Go ahead and start. Welcome, everyone. First of all, I wanted to thank the Jefferies team for inviting us to provide an up—oh, I need to find the way—an update on KALA. And remind everyone there will be likely some forward-looking statements. KALA is a leader in the emerging field of mesenchymal stem cell secretomes, and our focus is on rare ophthalmic diseases. We have an ongoing pivotal trial with our lead product, KPI-012, for the treatment of persistent corneal epithelial defects, which is a rare and vision-threatening condition for which there are significant unmet needs. We feel this could be a billion-dollar-plus opportunity based on a number of factors, first of which the only approved product in this space, OXERVATE, which is marketed by a small private Italian company, had sales of $820 million in 2023, and we speculate that it's eclipsed a billion dollars in sales. It is indicated for neurotrophic keratitis, which only represents about a third of the patients with persistent corneal epithelial defects. We are pursuing a broad indication for persistent corneal defects, and that would cover not only that third of patients that OXERVATE covers, but also the additional two-thirds of patients. We are doing that because of our unique multifactorial mechanism of action and the results of our phase IB study. In addition, for the third of patients with the neurotrophic keratitis etiology, we feel that we could have some significant benefits over OXERVATE with regards to dosing. They dose six times a day, with regards to tolerability, and with regards to the overall patient experience. We are making good progress in our development program and are targeting top-line data for our ongoing pivotal trial in Q3 of this year. We have a strong and experienced leadership team. They've been working together for some time, and KALA has successfully developed and obtained FDA approval for two ophthalmic products: one for dry eye disease, one for inflammation following ocular surgery, and those were divested to Alcon to allow us to focus on our mesenchymal stem cell secretome platform. This platform is a proprietary—we call them MSC secretome platform—is a cell-free regenerative approach to disease management. Secretomes are produced by collecting the biomolecules that are secreted by cells into the extracellular space. Generally, these proteins, these biomolecules, are secreted to support the health and viability of the cells. In our case, we start with human bone marrow-derived mesenchymal stem cells. We have a master cell bank, which is sufficient to get us through development and through commercialization. We manufacture our secretome by culturing those under GMP conditions for a controlled amount of time, giving them time to secrete the variety of biomolecules, growth factors, protease inhibitors, neurotrophic factors, and others. We separate the cells from the supernatant and are left with an aqueous solution that contains this variety of important biomolecules. We think one of the advantages of secretome is that you can get a similar effect to that of cell therapy without having to administer cells. There has been a good deal of work done in the literature about the role of secretomes and the positive effects on ophthalmic diseases such as corneal injury, retinal degenerations, glaucoma, and others. The primary mechanisms of action in our case are wound healing, tissue repair, anti-inflammatory, anti-immunomodulatory effects, and neuroprotective and neurotrophic effects. We feel that this platform has the ability to address a number of rare ocular diseases, and we've chosen persistent corneal epithelial defects, which we call PCEDs, as our first indication, and we'll talk a deal about that. We also see other potential areas: limbal stem cell deficiency, which is, again, a rare and life and sight-threatening disease for which there are no therapies, and a variety of others. We also have a preclinical program looking at different iterations of the secretome for the treatment of retinal diseases, primarily through upregulating neurotrophic factors and antioxidant factors. Our first lead product, KPI-012, is composed of a variety of biomolecules that are produced by the mesenchymal stem cells and that we formulate into a fairly simple ophthalmic formulation, which makes it easy for patients to administer. It contains key classes of biomolecules that we know are associated with corneal wound healing. These include growth factors, neurotrophic factors, protease inhibitors, and matrix proteins, and we'll go through that mechanism a little more in a second. We're currently, as I said, in a pivotal trial for PCED with a goal of complete healing of the lesion, and we'll talk a second about why that is so important. We have Orphan Drug and Fast Track designation from the FDA. Persistent corneal epithelial defects, or PCEDs, are defined as a corneal wound or defect that is refractive to current therapy and hasn't healed for a period of 10 to 14 days. We define it in our clinical trial as a defect that hasn't healed for at least 14 days. As you might expect, and you can see on the right-hand panel, this is really an area of denuded epithelium. We know the epithelium is a protective barrier. We also know that the cornea is the most highly innervated organ in the body. When you have an area that does not have coverage by epithelium, you will have a significant number of patient symptoms, primarily pain in many cases, visual impairment, and often these lesions are in the visual axis. You get a significant amount of vision loss. Equally important, as we talk to clinicians that manage this disease, is if you do not heal this lesion quickly, you have a high risk of infection that can lead to significant sequela, including loss of the eye. There is a high probability that if you cannot heal this lesion, it will continue to degrade into other areas of the cornea. You can get corneal scarring, you can get stromal thinning, you can actually get perforation of the cornea, which again can lead to the loss of vision, in many cases the loss of an eye. The one thing that we know about this condition is there's a variety of etiologies that can lead to it. One of those, of course, is neurotrophic keratitis, which is the only etiology for which there's an approved product and the one that's treated with OXERVATE, but there's a variety of other etiologies that can cause this, including trauma, diabetic keratopathy, severe ocular surface disease, infectious keratitis. Herpes keratitis is a very common cause of this disease, and patients often have more than one underlying etiology, which makes it particularly difficult to treat. We think because of our unique multifactorial mechanism of action, we can address the pathways that are the cause of the lesion and the impaired healing in all these etiologies. The prevalence is estimated to be about 100,000 patients in the U.S., and so it is a rare disease. It is an orphan drug, and we'll share in a second the results of a phase I.B. clinical trial in patients with PCED, where we had very good results that have led us into this pivotal trial. As I said, this is an underserved market with a lot of unmet needs, and a few of the needs that we think are important are a single therapy that addresses all etiologies. As I said, OXERVATE, which sold over $800 million in 2023 and probably has exceeded $1 billion, is only indicated for PCEDs that are secondary to neurotrophic keratitis. Our epidemiology data and that from other sources indicate that that's about a third of all PCED patients. You have two-thirds of patients that really have no approved therapy. We think there's a significant opportunity for a product that can address the other etiologies. OXERVATE also is not always patient-friendly. It has to be dosed six times a day. It requires a very complicated reconstitution by the patient. It comes frozen. They have to reconstitute it daily, and then they dose themselves with a glass pipette, basically. That is an experience that's difficult. Our product will have a very simple single-dose unit that these patients are familiar with from other products they've taken. They can just take one of those, put it in the eye, throw it away, and then do the next one the next day. We also know that approximately 16% have been reported, and when we talk to clinicians higher than that, that take OXERVATE, experience a very significant corneal pain, and that's not a pain upon administration. It appears to be a neuropathic pain that it's thought to be caused by a couple of reasons. One is the fact that it drives healing in neurotrophic keratitis by healing the nerves or by stimulating the nerves. You get the nerves regenerating or re-energizing while the epithelium is still denuded. You have nerves that are firing, and you do not have an epithelium. There is also a good deal of data that suggests that nerve growth factor has a direct effect on pain receptors. It may well be a direct effect from the active in OXERVATE, which we have not found data to suggest that happens with the neurotrophic agents that we have in our product that include PEDF and BDNF and others. We think there is significant opportunity here for not only the third of patients that have neurotrophic keratitis, but also the other two-thirds of patients that have different etiologies. Our goal, if we're successful, would be the first approved product with a broad indication to cover all conditions of persistent epithelial defects. It's a typical sort of rare disease type program. Most of these patients are seen by corneal specialists. There's about 1,800 of those in the U.S. The marketing effort, the sales effort to cover that is manageable for a company of our size. A little bit about the mechanism of action of our product. We know a lot from the literature over the last 40 years on the mechanisms and the pathways associated with corneal wound healing. Generally, when you have a defect or a wound where you lose the epithelium, what needs to happen is epithelial cells need to differentiate, migrate to the wound bed, and adhere to the matrix. You also have to have an intact basement membrane. You can still have a number of epithelial cells in overabundance, but if they do not attach to the basement membrane, then you lack that scaffold to start reproducing and healing the wound. We attack this problem from a variety of different regions. We know that some of the pathways, or the majority of pathways that are impaired in areas of poor or impaired corneal healing, such as you see in PCED, are responsive to factors we have in there. One of those pathways is impaired epithelial cell availability, differentiation, and migration. If you do not have enough epithelial cells, you cannot heal the wound because there is not enough to fill the wound bed and start the process. Secondly, we know that in many of these conditions, particularly if you have a significant amount of inflammation, you get a great deal of protease activity. Proteolysis tends to chew up the basement membrane, so you lose that ability of epithelial cells to adhere even if you have enough epithelial cells. There is also an interesting crosstalk between the nerves and the healing process. It is an evolutionary process. As I said, the cornea is the most highly innervated organ in the body and is essential for survival. This crosstalk has happened so that if you have a wound or any sort of defect on the surface of the eye, it signals the healing process to start healing, start all these pathways to start healing. If those neurons, if those nerves are downregulated or not functioning, you lose that crosstalk, so you do not get that stimulation. You have people that have significant pain. You have people that have these defects, but the nerves are not telling the rest of the healing process to kick in. The factors that we have in our product that we think addresses each of these, we have growth factors, for example, hepatocyte growth factor, pigment epithelium-derived factor, and others that promote the epithelial differentiation and proliferation and migration. That would address those pathways and those etiologies that involve insufficient epithelial cells, such as limbal stem cell deficiency and others. We also have protease inhibitors, including TIMP-1 and a number of SERPINs, and those are able to inhibit the proteases that degrade the basement membrane. For those conditions that involve an impaired basement membrane due to proteolytic activity, we feel that we can address those through our protease inhibitors. We are also supplying matrix proteins such as fibronectin and collagen to help rebuild that scaffold, to help rebuild that matrix to allow a basement membrane to which epithelial cells can attach and proliferate and start the healing process. We also have neurotrophic agents. PEDF is one, BDNF, and others, and they support re-innervation of the cornea and help reestablish that crosstalk between the nerves and the epithelial surface. We have conducted a phase I B trial a couple of years ago. This started out with a safety cohort of three patients. These were not patients with corneal disease, and we found no significant tolerability issues or no significant safety issues. We moved into eight patients with diagnosed persistent epithelial defects and were required to have shown no improvement over the preceding one or two weeks. We dosed them for a variety of different times and durations. Of the eight PCED patients that were treated in the trial, all eight of them showed improvement, showed some healing, and six of eight showed complete healing of the lesion. That is important for a couple of reasons. First of all, as I said before, that is the first thing clinicians want. They know the first thing they have to do when they see this condition is heal the cornea, because if they heal the cornea, the rest will often take care of itself. Secondly, that's the endpoint that FDA has indicated they want to see for demonstration of efficacy in our pivotal trials. We think it's very important that we've been able to show this. They all remained healed through the end of follow-up and again had no significant tolerability issues. This is a rather complicated slide, but it sort of illustrates the eight PCED patients that were treated in the trial. The green line is the duration of treatment. In the first few patients, we only dosed for a short amount of time to help establish the safety profile. The green dots are the point in time where complete healing, which was based on photography of the lesion, occurred. The gray line and the gray dot represent the follow-up. As you see, again, six of eight of these completely healed and remained healed throughout the follow-up period that ranged anywhere from eight to 19 weeks. We thought that was important that you could heal the wounds and they would remain healed. We also saw significant pain reduction in this trial. I mentioned that OXERVATE has a pain response that appears to be an adverse event. We talked a little while that occurred. In six of eight of the patients that were in this trial, they had significant pain going in. Some were greater than five on a visual analog scale, which is fairly significant. Upon treatment with our product, we showed that those had all returned to baseline within three weeks. A significant impact on pain. We think that's probably a good surrogate for the healing of the cornea because we know much of the pain is because of the areas of denuded cornea and the nerve sparring. Based on that, we've moved forward with our development program. We had a good pre-IND meeting with the FDA. They indicated they were open to a PCED indication, advised us that if we enrolled a trial and allowed all etiologies to be in the trial, that they would, if that trial was successful, not for each etiology, but as a whole, then they would be open to a broad indication for treatment of PCED. They also provided excellent guidance on their CMC clinical trial design and the endpoints, which we'll talk in a minute. As I said, we had a warfarin and Fast Track. We filed an IND in the U.S. in December of 2022, and that was accepted within the 30 days. The FDA did ask us to run a small safety cohort. Our initial study was done at a one-unit dose. Our current study is at a one and a three-unit dose. Despite having two large, very safe toxicology studies, they asked for a small, we negotiated for a small safety cohort. During that, as you'll see, we saw no significant tolerability or toxicology. One of the questions commonly asked is about the CMC program. We are manufacturing the secretome at full commercial scale. The drug product for our phase II trial was made at limited, not at commercial scale, but it's a very simple process, and we're in the process of scaling that up. One of the big challenges for us initially was developing a potency assay program. We do that through a matrix approach where we're measuring CQAs, as we call them, by ELISA of some of the key proteins, HGF, PEDF, and others, by ELISAs. We have cell-based potency assays. One of those that's one of the original ones is a scratch assay where we take human immortalized corneal epithelial cells. We do a very controlled scratch or wound in the eye, and then we can watch the rate at which that wound heals. We also have potency assays that look at attachment of epithelial cells to a matrix with and without our product. We have a potency assay that looks at inhibition of proteases. Last year, we had a Type C meeting with FDA. We presented where we were and what our proposal was for our potency assay program, and they agreed basically to everything we recommended. It was a 13-minute meeting because they agreed to everything. We felt very good about that, and we're in the process of validating those assays to be in a position to be ready for a BLA going forward. We also, with our current product, talked about other indications. We think with a current product, we could go directly into clinical trials for a second indication just by referencing everything that we've generated for the first study. Based on that, as I said, we moved into the phase II B trial. It's a pivotal trial. It's designed as a pivotal trial. It's referred to as phase II B because we weren't at full scale for the drug product. As I said, we were for the drug substance, the secretome. We did the initial run-in or the initial tolerability in two patients at the higher dose, three-unit dose, and saw no safety or tolerability problems at all. We moved into the current trial, which we're studying the one-unit, three-unit dose versus vehicle, one-to-one-to-one randomization in a 90-patient multicenter randomized trial. We powered the trial based on the results from the OXERVATE trials, particularly the U.S. trial, which was virtually an identical design. If we assume we have the same treatment effect they had, which was 65% healing in the drug-treated arm, 17% in the vehicle arm, then we would have greater than 98% power to achieve a P-value of less than 0.05. The powering is, I think, enhanced by the fact that, as we'll talk about, the endpoint is very objective. It is an eight-week treatment period followed by a two-week follow-on. The endpoint is complete healing of the lesion at eight weeks, and then it remains healed at 10 weeks based on corneal fluorescein staining. That is a very common technique. You put a drop of fluorescein in the eye. It adheres to denuded epithelium. You can see it through a camera. You take photographs of it. Those go to a central reading center, and we do not say blind it in a mass fashion. The reading center makes a determination. Is it healed or is it not healed? Is there any staining in the original area of the lesion? In that case, it would not be healed. If it is devoid of staining, then it is healed. The primary endpoint, again, is at eight weeks, and then continue at 10 weeks. As I said, top-line data is targeted for the end of Q3. We are excited to see the results. As always, a little anxious. I look forward to updating everyone once we get our final results. Thanks again. If you have any questions, I'm happy to answer. Yes. Enrollment is not yet completed. We have completed the original 90 patients we targeted, but because of the way we had to run the trial, the patients come in, are screened by the investigator. We run them in for a week on nothing but artificial tears and antibiotic to protect against infection. Then they go in the randomized. When we talked to investigators initially, they said they were not able, because of the urgency to treat, they would not be able and weren't willing to wait the three, four, or five weeks for the reading centers to confirm. The initial randomization was based on the judgment of the photographs taken by the investigator. As we've gone back and looked at the reading center, there is a certain percentage of patients. We originally announced 13. There are a few more that weren't confirmed by the reading center. We determined that those would not be appropriate to include in the final analysis. We will have a full analysis set that includes those patients that were randomized and that were confirmed by the reading center. We are continuing to roll beyond the 90 patients originally. We are at triple digits now to help make up for those patients. Yes. Those patients will be maintained in safety. You'll have additional patient data there. For the efficacy, it'll be the. They were all followed for the eight weeks throughout the course of the trial. Maybe finally, any feedback on KOLs on PCED has more etiologies than NK. Any feedback from them on if they think your product will work across all the broad etiologies? Yes. I mean, they understand that each etiology involves typically a different pathway that's impaired. The feedback we've gotten has been very good. They think that this multifactorial approach to treating this would be very helpful. As I said, they have really no approved products for the non-NK patients. They would welcome something that works in all patients. If our tolerability holds up, we could capture a large part of that NK population as well. Amazing. Thank you so much. My pleasure.