All right, welcome everybody to the JP Morgan Healthcare Conference. My name is Anupam Rama. I'm one of the senior biotech analysts here at JP Morgan. I'm joined by my squad, Priyanka Grover, Madhav Kukreja, and Ritika Pai. Our next presenting company is Kodiak Sciences, and presenting on behalf of the company, we have CEO Victor Perlroth. Victor.
Thanks, Anupam. Pleasure to be here again at JP Morgan. Look forward to telling you about Kodiak Sciences today. Please pay careful attention to our forward-looking statements given the many risks inherent to biotechs and drug development. So I thought I would start by talking a little bit about what is the opportunity for Kodiak. After that, we'll talk a little bit about where we are today at Kodiak, and then we'll have a little bit of a data snapshot into our third program, the KSI-101. Then we'll close the loop there, and we'll have some time for discussion and questions with Anupam. So the Kodiak opportunity, let's just remind ourselves for a minute what we're doing and why we're doing it. So retinal vascular diseases remain a large and growing market driven by aging populations and the increased prevalence of diabetes.
Within the retinal vascular diseases, we're targeting a 10 million-15 million set of patients in the United States, so 1.5 million- 2 million wet AMD patients, really as many as eight million diabetic retinopathy patients, and 1.5 million- 2 million RVO patients. With global sales of branded biologics for the retinal vascular diseases, say in the range of $14 billion and potentially growing towards $20 billion. It's a large market, and the U.S. remains the mainstay of the market, but there's still quite attractive ex-U.S. opportunities. In wet AMD, the established what we call Gen 1.0 anti-VEGF agents are achieving modest vision gains in the real world, and they require frequent injections to maintain the vision.
The Gen 1.0 anti-VEGF agents achieve only modest gains in year one despite frequent injections, seven injections with a mean interval of seven weeks in between them in the real world. And interestingly, the frequent injections are not sustained over the long term, which leads to significant vision loss over time for patients looking here on the right. Now we have in the marketplace new agents of Vabysmo from Roche and Eylea HD from Regeneron, but the Gen 1.5 agents, anti-VEGF agents, provide modest dosing interval extension in the real world. So for example, in the phase III Tenaya and Lucerne studies for faricimab, Vabysmo, the pooled analysis across the studies demonstrated half the patients, approximately 45%, were in their Q16 week dosing arm.
But in the real world, interestingly, in independent U.K. real world data, in one study here, only 18 patients were really put on the Q16-week and sustained their regimen for faricimab. And in another study, 0% of the patients actually were able to be put onto the Q16-week regimen. So the real world data for durability of faricimab does not match that demonstrated in the phase three studies. So durability remains a key or the leading unmet need even with faricimab and aflibercept HD now on the market. Patients switching to faricimab, another way of looking at their durability, achieve only a modest extension in dosing. So in clinical trials, fewer than half the patients achieve the four-month dosing in year one.
The real-world evidence shows that switching anti-VEGF experienced patients to faricimab achieves very modest extension, in this case an average of seven-and-a-half-day extension in durability. That's looking at wet AMD around eight-day extension, DME 4.8, and RVO, which is a hard disease, 0.8-day extension. The Gen 1.5 anti-VEGF agents also don't provide any additional vision benefits in the real world over Gen 1.0 agents in wet AMD. Looking at the market a little bit differently at the diabetic retinopathy component of the market, as I mentioned, the U.S. prevalence being quite attractive at eight million subjects, actually fewer than 1% of these are currently treated with anti-VEGF agents due to treatment burden with the existing Gen 1 and 1.5 agents.
Currently patients with diabetic retinopathy are generally not treated because of the treatment burden, and the watch and wait approach, which is what people do today, results in progression of that retinopathy and development of vision-threatening complications in the patients. For example, left untreated, 57% of patients with diabetic retinopathy progressed to advanced disease such as proliferative diabetic retinopathy or developed diabetic macular edema in the center of their vision over a four-year period. When we think about the Kodiak opportunity then, what are we thinking about here and what's the potential? We're developing our two lead agents, our antibody biopolymer conjugates, tarcocimab, our anti-VEGF, and KSI-501, our bispecific conjugate. They're being developed as mainstay biologic intravitreal monotherapies that can provide both high efficacy and high durability with a flexible one month through six month label.
So on the left axis in this four quadrant analysis, we see the efficacy with Gen 1 and 1.5 anti-VEGF agents as biologics, whether it's Eylea or Lucentis or Vabysmo or Eylea HD, delivering high efficacy and high immediacy. And as we've discussed, fairly mild or modest improvements in durability in this upper left quadrant. In the bottom right, where we have fairly low efficacy, let's say, or modest efficacy and activity and immediacy, yet perhaps we have the potential for agents that can deliver long durability such as TKI implants or perhaps gene therapy. So these are alternative therapies for different maybe subsets of the patients after evaluating the mainstay biologics. For example, these may be maintenance agents that are used in subsets of patients after the intravitreal mainstay biologics have already established disease control in the patients.
But what we're trying to do at Kodiak and what is fundamentally the Kodiak opportunity is the ability to make what we call true Gen 2 agents that are biologics, soluble agents that are intravitreally injected that are monotherapies, either single inhibitors through tarcocimab or dual inhibitors through KSI-501 that have both strong immediacy and efficacy and the longest durability and are eligible for all patients given that we're enrolling all treatment-naive patients of all types in our studies, and in KSI-501, the opportunity with a dual inhibitor of IL-6 and VEGF with the potential for additional efficacy beyond anti-VEGF monotherapies while also maintaining the signature durability of our ABC platform, so we're really looking, and it's really amazing thinking about the approval of Lucentis back in 2006 that we're nearly 20 years later, and this upper right quadrant, this bucket is still not serviced.
If we think about where the opportunity for Kodiak is, the question is, well, is it achievable? Is it possible? Is there potential for Kodiak with tarcocimab and/or 501 to finally fill the upper right quadrant here? Despite limited differentiation and the label limitations of the Gen 1 and the Gen 1.5 agents, let's just also recognize that each incremental improvement in the medicines has resulted in blockbuster commercial opportunities for the mainstay biologics in their application to all patients. So whether it's Lucentis, whether it's Eylea, whether it's Vabysmo, or the new Eylea HD, we see very attractive worldwide net sales and attractive growth.
So the opportunity therefore for Kodiak as a Gen 2 agent with tarcocimab and 501 to bring strong efficacy and the best durability up in that upper right quadrant is really important with each 1% share in market gain estimated to translate into many hundreds of millions of dollars of net sales. But let's not forget actually that Kodiak has broadened its pipeline. We've added a third novel agent into the pipeline, KSI-101. And KSI-101 has the potential to be an important and differentiated medicine in retinal inflammatory conditions, which is a greenfield market segment. So just to step back for a second and say, well, what does that mean to go into a greenfield market segment? Well, a relevant case study would be Tepezza in thyroid eye disease.
Not pretending to be Horizon, but Tepezza was launched as an anti-inflammatory biologic, a targeted therapy into a non-existent market with high unmet need and no approved therapy. Sales approach blockbuster status even in the first year of launch, substantially outperforming management expectation of $30 million-$40 million. So the opportunity here for KSI-101 is a similar greenfield market opportunity. There's a broad patient population, a high unmet need with no approved intravitreal biologics. And we even see the potential for the indication macular edema secondary to inflammation really to be a gateway indication for us into a broader set of diseases that could include all retinal diseases with "macular edema." So the difference here with KSI-101, it's a dual inhibitor, it's a protein, it's an inhibitor of IL-6 and VEGF.
They have a synergistic effect, the two biologics, a normalizing blood-retinal barrier function versus anti-IL-6 monotherapy alone. It's a high-strength formulation at 100 mg/mL. It's highly potent and provides a lot of firepower needed to treat the angry type of retinal inflammation and macular edema seen in this very interesting patient population. And we're exploring different types of accelerated development opportunities with KSI-101. So again, as we take another step back and think a little bit about the Kodiak opportunity, where is Kodiak? Well, interestingly, our clinical portfolio is at this late stage, has the potential to provide continued revenue stream starting from 2027 with built-in lifecycle management and risk diversification. Starting here with tarcocimab with the potential to be in that upper right quadrant with the best durability and strong immediacy and incremental share translating into meaningful revenue immediately.
And then we have the potential with KSI-501 for the best efficacy and durability and as a next-gen product that can fast follow our own tarcocimab. And with KSI-101, we have a very interesting diversified revenue opportunity, diversified away from tarcocimab and KSI-501. And let's not forget that Kodiak owns full commercial rights to our whole portfolio, which allows us the flexibility in our commercialization decisions to support adoption of our products. And we've invested and we have a mature, we have a longstanding and significant investment in commercial manufacturing, which positions Kodiak well to launch multiple conjugate products into large and growing markets. So our Ursus commercial facility dedicated to the manufacture of our conjugates was custom designed for large-scale premium manufacturing of complex antibody conjugate therapies. Mechanical completion was in 2022. It was commissioned as a GMP facility in January 2023.
We completed a commercial scale batch, a cGMP of our tarcocimab enhanced formulation in November of 2023. And further to support the Kodiak commercial franchise, we've even invested and made tremendous technical progress on an OCT goggles that we could together with tarcocimab drive home monitoring for tarcocimab treated patients together with physicians in terms of OCT scanning with our VERDI tool, the OCT goggles. So another interesting kind of complementary component of the Kodiak opportunity. Okay, so where is Kodiak today? Well, we believe Kodiak is primed for near-term and long-term success. So we have an agile mindset that we put our heads to work over the last 12 to 18 months. We've made really important course corrections and implemented these course corrections into our late-stage studies in a fairly aggressive time. Okay.
As a company that has engaged in complex retina clinical and manufacturing development, we've run and are running eight pivotal studies. We have more than 2,500 patient years of clinical experience. We've injected nearly 14,000 intravitreal injections of our conjugates into patients and supervised more than 55,000 clinical study visits. And we have technical ownership and leadership in-house across the board, enabling timely and cost-effective decisions. And we've diversified our late-stage pipeline. So we have two late-stage products, tarcocimab and KSI-501 in pivotal studies, and our KSI-101, we're working hard to accelerate that into pivotal studies this year. So a pipeline with three shots on goal, each in a BLA-facing development plan with filing of tarcocimab based on five successful studies as early as 2026. And we retain our independence, which allows us the flexibility to make each right choice for Kodiak shareholders.
We have a cash runway expected to support our operations into 2026. Looking backwards, looking where we are today and how does that bridge into the future. We strive to be a learning organization. Through our journey, we've gathered key insights and transformed these learnings into actions listed here on the left. What are the positives? Well, tarcocimab and the platform is very well tolerated in patients in terms of safety. We have a differentiated six-month durability across indications that's real as driven by the true science of our durability. We have animal as well as now human ocular PK data supporting a signature durability that represents at least a 3x advance over the next best biologic. The ABC Platform is a true medicinal platform. At the same time, over the past three to five years, we've identified issues.
An immediacy deficit that we saw in wet patients with our conjugates. We saw an increased cataract rate specific to DME, and we had fairly aggressive study designs. So we've learned from these and we've taken the following actions. We've built enhanced formulations for tarcocimab and KSI-501 to course correct issues identified in wet AMD and DME. We have new study designs educated from prior studies, and we anticipate the new GLOW2 and the new Daybreak pivotal phase III studies to have high probability of success, and we've diversified our portfolio to include also, as I mentioned, the KSI-101, a superior product, we hope, in a greenfield market opportunity where we're running up against sham comparators. Here's a summary of today's clinical programs and timeline of anticipated milestones for Kodiak's three "late-stage programs," so we have tarcocimab in the phase III GLOW2 study.
The GLOW2 study is in diabetic retinopathy. It's a repeat of the GLOW1 study with some enhancements. GLOW2 is nearly fully enrolled, and we hope to complete enrollment in the next 30 to 45 days. It's a 48-week study, primary endpoint with readouts, let's say, very close to one year from today. At the same time, we're testing tarcocimab as well as the KSI-501 in the new phase III Daybreak study in wet AMD. That study is enrolling well and will complete enrollment in the first half of this year, again with a 48-week endpoint in a readout, let's say, in Q2 of 2026. And with our KSI-101 molecule in macular edema secondary to inflammation, MESI, we're actively enrolling patients in our phase Ib Apex study.
We're looking to look for bioactivity and efficacy, let's say, across the different dose levels and to select two dose levels that we want to progress into the pivotal program, which we hope to start as early as the second quarter of this year, so we'll look at some early data in a few minutes, and from there, we'll be dose selecting two dose levels to begin enrollment in the Peak or Pinnacle study, which we hope to begin shortly, so let's take a little bit of a deep dive for a couple of minutes into KSI-101, speaking quickly, so we've diversified the portfolio, as I mentioned, with our third program. So it's a bispecific protein. It's not a conjugate, and it's a first-in-class protein in a greenfield market with a combination of the anti-VEGF here and the anti-IL-6 here.
So we're developing this in an indication that we call macular edema secondary to inflammation. So macular edema, fluid in the retina and the center of the retina, is the leading cause of vision loss in patients with intraocular inflammation. So intraocular inflammation is the fourth leading cause of vision loss in the developed world. And one-third of patients with intraocular inflammation develop this finding of macular edema as a result of the inflammation. That represents approximately 110,000 patients in the United States. And studies show that inflammation and vascular permeability, which leads to fluid, have a synergistic effect on driving the progression of the disease and the vision loss due to the macular edema. But there are no approved therapies that target both of these drivers of the disease.
The current treatment algorithm for macular edema secondary to inflammation and the unmet need. There is an unmet need for safer therapies that target the underlying mechanisms of the disease. The first-line treatment for these patients is local or systemic steroids, but many patients don't respond well, at least 30%-40%. More importantly, these are associated with elevated intraocular pressure or glaucoma that often requires therapy, even surgery, as well as cataract progression. Second line is more complex and dangerous, let's say, systemic immunomodulators such as cyclophosphamide. Up to 50% of patients do not have macular edema resolved. About a third of the patients don't experience improvement in their macular edema at all. Second or third line is systemic biologics such as Humira, but 55% of patients experience treatment failure.
And actually, Humira has no significant impact on the macular edema in the eye and are associated with various side effects of systemic immunomodulatory therapy. Third or fourth line would be the use of anti-VEGF biologics in the eye, but they don't work in very many patients. And the underlying inflammatory component of the pathophysiology is not addressed by inhibiting with anti-VEGF alone. So there's an unmet need for minimally invasive, potent targeted therapies with a better safety profile. Now, Roche is developing the vamikibart, which is an anti-IL-6 antibody, which is injected intravitreally in patients. And they've shown that anti-IL-6 monotherapy can provide visual and anatomical improvement in patients with inflammatory macular edema. And they generated nice data across three different dose levels, about an N of 12 patients per dose, looking here at the vision.
They show nice gains of vision in the five-to-10-letter range across these three different dose levels of 0.25, 1, and 2.5 milligrams. Concomitant nice improvement in OCT shows the macular edema disappearing. Of course, they show a bit of a dose response where their low dose achieves somewhat less drying and somewhat less resolution of the macular edema than their higher doses. It sets up a nice proof of concept for the mechanism in this difficult disease. At the same time, while their intravitreal anti-IL-6 monotherapy is useful for the patients, about half of the patients, 50%, still have persistent intraretinal fluid, which is similar actually to the overall failure rate of the systemic adalimumab, leaving room for improvement. Kodiak has been running our phase Ib Apex study in patients with macular edema secondary to inflammation.
It's a multiple dose study of KSI-101. Subjects with MESI or macular edema secondary to inflammation are put into groups at 2.5 milligrams, 5 milligrams, or 10 milligrams, and given a dose every month for four doses and then followed out to 24 weeks. We began enrolling and dosing patients with MESI last year. We'd like to present a little bit of patient case studies here. Then we'll continue to enroll more patients and to continue to present data as it becomes more meaningful and with a higher end over the course of the next several quarters. Just in summary, meaningful clinical response in both vision and retinal anatomy are being observed with all dose levels tested.
Our objective is to select two dose levels, low and high, to progress into the pivotal program for MESI, which we'd like to start in the second quarter of this year. Here are three. What we can see here is a 2.5 mg patient, a 5 mg patient, and a 10 mg patient who received KSI-101. These three patients represent the three furthest along patients, one from each of the three different dose levels. What we see is very strong treatment response at all three of these dose levels. For example, at the 2.5 mg dose level, we see a patient with macular edema secondary to inflammation with a very thick retina at baseline of 750 microns and a vision of 66 letters. They receive drug. We have data from week one. We look at week four, week eight, and week 12.
We see nice improvement of vision with the 2.5 mg dose plus nine letters. And we see very nice resolution of the macular edema, normalizing the retina with a CST improvement of minus 541 microns over 12 weeks. At the middle dose, the five milligram dose, again, we see a very sick patient with a baseline OCT or CST of 778 microns and a very nasty looking macula. And we see through the course of these treatments, through week eight, the furthest along that we have this patient, again, full resolution of the retinal thickness with minus 520 microns and a vision gain of 10 letters. And we see a 10 milligram patient who's only achieved the week one as of the data cutoff of January 13th, but with a starting baseline OCT of 517, and we see normalization of the retina with a vision gain of plus 18 letters.
We're very pleased with this early data with KSI-101. A primary objective of the Apex study was to explore these three dose levels to be able to help us select which two dose levels we would want to move forward into pivotal studies, and of course, to be able to feel comfortable that the asset can deliver on vision gain and on OCT resolution of the macular edema in the population, and we look forward to continuing to follow these patients. As I said, this is week 12, but we'll continue to follow the patients out to week 24, and we'll continue to add more patients to each of the different dose cohorts so we can actually generate, let's say, more robust data, but at a phase one level, we're already very pleased.
We've already engaged with FDA on what a pivotal program for KSI-101 in MESI can look like. And a key will be running a pivotal phase IIb/III study with a primary endpoint at week 16, safety out to week 48, and a low dose, high dose versus sham with four initiating doses once a month and a primary endpoint at week 16. So we're excited to see the early data and the very nice bioactivity at the three dose levels because we're already now leaning in towards clinical operations activities towards activation of a pivotal study here. At the same time, as we think about, well, what set of studies do we want to run towards KSI-101 approval, we believe that it has the potential also to be an important medicine in treating pediatric patients with intraocular inflammation and macular edema.
Up to 15% of patients referred to tertiary uveitis clinics are pediatric or adolescent pediatric patients. Like adults, macular edema is a major vision-threatening complication in children with uveitis. We're exploring whether our second pivotal study could be run in the pediatric and/or adolescent setting. In particular, management of these pediatric patients presents unique challenges today for clinicians. Diagnosis is often delayed with complications such as macular edema already present. The inflammation is more likely to be recurrent or chronic and can persist into adulthood. The risk of macular edema may increase over time with persistent disease in some patients. Systemic and local corticosteroids, immunosuppressants, and biologics are often needed to treat the macular edema, which can take, according to today's available therapies, often more than two years to resolve. The macular edema can be refractory to existing therapies.
Importantly, systemic use of steroids or immunosuppressive agents have limited utility because they have adverse effects on growth, nutrition, infectious disease, and fertility. There's a significant unmet need for effective and safe targeted therapies that are useful for the underlying disease mechanisms in this vulnerable patient population. In summary, where are we with Kodiak? We have three clinical programs leveraging our 15 years of learning. We are at a decisive moment. We're in motion and accelerating, and we hope that we represent an exciting investment opportunity. We have tarcocimab in phase III, a Gen II intravitreal biologic for all patients. We have an enhanced formulation of tarcocimab to bring both high immediacy and high durability and to definitively define our location in that upper right quadrant.
We're tracking towards a registration package in mid-2026 or in 2026 anyway that would include three major diseases: wet AMD, retinal vein occlusion, and diabetic retinopathy. We're developing tarcocimab as a mainstay biologic towards a $14-plus billion growing market. We're nearing completion of enrollment in the GLOW2 study, and we're driving hard for completing enrollment in our Daybreak study, targeting top-line data in, say, Q1 and Q2 of 2026 for tarcocimab. We're running KSI-501, our second late-phase asset, which is an enhanced anti-IL-6, anti-VEGF, bispecific ABC with the potential that the combination of improved efficacy based on the dual mechanisms and our signature six-month predominant durability profile based on the ABC platform to really deliver as a fast-follow agent for Kodiak. Upcoming milestone includes completing enrollment in Daybreak and looking at Daybreak top-line data in early 2026.
With KSI-101, sort of our third asset, our unconjugated protein for inflammatory retinal diseases, we shared some exciting new phase Ib data across the three different dose levels in very sick patients with very nice responses. We're setting ourselves up nicely to select two dose levels to progress into our first pivotal. It's a greenfield commercial opportunity: macular edema secondary to inflammation with risks uncorrelated to our ABC investigational medicines. The phase Ib Apex clinical cases show excellent treatment response at all three dose levels, driving, we hope, a program acceleration. Upcoming milestones will include presentation of more full data sets as our cohorts in the phase Ib open label study progress and phase III initiation, hopefully in the first half of this year. What is our vision for 2026 for Kodiak, which is really right around the corner?
A BLA filing for tarcocimab in diabetic retinopathy, retinal vein occlusion, and wet AMD, supported by five successful clinical studies and our commercial manufacturing facility versus KSI-501, based on hopefully successful Daybreak data, will be one study away from registration. KSI-101 will be looking towards top-line data readouts from two pivotal studies in MESI and BLA in preparation. Currently, well, we have cash equivalents of $200 million as of the end of the third quarter of 2024, which supports Kodiak operations, our guidance into 2026. Thank you very much.
Thanks. Thanks, Victor. I just want to remind folks that there are three ways to ask a question, right? So you can raise your hand, old school way. I'll call on you. There's a question portal. Or you could just email me, and I'll ask it on your behalf. But I'll just kick off here. In the new KSI-101 data, it looks like a small number, small follow-up, but it looks like you are seeing a little bit of a dose response. Based on what Roche showed, what would you be looking for on BCVA to really have a compelling story here? Is it a two-line gain, or how should we think about that?
One view of the primary endpoint in a pivotal would be use of 15-letter gainers as an event to compare against the placebo group to look for superiority.
15-letter gainers?
Yeah, 15-letter. Oh, 15-letter gainers. Yeah. So that's one way to look at it. I think what's important at this stage, I mean, these are quite sick patients, so we have CST baselines of over 750 microns for two of the patients. So I think we believe these are very strong responses. I think the mean change that Roche saw in their Dovetail study was in the range of around seven to eight letters across the three different dose levels. So we think these are attractive BCVA gains for these three early patients, and we think the drug looks really solid.
Of course, we're going to continue to dose more patients. The objective with this small N of these types of studies needs to be carefully considered that we don't overdo kind of the cross-trial comparisons. I think, like we did say from the Dovetail data, that 50% of the patients still had residual intraretinal fluid. So that will be something over the course of the 36 plus or minus patients that we may enroll in Apex. We can take a look at that.
From the audience?
Hey, thanks for presenting the data. It's very encouraging.
Oh, sorry.
Even better. Hi, I'm Alex from Driehaus in Chicago. Can you characterize how many patients have been treated at each dose? And are these the best that you've seen, or are they representative of the overall number of patients who've been treated at each doses?
Yeah, no, these are just the first patient at each dose level that was treated. So we didn't really grab our favorite patient. This just represents the first at each dose. We've, I think at this point, enrolled 11 patients, and we're continuing to screen and enroll patients basically every day. And we started at the 2.5 milligram dose, quickly progressed to five and 10, and now we're backfilling at every dose level, consistent with kind of our dose escalation paradigm.
Sorry, can I follow up on that? I would normally think for a dose escalation that you would do it on a cohort level where you would enroll an entire cohort before you would clear that cohort and then go to a higher cohort. So I would imagine that you have more patients at 2.5 and then 5 and then the fewest at 10. So at the risk of asking a similar-sounding question, and I beg your pardon, A, is that right? And if so, then B, do the patients all of whom were treated at 2.5 have had a similar experience and at 5 versus 10? And sorry for taking up everyone's time.
Yeah. Well, we are not doing a traditional SAD-type dose escalation. Our objective in Apex is to enroll up to 12 patients per dose level, so for a total of 36 patients. But we didn't want to enroll 12 at 2.5 and then 12 at 5 and then 12 at 10. So after a couple of patients at 2.5, we dose escalated to 5 and then 10, and then now we're kind of backfilling. So we have reasonably small N at each of the three dose levels today.
But the goal is to enroll, let's say, 8 to 12 at each dose level so that we can show curves and have a little bit more of a maybe view into dose escalation. What's also important is to say, wow, we have really wonderful bioactivity in these very sick patients fairly early in the program, and then that gives us a nice confidence to begin towards operational activities in preparation for the pivotals.
The other side of the equation is I know you'll probably present this in follow-up updates, but anything on the safety side that you would anecdotally highlight?
No, we're pleased with the tolerability profile, and we believe that it's very supportive of moving the program in an accelerated manner forwards.
And then you have a series of updates for this program. I think the slide said one first quarter, second quarter, and I think you previously even talked about third quarter. Should we just assume that these data are going to be presented in conjunction with medical meetings that align?
Yeah, one of our thoughts was we might do an earnings discussion or webinar, which would be, I think, in the end of March. So we could see where we are two and a half months from now with patients. I think we do want to think about. I believe Kodiak has actually a tremendous amount of science that we do want to be presenting at the medical meetings. And so we were quite busy over the last, say, 12 to 18 months really thinking about what's our plan, what's the execution, and moving all of these pieces on the chessboard to get this framework of activities moving, which I think we've done well. This year, key elements will be medical meetings and also thinking about publications and that kind of thing.
Just wondering how you would characterize kind of what the total addressable market TAM is here?
About a third of uveitis patients do get macular edema. In the United States, that represents somewhere north of 110,000 patients. That's a very good patient group. The macular edema does drive fairly bad outcomes for the patients. These are very sick patients. Macular edema secondary to inflammation represents really many different feeders. In this case, I believe these three patients were idiopathic MESI patients. That meant that this was inflammation just in the eye, and it wasn't the result of systemic autoimmune disease, which is also a big driver. I guess there are a lot of different choices as one thinks about pricing into this kind of indication area.
But I do think we believe that this is a molecule with blockbuster economic potential based on the size of the number of patients, the severity of the disease, the lack of any alternative therapies, and the fact that this will be an attractive drug both for uveitis as well as retina physicians in the United States and globally.
Any final questions from the audience? Thanks so much, Victor.
Cool. Thank you. Thanks a lot.