Good afternoon. I'm Larry Biegelsen, the medical device analyst at Wells Fargo. Welcome to the next call in our 2026 MedTech Innovation Spotlight call series. I'm pleased to have the management team from Bausch + Lomb. Speakers for this call will include Dr. Yehia Hashad, Executive Vice President of R&D and Chief Medical Officer, Dr. Mayssa Attar, Senior Vice President of Pharmaceuticals and Consumer R&D, Dr. Kelly Swaim, a Senior Vice President of Surgical R&D, and Dr. Cathleen McCabe, an ophthalmologist and cataract surgeon who's a strategic medical advisor to Bausch + Lomb. Additional participants from the company include Brent Saunders, Chairman and CEO, Sam Eldessouky, Executive Vice President and CFO, and Andrew Stewart, Global Pharmaceuticals and International Consumer President. On today's call, we will focus on Bausch + Lomb's exciting glaucoma pipeline, specifically BL 1107, its alpha-2B agonist, and ELIOS, an excimer laser for glaucoma. We'll start with a presentation by the company that summarizes the overall market and opportunity, the products and their mechanism of action and development updates. We'll then proceed to Q&A. If anyone has a question they want me to ask on their behalf, please email it to me. Everyone on the line from Bausch + Lomb, thank you for the opportunity to host this call. At this time, I'd like to turn the call over to Dr. Hashad. Thank you very much, Larry, for the opportunity and for hosting us. I actually will start by a very brief introduction, then I will hand over to my colleagues to give you the details about the projects. Can we go for the next slide, please? I think we covered who will be attending. I just remind everyone, obviously end of last year at the Investor Day, we presented our pipeline. Earlier this year at J.P. Morgan Healthcare, we also presented the key milestones that we will have in 2026 for our robust portfolio of pipeline. I think today we are going to focus on the glaucoma assets, which are highlighted here in yellow. One is related to BL 1107, the first glaucoma neuroprotective product, lowering intraocular pressure and addressing also functional outcome. ELIOS, the laser trabeculostomy, we will explain also, and its targeted approval also in the second half of this year. The rest of all other products are tracking well for this year towards achieving their corresponding timelines and milestones. Next slide, please. Before I turn it over to my colleagues, I just would like to give a very brief information on glaucoma. What is glaucoma? What are the types of glaucoma? How we manage glaucoma, and also speaking about some numbers related to the prevalence and incidence. Glaucoma is defined as a chronic neurodegenerative condition. In fact, this is even considered a new definition because in the past, glaucoma was defined in relation to intraocular pressure. What happened is that we found out that there is a lot of people that could be also having a normal intraocular pressure, but still have neurodegenerative condition that is very similar to what we see with the elevated intraocular pressure. That's why became the intraocular pressure as a risk factor that cause neurodegenerative changes at the level of the retina, primarily at the level of the photoreceptors, the nerve fiber layer, and the optic nerve. This results in a late functional disability. In other words, the glaucoma progresses very slowly to the extent that the majority of patients are not aware of glaucoma at the early stages. They usually, when they are aware of the symptom, it's too late because about 40%-60% of the neurodegeneration have already been happened. The key part of the treating glaucoma is to try to treat the glaucoma at the earliest stage possible before the complete damage happen. How glaucoma is being developed? We know very well that the intraocular pressure is maintained by a fluid inside the eye, we call it aqueous humor. This fluid is produced by area. If you look to the upper right corner picture image, it's a magnified image showing a structure called the ciliary body. The ciliary body has ciliary processes. These are the area where the production of aqueous happened. The aqueous travel, if you follow the arrows on the same picture, they release from the ciliary body, they go in front of the lens, they cross to the pupil over the iris, and then they go through a multiple channels, starting from what is called trabecular meshwork, then canal of Schlemm, then collecting canals, then to the venous system. This aqueous fluid is responsible for the pressure inside the eye. In other words, if there is an increased production of aqueous from the ciliary body, this can result in an increased intraocular pressure. Or, more commonly, there is a normal secretion of aqueous, but the outflow at the trabecular meshwork and the other areas is being obstructed or actually is reduced. That's why the majority of treatments for glaucoma are focusing on one of two things. Either you try to reduce the production of aqueous humor through addressing the ciliary body, or try to facilitate the outflow of aqueous from the eye through multiple procedures or treatments that addresses the enhancement of the outflow from the eye. There are two types of glaucoma, what we call open-angle glaucoma or angle-closure glaucoma. Luckily enough, the angle-closure glaucoma is a very severe condition. It's an emergency and really it's this is the one that is associated with a lot of systemic even symptoms in the form of headache, nausea, vomiting. It's, as I mentioned, it's an emergency. It requires immediate presence in the ER. There are some procedures need to be done in order to reduce immediately the intraocular pressure, and later majority of these patients require surgical intervention. The most common type is what we call open-angle. When we speak about the angle, it's the angle between the back of the cornea and the iris. The narrower this angle is, the more patients are liable to increase intraocular pressure and forming glaucoma. That's the two types are known, primary open-angle glaucoma and the angle-closure glaucoma. How we manage it, I mentioned the concepts is really very simple. Either we try to reduce the production of aqueous or try to facilitate the outflow of aqueous from the eye. We can do both by either medical, eye drops for example, or sometimes now we can use eye implants inside the anterior chamber to reduce the intraocular pressure. We do laser, and the laser treatment usually focusing towards the trabecular meshwork to create like small holes where it can add to the outflow of aqueous from the eye, or also MIGS. The MIGS, this is the area that witnessed a lot of innovation over the last, I would say, 7 years-8 years because it's characterized by simple operations, by very good safety profile for majority of the MIGS. More importantly, they are divided also about whether we are following the same outflow of the eye from through the trabecular meshwork, which actually should be the best way, or try to create an alternative channels. In other words, you make bridges from inside the eye to the outside in order that the aqueous can exit the eye. We have also major surgical interventions like trabeculectomy. This is the one is known as the gold standard for surgical procedure. In very severe cases, we have also shunt operations, which really, it's for final stages when all the other measures have failed. Next slide. The last point I want to address is the prevalence and the incidence. Glaucoma is a very common disease, and as I mentioned, they call it the thief of sight because majority of the patients don't really know, and they lose vision very gradually, and they don't feel it because it does not affect the visual acuity, it affect visual field. Majority of patient could hold good visual acuity up to late stages, and only the visual field restriction happen from the sides goes very gradually, so they don't realize it. However, those patients that reach to the irreversible damage or reach to a late stage of visual affections is about 35%. The best way to treat these patients that have visual acuity is to try to treat them early. Thanks to a lot of diagnostic modalities like OCT, like many other things, we can diagnose anatomical changes before the functional changes happen. Consequently, we can target the 4.2 million population before they get to the late stage of the visual affection. Because half of this 35 that for patients of glaucoma with vision affection, half of them have an irreversible damage and probably irreversible vision loss. That's why we need to focus more on the earlier stages before reaching. Unfortunately also we don't know which patient will move into those are having the severe visual affection. That's really where we are trying to play with the glaucoma neuroprotection. That's why you will hear glaucoma neuroprotection is became of one of the major unmet medical need in glaucoma. Many now are trying, but I think we are having the advantage. It's going to be the only product with a dual mechanism of action, lowering intraocular pressure, as well as affecting the neurodegenerative component of the eye. Now, I will hand over to my colleague, Mayssa Attar, to tell you about the BL 1107 and how it will address that. Great. Thanks, Yehia. Where I want to start is talking a little more and building on what Yehia just talked about and why we think BL 1107 is the right therapeutic strategy. Glaucoma, as we've heard, is a multifactorial optic neuropathy that's characterized by distinct pathological pathways that all converge on neurodegeneration. What that means is retinal ganglion cells and their axons sustain injury from various physiological insults. As we just heard, the risk factor we most commonly recognize is elevated intraocular pressure, which causes mechanical damage. There are other important disease pathways, as depicted on the right of this slide, for which there is no treatment. These pathological pathways lead to cellular dysfunction, and ultimately, when left untreated, the cells die. Because the neurons cannot regenerate, the resulting vision loss is permanent, making glaucoma a leading cause of irreversible blindness worldwide. Preclinical and clinical data suggest that alpha-2 adrenergic agonists may help treat injured cells before the damage becomes irreversible. Under normal conditions, activation of alpha-2 adrenergic receptors helps regulate the sympathetic nervous system by reducing release of neurotransmitters such as norepinephrine that's released during stress responses. An alpha-2 agonist drug leverages this natural mechanism, and in glaucoma specifically, may help suppress these neurodegenerative pathways to support neuronal survival and functioning. Again, while today we treat the risk factor of elevated IOP, glaucoma is ultimately a neurodegenerative disease. Studies have shown that most patients with mild to moderate glaucoma have macular damage and difficulty seeing in low light. What that means, as Yehia has just said, you want to intervene earlier. This is the stage where you might have injured cells, so you can still see that they're not functioning as well. There is no therapy approved to treat or prevent this vision loss associated with glaucoma. Now, the LoGTS study showed that glaucoma patients treated with brimonidine were less likely to develop visual field loss compared to those patients treated with timolol, even when IOP was decreased to the same extent. Brimonidine is an alpha-2 adrenergic receptor agonist, and alpha-2 adrenergic receptor agonists are thought to preserve and improve vision via two mechanisms. First, neurofunctional enhancement, and second, neuroprotection. Our goal with BL 1107, which is a next-generation alpha-2 agonist, is to fully realize the potential of these mechanisms. BL 1107 is a molecule that's designed to treat and target vision-threatening disease. The graphs at the top of the slide show non-clinical pharmacokinetic data that demonstrate when BL 1107 is administered as an eye drop, we detect the prodrug and little active drug in the tears. That means the prodrug is available to penetrate deep into ocular tissues, delivering the active drug to the retina, as shown in the second graph, where you see the majority of the drug detected in the retina is the active moiety. Another BL 1107 attribute is its receptor cell activity and potency, which is depicted at the bottom of the slide. The lower graphs compare potency to two different alpha-2 adrenergic receptors, alpha-2A and alpha-2B, for BL 1107 versus brimonidine. BL 1107 is more selective and potent to alpha-2B, while brimonidine is more selective and potent to alpha-2A. This is important since alpha-2B is the most widely expressed alpha receptor in the retina, where we need the drug to act to improve and protect vision. It's BL 1107's molecular attributes of enhanced retinal penetration combined with selective and potent alpha-2B agonism that should maximize vision benefits. To that end, Bausch + Lomb scientists have continued to generate data to demonstrate how the active moiety of BL 1107 protects retinal cells from neurodegeneration. What you're seeing here in this slide are data from an animal model, where rats are exposed to a phototoxic blue light, and we're able to assess the effects of this injury with and without BL 1107 active drug. If we focus on the graph in the middle of the slide, we are monitoring structural effects on the retina using Spectral Domain OCT. The Y-axis of the graph measures retina thickness, and the first column with the gray dots depicts normal thickness in a rat's retina when they have no blue light exposure. The next column shows structural damage after blue light exposure, which shows up as a thinning of the retina. In the last column, we see that when we have BL 1107 active drug on board, the retina is able to maintain normal thickness, so it protects those neurons in the retina. If we move to the graph on the far right, this depicts a functional measure. Specifically here, we're measuring electrical signaling in the retina, and the Y-axis depicts the amplitude or the strength of that signal. The top gray line shows normal signaling when no blue light exposure is experienced. If you look at the very bottom green line, it depicts the diminished signal after blue light exposure with no active BL 1107. The green line that's just below the normal gray line depicts how signaling is maintained when active BL 1107 is on board. What these data demonstrate is that BL 1107 active drug preserves both retinal structure and function following a blue light damage. These mechanistic data that I just walked through underlie the positive proof of concept clinical data we've seen in glaucoma patients treated with BL1107. In addition to lowering IOP, for the first time, we have clinical data that show 15-letter gains, which again is an approvable endpoint. The graphs on the left show that under low light conditions, patients treated with BL 1107 show a greater proportion of 15-letter gainers than patients treated with timolol in both the study eye and the treated fellow eye. The top graph depicts the study eye, and the lower graphs are the treated fellow eye. You can see the green bars that represent two BL 1107 doses on day one, four, and 14. You can see that the percentage of patients gaining vision, and the gray bars represent vision gains with timolol. What you can clearly see is more patients are gaining vision with BL 1107 treatment. If we move to the graph to the right, we see that patients treated with BL 1107 showed statistically significant improvement in visual field mean deviation on day 14 as compared to timolol. Recall, Yehia said this is one of those early functional measures that you see. Here we're seeing BL 1107 again being protective. These unprecedented data led us to run a larger phase II study, which is ongoing to demonstrate these visual neural enhancement effects. The ongoing study is a randomized double-masked parallel group study with approximately 159 patients. It's a phase II study that's designed to replicate the clinical POC data with refined study elements, such as powering for vision endpoints. We anticipate in the second half of the year to have data from this study. These data will guide the phase III study design. If approved, BL 1107 could define an entirely new category of glaucoma therapy. It would be the first with a neuroenhancement mechanism of action aimed at protecting and improving vision while also lowering IOP. BL 1107 has a robust future. Like we said, the phase II study that we're currently running reads out at the end of the second half of this year. With this powerful pharmacology, we are also exploring indication expansion opportunities for BL 1107, such as in retina. To that end, there's ongoing efforts to develop an intraocular sustained release BL 1107 formulation. The key takeaways are there are no current glaucoma therapies that address the underlying neurodegenerative pathology that threatens vision. BL 1107 has the potential to establish a completely new class of treatment, the first therapy with neuroenhancement mechanism of action in addition to IOP lowering. The clinical proof of concept has already shown BL 1107 improves vision in glaucoma patients, and the ongoing phase II trial, where we will replicate those findings, is expected to read out in the second half of this year. Thanks. At this point, I want to hand off to my colleague, Kelly Swaim. Thank you, Mayssa. As Yehia mentioned at the beginning of this presentation on the anatomy and physiology, I'll dive a little bit more into detail on the MIGS procedures. MIGS procedures lower intraocular pressure by enhancing the eye's natural aqueous humor outflow pathways, either through the trabecular meshwork into the suprachoroidal space or into the subconjunctival space. There are also some approaches that reduce aqueous production via ciliary body treatment, as Yehia mentioned. As we'll discuss further, ELIOS, our laser procedure, works through the trabecular meshwork. MIGS generally are characterized by a favorable safety profile with minimal tissue disruption compared to traditional, more sort of intense glaucoma surgeries and a meaningful IOP lowering effect that is relatively easy for both patients and physicians. To that end, I'd like to ask Dr. McCabe how MIGS has changed her treatment of cataract patients who have glaucoma. Yes. Thank you, Kelly. It's been a game changer in how we view cataract surgery along with the whole picture of a patient who has glaucoma. Now that we have h ighly safe and efficacious treatments to use at the same time as cataract surgery that also address a patient's risk of going on to having further vision loss with glaucoma. It becomes part of the paradigm of how we intend to treat those patients. We don't just view them as something that we need to do to improve their vision with cataract surgery, but we can also improve their quality of life and their risk profile for progression with glaucoma by addressing their glaucoma with a MIGS procedure. Thank you. Go to the next slide. ELIOS is well-positioned to expand this market, particularly since around 20% of patients who have cataract surgery also have glaucoma, and currently less than half of all cataract surgeons are performing minimally invasive surgery for glaucoma. As mentioned earlier, ELIOS will be our first clinically validated excimer laser in this space and will provide new options for physicians and patients. Again, Dr. McCabe, if you don't mind, as more physicians adopt MIGS procedures, how do you think they will decide which procedures will be best for their patients? Yeah. It's gonna be looking at the two most important things, which are efficacy and safety, along with their ability to quickly and effectively adopt the surgical procedure that's needed. I think these are all areas where ELIOS will help expand the number of surgeons who feel comfortable with the procedure because the techniques that are needed to be effective are readily available techniques to anterior segment cataract surgeons, and because we don't have to worry so much about positioning in the proper space a device that needs to be left behind. I know you're gonna cover that a little bit more, but that's a key part of the differentiation of this technology. Perfect. Let's go right to the next slide. We can talk about that. Our excimer laser provides a precise implant-free approach with several features that do distinguish it from other MIGS. One is the ablative laser creates 10 microchannels in the trabecular meshwork to decrease restrictive outflow. Two, the implant-free procedure reduces the risks of poor placement and leaves the trabecular meshwork largely intact to preserve its biomechanics. As we mentioned previously in the Investor Day in November, this innovative approach offers an opportunity for cataract surgeons who were not previously performing this procedure to do so relatively easily. Then finally, the procedure allows for further interventions for refractive cases because, as mentioned before, that anatomy is largely intact. I guess, Dr. McCabe, which of these features, you mentioned a little briefly, but which of these features do you think resonates most with surgeons? Yeah. I mean, I've been involved in the MIGS space since pretty much it was developed, and I've helped bring different technologies to market and teach a lot of different surgeons how to use different devices and things. There are a few things that are part of the hurdles that block adoption, and one of those is really where do I put an implant? Most of the MIGS procedures that were early to the market involve leaving something in the eye. The problem with that is if you don't put it in the right place or you don't put it in the right way, it's not effective. Beyond that, you can actually have some more long-term effects of leaving it in the wrong place. Doctors don't wanna complicate something that they feel very successful with already, which is cataract surgery. I think, you know, having something that's implant-free, that's readily adoptable in an area that they understand, the trabecular meshwork, most can identify very readily. I think those kinds of things, that simplicity of the procedure, are really the things that are gonna decrease some of the barriers that surgeons currently feel. Right. Thank you. If we go to the next slide. As you've seen in the press release this morning, we're very pleased to announce positive data from our U.S. pivotal study where we met our primary endpoints, which is very exciting. As you can see on the left, there was sustained IOP reduction by over 20% over the course of two years. On the right, you can see the reduction in medication burden as well with over 80% of patients that were medication-free. Obviously, we're pleased with these results, and they are consistent with other studies in the EU, where we have eight years of long-term data showing the durability of effect as well. This is all very consistent data of what we've seen before, but we're very excited for this well-controlled study to read out positive. We'll have full results that will be published and released in the coming months. Related to this, Cathy, if you'd like to talk about the data, what's most impressive to you, that'd be great. Yeah. I mean, there's two kind of things that we look for. Of course, we want rigorous data that's collected in a clinical trial setting and showing that there is meaningful and effective pressure lowering and medication reduction. The thing that matters most to patients is medication reduction, really. That's what changes their lifestyle. That's what changes compliance and therefore efficacy. But the other thing is what happens in a real-world setting, and is that durable? Is that something that's gonna last longer than the 2 years that we currently think? You know, they could even get an effective pressure lowering from cataract surgery alone. What we see is not only is the amount and effectiveness that we see at the 2-year data mirrored by what we see in that 8-year data, but it is durable across the 8 years. I think this is really exciting data. I think people will really be moved by that. Some of the data that we currently have for other devices really goes out to five years, so having eight-year data already is very meaningful. Great. Go to the next slide. You know, just the key takeaways I'll highlight again is. We really know ELIOS is positioned to expand the MIGS market by providing a glaucoma intervention that can be performed with cataract surgery. We also know that fewer than 50% of cataract surgeons are performing MIGS today, and so there's a huge opportunity there. Of course, we have our first clinically validated excimer laser offering a highly precise implant-free approach now with two-year data, and we expect U.S. approval in second half 2026. If you go to the next slide, I think I'll turn it back to Yehia. Yehia, you're on mute. Thank you. Obviously just to conclude on these two products. Obviously glaucoma still have a lot of unmet medical need that we need to look at the neuroprotective and the neurodegenerative part of the disease. This is where BL 1107 really, hopefully if the results come as we wish, that could change the way we are treating the glaucoma from a medical perspective. Similarly, on the ELIOS side, it's going to be the first clinically validated implant-free excimer laser technology, which again addresses a lot of areas, especially with relation to the technology itself that currently does not exist on the market. So far we are on track actually for the launch dates for ELIOS as well as for the data, top line on the second half of this year for the BL 1107. With that, actually, I will give it back to you, Larry, if you want to discuss the questions, if there are questions on both programs, and we'll be very happy to answer with the team here. Great. Thanks, Yehia, and thank you to the team here for the excellent overview. Again, if anyone has a question they want me to ask on their behalf, please email it to me. I thought I would start with BL 1107 and then go into ELIOS. Starting with the BL 1107, what have you learned from the proof-of-concept study that gives you confidence in the phase II study, and what are the study design elements that you refined for phase II? Yeah, maybe this question I will direct it to Mayssa, if you would like to comment on this. Sure. Our confidence is really based on the clinical findings that demonstrate beyond reduced IOP, BL 1107-treated patients showed statistically significant improvement in visual field mean deviation, when compared to timolol. Importantly, we also saw those 15-letter gains, which are clinically meaningful. You know, if this is reproduced in a phase III study, it's an endpoint that supports approvability. If you recall, under the low light conditions, we saw that patients treated with BL 1107, a higher proportion, achieved 15-letter gains than those treated with timolol. Those two findings, with the understanding of how this drug is designed to achieve the findings, as well as mechanistically the way it's supposed to work, gives us a lot of confidence. That's helpful. Did you want to add, Yehia? Yeah, I was just going to say also, overall, I think there has been in the past a long history, multiple attempts to address this area. Currently, there has been a lot of new innovations in diagnosis as well as new endpoints, like the low luminance endpoints. Those allow us to detect patients at an earlier stage. This gives us a bigger opportunity now with the characteristics of the products that Mayssa said, plus the data we have from preclinical and clinical to make that this product can work in a better way, so or a better population. We hope that this also translate into our results that we are hoping for all. When can we see the phase II readout? Sounds like it's top-line the second half of the year. I don't know, full presentation maybe at AAO. How quickly can you move to phase III? Again, Mayssa, you can answer how quickly we'll move to phase III. Then obviously for the top line, yes, second half, and hopefully by the academy, hopefully we will have some results there. Yeah. We obviously recognize that this would be a tremendous opportunity for patients. After the data readout, our goal would be to implement the new tools we have at Bausch + Lomb to get into phase III as soon as possible. You would see us back in the clinic within a quarter or two of the study readout. Got it. What is the regulatory pathway and in broad strokes, the timeline you've shared with us in the past? Do you want me to take this, Yehia? Yeah. Okay. In terms of the, it's a new drug application pathway that we would take through to go through that. Now, having said that, we also recognize that glaucoma is a serious vision-threatening disease. When a glaucoma patient experiences vision loss, it's irreversible. We would actually also consider, depending on the data that come out, filing for Breakthrough Designation. Why that's important is, if we're able to do that, we'll be able to have an even faster development pathway. Right now, with a normal pathway, we're anticipating. I believe we've communicated 2031. Our goal, again, depending on the data that we receive, is to accelerate this in every way possible. Got it. How much if you have breakthrough here, how much time does that save? Well, the evaluation by the FDA itself could be approximately 6 months saving from the whole evaluation process, because it could normally take 1 year. It could be like 6 months rapid review cycle. Obviously with the breakthrough technology, you have to do only one study. This can also save some time, because if doing one study versus two pivotal could be a big difference in terms of recruitment time and things like that. We could save some time there as well. Okay. Broad strokes, maybe potentially saving 2 years in total. Is that- Yeah, this would be a little bit of a stretch, but around, yeah, maybe a year, a year and a half could save that. Okay. You showed some impressive data from the proof of concept study. Put that into context for us in terms of how it compares to other glaucoma drops in terms of efficacy and safety. Obviously you talked about brimonidine, another, an alpha-2A agonist. I know it's not an alpha-2B agonist, but how does it compare? That's ALPHAGAN, COMBIGAN, the brand names that are on the market. How would this compare? Mayssa, would you like to comment on this? Sure. That's a great question. Brimonidine is a drug that's been on the market for a long time, and it's always had hints of neuroprotection, right? It has been unsuccessful because the clinical effect size is small to actually gain it as an indication, right? How BL 1107 compares to brimonidine, and for that matter, to any other drug, is that in addition to lowering IOP, which it does, just like any of the other IOP-lowering drugs, it actually has, because of its design, it's able to elicit clinically meaningful, statistically significant effects on vision. That is unprecedented. Nothing compares like BL 1107, including brimonidine. BL 1107, its design is a better design to treat vision-threatening disease than brimonidine, although it does harness the same pharmacology, but more effectively. Can I add a little bit to that as well? It's just that I want to say how important it is, a 15-letter improvement in vision. Clinically, if you think about that's three lines. That's like taking somebody who sees their best corrected vision 20/25, which is near perfect in the way we think about vision, and then having them, if they're 20/50, a three-line worsening, they will be no longer able to pass a driver's test. Hugely impactful on their independence. If we can instead bring them back to 20/25 vision, an improvement in 15 letters or three lines, they then have all that functionality again. A three-line improvement is a massive improvement in how it affects their quality of life. Yeah. I think Mayssa mentioned it during the presentation as well, but I really would like to emphasize, we do believe that our molecule, because of being a prodrug, and the prodrug has a lot of advantages because the normal drugs, when you just pass through the cornea, the majority is being absorbed by the cornea. The amount reaching to the eye itself usually is much less. Here with the prodrug, the active drug happens inside the eye, so it really gives you a much better targeting and focus inside the eye for the target tissue. Additionally, we said also, I think Mayssa mentioned, the potency of this product is really pretty impressive on the retinal cells. At least this is what we saw from the preclinical data on animals. We hope this translate as well into the human. The preliminary one from the clinical study still showing that. That's the difference. You know, I was surprised to see a 15-line improvement in vision at, you know, by day 14. I think about glaucoma as a slow progressive disease. How do you show an improvement in vision so early, so quickly? Yeah. Yeah. You would like to comment on this? This is a great question. Mayssa, would you like to- It is a great question. This goes back to this concept of neurofunctional enhancement. If you recall, the reason you lose vision is first the cells experience because of these neurodegenerative stressors. They become sick, right? They have subcellular dysfunction, and if left untreated, they go on to die, and then you can't do anything. What our data suggests is we're intervening early enough that we are treating those sick cells to turn down those stress pathways so that they can go back to functioning and seeing again. Essentially, that's the neurofunctional enhancement aspect. If you're doing that chronically, what it will do is it will protect the cells from dying. That's the neuroprotection aspect. That's how we are able to see it so early. Non-functioning cells are not necessarily dead cells. Yeah. They may become dead cells, but if we can bring them back to function, they won't. Yeah. You think of them as lazy cells. They are unable to perform the function. You want to prevent them from moving from lazy to dead cells, and you're trying to catch them at the lazy stage where you just try to activate them to be just the normal cells again. That's really what we are trying in a very simple terms. Okay. That's super helpful. We've got about 17 minutes left. Maybe we can transition to ELIOS, and if we have time, we'll come back to BL 1107. ELIOS is the more near-term opportunity. Obviously I'm primarily a device analyst. This is probably a little bit closer to home for me. Maybe let's start with where you see ELIOS being positioned in the current treatment landscape. I don't know if that's a question for Dr. McCabe or whoever wants to take it. I think Dr. McCabe would be the best to answer this one. Yeah. I'm happy to answer it because, you know, I see ELIOS as the go-to interventional glaucoma device that surgeons are going to use in conjunction with cataract surgery. We really have a mindset that's changed a lot over the last years in that if we have the opportunity to get a patient to have IOP control with minimal medicine intervention, that decreases their burden, cost and compliance-wise, and increases the likelihood of efficacy and protection from further visual loss in the future. Because ELIOS has excimer laser, which is very precise, and we really feel that. We use excimer laser for LASIK. We understand how precise it is. We know it's a non-thermal laser, and it creates more openings in the trabecular meshwork than any other thing that we have, while preserving normal tissue for further intervention, and the technique needed to do that is very accessible. I think it will be the go-to device that we usually think about, let's have one thing in our back pocket that we really feel good about, that we know we're gonna be able to effectively do, that we're going to have the least side effects, the least risk of complications, and I think this will be the device that people look to do that. There are other laser technologies out in the market today for full glaucoma, SLT, for example. How is this different? I'm happy to take that, and yeah, if you wanna jump in, too. You know, DSLT is different. It's a different market. It's for earlier intervention. It's an in-office procedure and has more of a variable response. I think one of the things we're most excited about ELIOS is the short learning curve that Cathy's spoken about, as well as even for those who are not as experienced with MIGS procedures, and the favorable reimbursement profile of this product. So we're excited for that. As mentioned before, the precision with the excimer laser itself. Got it. You showed the two-year data, Kelly, today for the first time. I haven't had a chance to look and see how that compares to the other MIGS. There's a lot out there. You know, I mean, I think people are probably most interested in iStent since that's the biggest. If you want to put that into context with goniotomy, you know, canaloplasty, et cetera, that would be helpful. Absolutely. Happy to give a little bit of overview and reinforce some of those points. Yehia, please jump in, and Dr. McCabe as well. As mentioned, we, you know, we shared the positive 24-month data on ELIOS today. The safety and effectiveness of this data is similar to that of other MIGS devices, but without leaving an implant behind. I think that's one of the really exciting things about this data. We met our primary effectiveness endpoints, demonstrating both statistically significant and clinically meaningful IOP reduction. The unmedicated diurnal IOP was reduced by 20% or greater in 76% of the patients, so the majority of patients saw that effect. Patients experienced an average of 7.4 mm of mercury decrease in unmedicated diurnal IOP. The average number of medications went from 1.5 at screening down to 0.3, you know, at 23 months, so a very large reduction there. You know, no intraoperative complications seen during the procedure, and a similar postoperative adverse event profile from cataract surgery alone. I think all in all, the data is consistent with what we've seen outside of the U.S., but even more reinforced with the well-controlled study that was run. Dr. McCabe, if you have anything to add or. Yeah. You know, the only thing I would also add is that the two-year data that we see in that eight-year published real world data is very, very similar. One of the things we saw early on with iStent-based MIGS interventions was it looked like sometimes the efficacy was not quite as good, and that's because a lot of those stents you can actually put in the eye, they'll stay in the eye, but they're not necessarily in the tissue they're supposed to be. I think one other thing that's gonna be a real advantage to this is it is a more direct application right to the trabecular meshwork, where you know that you've done the treatment where it needs to be, and you have 10 rather than, you know, one, two or three fenestrations that you've created, but without destroying all of the anatomy, which is what a large goniotomy does. Dr. McCabe, what's the learning curve here? You talked about it earlier. You said efficacy and safety are really important, but so is ease of use, and I'm paraphrasing what you said. How does the ease of use and the learning curve stack up to other MIGS procedures? Yeah. I've had the opportunity to do a lot of training on lots of different MIGS devices, but I've observed a lot of people who have used ELIOS as the first time that they've used it, and it could be very experienced glaucoma surgeons, experienced in the angle. Some of those doctors were doctors who had started off with stents and then just gave up on it because they didn't feel comfortable with it. Other doctors that I observed were new users in the angle of MIGS procedures, and all of them found that it was very accessible, very similar to other things that we need to do as far as how you move the instruments in the eye. It's just simply a probe. We use probes for lots of things, and you just need to identify the trabecular meshwork, which is easily identifiable. Every single one of the doctors I observed, and myself as I learned this procedure as well, found it to be, you know, very, very straightforward. I think the learning curve is going to be very easy. That's helpful. Maybe another one for Kelly. How confident are you in obtaining regulatory approval and launching ELIOS in the second half of this year? We remain confident and look forward to the launch. Yes, second half. Okay. You talked about reimbursement. Somebody mentioned reimbursement. This is a space that's had a lot of volatility to put it mildly. Forgive me, on the pivotal trial, was it a single arm trial, or was it an RCT? How do you expect the reimbursement to shake out, compared to other MIGS? I actually think it has a specific reimbursement code as a procedure. That's actually one of the biggest thing that we always look at, and ELIOS has already won. I think the trial to answer your question, it was actually a trial that had a single arm. It was a single arm of doing combined cataracts and glaucoma surgery. I think you know, I think we have a very good reimbursement structure so far present. I actually wish that we had somebody from the commercial to speak more to this. Generally speaking, I think the reimbursement is based on even the trial that we have. We think we have a very good chance to achieve the desired reimbursement for the product. You know we have a strong reimbursement team that understands procedural codes and understands procedures such as this. We have confidence in the procedural code that we will use at launch, and so we know that this will be a competitive product within the space and certainly competitive with all the other MIGS devices that exist today. Okay. I mean, with this code that you have, do you have any advantages on the reimbursement side compared to other technology that we should be aware of? Do you think it'll be competitive, Yehia, to other, like, iStent or do you have advantages on the physician fee or I cannot comment on the competitive part, but I know it's going to be very good in terms of the reimbursement part for ELIOS. Yes. That's, that's- It's an R&D call, so we'll follow up with the details on the. Yes, I think that's the best way. Yeah. We all know on this call how important, you know, the reimbursement is in this space. I would just say that the reimbursement the way we anticipate will be able to support the enthusiasm that we expect surgeons to have for the technology. Sometimes it's a barrier. We don't think reimbursement will be a barrier. It will just support that enthusiasm. That's good. That's good to hear. Is there an opportunity here as a stand-alone procedure for ELIOS, or do you envision this mostly as a, you know, done in combo cataract? Yeah. It's like for now it's a combo cataract. That's what we studied in. Is there a plan or hope to study it as a stand-alone procedure, going forward? Right now we don't have plans for that, but we are looking into that as a future development. Got it. Before I go back to BL 1107, just the $175 million peak sales, would anybody care to kind of characterize how to think about the ramp? Are there any analogs you would point to, Yehia? Is this going to be fast, slow? Any- Yeah, Larry, maybe I'll answer that one. I'll jump in here. You know, we do anticipate the approval in the back half of this year. I really think you're going to see the impact in our P&L in 2027, and ramp nicely in 2027 into 2028. I think given the learning curve that Dr. McCabe described, I think it will ramp more quickly than other MIGS, but it will still really be a 2027 P&L impact for us in a positive way. Yeah. Got it. Thank you. That's helpful. Going back to BL 1107, we didn't talk about the sustained release formulation. There's a lot of excitement with the success, you know, iDose is having. We have DURYSTA out there. Talk about the status of the sustained release formulation and how it might compare to, you know, the incumbents. Yeah. I think I will hand over also to Mayssa to give a overview of this. Before I hand over to Mayssa, I just would like to mention if the study results by the second half of the year comes as we expect, this will open the door for multiple other indications. It's important for us also to start to think about other formulations, other than the eye drop, and this is where we also started to focus on drug delivery system, long-acting. I think I'll just hand over to Mayssa to give you also a perspective on this program that we are doing. So, uh- Mayssa? Yeah.Sure. In terms of our work on the sustained release, it's the data so far in our hands are very promising and support entering development at the end of this coming year. Oh, that's right, at the end of this year, 2026. How we compare, I think it's inherent to the molecule that we're formulating. If you recall, we also have a partnership with Ripple that really has best in class approach for long-acting injectables. Because this would be the first molecule that's being formulated to lower IOP as well as protect cells in the retina, nothing can compare with it, and the doors it could open, it could be a long-acting glaucoma treatment. It could be a long-acting retina, like geographic atrophy treatment. There's so many things we could do with a formulation that was long acting. Again, I don't think there's anything like it right now, and it really comes back to what we see in this first clinical study that's going to read out later on this year to confirm mechanistically it's doing what we have seen it do so far. We are very excited at the opportunities that will open for us. Maybe lastly, could someone talk about the IP and the patents you have around BL 1107, please, and how long they go out? I think for the BL 1107, we actually have numerous pending families around the world, with several have been issued. We also have a lot of new applications for composition of matter, pharmaceutical composition of claims, methods of treatments, new mechanisms, potential other indications. We have a very wide patent portfolio for BL 1107. It goes all the way up to 2046. Actually we are actually some of them are pending, but some of them have been already granted. That's we are moving in a very good direction with this one in terms of patent. I think Brent mentioned also at the J.P. Morgan that one of the areas that we're focusing on across all our new pipeline is patents, and this is an area we have seen a dramatic increase. Unprecedented number of new patents we have applied for all our products during the last year and this year we continue to do the same. For BL 1107 particular, we are very confident, and it goes up all the way up to 2046. That's helpful. Three minutes left. You know, I wanted Yehia to give you kind of an opportunity to add anything that we didn't discuss that you want to highlight or to summarize. If I do the math here, these two assets, it's about $1 billion peak, you know, $800 million, I think you have for BL 1107, $175 million for ELIOS. I'm rounding up a little bit. Obviously, you know, big opportunity here for Bausch + Lomb. You know, thank you again for the opportunity to host this. Yehia, I'll give you the last couple minutes here. Thank you very much. We really appreciate the opportunity, Larry. Again, we are really very excited about our pipeline overall. I think we are really trying to target areas that have been known to be a high unmet medical need. There is not a lot of approved treatments currently. If we speak about the neuroprotection piece, we think that this is an area obviously a lot of companies looking, but this will be the first product that have dual mechanism of action to address the IOP as well as the neuroprotection piece of glaucoma. Similarly, also, I think for the cataract surgeons that are looking for a quick, fast MIGS procedure without leaving an implant behind, with a very high precision, a very rapid process, and also a very effective for a very long period of time, the ELIOS is a great approach to that. I think we are actually trying to find out even more to increase our pipeline with such things that are unique, differentiated, and addressing big areas of unmet medical need that we are still not addressing. That's really where we are focusing with our pipeline, and we will have more sessions like this for other products, I hope in the near future as well. Sounds good. Well, with that, we'll end it. Appreciate everybody's time today, and hope everybody on the line found it useful. With that, we'll end the call, and see everybody soon. Thank you. Thank you. Thank you.