All right, welcome everyone to the 44th Annual J.P. Morgan Healthcare Conference. My name is Anupam Rama. I'm one of the Senior Biotech Analysts here at J.P. Morgan. I'm joined by my squad, Priyanka Grover, Joyce Zhou, and Ratih Pinhai. Our next presenting company is Kodiak. I'm presenting on behalf of the company. We have CEO Victor Perlroth. Victor.
Thank you, Anupam. Well, each year at the J.P. Morgan, the metronome of the different years, it's great to be here. Thank you. But I also remember the R&D Day that Kodiak had in July of last year. I think at that time I said I couldn't be more excited and enthusiastic about what we had in front of us. And now, looking six months later, we've made tremendous progress on the plans that we articulated at that time. I think what I also like to say is, you know, many good things that could have happened did happen, and many bad things that could have happened didn't. I think as I look, and as we look at Kodiak to 2026 and into 2027, it's a tremendously exciting time for us. I continue to be very pleased with all of the progress and everything that I see at the company.
We're going to, as usual, run through quite a lot of content. There is a lot under the hood at Kodiak, and we'll try to do that in a time-efficient manner. First, remember our forward-looking statements. Please read carefully all of the SEC documentation, including the recent materials in the last quarter associated with our capital raising. So at Kodiak, as you know, we're now a definitively pre-commercial stage retina-focused biotech.
We have our KSI-101 asset, which provides in and of itself a very simple reason to believe in the potential for Kodiak and for value creation with very strong data out of our APEX studies, a mechanism of action around IL-6 and IL-6 plus VEGF that's highly validated now within the scientific community, Phase III PEAK and PINNACLE studies that are enrolling quickly and ahead of our expectations, with top-line data expected in the fourth quarter of this year and into 2027, and a tremendously interesting commercial opportunity for this bispecific protein asset. So a very interesting reason to believe in Kodiak. Don't forget, though, tarcocimab and KSI-501 are conjugates. So we look at them as science-based heavyweights. Tarcocimab is targeting a BLA in mid-2026, let's say after the readout in the DAYBREAK study in three different retinal diseases.
Retinal vein occlusion, a very exciting and fairly large, let's say $3 billion opportunity, tarcocimab being a medicine that in the BEACON study showed very strong data, both in terms of its power and in terms of its unusual durability head-to-head against Eylea. And then, of course, in diabetic retinopathy, we'll have the GLOW1 and GLOW2 readouts. GLOW1 previously and GLOW2 in March, let's say, of 2026, and the wet AMD readout in the DAYBREAK study in the third quarter. And 501, a bispecific conjugate with our science of ABC. We hope the VEGF trap and the IL-6 will deliver something special for that molecule in the retinal vascular diseases. So two very interesting assets.
They're not super. I would say that the potential value and opportunity of these assets is underappreciated, but it's a show-me business, and we're going to generate data in GLOW2, and we're going to generate and share the data in DAYBREAK, and we'll all turn those data charts together and see the value of those programs in the context of Kodiak's portfolio of three programs. And deeper in our pipeline, we have additional bispecifics around KSI-102 and KSI-103 that we're excited about. In inflammation, we have very interesting bioconjugate-based programs in massive disease areas to come, such as glaucoma of the retina and also geographic atrophy of the retina. We don't talk a lot, but we have had tremendous progress in our RNAi assets. And we also, of course, have Kodiak's commercial manufacturing facility partnered with Lonza, the Ursus facility.
We completed our validation batches and released those for the antibody, for the polymer, and for the conjugates. Tremendous progress within Kodiak, a very interesting portfolio of assets with four Phase III programs in progress, three Phase III programs on track for readouts this year. Wow. As a reminder, three Phase III programs in retina. They really follow scientifically from Kodiak's approach to drug development. We're at a decisive moment today. As I mentioned six months ago, tremendous progress since then. I still believe we represent a very compelling investment opportunity for all of you. This is a nice slide, slide four, where we list our expected catalysts. On the KSI-101 program, we'll have 24-week data from the Phase I APIC study in February of this year.
We'll have top-line data expected for the Phase III PEAK study in MESI in the fourth quarter of this year. And we'll have top-line data from the Phase III PINNACLE study expected, let's say, in Q2 of 2027. So an exciting program and an exciting set of catalysts. For tarcocimab, we'll have top-line data from the repeat GLOW2 study this quarter. That's our expectation. We'll have top-line data from the Phase III DAYBREAK study in wet AMD in the third quarter. And we expect to closely thereafter file the BLA for tarcocimab in wet AMD, diabetic retinopathy, and retinal vein occlusion. And the KSI-501, as you know, we'll have the same top-line data from the Phase III DAYBREAK study in the third quarter.
We look to the VEGF trap and the anti-IL-6 antibody in the context of our conjugate to explore the potential for improved efficacy beyond anti-VEGF monotherapy to show strong immediacy and to show an industry-leading durability. So with 101, we're looking at a greenfield market opportunity in very sick patients, very attractive opportunity. With tarcocimab and 501, we call that the quadrant of core unmet need, where as a biologic, we want to be able to deliver strong immediacy and an industry-leading durability as a biologic in the same therapy at the same time. Very unique. It's an area like the Wayne Gretzky. We're still trying to skate to where the puck wants to be. And I think with our bioconjugate portfolio and the studies we're running, we're going to turn those data cards and we'll find out whether we're there. And we very well may be.
That would be very exciting. So as I mentioned, the assets are on track for top-line data readouts in 2026 and into 2027. When you look at Kodiak, as we call ourselves, pre-commercial, what does that really mean? Well, being in retina, there's not that many companies in retina. And with retinal biologics and with the three different programs, there's a very interesting potential for Kodiak to begin to see a sustainable revenue drip beginning in 2027 that can grow aggressively across the three different assets. Let's stay tuned. And on slide seven, just a reminder that within our bioconjugate technology, we also have next-generation versions of that where we bring not just antibodies as conjugates, but also small molecules and RNAi and a variety of different types of diverse APIs into the polymer conjugate, in particular for retina, but some early activities systemically.
As drug developers in biotech and pharma, the concept of having a proprietary platform where we can really do multifunctional and modular drug development across a diverse set of APIs in parallel is very interesting, very unique, and I think part of a longer-term value build for Kodiak. So as I mentioned, we have three Phase III programs. We have a variety of earlier pipeline assets, all designed to address the leading causes of vision loss. So obviously, our KSI-101 in MESI and our tarcocimab and KSI-501 in the retinal vascular diseases. As I mentioned, I'm quite excited about the potential for our glaucoma duet, including an NLRP3 inhibitor that's quite potent, designed in-house, and also IOP lowering elements together, and also some earlier GA duets, which of course also represents large opportunities for Kodiak as a retina-focused franchise company. What about tarcocimab and 501, very briefly?
There remains, despite commercial complexity, valuable open space in the $15 billion retinal vascular diseases market, despite the availability of approved biologics and despite clinical trials of new exploratory technologies. The concept of an upper right quadrant medicine, a biologic that can provide both high immediacy and high durability at the same time and in the same product. There are technologies, what I call sort of lower right quadrant molecules that are being explored in clinical trials, including implants, gene therapies that are engineering for high durability, but importantly, lack any concept or potential for immediacy. Those really are maintenance agents that will end up being used in subsets of patients, but they'll always be relying on the mainstay biologics such as ours to establish and to reestablish disease control.
There's a very interesting open space in the market for a biologic that can provide high immediacy and high durability at the same time in the same therapy. That's what we're trying to develop with our ABC platform. If you look here on the right, the concept of having a bolus and a basal delivery, a strong early pulse and longest possible durability in the same medicine. That's what Kodiak's been trying to do. Here, slide 18, what we see is that immediacy with intravitreal biologics is achieved with lower molecular weight biologics, but the durability increases as the molecular weight increases. Of course, our conjugated antibody biopolymer conjugates are quite large. We prove definitively that our conjugates have the longest half-life as a biologic.
We have tarcocimab, a mean ocular half-life in humans of 20 days, which is threefold longer than, say, intravitreal biologics such as faricimab. Very interesting and very compelling data in humans. We generated that in sophisticated studies on slide 20 and slide 21, and it's very interesting science. We demonstrated that the 20-day half-life, which, as I mentioned, is three times longer than the smaller biologics like Eylea and faricimab, was consistent across the three major retinal vascular diseases. As we look backwards, right, did this three times longer durability come at a cost? It seemed, yes. The immediacy seemed to be the cost. In the wet AMD monthly DAYLIGHT study that we ran with the pre-changed tarcocimab formulation, we saw a deficit in the loading phase, right, in the immediacy of the effect.
After the loading phase, the drawing potential of the potency was comparable. To fix that, looking backwards, we decided to add free protein and conjugated protein together into our commercial formulations for both tarcocimab and KSI-501. For tarcocimab, we have still a 5-mg dose, but 4 mg of conjugate, but we added 1 mg of the free protein. We applied that platform upgrade into the KSI-501 program as well. In this case, 1.5 mg of the KSI-101 equivalent, right, of the free protein, and then 3.5 mg of the conjugated. That was designed to confer a number of manufacturing and safety benefits and, importantly, improved immediacy. The unconjugated portion of this commercial formulation for tarcocimab itself contains a high molar equivalent just of the unconjugated portion to approved intravitreal biologics.
So the 1-mg is equivalent to a 0.7 equivalent molar dose, which is the same as a 0.7-mg dose of Lucentis, with its marketed dose being 0.5, or a 1.3-mg dose of Eylea with its marketed dose being 2 mg, or a 2-mg equivalent dose of faricimab with its marketed dose being 6. So that's just the free protein portion. So it was added to bring a powerful and immediate disease control capability into the commercial formulation, while also improving manufacturability, dose administration, and patient safety. So we can apply that into some modeling where you can look at patients in retina that have either a short half-life and need monthly dosing, let's say, in the clinic, or an average patient that may need every 8 to 12-week dosing, or on the right, a patient that may do well on every 3 to 4-month dosing.
And in that case, our new formulations, our new generation of commercial formulations have free protein that can deliver something very similar to like an Eylea or faricimab. But we also have our conjugate that can deliver that much longer durability. And we can do that in each type of patient. We can deliver something better. And that's what we hope to be able to show in the DAYBREAK study. So again, our conjugates are designed now to bring the best of both worlds of an immediacy that's not weak, but is strong, and the best durability as a biologic at the same time and in the same therapy. So our ongoing and planned studies, we hope, will support a BLA for tarcocimab right after the DAYBREAK readout and a potential KSI-501 BLA, let's say, in 2027, while enabling complementary and potentially differentiated commercial profiles.
So let's remind ourselves, tarcocimab did show very successful data in the retinal vein occlusion area in the Phase III BEACON study. RVO is a $3 billion market today. And the current agents have failed to address the key unmet need for better efficacy and better durability. So we delivered six-month durability in 75% of the patients in RVO and BEACON. And we think tarcocimab can be an excellent drug for patients in RVO. And we did a head-to-head individualized dosing of tarcocimab in RVO and BEACON against aflibercept in the second six months in 75% of the patients. You can look at the vision or the OCT, did extremely well against Eylea head-to-head, and 75% of them had six-month or longer durability. So it shows you the power of the old tarcocimab and what the new tarcocimab can be even better.
Certainly, we demonstrated very high efficacy in industry-leading durability in diabetic retinopathy in the Phase III GLOW1 study, with 100% of the patients treated every six months. Actually, quite a large number of patients are seemingly treated with anti-VEGFs in the U.S. for diabetic retinopathy. In fact, recently, Roche is estimating as many as 850,000 patients. I like, on the slide 34, just a visualization. Why aren't more patients using anti-VEGFs when they have DR? I mean, if I had my eyeball on the left with all the hemorrhages and the clotting that's going to go on in the retina, I'd rather take twice-a-year tarcocimab and have my retina look like the one on the right. So we need to get through GLOW2. We need to get through our BLA, but we need to make tarcocimab available for these patients.
What are the potential implications and the upsides for tarcocimab in the GLOW2 study? The first thing, with top-line data expected at the end of Q1 2026, which is really right around the corner, it'll be the first Phase III readout using the commercial formulation for tarcocimab, providing important safety looking. It'll be the second pivotal superiority study with 100% of patients on every six-month, i.e., twice-a-year dosing versus sham. It'll be a repeat of that. We expect strong pivotal data and strong endpoint data for the primary and secondary endpoints, and it's a similar study design as the successful GLOW1 study, so if it's successful, we'll have a BLA-ready profile in DR and RVO.
Now, the ongoing Phase III DAYBREAK study in wet AMD explores in a definitive manner the immediacy through the loading phase, the real-world durability for tarcocimab, and also for KSI-501, the potential for showing better efficacy. So in DAYBREAK for wet AMD, what are the potential implications and upsides looking at the DAYBREAK top-line data readout for tarcocimab, which we expect in Q3? Well, we expect to show strong and immediate disease control in the loading phase, closing that gap, and at the same time, showing non-inferior visual acuity gains against Eylea q8, and also demonstrating long-interval dosing with a very flexible one-month through six-month label. So we kind of have an illustrative view. And what about for 501? What are the value implications of DAYBREAK? So it'll be year one top-line data in Q3. We'll be evaluating Q4, Q8, KSI-501, and wet AMD versus Eylea Q8.
There's the potential to show better visual acuity gains than anti-VEGF monotherapy. We don't know. Let's remember that we're seeing very powerful data with our dual IL-6 VEGF, KSI-101 in patients, very sick patients. There should be some translation into some of these wet AMD patients, but TBD. We hope to be able to show, of course, based on the commercial formulation, strong and immediate disease control. Revisiting the core unmet need and based on the science of high immediacy and high durability, we believe that our conjugates, tarcocimab and KSI-501, are poised to be credible contenders and/or to fill uniquely as Gen 2 agents, what we call this golden triangle. We'll be seeing that this year together.
Of course, we've been making and continue to make significant investments in commercial manufacturing, which positions us well to be able to launch multiple ABC products into these large and growing markets. I'm glad to report that in the last year or so, we've completed the BLA-facing commercial scale validation batches. We've manufactured those and released those for the antibody, the biopolymer, and the bioconjugates. Tremendous manufacturing progress in support of Kodiak's BLA. Moving quickly into one of our key assets, perhaps the most interesting asset from the standpoint of investors, KSI-101 and MESI.
We won't go through all of the background that we've been through over the last one or two quarters, but macular edema is a common clinical presentation of a wide spectrum of diseases caused by inflammation and/or VEGF overexpression, but it leads to a common phenotype of tremendous fluid under the retina, what you can see here. Now, what is MESI? Well, you can see these different visualizations on slide 45, whether it's anterior or intermediate, posterior or pan, or whether it's idiopathic or whether it's caused by unknown stimulus such as postoperative or juvenile idiopathic arthritis, for example. They all have a similar look. It's a leading cause of vision loss. And what causes it? Fundamentally, it's an autoimmune attack of the body against the retina, or in particular, against the barrier, the blood-retinal barrier.
And when that breaks down, you get IL-6 and VEGF that create a local amplification that leads to this fluid. So the unmet need is real. People are using corticosteroids today, mostly as intravitreal injections that can lead to permanent glaucoma and cataracts that are difficult to replace. So the slide 52 shows you some of the complexities of the surgical repairs, or slide 53 showing you some of these really horrific patient journeys for patients that are on a multi-procedure path towards blindness. So there is an unmet need for something that's safer and has high efficacy as a biologic. So IL-6, through a lot of the data that Roche generated in patients, is a validated mechanism through their Phase I data in DOVETAIL and generally repeated into their Phase III.
While intravitreal IL-6 monotherapy is helpful, 50% of the patients still have persistent fluid, leaving room for a more potent and/or broader spectrum therapy. So luckily, no on-target adverse events really associated with IL-6 biologic inhibition by Roche were noted in their pivotal studies, de-risking IL-6 inhibition in inflammatory macular edema. So how can the unmet need be addressed by Kodiak? Well, our KSI-101 molecule design, a very nice bispecific program. So it has a VEGF trap in line with an anti-IL-6 antibody. We formulate that to 100 mg per mL for a 50 and 100 microliters dosing, testing five milligrams and 10 milligrams in patients with modified Fc. So it's immunologically inert. It's very potent. It improves the tight junctions that are, as I mentioned, the core problem is the breakdown of the barrier. So dual inhibition by 101 confers superior normalization of the tight junction barrier.
There's a synergistic effect that we've seen. In fact, it can restore the barrier resistance from strong pre-existing insult, better than can be done by anti-IL-6 or anti-VEGF monotherapies alone. We think here it's poised to fill a very interesting unmet need in a greenfield market opportunity where patients are being given horrific therapies, intravitreal steroids that are creating tremendous side effects. Our drug, so far, knock on wood, doesn't seem to have any of those issues. We've shown 20-week data in the Phase I APIC study. The data look very strong. Very interestingly, we dose once a month, 0.4, 0.8, 1.2. Even though we stopped dosing, we see through weeks 16 and 20 a continuous improvement in the vision, in the mean change, and in the observed vision over time.
So we're planning to share the 24-week data at the Angiogenesis meeting, I believe, in early February. Fundamentally, the safety continues to look very good. So what we would anticipate to see at angiogenesis, whether the vision begins to go down or whether the vision continues to improve, they're both great outcomes for the therapy. More than half of the patients are achieving the greater than 15 or equal letter gain, which is critical to the key secondary endpoint in our PEAK and PINNACLE studies. And we're seeing very strong, very rapid improvement in the fluid in the patients. And importantly, more than 90% of the patients are achieving absence of any retinal fluid. So it's showing itself to be a very strong agent and very good safety. How it fits in? Well, Roche generated nice data in Phase I. We generated what looks to be stronger data.
When we do a comparison against Roche's DOVETAIL program, a single dose of our agent seems to deliver the majority of the response. And as we give several additional monthly doses of our agent, we get deep into this dryness corridor where multiple doses of the Roche anti-IL-6 doesn't quite take the patient where they really need to go. I think that picture speaks a thousand words, basically. So what about the Phase III programs that are enrolling now, PEAK and PINNACLE, looking at two dose levels, 5 mg and 10 milligrams against sham, fixed monthly dosing through week 20 and 24, and then individualized dosing through weeks 48? They're actively enrolling now on a global basis.
Importantly, as we looked at the Roche data, we decided that it would be useful for us, also because the programs are enrolling more rapidly, let's say, than we had thought. We're going to make the studies larger. Also, we've clarified through Type C meeting with FDA, both on the primary endpoint, but more importantly, on the key secondary endpoint for the programs, which I detail here. The populations are a little bit different. They're both very attractive for drug development in MESI. As I mentioned, we've increased the size of the PEAK and PINNACLE program here on slide 92. Patient enrollment is faster than expected. We don't expect major changes to the expected timelines based on increasing the size of the studies. As I mentioned, we've aligned the program with FDA and Type C meeting.
Our original idea around PEAK, separate from PINNACLE, we've decided to make PEAK larger in and of itself and also to extend that to a larger number of patients. Initially, our thought was maybe 150 patients, but now we're looking at for the PEAK core group to be 300 after we've finished enrolling that because PEAK's generally enrolling three to two to PINNACLE. We'll continue to enroll patients into what we call sort of PEAK two. Then we'll combine the PEAK two population with the PINNACLE population to create a second study, which we call pivotal analysis two, and that will be ready in the second quarter of 2027. Not spending a lot of time to talk about the economic opportunity for 101, but I think it is important that ocular inflammation is the fourth leading cause of blindness among working-age adults in the developed world.
MESI, which is a serious complication of ocular inflammation, is the primary contributor to vision loss and blindness, so there's a tremendous unmet need. There is no biologic available today. We have a pretty attractive initial KSI-101 addressable MESI population in the United States, of north of 150,000 patients, a very interesting and differentiated, potent, high-strength dual MOA biologic generating very strong data, exciting data, and very safe data so far in patients, and we're putting those into a larger pivotal program, and we're expecting top-line data there in the fourth quarter of this year and then into the first half of 2027.
So in summary, looking back six months and looking to where we are today and then thinking about where we're going to be in six months and 12 months or perhaps at next year's meeting, I hope that we'll be able to say that we're achieving this amazing curve of value because we're able to turn the Phase III data cards on these three very interesting molecules and generate data that's important for patients and therefore for Kodiak and our investors. Thank you very much.
Thank you. I'll ask the first couple of questions, but there'll be an opportunity for folks in the audience to ask a question as well. So feel free to raise your hand. Victor, I wondered on KSI-101, on PEAK and PINNACLE, if you could expand a little bit more on the rationale for the enrollment dynamic that you talked about. And was that any at all driven by what you learned from Roche and their update?
Yeah, thanks. Yeah, we spend a lot of time. We do spend a lot of time on the KSI-101 program and on the PEAK and PINNACLE studies. We're engaged in a zone of rapid site activation. We're enrolling a lot of patients, and we're treating a lot of patients. And under this master protocol concept that we have, we're essentially PEAK and PINNACLE are under one master protocol. And as I mentioned, we're seeing about three PEAK patients randomized to every two PINNACLE patients. Obviously, when you look at the Phase I APIC data, the PEAK equivalent patients had around, let's say, 80% three-line gain rate. And the APIC patients that were the PINNACLE equivalent patients were lower in terms of their three-line gain rate. That's really the critical key secondary endpoint from an FDA reg standpoint.
As we look at KSI-101, we need to make sure that we're going to deliver that as an approvable molecule for patients and for Kodiak. The first thing that we did when we looked at the Roche study is I think that their Phase IIIs replicated their Phase I DOVETAIL where they had 25%-30% three-line gain rate with that asset, anti-IL-6 only at a low dose. But then maybe their studies weren't powered properly for a placebo rate of, say, 15%. As we looked at PEAK, we think PEAK's highly powered, but we didn't want to have any risks. Rather than being N equals 50 per group, we decided to go to N equals 100 per group to be fully powered.
I mean, they would have achieved their endpoint had they been at 100 patients per group, even though I think we have a much more potent and a more powerful molecule. So we took PEAK to 300. Then at the same time, once we do that, we know that we're going to continue to have PEAK patients that are coming into the master protocol for screening. So we don't want to throw those away. So we decided just to what we'll define our preliminary analysis of the first, say, nominally 300 patients, but we'll continue to enroll patients into PEAK. And then meanwhile, PINNACLE is enrolling. So we'll wrap those together and have a hierarchical alpha that looks at PEAK then into the total population. So we think that's not too dissimilar from what we did in our BEACON study where we had a combination of the BRVO, CRVO populations.
But we think this is almost you can't say risk-free in the business, but this is looking at the Roche data, looking at what happened to them from Phase I into Phase III, where their SANDCAT study didn't meet the endpoint. But we, of course, have a much stronger molecule. But we didn't want to rest on that alone. We decided to flow all of these ideas into sort of an enhanced pivotal program in the context of the master protocol that gives us PEAK and then PEAK plus PINNACLE together with a very high confidence that we can deliver the molecule to the investment community and to the patients.
Just on PEAK and PINNACLE, though, can you talk to us about the patient populations being enrolled in both in this dynamic of three-line gainer versus three-line preservation, right? And why that's important?
Yeah, well, what we decided to do is to really power the studies for three-line gain and not necessarily have to rely on preservation of preventing three-line loss because we have data from APEX in three-line gain, and of course, Roche has data in three-line gain, but we didn't have specific data, let's say, on preservation, preventing three-line loss, so we do believe that's important and powerful, but we decided we didn't need to take any risks of assuming anything in the PINNACLE, and we decided to power that analysis for three-line gain, so really, it's like a risk minimization. We have data towards one. We didn't have data towards the other. We decided to dig deeper in the one where we have the data.
Question from the audience? Feel free to raise your hand.
Just remind us on tarcocimab, BLA is being filed in 3Q26. So it's going to be the spectrum of indications, RVO, wet AMD, and DR? Yep?
That's correct. I think it's interesting now because we're just right in front of the data from GLOW2 that we should evaluate in that moment, what is tarcocimab coming out of GLOW2? Because we won't have the DAYBREAK data yet in wet AMD. I think tarcocimab can generate from the GLOW2 a profile that in and of itself should be very valuable. Two positive, let's hope, studies in DR, right? Nice safety of this post-change formulation and bringing through the BEACON study, the RVO indication. So we could file. That's a filable profile. It doesn't matter what happens in wet AMD with DAYBREAK. Obviously, we're very excited and very optimistic about DAYBREAK.
But to be honest, like a twice-a-year biologic for DR that really opens that up and also has three loading doses, so it could be used in DME patients and the DR twice-a-year profile and the ability to sell into RVO where we have a very powerful action, and we had 75% of the patients giving the same outcome as Eylea in the second six months. So I think it's a very valuable profile. In those two diseases, of course, we'll finish some of the drug product manufacturing, and we'll wait for DAYBREAK because we're optimistic, and then we'll be essentially ready to rapidly throw that clinical data from DAYBREAK into an integrated efficacy and safety and file the BLA very shortly after, let's hope, for a mid-September top-line data readout for DAYBREAK.
And then just remind us what you think a win scenario here is in GLOW2? You reviewed GLOW1 was positive. You've made some changes. Is it broadly replication of what we already know, or would you be looking for something a little bit different given the changes?
The most important is to have a very strong, statistically significant superiority on the primary endpoint. Also to show good strength on the key secondary endpoint of preventing the sight-threatening complications. But I think we hopefully will achieve that. I think showing nice safety of the post-change formulation will be important. We have that third loading dose. The populations are a little bit different between the GLOW1 and the GLOW2 studies. But I think we shouldn't get lost in what the different percentages are. I think it shouldn't be a close win, the superiority. Just like in GLOW1, it should be a definitive statistical win for tarcocimab in DR plus very good safety that signals that we've made some nice safety changes into the formulation.
Safety and a definitive statistical superiority on the primary and key secondary endpoint, I think, will be very valuable and should be good enough.
Questions from the audience?
How should we think about this dynamic of tarcocimab and the data you're going to have there and the 501 data? Both of these products eventually come to market, right? How does Kodiak do you market both? What do you do?
We see sort of KSI-101 and KSI-501 a little bit as being like a franchise, and then the tarcocimab versus the KSI-501, that's just different optionality, and lucky we're in control of how we do our own lifecycle management, so what's important for KSI-501? I mean, first of all, it'll be interesting with FDA. Is it true that maybe there's a possibility to file for approval based on single studies that are adequate, well-controlled, and definitive? If that were true, there's no company better, in my view, than Kodiak to profit from that because we'll have tarcocimab, of course, with many studies, but we'll have the DAYBREAK study with KSI-501, which is a singleton study in wet AMD. We'll, of course, have PEAK at the end of this year, a singleton study that feeds into PINNACLE.
We are thinking about, well, for KSI-501, what additional studies and indications should we study? We're nominally thinking about initiating pivotal or pivotals in the second quarter of this year to help feed how we think about the evolution of the KSI-501 asset within the retinal vascular diseases. I mean, the simple answer is that we control both molecules. We haven't partnered them, and we'll be able to use them commercially to maximize, let's say, the patient outcomes and the revenue.
Maybe final.
It's a good problem to have if it looks good.
Maybe final question for me. You recently did financing. You've got these catalysts coming up. I'm assuming all the milestones are covered, but what isn't covered and as you head into important readouts?
Right. Well, we were very pleased with the financing that we did, and in particular, the participation by very high-quality investor groups. I think what we wanted to do as a key objective was to rebuild the Kodiak cap table to try to get us closer to where we had been before, okay, such that we have the quality that can really build Kodiak from, say, a $20-a-share company to, I don't know, $50 or $100. I have no idea. So I think we achieved that, and we also recapitalized the company, raised a bit more capital than we had anticipated, and that's a very good thing. So we definitively have capital through the GLOW2, DAYBREAK, and PEAK readouts. I think based on operational discipline, we could get through the PINNACLE readout.
But we have to believe that we will be achieving some of our science-based outcomes in the pivotals and that those will provide additional opportunities for raising incremental capital along the way.
Thank you, Victor.
Cool. Okay. Well, thanks a lot, Anupam. Thanks, everybody. We'll see you next year.