Where Kodiak stands today, with respect to its three lead programs.
Perfect. Yeah, that's a great question. Well, we're very pleased, actually, to be in the position that we are, I would say, from the standpoint of the science that we have, the molecules that we have, and also the capital that we have, together with the experience and capabilities of our team, and also our focus in retina over, say, a 10+ year period. So when we put all of those pieces together, it's potentially quite powerful. So over the last, let's say, really wanted to do a bit of soul searching to what we should be doing. We have a tremendous amount of data that we've generated as well. So something like over 55,000 patient visits in our pivotal program that we've overseen.
And with the tarcocimab program, more than 2,500 patient years of exposure of the medicine to patients across the retinal vascular diseases. We also have the Ursus commercial manufacturing facility, together with Lonza, which we built and finished and is approved and is manufacturing commercial-scale product of tarcocimab, but the suite is also an ABC Medicines manufacturing suite, so relevant for all of our ABC Medicines. And of course, a lot of expertise, not just with the conjugates, but of course, conjugates are antibody biopolymer conjugates. So we make the antibodies, and then separately we make the biopolymers, and then we attach them together, and then we concentrate those and then prepare them, you know, for drug product for retina, which is difficult to do.
We've done a very good job, I would say, over the years, and also focusing on the high concentration of our formulations. So at the same time, we take a close look at the commercial landscape and also the development landscape for retina. I was just at the Clinical Trials at the Summit meeting last weekend, which is perhaps a more predominant retina KOL-type meeting. There's a real shotgun kind of four-minute talks across the whole day, starting at 7:00 A.M., I think, all the way through, say, 5:00 or 5:30 P.M. So there's quite a lot of breadth of exposure to what's happening, what has happened in the field, let's say, over the last year, what's currently happening, and where people think the field's gonna go.
It's a nice meeting 'cause it's a bit small, but it's well attended. I would, I would say, from the standpoint of different types of experts. My sense from participating in the meeting and communicating with a lot of the different people there is that where Kodiak is now poised to be and to go is a tremendous opportunity for Kodiak and also, I think, for patients and the retina community. So we've been quiet over the last, say, six+ months as we were thoughtful about what it is we, we wanted to do. Part of it was, as I said, taking a look in detail at the data. And part of it also was engagement with the regulatory folks. But we've largely completed that analysis and set of interactions. So I think we're, we're poised now.
And so now is the time for us, and that's why, Andrea, this is a very good moment in time for us to begin opening up about what are the details of our plan on a going-forward basis, why is it supported, across these sort of many underlying pillars of experience, capability, where the molecules are, where the field is, you know, where we think we are with the agency, and the unmet need, let's say, in the sector. So with all of that introduction, you know, I think we're in a wonderful spot. We have two medicines that are designed on the ABC platform, the tarcocimab as well as the KSI-501, and they're a bit complementary to each other, and we can talk about that.
And then, of course, we have our third program, which is the naked antibody, the KSI-501 program, that we're targeting to put in a very different kind of indication space within retina that doesn't have any approved biologics today, and is an important unmet need area, and where we can have early primary endpoint data, say, 16-week primary endpoint, against sham. So going against sham, obviously, is a wonderful way to go as opposed to banging it out against aflibercept in head-to-head studies. So we're excited about that third piece of the pipeline because I see it both as important for patients, right? The KSI-101 is the anti-IL-6, anti-VEGF bispecific antibody. One thing that's nice about it from a portfolio standpoint is it doesn't have any of the ABC Platform in it.
And so it's a different kind of development, and also it's a different kind of risk profile. We're a little bit fast-following the Roche anti-IL-6 program. We call it macular edema secondary to inflammation. In patients in retina with severe inflammation in the eye, macular edema is the leading cause of vision loss. And there are no locally administered, you know, intravitreal biologics for this area. So it represents a very nice and very interesting market, you know, commercial opportunity, patient opportunity, and development opportunity. And so that, of course, is the same antibody that formed part of the KSI-501 program. In this case, it's formulated, you know, let's say, to 100 mg/mL formulation strength, the KSI-101.
Really, it's, it's a bit of a sledgehammer type potential for patients with angry inflammation disease in the eye, and it'll be a unique asset with the dual mechanism of action. Preclinically, that molecule with the dual inhibition of the VEGF and the IL-6 has shown very interesting synergy in different types of barrier biology, you know, blood-retinal barrier, for example, where you can have superior normalization of that with the two mechanisms inhibited that one cannot achieve with either of those mechanisms alone. So there's the possibility that it could even, you know, advance to be more of a disease-modifying therapy for inflammation and macular edema. It's an area where we'll have a unique asset. That can move very quickly.
That's gonna move into a multiple-dose phase 1B study starting within the next few weeks, in patients with macular edema secondary to inflammation. The objective of that is to look across several different dose levels and then to choose two dose levels to move into dual pivotal. So the dual pivotal, they're called PEAK and PINNACLE, and those, we expect to start later this year after we have a little bit more visibility into what two dose levels. The study designs are, very advanced, I would say, at this point, with 16-week primary endpoints, across two, matched studies. And again, as I mentioned, with the 100 mg/mL kind of high-strength formulation.
So that's a very exciting asset for Kodiak in and of itself. And that doesn't take anything away from the two, let's say, lead programs that are built on the ABC Platform. So tarcocimab, of course, and then KSI-501. So there's a lot of learnings from the, you know, the many thousands of patients that we've dosed with our ABC Medicines and, in particular, tarcocimab over the past few years. So, you know, at the, the Clinical Trial at the Summit meeting, it was still very apparent that the two key unmet needs in retina are still unmet.
The first is durability, and the second is, you know, better durability, and the second is better efficacy for patients. So for the durability, there over the last 10 years, let's say, there's been a search for different approaches to bring better durability. No approach has delivered yet. And, the approaches go from, you know, the more vanilla, which are biologics-based, all the way through more exotic, which are surgical-type approaches or gene therapy or different types of, drug delivery.
On the biologic side, of course, we have Vabysmo and Eylea HD. And through their clinical trials, they've shown the ability to go out to, say, every 12 weeks or every 16 weeks. Vabysmo, of course, is a bispecific antibody, but but in direct head-to-head studies with fixed dosing, with a high level of dosing, didn't show any improvement over the aflibercept in those studies. And there's a lot of post-hoc analysis now trying to look at different types of sub-analyses to show that it was superior in certain areas. But fundamentally, it's an exciting asset for Roche, who didn't have globally an anti-VEGF biologic, and they they do now. I think commercially, Vabysmo is very exciting for Roche.
It's exciting for the whole retina field because I think what it demonstrates is even within the complex commercial environment for anti-VEGF therapies in retina, a new medicine that physicians can get excited about can actually show multibillion-dollar potential and show fairly rapid growth on a global basis. So it still shows the power of the large anti-VEGF market and the desire of the retina community from all perspectives to lean into innovation for patients and then the pharma company to be able to really drive important new levels of revenue in what's a massive market, even in the context of biosimilars, right, which are emerging more for Lucentis and also in the context of even, say, like Eylea HD. So for Eylea HD, of course, I think we still have to see what kind of growth, revenue growth potential Regeneron will achieve there.
I think they're just getting their J code. They don't have a label for monthly dosing, which is hurting them. And of course, commercially, they don't have a strong need to migrate patients onto HD from Eylea itself. And very interestingly, they've had very good success, I would say, in the patent office, with the potential for biosimilars against Eylea to be pushed out, it seems like, maybe into 2027. And I like that to the extent that their strong science, you know, around their formulation, has, you know, been shown to be important from a patent standpoint. And of course, we always like victory of science, because we like to think that we play, you know, within the deep science space.
So, you know, Eylea HD is, in, in our view, of course, not very innovative. So it's a bit more of the drug. I think what their phase 3 studies showed is that, for example, through the loading phase, you don't get any better vision or any better drying in the retina by having more drug. And so it's a bit, and I would say that was a bit of a shocking result. And, you know, scientifically also, very interesting.
So I guess we think that, you know, Vabysmo and Eylea HD, I sort of call them Gen 1.5 anti-VEGF medicines. You know, they were trying to bring better efficacy with Vabysmo and better durability with Eylea HD. I think they end up, you know, still in the realm of more efficacy, not so much more durability. And even in the context of efficacy, as I mentioned, Vabysmo didn't show that, and Eylea HD didn't really show it either.
So they leave, you know, the unmet need for better efficacy and the unmet need for better durability unmet in the market on the one side, right, starting from the vanilla. And then if you flip to the other side, looking at surgical solutions, you know, like the Roche Port Delivery System or subretinal, gene therapy surgical, or from a gene therapy standpoint, like intravitreal or supracoroidal, all of those more exotic solutions continue to have, you know, either a very small amount of data or, if they have a lot of data, show, you know, a lot of warts and a lot of complexities.
And there's still a lot of work to do. And I guess nobody knows better than Kodiak the types of surprises one can have when you move into tens of thousands of patient visits and, thousands of years of patient exposure. I think our surprises that we have had, because we've had with tarcocimab six successful pivotal studies, I mean, six successful or six studies that we've run phase 3s, with three of them meeting the endpoint and three of them not meeting the endpoint, important data was generated in, in the three studies where we didn't meet the endpoint. The first study was our DAZZLE study in wet AMD, where we went for durability out the gate.
So it was sort of a phase 2b/3 study, our first big pivotal. And some important learnings, and we can talk about that. And then, of course, last year, we had the dual pivotals in DME, GLEAM and GLIMMER, which did really well, out the gates. And I would say scientifically, our, our conjugate, did an excellent job of being potent and delivering six-month durability for the majority of the patients.
But we had cataracts, you know, adverse event imbalance, really in the last third of the study, where we had, say, 89 events, and the aflibercept group had 45. But within our 90, you know, it caused, let's say, 30 or so patients to lose a lot of vision. And then that really impacted the non-inferiority at the end of the study. So that type of surprise was horrible, and that's part of the drug development process. But rather than crying about it, as I said, we really dug deep into the data. So what have we learned about the ABC Medicines and how is it relevant for tarcocimab and for KSI-501, and why is Kodiak relevant? Well, you know, we start with the antibody and we form the conjugates. We're a locally administered biologic.
So we kind of stand on top of, you know, the history of the anti-VEGF biologics, and yet we're still an intravitreal biologic. So, you know, we're, we're vanilla, okay? Perhaps by bringing the biopolymer and the conjugate, it got a little bit strawberry in a way. But we're not exotic. Tarcocimab's objective is to really bring true long-interval, 6-month predominant durability. And we don't want to sacrifice immediacy or clinical efficacy in order to get there. So that's the critical element of tarcocimab. And we can talk about, well, why do we think where we were and where we are now, why can we achieve that? Why do we have confidence that we can do that? And why should we be able to shout that a bit more from the rooftops?
Because it's really driven by the data and by some of the course corrections that we've made that we can have that level of confidence. And for 501, the objective, I would say, is a higher level of efficacy predominant while also bringing the durability from the ABC Platform. So that complementarity is there. And that's why we're leaning into running both tarcocimab and 501 together in a single study against aflibercept and Wet AMD as a next study where we should be dosing, dosing patients, let's say, in the next few weeks or month or so.
That will be really exciting for us to be able to showcase, you know, six-month or long-interval predominant durability, the question of whether we have solved the early immediacy deficit that we've seen with the ABC Platform, in particular tarcocimab, and then with 5, with tarcocimab, and then with 501 to really have a study design that tries to go a little bit like what Roche tried to do with Vabysmo, where they went for, you know, high-intensity dosing, let's say, against Eylea in their RHINE and YOSEMITE studies, to try to see whether there's a trend for better efficacy or whether they could actually go for superiority. So our idea with 501 is to focus a bit less on the durability and to focus a bit more on the potential for superior efficacy or trending towards better efficacy.
So, what is it about our view of our science, right, and our course corrections that suggests to us that we, you know, as an innovator company in the space, through all of the work and design and manufacturing and Clinical Trial, you know, execution, why do we think we, as an innovator, you know, have learned the right lessons so that we can avoid another surprise? I think Kodiak's struggling, I would say, from the investor market standpoint. First, people thought, well, you know, was Kodiak going to shut down, right? Did they think, well, the science has been played out and it doesn't have anything left? And they didn't know what our plans necessarily were because we didn't know what our plans were.
Then, you know, if we wanted to make any changes, right, do we have the blessing of the agency or not, right? What are the plans going to be and how do we execute those and how much capital do we have? I think whether we want to start on the simple thing at the top or whether we want to start from bottoms-up build and looking at the science, you know, either approach can be discussed, you know, simply to understand where we are. For me, just starting with the science of it, we have really two, I think, really important science updates that we understand the data across the pivotal program. I mean, the first is that we built our conjugate platform, the ABC Platform, for durability from the beginning, right?
It's a design for durability, not just increasing the molar dose or, or something or trying to bring another mechanism that, in theory, mechanistically can bring more durability. We started out with the goal of we're going to be an intravitreal biologic. That's vanilla, right? We're going to modify the antibody so it can have longer durability. We do that by making it larger using our proprietary polymer. And when you make something larger in retina, the data all show, you know, that you're going to have a longer, you know, diffusion time and, it'll distribute more slowly and the exit from the eye is going to be slower. So that's the design concept. And, you know, you need it to stay potent. And our conjugates are very potent. They're the same potency as the naked mAbs.
And then you want to show, well, can you have a longer, you know, exit, ocular exit in animals? And we have the best ocular exit for a biologic by, say, 3-4x over Vabysmo and Eylea. So check that box. And then now we've really begun to pull samples from some of our earlier clinical studies to look at the human ocular exit. And that data is very exciting. We're seeing, again, a multiple of the ocular exit, the ocular half-life over the data reported by, say, Vabysmo and aflibercept and Eylea. So, you know, check those boxes. We do have the design, we have the size, and we have the best durability in the business that can support a six-month predominant profile in humans. And we have very strong potency in the majority of patients across all of our studies.
We can go through that in more detail over the next few months or etc. with Kodiak. I think clearly, though, that wasn't enough. That's not enough. Physicians, with, you know, biologics available like Eylea and Vabysmo that have high efficacy, let's say, yeah, maybe they don't have true durability, right? There's a bit of gamesmanship in the clinical trials and whether it's Q8, Q12, Q16, and how you decide that. It's durability that's incremental over the, you know, their earlier products. But what they have is powerful efficacy. And physicians don't want to try to get to what I call the promised land of six-month dosing by sacrificing early efficacy in the patient, especially in Wet AMD where you don't want to get behind the disease.
So if we look at the scientific data and we look at, say, our phase 1b study with tarcocimab, we were a bit weak in the loading phase. Okay, let's say, you know, tarcocimab was about -100 microns mean change from baseline in OCT through week 12 through a 3-month loading phase. Well, we saw that again, you know, in DAZZLE around -100. And we saw it again in the DAYLIGHT study, right? Our monthly study where we showed tremendously strong safety and we showed non-inferior efficacy. But all three of those wet AMD studies showed that we're weak in the loading phase as a mean and maybe even as a median. So maybe -100. And the aflibercept, you know, through that period is, say, minus like 135 or 140 or something.
So we had maybe a, you know, a deficit or a gap of about like, I don't know, 30-50 microns. And, you know, as I said, Eylea HD at 8 mg showed the same data as Eylea 2 mg. That kind of sets the threshold or the bar for where you want to be for not being weak. I don't know if through DAYBREAK, you know, our new Wet AMD study with 501 and tarcocimab, we need to exactly achieve that, but we, we want to be very close or to achieve that. And of course, brolucizumab, which was, you know, a single-chain FV that's 27,000, which is very small, you know, it can go, let's say, I don't remember exactly, but maybe it's, you know, -180 or something or -175 through the loading phase.
So it shows that with big size, you know, we know we can achieve better durability. We have the science for that. But there's some sort of size filter, not really for penetration into the retina because our conjugates have very, very good penetration deep into the retina. But it's sort of like some of the VEGF must be on deep on the cell surface. And so there's a size filter that things like brolucizumab that are very small can grab that VEGF and inactivate it. Eylea does it to an intermediate level, but certainly well enough for the patient. HD doesn't give you more power because it's the same size. You have more of something, but it can't really reach into that kind of gopher hole. And our conjugates were bigger.
And so, you know, some of the VEGF that's accessible by, you know, Eylea, we're not able to get, let's say. So how to solve that important problem, from a, you know, a platform perspective? And it's actually quite easy to do because we make the antibody, we make the biopolymer and we put them together. And so then what we can do is, well, we can actually just leave a defined amount of free antibody that's not conjugated. And the antibody is around the same size as Eylea, a little bit bigger. Or it's, well, the same size as faricimab. Exactly.
And so by leaving enough antibody that alone, it has a pharmacologic effect, plus the majority conjugate, you know, we have a formulation, whether you want to call it enhanced, etc., that we actually initially built, for the commercial scale-up in our commercial facility because the gel was a bit, I mean, the drug was a bit like a gel. And as you scale up manufacturing, that's quite hard to work with. And so by adding more free antibody and decreasing the amount of the biopolymer mass in the formulation, we can, you know, kill many birds with one stone in a sense. So first we have enough free antibody to drive the early pharmacology to normalize through that early loading phase and still have a majority of the conjugate. So we balance towards durability and have that early efficacy.
So that's what we say, you know, we're a learning organization that can look deeply at the data. We can make small but really important course corrections. We can communicate with the agency to make sure that if we do these kind of changes, how do we bridge that? And in fact, although we could have bridged through one phase 3 additional study, we're actually going to bridge through two. Okay. We're going to really solve that early immediacy, and still retain that dominant, you know, long-interval durability profile for tarcocimab. So there's a lot of depth in that and there's a lot more that we can talk about. And we've applied that same learning to the KSI-501 program where we're also going to have a significant amount of free bispecific antibody combined with the conjugate.
So, you know, in, you know, say diabetes, somebody might have a basal insulin and a bolus, right? And they take that as different shots during the day. But for retina, obviously, where you want to do an intravitreal injection in the majority of the patients every six months, that's what we know we can achieve. We've shown that across multiple different retina disease indications that the six-month predominant is super, but you can't do like, you know, multiple injections. So the beauty is that with our biopolymer and the conjugate that drives the stability of the mAb as conjugated and alone, we've co-formulated that and a single injection gives you the right balance. So, that's really critical.
And the other, you know, nice benefit of decreasing the total mass of the biopolymer by increasing the amount of the free antibody for both tarcocimab and 501 is that the drug's not a gel really anymore. It's much more liquid. And so, it's much more dispersive. So that's really important for the safety, you know, of the cataracts that we saw. So whether or not we want to consider a cataract to be, you know, a real safety finding, because, you know, 80% of the diabetic patients already have a cataract, you know, when you enroll them in the study, you know, and all diabetics over time will get a cataract. But you don't want to have adverse events of cataract in phase three studies that can impact the vision when your endpoint, you know, is vision.
So by decreasing the mass, modifying the formulation, increasing the level of the free antibody, we make the drug more watery so that the injection time goes from, say, 10 seconds to 2 to 3 seconds. And also the drug, when you inject it, is much more dispersive. So it doesn't really stay as like a, as like kind of a goop that you can see through that goop, but rather you'd rather that it disperse and be sort of more vanilla, like I call it, like a Lucentis or an Eylea. And, you know, we, we believe that will also have an impact on the cataracts. Now, it's important to remember on the safety, you know, like I said, we have 2,500 patient years of safety and the safety is very strong.
We never had a case of occlusive vasculitis or any of the horrible blinding inflammation that a number of the other medicines suffer from. So that's superb. And from the standpoint of the cataracts, you know, in the DAYLIGHT study where we dose monthly against aflibercept every other month, we actually have fewer cataract adverse events than Eylea. And so therefore it's not some fundamental concept of the medicine across the diseases. It was really only in the diabetic macular edema study where it had an impact. And, you know, we believe that by modifying the formulation to make it, you know, faster to dose, you keep that needle away from the lens, with the eyes moving in the patients. And we've made the drug a lot more dispersive.
We believe we can bring that rate down, you know, into background because a lot of the patients have cataracts. So on those same principles, which apply to tarcocimab, also apply into the KSI-501 program. So that's a lot of words, but I think we are planning to put tarcocimab into two new Phase 3 studies. The first one is a repeat of the very successful GLOW1 study in diabetic retinopathy where 100% of the patients were on six-month dosing. The data we generated in the DR indication is phenomenally strong data. It's important for patients. Other more exotic approaches are trying to go into diabetic retinopathy.
But why would a physician want to go for an exotic approach when a biologic-based approach can bring all the patients to six months with extremely strong, you know, data, both on the primary endpoint, you know, of improving the disease level, what's called the DRSS level in the patient, but also, in what's decreasing the sight-threatening complications by almost 10x, you know, in those patients when they're dosed every six months. So where is really the opportunity for exotic approaches when a more vanilla approach like ours is generating phenomenal data? Plus the GLOW2 study, which we need for approval, we need two studies and one indication is a repeat of GLOW1. So we see it as having very high probability of success.
And then the DAYBREAK study, which we're, as I mentioned, we're going to put tarcocimab and 501 against the aflibercept in the wet AMD, allows us to further bridge, you know, the new formulation, also to really be able to demonstrate what the free MAB together with the conjugated MAB can do in the loading phase for both tarcocimab and 501 to really fundamentally solve that and to grab that by the horns and to demonstrate to the community, well, what, you know, a strong science in the design and execution can deliver for the patient. I believe we have still the potential, you know, to have a first-line therapy, you know, both with tarcocimab or 501. And, you know, some of the physicians or one of them, here's a quote that was quite nice.
It said, "My experience with tarcocimab treated patients in your trial is you have the durability, but you didn't dry as well in the loading phase. But with the formulation of conjugated and unconjugated antibody, then you have fixed that and you have a drug that primes itself and then takes longer. Together with monthly reimbursement, which you have from your DAYLIGHT study where needed, I don't know why you wouldn't be a contender for first-line after step therapy from Avastin." And that's for tarcocimab. And if you bring all of that science and learning and the studies that we're going to be running with 501 and the potential to really bring all of that plus, you know, better or superior efficacy, I think I'm very excited about, you know, where we are and about what we're doing.
And then you bring the KSI-101, as I said, sort of an uncorrelated asset going against sham as a powerful antibody in an area of high unmet need, you know, into 16-week primary endpoint studies. And, you know, financially, Kodiak's in a strong spot, right? We had close to $250 million in capital recently. We're moving into, you know, a strong set of phase 3 studies, right? With BLA-facing studies for all three molecules should be in progress this year. So, of course, another element I think is, you know, the market doesn't understand where Kodiak is today.
We're really beginning to tell this story and we'll further support our views of the science, in some detail. And also, you know, as I said, from the other side, you know, commercially, why we think we're, we're relevant and from an investor standpoint. But I think there's also a view that there's a financial overhang for Kodiak, you know, with the number of phase 3 studies that we're running. You know, we accept that. What we want to do is to get these pivotals structured, enrolling, right? GLOW2 is already enrolling. DAYBREAK will be enrolling shortly. The 101 study for KSI 101, the 1B will be enrolling shortly, and we'll be transitioning into the PEAK and PINNACLE phase 3s later this year.
Our objective is to get these studies active and enrolling, take a look at the enrollment rates. At that point, we'll really understand, you know, we know that we have the runway to finish these studies, but of course, it's about, you know, when we turn the data cards on these studies, how much capital does Kodiak have at that time? You know, is that an acceptable? But we're committed to doing that. And that's an update in the interim. There's a lot there.
With that, that was very comprehensive. So thank you, Victor. Maybe I can just ask you more granularly there. You know, as you mentioned, the cash runway is a question that comes up and, you've guided to being able to get to the other side of these trials. But maybe help us understand, is that in the 25, 26 range? Is it in the 27 range? Like maybe put some guardrails around that.
Right. Well, just to give you a quick view, the GLOW2 study, we hope to complete enrollment this year and it's a 48-week primary endpoint. And I would say in our prior phase threes towards the latter end of the six we ran, you know, we were unmasking the, you know, the data. Let's hope, you know, let's say, within 6 weeks of last visit. So personally, my own personal target, you know, aspirationally, and we, we drive hard is that we can be, at the end of 2025 with the data from GLOW2. DAYBREAK's only a 40-week endpoint, and it'll start enrolling a bit later, but we're really the, the most credible treatment naive Wet AMD study enrolling.
And so I think also that can be, you know, unmasking data in a similar timeframe as GLOW2. So, you know, I don't know whether we achieve end of 2025 or whether it's early 2026, but we have capital through that window. And then it, like I said, it's a question of runway at that time.
Well, with that, Victor, we'll have to, we'll have to do more follow-ups after this. But thank you so much for the overview.
Yeah, let's definitely do that because there's a tremendous amount under the hood. If we address each one of those items, I think that the package is very compelling that, you know, to investors to give them the best opportunity to make, you know, the best investment decision. Hopefully our, our stock when we look 12 months from now or 24 months from now, we'll see it as having been a great bargain. So you can help us tell that story.
Well, thank you, Victor. Thank you, everyone.