Thank you. We'll get started. Thanks for having me at the meeting. Please note my comments today will contain forward-looking statements, so please refer to our SEC filings, both Form 10-Q and 10-K. Kodiak is fundamentally a vision sciences company. The eye is how we experience the world, and at Kodiak, we're privileged to have been focused on this area for over 15 years now. Unlike oncology or immunology, there are very few companies doing this work. At Kodiak, we have both a late-stage clinical portfolio and an emerging pipeline that span multiple retina mechanisms of action, mostly bispecifics and multi-mechanism medicines. Multiple indications, mostly high prevalence disease, and also multiple different drug types in the pipeline and portfolio, mostly conjugates, as well as bispecific antibodies. Today, I'll focus most of my comments on our late-stage pipeline. Our three late-stage clinical assets are bringing new science to the major causes of vision loss in the developed world and globally, and representing an opportunity for many millions of patients. We're at a very interesting moment in the company. As we've said before, it's a pivotal moment. All three clinical programs are in phase III, with top-line data expected in 2026. Zenkuda is BLA-ready. It's a little bit difficult sometimes. Some investors are very knowledgeable about the scientific history of Kodiak, whereas other ones, based on the stock, let's say in the last year, are new to the Kodiak story. We'll try to run through at a high level, but also in some detail to try to hit the highlights actually for all interested investors. Just looking quickly here on the slide, we have KSI-101, which is our bispecific protein. We're developing that in the disease that we call MESI, macular edema secondary to inflammation, and we'll talk more about that. We had very nice phase I-B data in patients in our APEX study in MESI. The phase III PEAK and PINNACLE studies are actively enrolling quite well. We're expecting to announce PEAK top-line data this year, let's say in December before Christmas. The Zenkuda, or tarcocimab, as previously called, is our anti-VEGF, antibody biopolymer conjugate, ABC. We've run four successful pivotal studies with positive top-line data with tarcocimab. We're BLA-ready for that molecule in diabetic retinopathy, retinal vein occlusion, and also in wet AMD. We're running the phase III DAYBREAK study in wet AMD, and we expect top-line data for tarcocimab in the study, let's say in late September of this year. We expect to file a BLA shortly thereafter this year. We're also running in the same DAYBREAK study, the KSI-501, which is a conjugated form of an anti-IL-6 VEGF bispecific biologic or inhibitor. In the DAYBREAK study, we're looking to see whether or not the combination of the IL-6 with the VEGF as a conjugate can give us a differentiated kind of efficacy in context of vision. That study also, the 501 will read out together with Zenkuda, and we anticipate late September, as I mentioned, for the readout. As I mentioned, we have four phase III readouts in calendar year 2026. If successful, that will position us very well to file three BLAs in calendar year 2026 and 2027. First of all, we had previously the BEACON study and the GLOW 1 study and the DAYLIGHT study with Zenkuda that were successful. Earlier this year, we had a very successful readout in diabetic retinopathy in the GLOW 2 study. We're anticipating with Zenkuda with keen interest, the DAYBREAK readout, as I said, in late September, followed quickly by a BLA. Within a couple of months, we anticipate and are on track for the PEAK 1 readout in MESI with KSI-101, we believe before Christmas. We hope that we'd be able to file a BLA, if not based on that readout, but then based on the PINNACLE or the PEAK 2 and PINNACLE readout, which we anticipate in the second quarter of 2027. As I mentioned before, the KSI-501 also reading out in the DAYBREAK study in September timeframe. Also, we're very close to first patient in for a new DME study with KSI-501, which will be a fairly large study. We hope that we'll be able to explore the potential for superiority of KSI-501 in DME population, and also look to explore some aspects of the durability of the KSI-501 in DME. It's an exciting year in 2026 and an exciting next six, 12, and 18 months for the company. At the same time, when we think about Kodiak at a high level, we have made significant investments in our clinical and commercial stage manufacturing capability, together with our Swissmedic-approved commercial facility, together with Lonza. Let's take a step back and we'll spend most of the time today talking about our late-stage pipeline. Let's first talk a little bit and remind ourselves about some of the science that sits underneath our two conjugates, Zenkuda and KSI-501, because there's quite a lot of questions in anticipation of the DAYBREAK readout in just a couple of months. First, let's remember that our ABC Platform, our antibody biopolymer conjugate platform, is composed of a co-formulation, really, or a mixture, of biologic medicines, both an antibody to drive the immediacy of effect, as well as a conjugated form of the antibody to drive a long interval durability of effect. From the standpoint of the design, the potency, the animal work, as well as now significant human work, we feel that we've built a very special capability for retina, which is proprietary, both from a patent standpoint, but also there's quite a lot of capability and knowledge in the manufacturing. Let's just talk briefly about durability. Our ABC medicines are designed for longer durability. If you look on the left, you can see other predicate medicines with different sizes. These are antibodies or antibody fragments, largely. The smaller the antibody, maybe the deeper and faster it will go into the retina, but also the faster it leaves. Immediacy of effect is driven largely by a small size of these biologics. On the right, we have Kodiak's antibody biopolymer conjugates that are quite large, and by virtue of their large size, will have much longer dwell time in the eye in terms of how long they take to distribute and how long they'll stick around. We prove this definitively looking at around 50 patients, let's say, and doing sampling of their front of the eye as the drug is injected into the back, and then it will exit partially through the front. When we do that analysis and look at Zenkuda compared to, say, faricimab, Roche's Vabysmo, we see that we have a mean of 20-day half-life for our conjugate versus a mean of faricimab or EYLEA or other antibody-sized medicines in the eye of 20 days versus, say, seven and a half days. With a fairly broad range, actually, but we have over 80% of our patients had a half-life of greater than 11 days, whereas, say, other predicate biologics such as faricimab, really only 10% of the patients had a half-life over 11 days. Something significantly different. What we learned over the years when we think historically in the earlier studies is that having long durability works well in the majority of the patients. Actually, in a small minority of patients, is it 10% or maybe 20% of the patients, having that large conjugate only meant that in early dosing in the patients, we were maybe weak in terms of the speed or the immediacy of that efficacy. We didn't want to just have a maintenance therapy for patients. We wanted to have a biologic therapy that could be used first out the gate or first out of the fridge or as a first-line therapy for all patients. What we did is we thought, "Why don't we just combine a defined amount of the unconjugated protein, the antibody, together with a defined amount of the conjugated form of the antibody?" That's what we've now set as a new standard for our ABC Platform. For Zenkuda at a 5-milligram dose, we have one milligram of the unconjugated antibody and four milligrams of conjugated. For the KSI-501, which is a bit larger protein, say around 200,000 versus the 150,000 of Zenkuda antibody to antibody, we decided to have 1.5 milligrams of the unconjugated to drive that immediate effect and 3.5 milligrams of the conjugated. It's a single biologic engineered for high durability. Why is that useful? The reason is there are very good predicate agents that are already in the market, EYLEA and Lucentis, for example. Okay. Even more recently, we have what we call Gen 1.5 agents, Roche's Vabysmo or Regeneron's EYLEA HD. Despite the Gen 1 and the Gen 1.5, there remains a valuable open space in the large, say, $15 billion retinal vascular disease market. That opportunity would be for a biologic that has both high immediacy and efficacy, as well as a truly longer high durability in a single biologic. I call on this four-quadrant axis the upper right quadrant. The Gen 1 biologics provide immediacy, and let's say the Gen 1.5s provide immediacy and more of an incremental durability. They're meaningful for patients. Even based on that incremental durability, they're commercially very successful. Despite that success, most patients in the real world are actually still being treated on a Q8 week or a Q12 week regimen. There are new technologies that are being explored in clinical trials, including implants and gene therapies. They're engineering for high durability, but they're lacking immediacy, and they're generally relying on mainstay biologics such as EYLEA or Lucentis or Vabysmo to establish disease control and to bring immediacy as part of a different type of therapy. For Zenkuda and KSI-501, we're trying to bring a differentiated kind of immediacy combined with durability. For Zenkuda, we're looking for non-inferior efficacy with good immediacy and the best durability. For 501 in the DAYBREAK study, we're trying to look for, well, what is the potential improvement in efficacy, i.e. vision, that an anti-IL-6 and VEGF trap bispecific conjugate can bring to the patient, as well as having strong immediacy and industry-leading durability. We separately, previously, as I mentioned with Zenkuda, have successful studies phase III in retinal vein occlusion, our BEACON study, also successful diabetic retinopathy readouts in GLOW 1 and GLOW 2 phase IIIs, and also had a successful monthly wet AMD study, the DAYBREAK study, and we're waiting on the results from DAYBREAK. In KSI-501, DAYBREAK represents the first pivotal study, and we're looking forward to the readout shortly. As I mentioned, we're beginning a DME study as well. I think, well, obviously it will be important to see the results of DAYBREAK for tarcocimab, or Zenkuda. I think what's important to remember is we already have very successful readouts, and I think that our commercial profile already, based on the phase III that have read out so far, already positions Zenkuda to have a very interesting and important differentiated profile in the commercial marketplaces. For example, RVO represents about 20% of the Eylea sales, or let's say globally, around $3 billion out of the $15 billion anti-VEGF market. We demonstrated in our BEACON study a very strong efficacy while doubling the treatment interval, so Q8-week versus Q4. In the second six months of the study, we went head to head against Eylea and showed that 75% of our patients can achieve a six-month durability at year one and have overlapping vision in OCT as compared head to head against Eylea. Fewer doses, a head to head comparison, strong efficacy in the first six months where we doubled the interval, very strong 75% six-month durability in the RVO market. Very nice data, actually. Here's the overlapping in the first six months, the vision in OCT, then in the second six months, you can see directly overlapping vision in OCT on a matched criteria. A very interesting profile for Zenkuda in retinal vein occlusion using the old formulation, and I think it will be even stronger with the new formulation. Also in the GLOW 1 and GLOW 2 studies with Zenkuda, we generated very strong data in diabetic retinopathy, which is close to 10 million subjects in the U.S., of which maybe 20% have vision-threatening disease. Diabetic retinopathy can progress quickly into vision-threatening proliferative retinopathy or into DME. Very few of these patients are actually treated today. We showed very strong data in GLOW 1 and GLOW 2, with 100% of the patients essentially on six-month dosing at the endpoint. As I mentioned, very nice data in terms of clinical treatment and improvement, and also the key secondary endpoint, which is reducing the risk of developing sight-threatening complications by over 85% in both GLOW 1 and GLOW 2. I think for me, in terms of thinking about the opportunity for Zenkuda in diabetic retinopathy, I really think a picture is worth a thousand words. This is a baseline patient in GLOW 1 with microhemorrhages, as you can see on the left. After treatment with Zenkuda through the six-month interval, the patient has totally cleared the hemorrhages, and the retina looks quite beautiful. I think although diabetic retinopathy isn't a large established market in the retinal vascular disease area today, we believe it has a lot to do with the fact that today's agents have multiple loading doses and are dosed quite frequently. Whereas we've shown very compelling data in both GLOW 1 and GLOW 2 that on the six-month interval, we can treat the patient and also prevent worsening of disease. I think over time, the commercial opportunity for a drug like Zenkuda in this type of market is quite special. In any case, we're running the DAYBREAK study. We tried to put all of the new ideas of our learning, of our science in terms of the redesign of the molecules and of the platform, as I mentioned, tarcocimab and 501 with the new formulations. At the same time, we tried to design a clinical trial in DAYBREAK that's very conservative. We're not trying to throw the Hail Mary. We're not taking a very aggressive set of decisions in the design of the study. Rather, we took a very conservative view. We're doing four loading doses. Okay? With tarcocimab, we're allowing the patients to be treated every month or as infrequently as every six months, depending on whether or not the disease is reactivating in the patient's eye. In the KSI-501, we're doing, again, four loading doses, and we're dosing the patients every eight weeks. We do allow them to be treated monthly if they have disease reactivation. We're using an AI-based tool that precisely measures the fluid in the eye at each month. If fluid is present, the patient will be treated with active therapy. If disease is not present, then they will not be treated. For tarcocimab, that's going to let us assess durability in the patients up to six months. For KSI-501, that's going to let us evaluate the potential for intensive dosing. What kind of additional visual acuity or efficacy might we see with that IL-6 bispecific VEGF? Again, both of them have the mixtures of our unconjugated as well as conjugated for both tarcocimab and 501. This study will read out very shortly. I think we believe that the study, from what we see, is prosecuting or executing very well, and we'll be just as excited as all of you to see how the data come out when we take a look at the top-line data and share that. I think we are looking for tarcocimab and 501 to show nice safety in DAYBREAK. We're also looking for the new formulations to help us deliver strong fluid control through the loading doses and through the matched zone with Eylea to understand how powerful is the immediacy through the loading phase. Through the rest of the study and into the primary endpoint, we'd like to see nice durability with tarcocimab and good vision, non-inferior to Eylea. With 501, we're very curious to see whether, again, that combination of the IL-6 and the VEGF can deliver some kind of differentiated efficacy in patients. We're optimistic on the study, and we'll see what the readout is shortly. Again, we do believe that the data we've generated to date, say in RVO, in the BEACON study, does support strong immediacy and high durability, that the data in the GLOW 1, and particularly in GLOW 2, where we really think the strength of the new formulation and the safety of the new formulation is clearly shown in GLOW 2 with very strong data, that we see nice immediacy there and also strong durability in the diabetic retinopathy population, and a nice opportunity both in RVO and DR with Zenkuda to try to build a very interesting commercial franchise. DAYBREAK will help us understand the potential, both for tarcocimab and for KSI-501, and for our ABC Platform investments as well, help us really understand what the opportunity is for our ABC medicines and those two, our ABC Platform and those two medicines in treatment-naive wet AMD. Whether, in fact, people have been working, let's say, for 20 years since the introduction of Lucentis to really develop something that can service this upper right quadrant commercially as a biologic. We hope that based on the evolution of our science and our molecules and our clinical trial designs, that we're going to have and are running a definitive experiment in DAYBREAK. We hope that we'll be able to show nice safety, strong fluid control through the loading phase, and nice durability with Zenkuda, and also with 501, the opportunity to explore whether our bispecific can give something special in terms of efficacy as well. Let's move on to KSI-101. I think the DAYBREAK readout in late September, we're doing everything that we can, we're going to share the data in an objective manner when it comes, we're optimistic, why don't we all see together? Meanwhile, the KSI-101 is a different kind of molecule, we're running it in a different kind of indication. It's a new indication area where there are no therapies. The PEAK and PINNACLE pivotals are enrolling very well. As I said, we expect to announce top-line data for the KSI-101 PEAK 1 study this year. Let's get prepared for that amazing potential outcome. Macular edema, as you know, in retina, is the common clinical presentation of a wide spectrum of diseases that can be caused by inflammation and/or by VEGF overexpression. Macular edema and visual impairment are shared clinical features irrespective of the etiology or the location of the inflammation. For example, on the top, looking at the location of the inflammation, whether it's anterior, whether it's intermediate in the eye, whether it's posterior in the back of the eye, or whether you have a panuveitic pattern where you have inflammation across the eye. At the same time, you can have macular edema from different specific etiologies irrespective of the location. Whether it's idiopathic, meaning we don't know why the patient has inflammation, whether they might have juvenile arthritis, or whether they have focal inflammation, or whether they had severe inflammation for such a long time that they began to get angiogenesis in the eye in terms of PIC, or you might have had a post-operative, you might have had a procedure, either systemically, interestingly, or in the eye, and then you develop refractory inflammation afterwards. MASI, macular edema secondary to inflammation, is fundamentally caused by a three-step system. First, you have some sort of immune trigger. Okay? That causes the immune system, for whatever reason, to attack the eye, and in particular, it attacks the barrier between the blood and the retina. That barrier breaks down, you get macular edema, visual impairment, and worsening of inflammation, and then that leads to this IL-6 VEGF amplification cascade. Steroids are what people have traditionally been using for MESI, but they carry significant safety risks. Efficacy also can be limited. The adverse events from current MESI treatments, in particular the steroids, can lead to very complex problems for the patients, often leading to repeated surgeries and irreversible vision loss. Cataract repair, unlike in more ordinary people, in the context of severe inflammation, the repairs are usually delayed. The patients often can be blind for quite some time. Meanwhile, for example, intravitreal steroids, for example, RETISERT, as many as 60% of patients will require chronic pressure-lowering medications, and maybe a third of them will require complicated filtering procedures. Nearly all eyes are expected to develop cataracts. This is pretty complicated and not something that we want. There are very complicated patient journeys in MESI with many years of different types of failed treatments, in this case, adalimumab, methotrexate, CellCept, azathioprine, oral steroids, different types of eye drops, different types of intravitreal steroids, as well as many, in this case, repeated surgeries, either for cataracts and glaucoma and glaucoma shunts. It's pretty complicated. Most of these patients are going to go blind, and there really is no wonderful therapy, and there's certainly no biologic. KSI-101 is a first-in-class, high-strength intravitreal biologic designed to target IL-6-mediated inflammation and the VEGF-mediated vascular permeability at the same time. It's at a high formulation strength of 100 mg per mL. It's a bispecific protein with an anti-IL-6 antibody and a VEGF trap and a modified Fc so that it doesn't activate the complement in the eye. It's a very nice molecule. It's behaving well. It's very potent, and we're very excited about it. We know that IL-6 and VEGF, when they disrupt the barrier, they can do that independently, but when they're combined, they cause an even greater loss of barrier integrity. When we add KSI-101 to the mixture, it restores the barrier integrity to no exposure levels, whereas anti-VEGF or anti-IL-6 monotherapies only provide a partial restoration of the barrier. As I mentioned, we've tested 101 in MESI patients in the APEX study, and we had basically four different cohorts: 2.5 mg dose, 5 mg dose, 10 mg dose. Recently we ran an Asia cohort in preparation for Asian studies. We've tested around 41 patients in the U.S., plus or minus, and 13 in Asia. We saw very dramatic visual acuity gains, really in all four of the different cohorts, whether it's 2.5, 10 mg or the Asia patients through 24 weeks. You can look at that from a mean change approaching 15 letters or from an observed point of view, observed vision, where we're achieving 20/25 Snellen vision by week 20. Importantly, looking at 15 letter gain in patients, more than half of the patients, particularly at the 5 and 10 mg dose and also in the refractory Asia population, actually more than 50% of them gained three lines of vision. Importantly, we see very powerful fluid resolution actually within one week of treatment with KSI-101, bringing the patients into a deep, sustained dryness corridor through the duration of the study, and it's sustained even beyond the fourth dose at week 12 through week 24. Very strong one-week response and stable in that dryness corridor all the way through week 24. Importantly, we have more than 90% of the patients showing complete absence of intraretinal fluid. Also, we've shown very nice safety with the molecule. Single doses demonstrate rapid, meaningful responses in MESI, independent of the inflammation location or the macular edema etiology. In fact, with a single dose, we're seeing largely normalization of the retina. There are some nice comparisons on a single dose through one week versus Roche's anti-IL-6 vamikibart, where our drug is showing very rapid, very powerful response in fluid, whereas vamikibart is looking quite sluggish. We're running the PEAK and PINNACLE pivotal studies. As I mentioned, they're enrolling well, and we expect the PEAK1 readout before Christmas. We're running them in the context of our master protocol. The more sick patients or more severe disease, let's say, are enrolled into the PEAK study, and the slightly less severe patients are enrolled into the PINNACLE study. We've increased the size of the overall program to ensure success. The pivotal analysis one, which is coming out of PEAK of the first 300 patients, will read out before Christmas. The pivotal analysis two, which has an alpha hierarchy first of looking at the patient 301 through 600 of PEAK two, and then down into the combination of PEAK two plus PINNACLE. We believe that that will be ready for top-line data readout in the second quarter of 2027. Just a reminder that MESI is actually quite a large group of patients, and some of the epidemiology is in the corporate deck that you can look at. The initial addressable population is greater than 150,000 patients in the United States and actually may reflect as much as 20% of the retina practice volumes. I think that's why we're seeing such encouraging rate of enrollment in our PEAK and PINNACLE studies because there are quite a lot of messy patients out there. I don't think we'll spend too much time on our pipeline at this time. Suffice to say that we continue to build, I think, deep science, both from a bispecific antibody standpoint and also our new ABC medicine duets in large indications, expanding further into ocular inflammation with additional bispecifics and also very interesting duet-based medicines for glaucoma, looking at the optic neuropathy of glaucoma, as well as multi-mechanism medicines with long durability for geographic atrophy. I think I'll stop there, and thanks everybody for your attention. It's an exciting year. We have DAYBREAK coming up in a few months. It will be followed within a couple of months by the PEAK1 readout. We hope to file a BLA in that interregnum between DAYBREAK and PEAK1. Hopefully we'd be able to look towards an early BLA for KSI-101 in the first half of 2027 and perhaps two approvals by the end of 2027 for Little Kodiak. Thanks so much