Kodiak Sciences Inc. (KOD) June 2026 Conference Transcript

So, good morning and welcome to the Jeffrey's Global Healthcare Conference in New York. My name is Ryan Burns with the Jeffrey's Investment Banking Team, and it's my great pleasure to introduce Victor Perlroth, CEO of Kodiak Sciences.

Thanks. 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. And 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 three, with top-line data expected in 2026, and ZenCuda is BLA-ready. So with regards to, 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. So 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. So 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 1B data in patients in our APEX study in MESI. The Phase 3 peak and pinnacle studies are actively enrolling, enrolling quite well, and we're expecting to announce peak top-line data this year, let's say in December before Christmas. Zincuda, or Tarkosumab as previously called, is our anti-VEGF, anti-biopolymer conjugate, ABC. We've run four successful pivotal studies with positive top-line data with Tarkosumab. We're BLA-ready for that molecule in diabetic retinopathy, retinal vein occlusion, and also in wet AMD, and we're running the phase three daybreak study in wet AMD, and we expect top-line data for tarcosumab in the study, let's say in late September of this year, and we expect to file a BLA shortly thereafter this year. We're also running in the same daybreak study the KSI501, which is a conjugated form of an anti-IL-6 VEGF bispecific biologic or inhibitor, and 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, and that study also, the 501 will read out together with Zincuda, and we anticipate late September, as I mentioned, for the readout. So, as I mentioned, we have four phase three readouts in calendar year 2026. If successful, that will position us very well to file three BLAs in calendar year 2026 and 2027. So, first of all, we had previously the Beacon study and the GLOW-1 study and the Daylight study with Zincuda that were successful. And then earlier this year, we had a very successful readout in diabetic retinopathy in the GLOW-2 study. And we're anticipating with Zincuta the, you know, with keen interest, the daybreak readout, as I said, in late September, followed quickly by BLA. Then, within a couple of months, we anticipate and are on track for the Peak 1 readout in Messi with KSI 101, we believe, before Christmas. And 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. And as I mentioned before, the KSI-501, also reading out in the daybreak study in September timeframe, and 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 KSA 501 in DME population and also look to explore some aspects of the durability of the KSA 501 in DME. So it's an exciting year in 2026 and an exciting next 6, 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 Swiss medic approved commercial facility together with Lonzo. 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 in CUDA and KSA 501 because there's quite a lot of questions in anticipation of the daybreak readout. in just a couple of months. So first, let's remember that our platform, 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. And 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. So let's just talk briefly about durability. So 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. Immediately, there are very good predicate agents that are already in the market, ILEA and Lucentis, for example, okay? And even more recently, we have sort of what we call Gen 1.5 agents, Roches of Abismo or Regeneron's ILEA HD. So 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. And 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 sort of call on this four quadrant axis the upper right quadrant. So 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 and even based on that incremental durability they're commercially very successful. But despite that success, most patients in the real world are actually still being treated on a Q8 week or a Q12 week regimen. And there are new technologies that are being explored in clinical trials, including implants and gene therapies. And they're engineering for high durability, but they're lacking immediacy. And they're generally relying on mainstay biologics such as ILEA or Lucentis or Babismo to establish disease control and to bring immediacy as part of a different type of therapy. So for Zincuda and KSA 501, we're trying to bring a differentiated kind of immediacy combined with durability. And for Zincuda, we're looking for non-inferior efficacy with good immediacy and the best durability. And 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 by specific conjugate can bring to the patient, as well as having strong immediacy and industry-leading durability. So we separately, you know, previously, as I mentioned, with Zincuda, have successful studies, phase 3 in retinal vein occlusion, our BEACON study, also successful diabetic retinopathy readouts in GLO-1 and GLO-2 phase 3s, and also had a successful monthly wet AMD study, the Daylight Study, and we're waiting on the results from daybreak. And in KSI 501, daybreak represents the first pivotal study, and we're looking forward to the readout shortly. And as I mentioned, we're beginning a DME study as well. I think, you know, well, obviously it will be important to see the results of daybreak for torcosimab, but I think, or zincuda. But 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 threes that I've read out so far, already positions included have a very interesting and important differentiated profile in the commercial marketplaces. So, for example, RVO represents about 20 percent of the ILEA sales, or let's say globally around $3 billion out of the $15 billion anti-VEGF market. But we demonstrated in our Beacon study a very strong efficacy while doubling the treatment interval, so Q8 week versus Q4. And then in the second six months of the study, we went head-to-head against ILEA and showed that 75 percent of our patients can achieve a six-month durability at year one and have overlapping vision and OCT as compared head-to-head against ILEA. So fewer doses, a head-to-head comparison, strong efficacy in the first six months where we doubled the interval and very strong 75% six-month durability in the RVO market. And very nice data, actually. Here's sort of the overlapping in the first six months, the vision and the OCT. And then in the second six months, you can see directly overlapping vision and OCT on a matched criteria. So a very interesting profile for Zincuda in retinal vein occlusion using the old formulation. And I think it will be even stronger with the new formulation. Now, also in the GLO-1 and GLO-2 studies with Syncudo, we generated very strong data in diabetic retinopathy, which is close to 10 million subjects in the United States, of which maybe 20% have vision-threatening disease. So diabetic retinopathy can progress quickly into vision-threatening proliferative retinopathy or into DME. Very few of these patients are actually treated today. And we showed very strong data in GLO-1 and GLO-2 with 100% of the patients essentially on six-month dosing at the endpoint. So 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 site-threatening complications by over 85% in both GLO-1 and GLO-2. I think for me, in terms of thinking about the opportunity for Zincuda in diabetic retinopathy, I really think a picture is worth a thousand words. So this is a baseline patient in GLO1 with microhemorrhages, as you can see on the left. And after treatment with Zincuda through the six-month interval, the patient has totally cleared the hemorrhages and the retina looks quite beautiful. So I think although diabetic retinopathy isn't a large established market But 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 GLO-1 and GLO-2 that on a 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 Zincuda 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, Tercosimab and 501 with the new formulations. At the same time, we tried to design a clinical trial in Daybreak that's very conservative. So 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. So we're doing four loading doses, okay? Then with Tercosimab, 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. And in the KSI-501, we're doing, again, four loading doses, and we're dosing the patients every eight weeks. But we do allow them to be treated monthly if they have disease reactivation. And we're using an AI-based tool that precisely measures the fluid in the eye at each month. And if fluid is present, then the patient will be treated with active therapy. If disease is not present, then they will not be treated. So for tarcosimab, that's going to let us assess durability in the patients up to six months. And for KSA-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. And again, both of them have the mixtures of our unconjugated as well as conjugated for both Tarkosumab and 501. So, you know, this study we'll 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 tarcosimab 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 ILEA to understand how powerful is the immediacy through the loading phase. Then through the rest of the study and into the primary endpoint, we'd like to see nice durability with Tercosumab and good vision, non-inferior to ilea. And 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 you know that the 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 was in CUDA to try to build a very interesting commercial franchise. And Daybreak will help us understand the potential both for Tercosumab and for KSA501 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 and whether, in fact, you know, 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. And 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. And we hope that we'll be able to show nice safety, strong fluid control through the loading phase, and nice durability with Zincuda, 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, and we're going to share the data in an objective manner when it comes, and we're optimistic, and why don't we all see it together? Meanwhile, the KSI-101 is a different kind of molecule, and we're running it in a different kind of indication. It's a new indication area where there are no therapies, and the peak and pinnacle pivotals are enrolling very well, and as I said, we expect to announce top-line data for the KSI-101 Peak 1 study this year. So 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. And 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 pan-uveetic pattern where you have inflammation across the eye. But 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. Messy, macular edema secondary to inflammation, is fundamentally caused by like a three-step system. First, you have some sort of immune trigger. 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 sort of this IL-6 VEGF amplification cascade. So steroids are what people have traditionally been using for messy, but they carry significant safety risks. Efficacy also can be limited. So the adverse events from current messy 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 sort of more ordinary people, in the context of severe inflammation, the repairs are usually delayed. So the patients often can be blind for quite some time. And then meanwhile, for example, intravitreal steroids, for example, Red Assert, as many as 60% of patients will require chronic pressure-lowering medications. And maybe a third of them will require complicated filtering procedures. And nearly all eyes are expected to develop cataracts. So 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, celsept, 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. So 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. So 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 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. So 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-IL6 monotherapies only provide a partial restoration of the barrier. So as I mentioned, we've tested 101 in messy patients in the APEC study, and we had basically four different cohorts, 2.5-migdose, 5-migdose, 10-migdose, and recently we ran an ASIA cohort in preparation for Asian studies. And we've tested around 41 patients in the U.S., plus or minus, and 13 in Asia. And we saw very dramatic visual acuity gains, really, in all four of the different cohorts, whether it's 2.5, 5, 10 MIGs, 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, we're achieving 20-25 smell and vision by week 20. Importantly, looking at 15-letter gain in patients, more than half of the patients, particularly at the 5- and 10-meg 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. So very strong one-week response and stable in that dryness corridor all the way through week 24. And importantly, we have more than 90% of the patients showing complete absence of intraretinal fluid. Also, we've shown very, very nice safety with the molecule. And 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. And there are some nice comparisons on a single dose through one week versus Roche's anti-IL-6 famicobar, where our drug is showing very rapid, very powerful response in fluid, whereas Vimicabarth looking quite sluggish. We're running the peak and pinnacle pivotal studies. As I mentioned, they're enrolling well, and we expect the peak one readout before Christmas. We're running them in the context of a 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, and the pivotal analysis two, which has an alpha hierarchy first of looking at the 301 through patient, 301 through 600 of peak two, and then down into the combination of peak two plus pinnacle. And 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. And 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, and it will be followed within a couple of months by the Peak 1 readout. We hope to file a BLA in that interregnum between Daybreak and Peak 1, and then 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.