is planned for 2026 for the three disease indications supported by five pivotal studies in diabetic retinopathy, wet AMD, and RVO based on FDA alignment that we've had. Wet AMD from the DAYLIGHT study, retinal vein occlusion from BEACON, diabetic retinopathy from GLOW, and then two new phase III studies that are actively enrolling, the GLOW2 in diabetic retinopathy and the DAYBREAK study in wet AMD. Importantly, we have had very nice conversations with regulators on those study designs. The GLOW2 study repeats the successful GLOW1 study with the addition of an additional loading dose. As I mentioned, the DAYBREAK study design is a fairly innovative study design. It includes both tarcocimab and KSI-501 as compared against the aflibercept comparator in wet AMD. It is a one-year primary endpoint study, but it is a two-year study. The objective for tarcocimab is to show improved durability or strong durability and improved immediacy. It is to assess the six-month durability potential. For KSI-501, the objective is a bit different. So given that it has a second mechanism of action, we chose to make the KSI-501 objective to really explore the potential of the bispecific MOA, IL-6 and VEGF inhibition to deliver or to be able to tease out some ideas of improved efficacy in wet AMD, which is a very complicated disease where there is still a lot of high unmet need for patients. So DAYBREAK includes a number of corrections, let's say, for the study that we ran initially in wet AMD called the DAZZLE study, where we felt we had underdosed some of the patients. So we added a fourth loading dose. We allow shorter intervals of every month and every eight weeks as opposed to locking patients only into very long interval dosing. And we have flexible intervals. We have new reactive dosing criteria that are pretty impressive, actually. And we use fluid as a disease marker using AI tools for every patient. And also, whereas we were weak on the immediacy when we had the legacy formulation, we believe the new combination will drive a very interesting clinical profile. So for example, before, maybe we just used the central 1 mm to drive retreatments, whereas now we're using the central 3 mm, which is important and can drive more appropriate treatments. Furthermore, we have new tools and disease activity reports from each patient at every visit looking at the presence or absence of intraretinal and subretinal fluid to drive disease treatment for the disease activity criteria. So these represent a pretty complex set of science and a pretty complex set of learnings. And we're very pleased with the DAYBREAK study design, and the study is enrolling well. As I mentioned, our KSI-501 is a first-in-class bispecific conjugate, looking at the similar sets of diseases and hopefully trying to tease out the ability to have a higher level of efficacy in some useful percentage of the wet AMD patients. It has the same enhanced formulation benefits, and it has, as I mentioned, a similar arm in the DAYBREAK study looking for better efficacy. Our KSI-101 molecule is an element of having diversified our portfolio. It's an ABC Platform-independent first-in-class bispecific protein in a greenfield market, so it inhibits both inflammation as well as the elements of the VEGF permeability and fluid control. We call it MESI or macular edema secondary to inflammation, so as an unconjugated protein, it's more of a traditional intravitreal biologic with a profile that's uncorrelated to our other medicines. Macular edema is an important element for patients. It's the leading cause of vision loss in patients with intraocular inflammation. And that's really targeted by the anti-IL-6 component of the KSI-101. In the current treatment algorithm, steroids are the mainstay, then systemic immunomodulators, and then maybe systemic biologics. Anti-VEGF agents are sort of a last agent. But there's an unmet need for a minimally invasive potent therapy with a better safety profile. And that's what we're trying to develop with KSI-101. Roche is developing their anti-IL-6 antibody in the eye. They've generated impressive data, but they've also shown an important dose response. And they're actually developing their two lowest dose levels. And we think that leaves room for a higher dose in our agent as well as the bispecific mechanism of action with the VEGF and IL-6. So KSI-101 is being tested in our APEX phase I study. We'll be sharing data in Q1 and Q2 of next year. We look forward to that. We already have strong alignment with FDA on phase II-B/III studies, which we call PEAK and PINNACLE for KSI-101. We hope to start those studies mid-2025. We have three clinical programs advancing in parallel, collectively addressing the limitations of today's therapies across a broad spectrum of retinal diseases. That really represents the current state of the art of Kodiak. As I mentioned, pivotal studies and clinical studies for all three of these agents are ongoing and build from the strong science that we have been following these years. We think over the next six months and then over the next 18 months, it will be an important time to see how we bring all of these elements of science and execution together and see how that translates into value for Kodiak stakeholders, so thanks very much. Maybe just let me ask you one question. I think it's very important for investors to understand. You made some changes to your formulation. And how does that increase your confidence on improved efficacy and also safety? Yeah. Yeah, thanks, Kyle. Well, I think critically, the enhanced formulations have maybe five or 10 different benefits. So importantly, from an efficacy standpoint, we always have shown the strong durability. But I think that may be important and be able to show itself in 50% of the patients or 2/3 of the patients or maybe 80% of the patients. But the 10%-20% of very high-need patients are a difficult set of patients to treat. But we wanted to develop not just a maintenance therapy, which would be for like really good patients. We still believe that there's an opportunity to be a mainstay biologic, to be an heir kind of a parent to the EYLEA type franchise. In order to do that, we go after treatment naive patients. We really felt that we had to solve the immediacy gap that we showed in the DAZZLE study and even in the DAYLIGHT study. By bringing a certain amount of free protein that's unconjugated, but an amount that's sufficient pharmacologically really in and of itself, plus to bring a lot of our conjugate to the table, that combination is really powerful. It's an enhanced form of the medicine, but in all of the many thousands of patients that we've dosed and all of the clinical data we have at our disposal, both EYLEA as a control as well as tarcocimab, the legacy formulation. With the studies of that, what we believe is that this enhanced formulation can bring all of the key elements that are needed for our medicines to be like the winner in this really massive category of the retinal vascular diseases. So LUCENTIS was approved in 2006. EYLEA may be, you know, incrementally better. Vabysmo and EYLEA HD are maybe incrementally better than that, but they've still left open the prize. And so all of this learning and these sort of soft course correction that we made with the enhanced formulation have, you know, so many benefits. And we believe that both tarcocimab and also KSI-501, which then brings like another supplemental mechanism of action and, of course, being tested in the new DAYBREAK pivotal with what we think is a wonderful design. So that's why we say like our science is really coming full circle. And I think I'm quite excited that, you know, we can execute on the clinical trials. We've manufactured these enhanced formulations in our commercial facility, the Ursus, at commercial scale. And we're very late in the game here. So we're quite excited. And we think, you know, the next six months in terms of preparing on the execution and the timelines and last patient in for the pivotals, plus new data on the KSI-101, the clock kind of will then be started. And then it's more of a calendar thing through the 48-week primary endpoint for last patient, last visit. So it's pretty exciting. And we think both from an efficacy and also from a safety standpoint, the new formulation, which is not a gel anymore, it's really much more watery and aqueous. And we think that will improve dose handling, administration, and therefore improve safety. But it's important to remember that we already have like 13,000 injections in eyeballs and 2,500 patient years of safety exposure and tens of thousands of patient visits. And our safety profile is very, very excellent. So thanks a lot, Kyle. Cool. Great.