Good evening and welcome to the 43rd Annual J.P. Morgan Healthcare Conference. My name is Dave Parag, and I'm part of the Healthcare Investment Banking team here at J.P. Morgan. Today, I have the pleasure of introducing our speaker, Pravin Dugel, President and CEO of Ocular Therapeutix. And also here on the podium, we have CFO and COO Donald Notman, who will be participating in Q&A. In terms of the logistics for today, please reserve any questions for after the presentation. For those in the audience, a mic will be passed around. And for those viewing on the web, please submit your questions online, and I'll be able to view them through the iPad on stage. With that, take it away, Pravin.
And, David, thank you very much. And I'd like to first start by thanking the organizers for this opportunity and this wonderful meeting. And I want to thank all of you for being here this afternoon. Let me see if I can find the clicker. Oh, there we go. Our forward-looking statements are in our filings. So Ocular Therapeutix is a public company targeting wet macular degeneration with its lead product, AXPAXLI. So what is wet macular degeneration? Well, wet macular degeneration is the leading cause of blindness in this country. And if you were in this beautiful city and were looking at this beautiful bridge and had wet macular degeneration, this bridge wouldn't look like this, but unfortunately, it would look like this. We at Ocular Therapeutix have one goal, and that goal is very simple: to redefine the entire retina experience.
And we aim to do that by redefining three different portals. We will redefine treatment, we will redefine development, and we will redefine outcomes. And let me address each of these individually. First of all, redefining treatment. As mentioned, wet macular degeneration is the leading cause of blindness in this country, but it doesn't have to be. 1.6 million Americans suffer from wet macular degeneration in the United States alone. However, we have a proven target that we've known for many years, and that's VEGF. We also have proven treatments that we've had for several decades. That's the anti-VEGFs that are commercially available. So what's the problem? The problem you see is that 90% of patients, 90%, require an injection, a needle in the eye, once every one to three months. And that's simply not sustainable. So we have a problem with sustainability.
For that reason, understandably, but tragically, 40% of patients in the U.S. alone discontinue treatment in the first year and end up going blind. So you can imagine an elderly patient with wet macular degeneration has to come in to see a doctor like me once every month for an entire day. That's simply not sustainable. And because they're elderly, they oftentimes need a loved one or a caregiver as well. And that person, oftentimes of a working population, also has to take time off to bring this person in. And although there's effective treatment, it is tragic that 40% of patients in this country discontinue treatment in the first year and end up going blind. Now, to add salt to the wound, it gets even worse than that.
Those patients who are actually able to be on treatment, after about three to five years, end up losing vision anyway, and they lose vision because of the episodic nature of our treatment. When we give these injections every month or every other month, the back of the eye gets thick and thin and thick and thin, akin to having multiple concussions in the back of the eye, which causes scarring and atrophy, causing a loss of vision. At Ocular Therapeutix, our goal is to correct both of these problems. We intend to have a drug that's both sustainable as well as a drug that will provide better chronic visual outcomes, so what is the thirst for this? Well, history has shown us that incremental durability improvements deliver significant market opportunity, and let me show you this.
With Lucentis, there was a durability of 30 days, and the global market revenue was $1.8 billion. With Eylea. Now, seven years later, Eylea wasn't safer. It wasn't stronger. It simply lasted two weeks longer, so a total of 44 days. And the global revenue rose to $2.8 billion. Most recently is the second version of Lucentis, which is Vabysmo. And again, Vabysmo is not safer. It's not stronger. It simply lasts two weeks longer, so a total of 57 days. And the global market revenue, $4.3 billion. Now, when we talk about AXPAXLI, we're talking about a different orbit altogether. We're not talking about days. We're not talking about weeks. We're talking about lasting 6 to 12 months longer. So you can see the market opportunity here is enormous. So what is AXPAXLI? Well, AXPAXLI consists of two different components.
First is the drug itself, which is axitinib, which is a multi-target tyrosine kinase inhibitor. It is a highly selective pan-VEGF inhibitor. It's the most potent and selective TKI that's being tested. And this is placed in a proven platform, ELUTYX Technology, which is a bioresorbable sustained drug delivery platform. It's a proprietary hydrogel. And it's important to say here, this is not an implant. This is a hydrogel. It's versatile, it's biocompatible, and it's tunable. So AXPAXLI is a single injection, a single hydrogel. It provides continuous and consistent delivery for up to 12 months. It has complete and predictable bioresorption. Again, very importantly, this is not an implant. This is a hydrogel. So when the drug is gone, the hydrogel simply dissolves. There are no carcasses left behind. There's nothing floating around. There's no stacking issue whatsoever. When the drug is gone, the hydrogel is gone.
Now, redefining development. We have proof of concept data that has demonstrated very robustly that AXPAXLI has activity and durability. I'll feature two studies. The first is our study in the United States, in the U.S., that shows that with a single AXPAXLI injection, 100% of patients, 100% of patients were rescue-free per protocol at six months, and again, with a single injection of AXPAXLI, 80% of patients were rescue-free per protocol at 10 months. In our study in Australia, we were able to demonstrate substantial monotherapy activity in treatment-naive patients with wet AMD, and this is as monotherapy with AXPAXLI. Currently, we have two phase III registrational studies: the SOL-1 study, which is designed to show superiority with a single injection of AXPAXLI, and the SOLAR study, which is designed to show non-inferiority to standard of care with repeat dosing.
These studies are complementary and designed to show durability, repeatability, and flexibility. We're redefining development by redefining the process. We're de-risking the entire program. The main features here are compelling phase I data, de-risking of the phase III designs, and de-risking of the regulatory path. Let me first address SOL-1. SOL-1 is a superiority study comparing a single AXPAXLI dose to a single aflibercept or Eylea 2 mg dose. It is designed as a two-arm trial with 150 patients in each group. The primary endpoint is at week 36 and is designed to demonstrate that a single AXPAXLI dose is superior to a single aflibercept or Eylea 2 mg dose based on the proportion of patients who maintain visual acuity defined as losing less than 15 letters of vision at week 36.
The main features here are that we've de-risked this trial by de-risking the patient population by randomizing only those strong anti-VEGF responders. The trial is designed to establish AXPAXLI durability. It's also designed to enable a superiority claim on the label. Very importantly, this potentially would be the first and only superiority claim on the label in our field, and it's aligned with the FDA through a Special Protocol Assessment, or a SPA. Now, let me move to the second registrational study named SOLAR. This is a non-inferiority study comparing AXPAXLI given every six months to aflibercept 2 mg given every eight weeks. It's a three-arm trial with 825 total patients randomized in a ratio of 2:2:1 .
The primary endpoint is at week 56 and is designed to demonstrate that AXPAXLI is non-inferior to fixed-dose aflibercept 2 mg every eight weeks with respect to mean change in best-corrected visual acuity at week 56 from baseline in wet AMD patients. The main features here are that we've de-risked this trial by de-risking the patient population by randomizing reliable anti-VEGF responders. The study is designed to enable every six-month dosing on the label, and it provides commercially relevant data, and it's aligned with the FDA with a written Type C response. We have enrolled and randomized and completed SOL-1 very much ahead of schedule. We expect the top-line results to be in the fourth quarter of 2025. We have randomized over 300 patients, again, very much ahead of schedule. In regards to SOLAR, our second registrational study, this was conceived of in May of 2024.
From the time of conception to the study to the time of the enrollment of the first patient was less than 90 days, and that's remarkable, less than 90 days. A month later, we received a written Type C response from the FDA validating SOLAR as a registrational study, and since that time, we have been very actively and very successfully recruiting SOLAR. Today, I'm very pleased to announce to you that as of January 10th, we have currently enrolled 311 patients in SOLAR across various stages of loading and randomization, so let me repeat that. In a very short period of time, in this second registrational study, we have already enrolled 311 patients across various stages of loading and randomization. Now, let me switch to diabetic retinopathy. Diabetic retinopathy is a large and unrealized market opportunity.
Diabetic retinopathy is the leading cause of blindness in the working-age population in this country. About three-quarters of patients with diabetic retinopathy suffer from non-proliferative diabetic retinopathy. So that's more than six million patients in the United States alone. And here again, there's a known target, which is anti-VEGF, and there are known treatments that we've had for decades, which are the commercially available anti-VEGFs. But yet, in this blinding disorder, less than 1%, less than 1% of patients are actually being treated. And why is that? Well, the reason is the same as for wet AMD, and that's a matter of sustainability. It's simply not sustainable. And that's, again, a problem that we in Ocular Therapeutix look to correct. We have a study, a proof of concept study, a phase I study named HELIOS.
This was designed as a multi-center, double-masked, randomized parallel group study of AXPAXLI in moderate to severe non-proliferative diabetic retinopathy without center-involving diabetic macular edema. The primary endpoint was the safety and tolerability of AXPAXLI. The secondary endpoint, the changes in the Diabetic Retinopathy Severity Score, rescue therapy, vision and OCT, and most importantly, and most clinically relevantly, vision-threatening complications or the risk of losing vision and going blind. The results, in my opinion, are absolutely remarkable. First, look at the control arm, and what you'll see there is that at week 48 in the control arm, 37.5% of patients, so almost 40% of patients, developed vision-threatening complications, and this is in line with what we know about the natural history of this disease, that year upon year, 30%-40% of patients develop vision-threatening complications and risk blindness. Now, look at the treatment arm. That's what's remarkable.
With one injection of AXPAXLI, one injection, at week 48, that rate of vision-threatening complications was reduced literally to zero, to zero. So what does that mean? That means that I, as a retina physician, can be sitting across the table from a patient and say, "Mr. Smith, your risk with this blinding disorder of developing a vision-threatening complication year upon year is 30%-40%. And if you come to see me once a year, but once a year, much like you go to a dentist for teeth cleaning, I can reduce that risk literally to zero." That's powerful, and that's impactful. So AXPAXLI is not just preventative. In this study, we had patients with non-center-involving diabetic macular edema. And every single patient, every single patient with diabetic macular edema improved, every single patient.
Not only is AXPAXLI potentially preventative, but it is also therapeutic for patients who already suffer from vision-threatening complications. Now, let me switch to outcomes. What does all this mean to patients? Let me go back to wet macular degeneration. I said earlier that understandably, but tragically, 40% of patients in this country, despite a known treatment, drop out because of sustainability. With a more sustainable treatment regimen like AXPAXLI, if that 40% number was reduced by even 5% to 35%, that means that more than 50,000 patients in the U.S. alone could avoid vision loss. If that number was reduced to 25%, more than 150,000 patients in the U.S. alone could avoid vision loss. And if that number was reduced to 15%, astonishing, more than 250,000 patients in the U.S. alone could avoid vision loss. Those are pretty powerful numbers.
That's just the first problem that we will correct. The second problem is that of chronic visual acuity. By not having these oscillations in the back of the eye, by avoiding fibrosis and scarring, we believe that we'll have better chronic vision outcomes in both the patients who don't drop out as well as in the patients who are already on treatment. What is the market opportunity for this? Our ongoing registrational studies target wet macular degeneration. Despite the 40% dropout, that market is huge. Despite the 40% dropout, that market consists of 1.65 million patients in the U.S. alone. Soon, we'll be targeting non-proliferative diabetic retinopathy. That target is even bigger. Here that we're talking about 2.7 million patients in the U.S. alone. Future opportunities where VEGF is a known and proven target include retinal vein occlusion, which is 1.4 million patients in the U.S.
alone, proliferative diabetic retinopathy, 1.7 million patients in the U.S. alone, and diabetic macular edema, 1.7 million patients, again, in the U.S. alone. So a total market opportunity in the U.S. alone of 9.2 million patients. So as I mentioned, we will redefine the retina experience. We will redefine treatment. We will redefine development. We will redefine outcomes. AXPAXLI has the potential for up to 12-month dosing across all retinal vascular diseases. It has a proven mechanism of action with a proven delivery and compelling early results. We have redefined development by de-risking our registrational programs that SOL-1, which is a superiority trial, and SOLAR, which is a non-inferiority trial. We know from our experience practicing for decades that for a drug to be easily adopted in retina, it needs to be safe, it needs to be effective, it needs to be durable, and it needs to be flexible.
And AXPAXLI checks all of these boxes. As a company, we at Ocular Therapeutix are resourced for success. Infrastructure, we have clinical and commercial capabilities to execute successfully. Capital, we have a strong cash position, $427 million reported in September of 2024, expected to fund operations into 2028. And finally, expertise, and most importantly, expertise. We have a world-class team that has played key roles, leading roles in the approval of Lucentis, Eylea, and Vabysmo. Let me end where I began. We will redefine retina globally. We will redefine treatment. We will redefine development, and we will redefine outcomes. I'd like to thank the organizers for allowing me this opportunity, and I'd like to thank you for being here today, and thank you for your attention. I'm happy to take any questions.
Thanks, Pravin. I'll kick it off with the first question. So you kind of touched on this, but there are a few extended duration TKIs being developed in the wet AMD space, along with other long-acting approaches to treatment. Can you walk us through how Ocular's asset is differentiated from those in development?
Yeah, I certainly can. First of all, look, not all TKIs are the same, right? TKIs are a class of compounds that behave and act quite differently. What I can tell you is the TKI that we're using, axitinib, is known to be the most potent and most selective of the TKIs that are in development. And that is combined, as I mentioned, with a hydrogel. It's not an implant. It's a hydrogel that is tunable. So it's tuned to dissolve and go away when the drug goes away. It's targeted for 10 months, which is exactly what we want in a study that has a nine-month endpoint.
So in those ways, I think we're very much differentiated from any of the other products that are being studied right now, let alone the fact that our data is completely different. As you know, in diabetic retinopathy, this drug was used, as I mentioned, with HELIOS as the only drug with a single injection with the results at 48 weeks. And I showed you some of the results, but it's important to underscore that every single parameter we studied, and I mean absolutely every single parameter, was aligned in favor of the drug, every single one of them. And that doesn't happen by accident. Our regulatory pathway is differentiated. We have a very clear regulatory pathway where we've followed exactly what the FDA wants us to do.
And that's validated with a SPA with SOL-1 and a Type C written response in SOLAR. So we're differentiated in many ways from the data to the biology as well as the regulatory pathway. Couldn't be that clear. Somebody's got to have some question. Anything is fine. Yeah, shoot. Yeah.
Criteria for rescue. Different companies have different criteria for rescue. Is there a standard for rescue, whether it's vision loss, whether it's OCT, number of visits, all that kind of stuff? I'd love to get your latest thoughts on that.
Yeah, it's a great question. The question is, what are the standards for rescue? And I think those standards, quite honestly, are very clear. So let's do two things. Let's differentiate the superiority study from the non-inferiority study because the standards are different, okay?
So in our superiority study, which is SOL-1, the standard for rescue is very clear. It's loss of 15 letters of vision, right? So there's no question about that whatsoever. It's a single rescue, and that's considered a treatment failure. So when that occurs, that patient then goes on on-label Eylea from that point on, and that patient is counted as a treatment failure. And that patient is then part of the calculation in the primary analysis in the proportion of patients who maintain vision, Eylea versus AXPAXLI. So that's very clear, right? Now, a little bit more complicated is the rescue criteria for patients in the non-inferiority study. Now, that also is a discussion with the FDA.
Our expectation, we haven't guided you yet as to what the rescue criteria are for our non-inferiority study, which is called SOLAR, but it's going to be very different than SOL-1 because, again, this is a non-inferiority study. And my expectation is that that is going to be very much in line with the non-inferiority studies that have been done in the past historically. So very much in line with that. The other question that was raised. Which is what? BCVA or? Which is BCVA-OCT combination. That is correct, yeah. The other question that was raised, which was a little bit more nuanced, and I want to address this directly, was how many rescue injections can you have in a non-inferiority study and still be legitimate, right? And that was answered directly by our FDA director, Will Boyd.
What he said was, and I'm paraphrasing him very clearly, one rescue injection is allowed. More than one is under review. But what they don't want is they don't want a rescue injection to influence the primary endpoint. They consider the commercially available anti-VEGFs to last for about three months. So the bottom line is if you're giving a rescue injection within three months of the primary endpoint, that's going to be under review because that potentially can influence the primary endpoint. One rescue is okay, one rescue injection, but more than one is under review. Does that make sense?
Yes. Thank you.
Yep, shoot.
Are you bringing patients back monthly to look at the OCT thickness throughout the trials?
Yes. Yeah. I mean, that's pretty standard in all the trials, right? So we are. We have monthly visits that look at the OCT as well as the vision. I will tell you that if there are issues, for instance, particularly in SOL-1, and that was one of the concerns, and maybe that's what you're driving at, which is to say, what if there's thickening of the OCT, and this is a legitimate question, and I think you were going there. What if, and with your smile, I can see you probably were going there, which is actually a very fair question.
What if the OCT starts getting a little thicker, but the patient hasn't quite met rescue criteria, well, we have safeguards in place. We have two world-famous medical monitors, Baruch Kuppermann and Darius Moshfeghi, who are available pretty much 24/7 to guide people through that. The PIs can have the patient come back as often as they want.
They don't have to wait for a month. If they feel like this patient needs to be observed in a week, that patient can come back in a week. There's no issue with that whatsoever. And I will tell you, and let me be very clear, we're under masking right now. We are very, very, very, very happy with the conduct of the SOL-1 study. The on-protocol rescues are exactly what we would expect. We're very, very happy with that, and we're very happy with the conduct of the study. And that speaks to the study centers, our PIs, as well as our medical monitors. So again, the conduct of SOL-1, again, under masking, is something that we're absolutely thrilled with. Couldn't be that clear. Yeah, shoot.
So what was the controversy with superiority? Why would one entity do a superiority study versus another would do a non-inferiority? From a regulatory perspective, I know your strategies are a little unusual for not depending on who listens to you, so.
Yeah, so I can't speak for others, but I can speak for myself. What I can tell you is that in the 30, 35 years that I've been doing this, I don't think that I've ever been part of a group that has designed two studies that are so complementary and have worked so well for so many reasons. Okay, let me just describe some of them to you. Otherwise, I'll be here for like four hours. I think everybody expected us to do SOL-2. Maybe you did too, because that's the knee-jerk. That's what everybody does, right? There's ANCHOR and MARINA, there's HAWK and HARRIER, there's VIEW 1 and VIEW 2. The knee-jerk reaction is just to repeat the same study.
Now, the reason we did not do that is that it provides us logistic advantage, and I described that. It provides us a competitive commercial advantage, and it answers every single question the doctor wants to know, so logistically, when I came here, we already had SOL-1 going. What I said to the team, and remember, SOL-1 was set to be a study that was going to be impossible to recruit, right? We recruited it in record time, in historic time. I don't think there's another retina study that has ever recruited this quickly, and this was in a study that was impossible to recruit, right? We did that by having the best team that we possibly could that's ever been put together, in my opinion, on the planet.
One of my requirements when I came in, and we had to design the second registrational study, was to say, "Okay, here are the boxes that you've got to check." First of all, the second study actually has to help the recruitment of SOL-1, not just not cannibalize, but actually help, right? The second thing is the second study has to give us the best label any drug has ever had in this field, and the third thing is that everything has to be done in record time, right? And every question the doctor has has to be answered, so what we required of SOL-1 is that in the beginning, all the patients going to SOL-1 had to go through SOL-1, so that immediately increased the traffic in SOL-1, and those few patients that screen failed could then completely be swapped to SOL-1, and that's exactly what happened.
The second thing because of that was that at a certain point, what ends up happening is you don't want to over-recruit. The rule of thumb is that you recruit about maybe 10% more. That's what you're okay with, but not much more. So when you're getting close to the end of recruitment, you call your active sites and you say, "Look, we're kind of towards the end. Slow down a little bit." We never had to do that because the sites, and I've been one for 30 years, they stop, right? And then you stop, you go to a different study, you go to a different sponsor, and the second study, you got to ramp up again. So you get this bimodal thing. We don't want a bimodal thing. We wanted a rocket going like that. So here, what we did was say, "Keep on recruiting.
Never stop," and all those patients in the pipeline in SOL-1, as soon as SOL-1 was completely randomized, simply rolled over to SOL-1. That's why you see the numbers you saw today, 311 patients, right, in various stages of loading and randomization in a very short period of time. It worked. It worked extraordinarily well. Otherwise, we'd just be starting recruitment right now. We just rolled those patients directly over, right? As far as the commercial advantage and doctors are concerned, look, we'll answer every single question they want with these two studies. The first question, how long does AXPAXLI last? Does it really last for nine months? SOL-1 will answer that. Can it be repeated? SOL-1 will answer that. Can it be flexible on the label where I can use it on certain patients every six months and certain every nine months? The answer is yes.
With a combination of SOL-1 and SOLAR, we'll get that on the label. Most importantly, can it be a superiority label, the first one ever? And the answer is yes, potentially, with SOL-1. So these studies should never be looked at in isolation. They should be looked at together, and they're perfectly designed to complement each other and answer every single question and get us the very best label we can possibly get. And it's worked. That's why we have the numbers we have today. There's got to be some tough questions.
I have a more broad question.
So. Go ahead.
Yeah. Conducting trials with de-risk populations is pretty common around other therapeutic areas. Why has it taken it this long for a retina company to do it?
Yeah. It's a really important question. For those of you who are in retina or know and are interested in retina, that is the single most, in my opinion, the single most important topic that is simply not addressed. I think unless you've been in practice and you've seen these patients, we have no way of recognizing, and people have no way of recognizing how variable this disease is. For many of you who do other things like, say, colon cancer, if I came to you and I said, "Look, I have a drug for colon cancer," I mean, you would laugh me out of the room. You'd say, "What kind of colon cancer? What stage? What grade?" Because it's extraordinarily variable, right? I would argue with you that wet AMD is probably even more variable.
If you talk to your KOLs or to any retina specialist, they'll tell you there are some patients you've got to treat every two weeks. This is the extremes. There are others you can get away with every six months. We have no way of knowing who those patients are. We have no genetic markers. We have no anatomic markers. We have none of that, right? And all you need in any study is to have an unintended bias in one arm or the other, and your study is completely messed up in an unintended way from this variability that we can't account for, right? In the past, what big companies have done is they've simply just increased the numbers. If you look at the ANCHOR and MARINA studies or the VIEW 1 and VIEW 2 studies or HAWK and HARRIER, there are thousands of patients.
Now, we're not doing 2,000 patient studies. When you do a 300-patient study or 800-patient study, you've got to do everything you can possibly do to de-risk that patient population. And that's exactly what we've done. If you look at SOL-1, for instance, it's a superiority study. And what you want there is you want patients with the most amount of VEGF receptors that are active. If you look at the growth of the neovascular membrane, you get a huge stimulus. You get these VEGF receptors popping up, and then the membrane gets bigger and bigger and bigger. And those VEGF receptors, and here, the vision is good. And those VEGF receptors start involuting. You get the fibrosis receptors coming up. Here, the vision is bad. The neovascular membrane then involutes, becomes fibrotic, atrophies, and the vision is bad and goes away. Most studies recruit here.
We're recruiting here in the superiority study. When the vision is good, we're selecting those patients, but we're super selecting them not only by making sure that they have the most amount of VEGF receptors, but we're making sure those VEGF receptors are actually functional, that they respond by requiring that patients improve by at least 10 letters of vision or get to 20/20. So we're super selecting those patients for SOL-1. So we load them up, and then we go ahead and let them down once. They're perfectly selected for a superiority study. Now, that's in contradistinction to SOLAR, which is a non-inferiority study. That's not the patient population you want. In a non-inferiority study, you want an absolutely stable patient population. You don't want any movement whatsoever because stability is king. That's what wins, right?
We've got three loading doses, and we've built in two things, a period of time that nobody else has, which is two observation periods. We have two opportunities to observe the patients. What are we observing for? We're observing for fluctuations. Because as I said earlier on, there are these anti-VEGF addicts that will fluctuate. You don't want that in a non-inferiority study. We have two opportunities to go ahead and weed them out and then two more loading doses, and only then do we randomize. We specifically super select for stability in our non-inferiority studies. These are studies that are very, very well thought out, and these patients are de-risked in a bespoke manner that is specific to each study. Now, if you look at other trials, what you will see is that people mix treatment naive and previously treated patients.
They will randomize and then load. That all introduces variability. What we're doing is doing everything we can to de-risk the trial by decreasing the variability of the patient population in a bespoke manner.
Thanks, Pravin. And I guess switching gears a little bit, as it relates to NPDR, we saw in 2024 that a competitor, TKI, did not work in this indication. What did you see in the HELIOS data that gives you confidence going forward? And what do you plan to discuss with the FDA as part of the next steps?
Yeah, well, in the HELIOS data, as I said, I mean, I think that data set is absolutely remarkable. That was a safety study. It was a safety-only study. Patients weren't super selected like I described because that was not the intent of the study. But despite that, to have every single patient, and we showed every patient. We showed every single patient, every single eye, every single patient, to have every single patient perfectly aligned in favor of the drug doesn't happen by accident, right? I mean, that was remarkable at week 48 with a single injection.
Every single patient that improved was on the drug. Every single patient that deteriorated was not on the drug in every single parameter. But most importantly, exactly what I said, the vision-threatening complications part, and I talked to my colleagues, as I'm sure a lot of you do to your KOLs, and everybody has said that if we had this drug, if I had this drug today, I'd be using it today because these patients have no other option. As I showed, they're less than 1% of patients getting treated, right, and this is a huge problem. It's preventable. It's absolutely preventable, and there's no one else in the market.
And we intend to correct that, and we intend to take that over. But again, it's not just preventative. I also want to emphasize that every single patient with diabetic macular edema improved. So we firmly believe that it's also therapeutic. Our future opportunities include diabetic macular edema, retinal vein occlusion, diabetic retinopathy, proliferative diabetic retinopathy, on and on. So we see enormous opportunities for AXPAXLI, starting with wet macular degeneration, SOL-1 and SOLAR, going to diabetic retinopathy, and then the other proven targets thereafter. Any more questions from the audience? Well, maybe to close out, perhaps you can just remind us one more time why you think this is such an exciting time for ocular and why investors that are new to the story should start paying more attention now.
I mean, I think there's a lot of data that I presented today, but the one thing that I think people should look at is there's a difference between a drug that goes through regulatory and is a positive clinical trial and a drug that's adopted easily and quickly and seamlessly by the retina community. This drug will not only pass through the clinical trials, we believe, obviously, with a clear regulatory pathway, but very importantly, it'll be adopted by the retina community simply because nothing has to change there. Their workflow does not have to change. Their patients don't have to change. Their techs, their staff, their buildings, their parking lots, the size of their office, their workflow in general, nothing has to change. They simply can reach out and get a better drug and have much happier patients, have a much larger attachment.
And I think this is a win-win-win situation where the doctors will be happier, the payers will be happier because there'll be a lot more patients that will be treated, and the cost of blindness is enormous. And with a 40% dropout rate, that cost is huge. And I say the payers will be happier because patients drop out of the treatment. They don't drop out of the insurance plan. The insurance plan still has to cover them, and it's very, very expensive. So I think the doctors will be happier, the payers will be happier, and most importantly, the patients will be happier.
Thank you.
Thank you. I want to thank all of you for staying around, and thank you to the organizers for this opportunity, but thanks to all of you for your attention. Thank you. And thank you, David.