Hello, everyone, and welcome to the final day of the Jefferies Healthcare Conference. It is my great pleasure to introduce Chief Executive Officer, Eli de los Pinos. Eli? Thank you. It's a pleasure to be here. So Aura is a clinical-stage oncology company. We have a precision therapy platform, and we differentiate with a unique mechanism of action, where we have direct tumor cell killing and immune activation that leads to the opportunity to treat tumors focally and have durable responses. We have a late-stage clinical development pipeline with a phase 3 ongoing in primary uveal melanoma, and we have a SPA agreement that supports our endpoints. We're proud to address large areas of unmet medical need with two big market opportunities: in ocular oncology, broadly, with over 60,000 patients and no drugs approved, and in urologic oncology with over 500,000 patients globally. And we have key upcoming clinical milestones within the next 6-12 months. Most importantly, we're gonna be releasing our phase 1 bladder data. So this is our clinical pipeline. As I said, we have two therapeutic areas, ocular oncology and urologic oncology. As you can see, the planned milestones in the ocular oncology are gonna be the phase II data readout for primary uveal melanoma. That's gonna be in September at a medical conference. And then we're gonna have some early data of our second ocular oncology program, which is in metastasis to the choroid. As you can see, we're actively enrolling in our COMPASS study, which is a registration enabling for the approval in primary uveal melanoma. So how does bel-sar, our first VDC, work? So bel-sar is a virus-like drug conjugate, and a virus-like drug conjugate is similar to an antibody drug conjugate, but with a unique differentiation. Instead of an antibody, we have a virus-like particle that targets the unique specificity towards the tumor cell membrane. This virus-like particle binds heparan sulfate proteoglycans that are highly sulfated uniquely on the membrane of cancer cells and not on normal cells. So when a VDC is administered into a human, either locally into the bladder or locally into the eye, it will not bind any healthy tissue. It will just bind the membrane of the cancer cell. As a second step, we activate this VDC with infrared light, and what happens is that the cytotoxic payload that's conjugated to the virus-like particle is then activated and releases reactive oxygen species that are highly cytotoxic to the membrane of the cancer cell, and the cell goes into acute tumor necrosis. This mechanism of action is highly reproducible. It's genetic mutation agnostic, and it usually kills after cell death, so it's basically direct cell killing. So once it binds the cancer cell surface and it's activated by light, it will consistently create the necrosis. That's mechanism number one. Mechanism number two is an immunogenic cell death that's driven by the way we're killing the cancer cell, that liberates damage-associated molecular patterns, activates CD4 and CD8 T cells, and most importantly, these CD8 T cells have durable memory against the cancer. As we will see, this plays a unique role both in ocular and urologic oncology, as we then can treat focally and have durable responses. So what is the ocular oncology market opportunity? We believe this is one of the most unique unmet medical needs currently today, where we have 66,000 patients and no drugs approved. Primary uveal melanoma is just our initial path to market in ocular oncology, but we broadly can transform this entire medical field. What are the uniqueness? The unique approach from a commercial opportunity is that all of these cancers are seen by the exact same physicians, ocular oncologists, and there are only 50 in the U.S. and 50 in Europe. Local cancers in the eye are not seen by medical oncologists. Medical oncologists see metastatic disease. These types of cancers in the eye are seen by ocular oncologists and treated locally, and that's the opportunity that we have. Currently, the majority of these cancers are treated with radiotherapy that blinds patients, and obviously, we'll show you our clinical data, where we think we have a unique positioning to give bel-sar frontline and entirely transform this medical field. So let's look at a closer look at primary uveal melanoma. How is it diagnosed? How many patients do we really have in this early stage disease, and what are the differences between primary and metastatic? What you can see here is this is a disease that it's diagnosed early. Patients come with some blurred vision, some symptoms, or just with a tiny pigmented lesion in the back of the eye. That's what we call indeterminate lesions. But those patients are not healthy. Those patients have a life-threatening disease that if it's not treated, it will lead to metastasis, and, you know, the overall survival when you have metastatic disease is less than six months.... So there's a unique opportunity to actually not just diagnose early, but treat early. And why don't we do that today? The reason why a lot of these indeterminate lesions in patients with an early stage disease are not treated today is because the treatment today blinds patients. This is what we have today. We have plaque brachytherapy that requires two operating room procedures, at least leaves patients with irreversible blindness. So obviously, if you only have this type of approach, what happens in the early stage disease is the majority of the patients are in a watchful wait until the disease actually show signs of malignant transformation growth, and then patients receive radiotherapy. We believe we can change this, and bel-sar is uniquely positioned to make a difference in the frontline disease and capture all of these 8,000 patients. In fact, that's just an incidence of the disease. There is a very large prevalence of this early stage disease. So how can we provide a complete different approach to early stage intervention? We can deliver our drug with a very easy in-office procedure. Basically, with a suprachoroidal injection that delivers the drug right there, where the tumors start, and we can activate it with lasers that are already available in the majority of these ocular oncology services. Remember, this is not medical oncology. This is ocular oncology. What would be the goals of treatment? Would be local tumor control, basically the same that radiotherapy does, but with a unique, unique opportunity to preserve vision, to avoid the radiation-related morbidities, treat early, and reduce the risk of metastatic disease, with an overall improvement in the quality of life for the patient. Who would choose radiotherapy frontline if there is something that works just as good but preserves vision? That's the vision that we have, and that's the opportunity to transform this disease. So what data do we have, and what, how do we feel comfortable and confident that we have a really good opportunity to get this drug approved? So we run a phase II study, dose escalation and expansion with suprachoroidal administration, exactly the same as we want, or we are doing in phase III. We looked at three endpoints: tumor progression or lack of tumor progression, visual acuity loss, and the tumor thickness growth rate. It's very important because these tumors were actively growing at entry, and we can see the difference in the growth rate right after treatment to see if we have a definitive treatment that achieves a local cure or not. So as I present the data, I'm gonna compare these subtherapeutic regimens, where patients receive 1 or 2 injections, to those where the patients receive the full treatment cycle of which is 3 injections per cycle or the equivalent of 9 injections. So we're comparing 1 to 2 injections to 9 injections. So this is a summary of our phase II data. We have 80% tumor control rate. Again, this is the equivalent not just of stable disease. This is the equivalent of complete cessation of growth or the equivalent of a local cure for this early stage disease. So 80% of the patients receive 3 cycles of treatment and are completely, completely arrested. There's no further growth, and it's very durable to 12 months. That goes hand in hand with 90% visual acuity preservation. Unprecedented! We're treating tumors where they're right there under the fovea or the optic disc, and we do not blind anyone. In fact, not only we do not blind anyone, but the difference in, like, the letters is just 1 or 2 letters. So incredible visual acuity preservation, and all that with extreme safety. And that's really important because if you think about it, we're treating early stage disease. These patients are absolutely healthy. They're not gonna go to a systemic intervention. What they can go is to a local intervention that actually cures them without rarely having any side effect. What you can see here is Grade 1 adverse events of an anterior chamber cell, eye pain, Grade 1 in less than 10% of the patients. So again, an ideal target product profile to treat locally by ocular oncologists and capture all the early stage disease and really transform the treatment paradigm, avoid radiotherapy for the majority of these patients. Now, what's next? Actually, we are actively enrolling in the COMPASS study. This is already agreed with the FDA that this is a study that supports registration. It has 100 patients to support the safety database, and it is randomized 2 to 1 to 2. Why this? This, the FDA actually wanted a second arm to improve the masking of the study, but the statistical analysis of the primary endpoint will be the high dose, 80 micrograms of bel-sar versus sham. Primary endpoint, as you can see here, is the time to tumor progression, and the first key secondary endpoint is a time to composite, which it will include tumor progression or visual acuity failure. Obviously, with 80%, tumor control and 90% visual acuity in Phase II, this study is highly de-risked based on the Phase II data. So how would that—what does that mean? What if the Phase II data was analyzed as the primary endpoint and the key secondary?... Here is the Kaplan-Meier analysis simulating what would be if this was Phase 3. As you can see, the time to tumor progression just with 10 patients per arm has a p-value of 0.0012, and that's based on our current data, which has just 2 events in the treatment arm that happened very late, and the majority of events of the sub-therapeutic regimen, which is the equivalent of sham-like patients, having progression of the disease very early, between 6-9 months. So very exciting data, again, that supports the probability of success of the phase 3 study, which is currently enrolling. The COMPASS study has the majority of U.S. sites actively enrolling, and we're very excited because we're launching this study globally with a really good endorsement from the ocular oncology community. The next indication, actually, milestone this year, too, is metastasis to the choroid. That doubles the market opportunity with 20,000 patients. Again, these are cancers that start in the breast or the lung and metastasize to the eye, and they're also seen by the same ocular oncologist that see primary uveal melanoma. And these patients also are treated with radiotherapy, which is burdensome and leaves with blindness and radiation-related comorbidities, exactly the same as primary uveal melanoma. So we have a planned study. We have an open IND, and is the design of the study. It's a dose escalation, and we plan to have some early data before the end of the year. What are the interesting things of this study and this disease? While it's in the choroid, it's gonna be metastatic disease, so we have the possibility of seeing quicker endpoints, quicker readouts, much faster than what we do in primary uveal melanoma, which is primary disease. So here we have the opportunity to have some early readouts of efficacy in terms of tumor response, as well as seeing an improvement in visual acuity. Finally, there's a lot of excitement around our phase one bladder cancer study, and we're really excited, too. Obviously, it's a very different therapeutic area. Unfortunately for patients, this is a big, big unmet medical need just in terms of number of patients. 500,000 cases globally, not rare. 200,000 NMIBC between the U.S., Europe, and Asia, and over 60,000 muscle-invasive. A big, big unmet medical need where we think, we think that we can also make a big difference. So this will look familiar to the slide that I presented for ocular oncology. Very similar, we have an early diagnosis of non-muscle invasive bladder cancer. The cancer starts in the bladder, like in the eye. It starts small, it has not invaded the muscle yet. We have a lot of patients that are in low grade, low intermediate risk. What is the treatment, and what's the unmet medical need for these patients? Well, for these patients, we actually send them all to surgery. That is the mainstream of the frontline therapy for non-muscle invasive bladder cancer. And the problem with this surgery, which is called TURBT, is recurrence. There are many speculations on why patients recur after surgery when they have a papillary lesion, and, you know, a lot of the times is that the surgery is not clean enough, or maybe you're not removing what you cannot see. Some of the risk mitigations for this recurrence is to give additional chemotherapy or a very old immunotherapy called BCG, which is in scarcity. Some patients, the same as in the eye, instead of being low grade, are high risk, and immediately they receive the adjuvant therapy. And unfortunately, BCG, which is in scarcity, some patients are unresponsive to, and at that time, you know, the risk of just losing your entire bladder and the risk of metastasis is very high. So we can play a role in all of these disease stages, but obviously, the opportunity for our drug is to treat early when you have an intact immune system, especially in bladder cancer, which is, we know that this is a cancer that responds really well to immunotherapy. What an opportunity to treat with something that is highly pro-immunogenic. So that's where we see the opportunity and differentiation for bel-sar in NMIBC. First of all, let's think about the benefits or the opportunity for the urologist, right? We have a highly efficacious proimmunogenic type of drug, but it doesn't have any risk. There's no viral shedding. You can basically give it with gloves. The second is that it's activated. It's very safe, but it's activated with lasers, and it's administered with injections that actually are mainstream in the urologist office. Basically, the injections are used for Botox, for urinary incontinence, and lasers are used for kidney stones. So this is something that it's in the mainstream of the urologist practice. For the patient, there is such a unique benefit. We have the opportunity to treat focally, to treat the lesion, and to not only have a direct tumor cell kill that's consistent, that's genetic mutation agnostic, but also stimulate an antitumor specific T cell response against the tumor itself frontline. That should translate into durable responses, a reduction in the risk of recurrence, and importantly, why should we send the patients to the operating room when we can treat them in the office? And for the urologist, instead of treating 2 patients, now they can treat 30 patients in the office.... so it benefit both ends. Our phase one study is a window of opportunity study. We're treating 21 patients. We went very quickly with fast track designation from the ocular indication into the bladder indication. And, the FDA asked us a part one just to test the safety of bel-sar alone without light activation, which we did, and we've publicly announced the data. Bel-sar alone was extremely safe, with rarely no, treatment-related adverse events. Now we're in part two, which is really exciting because we're not just administering bel-sar, but we're also activating bel-sar focally. So we can look at what is that response in a window of opportunity, which means that we can treat and then do the TURBT, which is the standard of care, but get tissue after treatment so that we can look firsthand and see what's going on from a molecular perspective in the tumor response. So we'll have 10 patients in NMIBC and 6 patients in MIBC, and these are all comers, which means that, especially in the NMIBC, we can have patients that are low grade, intermediate risk, high risk, with a BCG refractory, even CIS. So it is going to be really important for us because we potentially can demonstrate that our mechanism of action of both direct cell kill and immune activation is disease stage-agnostic as well as tumor-agnostic. So what did we see in the first patient? Remember, this is single dose with a tiny, tiny dose that comes from the eye study. In the eye, we're giving 80 micrograms in 100 microliters. That's what we did in this much larger, much larger tumor. We injected focally. You can see the pre-treatment biopsy and the example of what is a papillary carcinoma. That's what it looks like. This is small, like cauliflower bumping up from the bladder wall. And we give a single dose with light activation. 7 days later, when the patient came back to do the standard of care, TURBT, basically everything was gone. There was no tumor. So the physician actually performed, you know, a full TURBT to see what was left, what happened, why did the tumor go away? What we see is that we've consistently seen this across so many different animal models, that a single dose is able to completely, completely have a clinical complete response with presence of necrosis. That's extremely safe because we only necrotize the tumor. But what you see here, right around the necrosis, is this massive immune infiltrate in just seven days. Rarely you see this kind of response, especially an adaptive immune response. You have to have an extraordinarily high pro-immunogenic cell death to recruit lymphocytes within seven days, and that's exactly what we saw. Obviously, it's really exciting. Why? Because this means that we could potentially treat these tumors frontline. Everyone with one injection, obviously, this study is just single dose, but we have the opportunity to see these dramatic responses where we could probably even do an immune ablation, which means that we could avoid TURBT for a lot of patients, especially if we look at that big bunch of patients, 80,000, that are in low risk or low intermediate risk. Why would we need to send them to the surgery when you have something that it can be treated focally, that it has no adverse events, that the urologist can do in the office, and not just, not just the standard chemotherapy? A very highly pro-immunogenic type of therapy that has this massive adaptive immune response should translate into very long and durable responses for patients that would benefit and then would avoid everything down the line and the cost to the system that that entails. So very early days, this is just an N of one. We're going to be, you know, our guidance is mid-year to provide additional data in this very exciting non-muscle invasive bladder cancer space, and we look forward to updating you on our progress. Thank you very much.