Morning, everyone, and welcome to day four, the final day here of the 43rd Annual J.P. Morgan Healthcare Conference. My name's Teyvon Wilson, and I'm an associate in the healthcare group based in New York. This morning, please introduce the team here at Protara Therapeutics. They'll provide a presentation on the company, and with the team, we'll have Jesse Shefferman, who's the Chief Executive Officer, as well as Protara's CFO, Pat Fabbio, and Chief Scientific Operations Officer, Jackie Zummo. With that, Jesse, take it away. Hey, thanks, Teyvon, and thanks to all of you for being here at 7:30 A.M. in the morning on day four of the J.P. Morgan Conference. We're grateful to J.P. Morgan for inviting us, and we'll spend some time talking through all three of our programs today. A lot of you may be familiar with our NMIBC program. We have a rare disease portfolio as well that is also in late stage. We want to make sure that we spend some time with that as well. So thank you for being here. Just a quick word, standard forward-looking statement, disclaimer, and we'll move on from that. So, as I mentioned, Protara has three different programs across oncology and rare disease. In oncology, we are in a phase two study that is designed to be registrational in non-muscle invasive bladder cancer for patients who are BCG-unresponsive. We are also enrolling a study in, or we plan to enroll a study in BCG naive patients in 2025. In addition, we will begin a program with systemic priming in BCG naive and BCG inadequately treated patients, where we will begin to explore the unique characteristics of 002 and its predecessor compound, OK-432, where this is the only bacterial immunopotentiator used as a therapeutic in the world that can be administered systemically, and we believe that that is a path to comparative and competitive advantage in NMIBC moving forward. We want to make sure that we spend some time on the rare disease programs. We have IV Choline Chloride for parenteral support. This is a phase three program where we are beginning to stand up sites for a pivotal study where the approvable primary endpoint is eight-week PK. This is a rare disease program that would address potentially as many as 40,000 patients in the U.S. and tens of more thousand patients around the world. We have orphan drug designation. We have IP to 2041, and again, an addressable patient population of about 40,000 in the U.S. We also have our TARA-002 program in lymphatic malformations. We'll go through this program, but lymphatic malformations are idiopathic malformations of the lymphatic system that happen in utero. It affects about 2,000 kids every year. And in Japan, the predecessor compound OK-432, also known as Picibanil, is the standard of care for lymphatic malformation patients. We have rare pediatric disease designation. So, upon approval for this product, which is currently in phase two, we would be awarded a priority review voucher. This gives a sort of a visual representation of how the portfolio stacks up. Obviously, a lot of work in the oncology setting, but I wanted to note that as you look across this portfolio, the sort of unifying factor is that all of these assets were brought into the Protara portfolio having generated data in humans before we took them on. These assets, in our view, are de-risked in some way or another, whether it's through human data. In the case of 002, the predecessor compound OK-432 has been utilized in 250,000 patients globally in oncology indications and also in structural malformations disorders. IV choline came to us with a phase 2 data package ready to go, and as we said, 002 has been utilized to treat lymphatic malformations patients in Japan since the mid-1990s. I'll pass the mic to Pat so he can kind of talk through our Catalyst Rich 2025 and beyond. Sure, thanks, Jesse. You'll see here that, you know, at the end of last year, the data that we announced really supports and drives a number of near-term milestones. Most notable mid-year will be interim data from our ADVANCED-2 study in 12-month evaluable patients. Then by the end of the year, we'll be reading out futility analysis, 25 BCG-unresponsive patients, six-month evaluable. We have a strong balance sheet with the cash from the recent financing at the end of last year, $102.7 million. We have runway into 2027, and we have common share equivalents of about 46.7 million shares. So, let's talk a little bit about the unique history of TARA-002. We're honored to have a member of our partner team, Chugai, joining us here in the audience today. TARA-002 is an investigational genetically distinct strain of Strep pyogenes that is inactivated while retaining its immune-stimulating properties. What makes that unique among the very few other bacterial therapeutics out there is that it is fully inactivated, meaning it's not attenuated. And of course, as you start talking about the utilization of a bacterial therapeutic in the NMIBC setting, that rhymes very closely with the standard of care, BCG. But one of the things that will start to build the case that this is a cousin too, not an identical treatment as BCG, TARA-002 and its predecessor, Picibanil OK-432, are fully inactivated, which means you can dose these systemically more than once. You can do a single priming dose of BCG, but you cannot do more than one systemic dose. We can utilize 002 systemically over and over again in the same patient. We manufacture 002 under GMP conditions from the same master cell bank as Chugai's originator therapy, OK-432, which is approved in Japan for lymphatic malformations, as well as a number of oncology indications, including head, neck, and thyroid, gastric, and lung cancers. One of the fun things that you can do is get on PubMed, type in OK-432, and there will be over 2,000 distinct articles and case series, case reports published on its use in oncology setting, as well as in structural malformations. Protara has worldwide rights to the utilization of that master cell bank, excluding Japan and Taiwan, which gives us significant freedom to operate. And again, we're grateful to our partners at Chugai for all of the support that we've had from them over the years. Maybe as we sort of start talking about data and mechanism, I would like to pass the microphone to our Chief Scientific Operations Officer and my co-founder, Jackie Zummo, to talk through why 002 is like BCG, but why it's not like BCG. Thanks, Jesse. So, mechanistically, 002 and BCG are similar. They both are bacterial immune potentiators that drive a TH1 pro-inflammatory response. They both have preference to M1 polarization. But where they differ is in that 002 is a NOD2 TLR2 agonist. BCG is a TLR4 agonist. We've actually conducted nonclinical studies to compare directly 002 to BCG. And what we found is that 002 results in a significantly stronger tumor cell killing compared to BCG, and it's got a higher upregulation of key pro-inflammatory cytokines and chemokines, including TNF alpha and interferon gamma. We believe that these important mechanistic differences between 002 and BCG support the meaningful efficacy that we've seen to date with 002, both in the BCG unresponsive as well as in the BCG naive setting. Thanks, Jackie. We'd like to now talk you through the data that we released most recently on December 5th at the SUO Conference, the Society of Urologic Oncology, where we published data on a pool of both BCG unresponsive and BCG naive patients. The data that we produced on the naive side is the first time a sponsor outside of immune checkpoint inhibitors in NMIBC has published on the naive setting, and so I'll have Jackie talk you through some of the findings of the data and some of the exciting opportunities that the data represents. The data set includes 20 patients who are evaluable at three, excuse me, at three months, 18 patients who are evaluable at six months, and three patients who are evaluable at nine months. There are five patients in the BCG-unresponsive cohort and 15 patients in the BCG-naive cohort. The time of this data cutoff was November 19th. Across all patients, 002 demonstrated a 72% six-month landmark complete response rate and a 70% complete response rate at any time. In the pivotal cohort of BCG-unresponsive patients, the CR rate was 100% at six months and 80% at any time. In the proof of concept cohort of BCG-naive patients, the complete response rate was 64% at six months and 67% at any time. While we don't expect that our response rates in the BCG-unresponsive setting will remain at 100%, as we enroll more patients, what we're encouraged by is that we do believe that even if it came down to where we are in the BCG-naive setting, this is still a very effective drug for non-muscle-invasive bladder cancer and is also very competitive in terms of what we've seen from other investigational drugs and also in line with the data that we know about BCG. So, why don't you talk us through the swimmers plot here? Yeah, so I think the important things to look at from the Swimmer's plot is that, you know, reinduction with this drug for patients who are not early responders at three months results in about 83% of patients being able to be salvaged and to be able to convert to month-six complete response. It's very encouraging to know that, you know, that opportunity exists for those patients. In addition to that, we did have those three nine-month patients, and those patients, two of three or 67% were continued responders at the month-nine time point. So, as we take a look at this, you know, one of the things that stands out to us is the power of reinduction salvage. You know, at 80%, that is miles higher than some of our competitors who tend to, you know, see reinduction salvage rates in the 50s. We believe that this may come in some, but note that every time you reinduce a patient, statistically, it's an independent event. You are no more likely to be reinduced because of what happened in the last patient that was reinduced. And so, we actually would feel, we feel that there's a chance that that reinduction salvage rate might carry itself through as the data set gets larger through 2025 and 2026. A quick word on safety? Sure. So, from a safety perspective, this is a very tolerable drug. We have seen most of our side effect profile is really attributed to, one, either mechanistic response that you would expect from an immune-potentiating drug like this, which is, you know, sort of flu-like symptoms. And then the fact that this is an intravesical administration, a lot of them are instrumentation related. So, very clean safety profile so far, and it's consistent with what we know about OK-432, which, as Jesse mentioned, has hundreds of thousands of patients that have been treated. A quick word on the interesting data in naives. I think we get a lot of questions, where does 002 kind of fit in in the NMIBC landscape? Of course, we know BCG unresponsive is a smaller EPI, and it's a more competitive landscape. You know, in that setting, we've got early data here, and we believe that we are beginning to make the case that we're through sort of a threshold of relevance as it relates to efficacy, and that if we can continue to sort of produce the type of results that we've seen so far in an earlier set of patients, that might put us in a very competitive stance relative to some of the further along novel therapeutics in the BCG unresponsive setting. But then the next question is, okay, you're generating data that is in line with, if not better than BCG itself in the BCG naive setting. So, is there an opportunity there? And I want to make sure that we're articulating sort of where we see that opportunity. I don't think you ever replace BCG, right? But based on claims analysis that we've run, we know that, you know, there's a little bit of COVID in this, but, you know, over the past several years, there's been roughly about 12,000 patients every year that either can't get, don't tolerate, or refuse BCG treatment. And so, our view is that the opportunity in the naive setting is as an alternative to BCG. And so, if you're thinking that your addressable patient population there is somewhere between 12 or 15 or 10,000 patients, and you can penetrate half of that, that's several thousands of patients in the naive setting where you are offering a real alternative to BCG. Remember, it's not just that the efficacy that we've demonstrated in naives is in line with BCG. We are safer and better tolerated than BCG and easier to administer for both the patient and the practice. And as we talk about those components, you start to, you know, touch on what we think answers the question that I'm sure that I know we get all the time, and it might be on everyone's mind is, you know, where does 002 fit in, right? You're about a year behind a couple of, you know, further along independent developers of non-muscle invasive bladder cancer treatments. You know, and what is it about 002 that differentiates it? Our observation from other sponsors out there developing drugs in the NMIBC setting is that there are sort of two plausible investment cases around NMIBC development assets: complex high response rate therapeutics and sort of easy low burden therapeutics, low burden on the practice, low burden on the patient, fast administration time geared towards the community. So, our administration time is 15 minutes. There's no thaw time. It can be administered, it is administered via catheter. So that is, you know, that obviates the need for the physician to actually be in the room and can be administered by a nurse. In fact, the administration of 002 is rate limited by how quickly a nurse can insert a Foley catheter, right? The patient doesn't have to stay for two hours after administration because, again, 002 is inactivated. There is not a risk of BCG-osis. There has never been a case, either in the U.S. or in Japan, of sepsis in the use of 002 or OK-432. So, from our perspective, the patient goes home, there's no urine bleaching, there's no special protocol post, and there's no special protocol pre-administration. So, we hit that, you know, sort of profile. And at the same time, we believe that we've started to make the case that we have efficacy rates that are in line with some of the competitors out there that are a little bit ahead of us. And so, as the only broad spectrum immunopotentiator being developed in this field, we offer a different mechanism than either the targeted immunotherapies or the, you know, enhanced chemotherapeutics that populate the development or approved armamentarium. Really, that's where we think we make the case for 002 as not just being another piece of the puzzle, but a highly competitive option for physicians in both the unresponsive and in the naive setting. Our plans, as we mentioned for 2025, is to continue accelerating enrollment of our BCG unresponsive patients to give a sense. The data that we presented in December came from seven sites. We now have 25 sites up and running and believe that that will create a hockey stick effect in our enrollment of BCG unresponsive patients. We need to confirm our protocol design for a registrational study for BCG naive patients and hope to have that confirmation from FDA in the first half of this year, enabling us to commence the BCG naive study by the middle of the year. Finally, where our blue sky opportunity exists is in systemic administration. Imagine a world where after we've demonstrated that a single priming dose followed by a normal induction course intravesically produces an earlier onset of therapeutic effect. If that acquaintance of the adaptive immune system with the antigens presented by 002 is active, imagine a world where you can take transurethral administration of maintenance doses off the table and replace that with subcutaneous doses of 002. That's the world we want to move towards because that's where once you're sparing lots of bladders, the residual unmet need is that the route of administration for bladder cancer is heavily burdensome to the patient. You know, how do you go from a part of the story to leading the story is you lean on competitive advantages like our ability to dose systemically. There'll be more to come on that in 2025 and beyond. So, with about 20 minutes left, I'd like to spend some time familiarizing everybody with another incredibly important and high-value component of the Protara portfolio, which is our two rare disease programs. I'll start with IV choline, and then we'll talk about lymphatic malformations, which is very near and dear to our heart. So, IV choline is the root substrate in the synthesis of phosphatidylcholine. Phosphatidylcholine is the most ubiquitous phospholipid in the body. For those of you that want to go back to your college biology, phospholipids are ubiquitous in the creation of membrane-like structures and cell structures, right? The cell membrane is constructed of phospholipids, and of those, a vast majority are phosphatidylcholine. You and I get choline sufficient enough to synthesize phosphatidylcholine from the food that we eat. But patients that are on parenteral nutrition, i.e., they receive their nutrition via a central line, do not get choline, and nor do they have the absorptive capacity in the small bowel to take in choline and synthesize it to phosphatidylcholine. There are a number of underlying etiologies that drive the need to be on parenteral support, but our estimate is that there are about 40,000 patients in the United States, about 35,000 adults, about 5,000 pediatric patients who are on what we would call chronic TPN, on parenteral support for more than three days a week and on for more than six months in a year. The most notable downstream clinical sequelae of choline deficiency is liver complications. That's because the very low-density lipoprotein particles that transport triglycerides out of the liver are wrapped in an envelope of phosphatidylcholine. If you have very, very low phosphatidylcholine, it's difficult for VLDL to transport liver triglycerides out of the liver. But there are other clinical sequelae as well associated with choline deficiency. But before we embarked on a clinical program, the FDA gave us the green light in 2018, actually, to go into a phase three study looking at liver endpoints. We wanted to make sure that we knew where these patients were and that they actually did demonstrate a homogeneous series of sequelae in the liver from choline deficiency. I'll have Jackie talk you through what we learned from an observational study aimed at finding these patients and understanding sort of what they need in terms of choline replacement therapy. We conducted an observational study, and we basically, as Jesse mentioned, a global study around the world to be able to, one, locate these patients, and then two, really be able to get a chance to understand whether or not they were choline deficient and what did that choline deficiency really mean for them in terms of other clinical manifestations. What we found was that approximately 78% of parenteral support patients that are dependent on it based on the criteria that Jesse mentioned, three days on and dependent for six months or more, that they were choline deficient. Of those 78%, about 63% of them had some form of liver damage. What we found was that the liver damage was actually heterogeneous. What I mean by that is that some patients had fat in the liver, others had cholestatic injury, others had, you know, hepatobiliary injury, some had all of those things or a mix of them. So, what that did for us was give us the opportunity to go back to the FDA and have a conversation around how to develop a phase 3 study and design it so that we could actually be able to power it appropriately and be able to, you know, meet the clinical benefit definitions that the agency requires for approval of drugs. We took those data, went back to the FDA, and what they decided was that an alternative path was appropriate for this drug. So, we are pursuing now and are beginning a phase 3, phase 2/3 registrational study with a source of choline as the primary indication. As Jesse mentioned earlier, our primary endpoint there is a PK endpoint at eight weeks. We will look at and measure over time the sequelae of liver dysfunction as well as other things associated with choline deficiency, including bone density, muscle strength, cognitive impairment, which is all linked to choline deficiency, and what the agency has told us is that, you know, if we can demonstrate clinical benefit there, that would be great, but really, what they're most concerned about is demonstrating that we can raise the levels of choline in these patients, knowing that it is an essential nutrient and plays a significant role in multiple processes in the body. As Jackie mentioned, this is a pretty large rare disease addressable population. What's interesting about IV choline replacement therapy is that both ASPEN and ESPEN, the U.S. and the European physician networks that treat patients with parenteral nutrition have already included recommendations for choline supplementation into guidelines. This is before we've even completed the phase three study. It gives you a sense of sort of the demand for new products as they are discovered into this parenteral support setting. These patients are pretty fragile, and if you can do something to, you know, stave off what most physicians think is an inevitable move towards liver dysfunction, that's a pretty good opportunity to meet an unmet need. Then sort of the cherry on the top, Jackie talked through the fact that we've actually already measured serum choline concentrations in parenteral nutrition patients in our phase two study. Yeah, so in our phase 2 study, we actually have data that demonstrates the not just clinically meaningful, but also statistically significant improvements that once choline is restored at a normal level in these patients, you do see a change or an improvement pretty quickly in fat being able to move out of the liver, but also in the cholestatic injury. And so, these two together, these two pathologies really are the hallmark pathologies of intestinal failure-associated liver disease. And so, we will continue to look at this as part of our secondary endpoints, and we do believe that there will be patients that come into our trial that actually meet both of these criteria and, you know, could potentially have a discussion with the agency about intestinal failure-associated liver disease improvements as well. So, where to from here on the choline program? As we mentioned, we're standing up sites today. These are all going to be academic centers of excellence because these patients tend to be concentrated to, you know, hospitals in that setting. It's probably about an 18-month-long study, but it has, as Jackie mentioned, it's a seamless phase 2b/3 design where in the 2b, we will measure three different doses just to confirm that we're utilizing the right dose from the phase 2 study. And we will be measuring exactly the primary endpoint of the RCT in those 24 patients that will be the first to be enrolled in this study. So, we'll get a look at whether or not these patients are demonstrating the primary endpoint of elevations of serum choline concentrations by the end of this year. Once, we'll take two of those doses from the dose confirmation arm of the study, again, seamlessly move into a 120-patient RCT, two-to-one randomized active to placebo, and again, we'll be able to start to measure achievement of primary endpoint at the eight-week time point in those patients as well, so finally, thank you to those of you that have had enough coffee to stick with us for the last 30 minutes. This program really is what animates us, and we know it animates our partners in Japan, Chugai, so OK-432 is the standard of care in a non-malignant structural malformations disorder called lymphatic malformations. These are rare non-malignant lesions consisting of dilated lymphatic fluid-filled sacs caused by abnormal development of the lymphatic endothelial system. This is driven by somatic mutations in the AKT PI3K-mTOR pathway. There's no familial pattern of inheritance, but they are driven by, you know, sort of genetic mutations that are predictable, if you will. There are no current treatment options, no approved products. The standard of care here is surgery, and as you can see in this de-identified patient, these lymphatic malformations tend to occur in very sensitive areas of the body. We are undertaking a phase two clinical study, and Jackie will talk you through that. We also have licensed in the rights in terms of data and regulatory package of a 550-patient study conducted in 27 centers utilizing OK-432 in lymphatic malformation patients, and that data set consisting of 500-plus patients, we believe over time will be supportive once we sort of demonstrate that the product we're manufacturing in Winston-Salem, North Carolina, is comparable to OK-432, and the FDA has already stated that that is the case. An interesting data point is our IND non-clinical package consists of non-clinical experiments that were conducted by Japanese scientists at Chugai in 1975. The quality of that non-clinical work was so good that it literally comprises our non-clinical section of our IND, and it just goes to reinforce the support and the partnership that we've had with Chugai over the years. A final note, I talked about the fact that you can type in OK-432 into PubMed and get 2,000 different sort of discrete case series or case studies. We know that in the literature, OK-432/002 has been utilized in as many as 8 to 12 other non-malignant maxillofacial cystic malformations, thyroglossal duct cysts, ranula, mucocele, salivary duct cysts. When you start adding up all of these maxillofacial cyst experiences where OK-432 has demonstrated equivalent efficacy as it does in LMs, that patient number in the United States alone is about 12.5 million. So, our strategy is get this product approved in the pediatric LMs indication, get the priority review voucher, and then begin to look at expanding into other indications where you already have data that demonstrates profound efficacy. And when we talk about profound efficacy of OK-432, we like to look at this slide. These are patients from the 550 Iowa-led study that achieved complete or substantial response after only four doses. In fact, we've recently published data of our own interrogation of lymphatic malformations patients and found that in two of three patients that actually were properly diagnosed, we achieved a complete response or complete resolution of the lesion after a single dose. So, you know, this is the kind of stuff that gets you into biotech to be able to help kids like this. I'm often focused on the young lady on the top right. That's a school-aged child whose experience outside of just her health, her physical health, but her mental health, her, you know, every aspect of her life is better because this drug was administered four doses, and that's a new kid. And that's the kind of impact we want to be having on patients and are honored to be able to, you know, interrogate this drug that our, again, our partners at Chugai demonstrated is a true game changer in the lymphatic malformations setting. So, with about seven minutes left, I would like Jackie to, you know, take all of that and put it into a quantitative view of how effective this drug is. This data is from the Iowa study. Remember, we're talking about 550 patients. Jackie, you want to talk through the observation? Sure. So, I mean, I think the pictures kind of say it all, but, you know, from a quantitative perspective, patients who were treated immediately with OK-432 had about 69% of those responded and had what we call substantial or complete response. Where this drug is most effective is in the macrocystic setting, when larger, the larger balloon-sized cysts. In that setting, 84% of patients had a complete or substantial response. And really, I think, you know, just looking at the pictures tells it all, but, you know, also very safe. This drug is very safe and appropriate for a pediatric population. And I think that, you know, we have a study that's going on right now. Our waitlists are full. We get calls constantly from centers around the country waiting to get newly diagnosed children into our study. As you think about the portfolio, we believe that there are multiple shots on goal where we've demonstrated effect size that says that there's a there there, whether that's in multiple different settings in NMIBC, our phase 3 study of choline chloride in parenteral support patients where, again, you have a PK-based endpoint for approval, and then in the lymphatic malformations program where we know this drug successfully treats hundreds of children every year in Japan, and we want to bring that experience to the U.S. and around the world. We'll open it up to questions. I think we've got about five minutes, but we are grateful for everyone's support and attendance today and look forward to continuing to meet more of you in 2025 as we get through a very catalyst-rich year. Thank you for your time. Thank you. I think that just seeing that photo of the young woman in the top right, I think that was pretty moving. I think that to your point, Jesse, this gets into why folks are so, you know, want to get into biotech and want to get into this. So, if there are any questions in the audience, again, please raise your hand. We have some prepared questions here. Also, if you're watching this through kind of the webinar, feel free to type those in, and we can, you know, answer this here as well. I guess to start, and maybe taking sort of a step back and kind of looking at the holistic sort of 2025 landscape, I think there was a milestone slide that you had earlier. Maybe just quickly talk about, you know, because it looks like it's going to be a very active year for Protara, right? Like there's going to be a lot of things we're looking forward to. What are you most excited about when you look at your upcoming milestones and maybe just talking to the audience through that? I think if you pulled each of the three of us up here, we'd all probably have a different answer. Look, I think in the NMIBC setting, where there remains sort of an unknown in terms of the competitive landscape is what is 12-month durability really going to be? We've had a couple of our, you know, further along co-sponsors in the NMIBC development space start to put out data that says, you know, something in the 40s in terms of a complete response rate or durable complete response of about 40% at 12 months, that's a game changer. You know, right now, as Jackie mentioned, the most far along patients we've been able to observe are nine-month patients, and there we're at 67% at nine months. So, we're intrigued for the mid-year data set. These patients that were primarily six-month evaluable in December will ostensibly be 12-month evaluable in June of 2025. And so, we might be able to and intend to actually answer the question, how durable is 002? And is that an opportunity to move beyond, again, a threshold of relevance to best in class? Yeah. So, I'm excited for that data set. And, you know, equally, I'm really excited to see where the STARBORN-1 interim data comes in. So, in the lymphatic malformations program, the way that it works is the agency's asking us to clear three patient safety sentinels stratified by three different age groups: 18- to six-year-olds, six- to two-year-olds, and two-year-olds to six-month-olds. If you think about it, we're through the older age cohort, and that took some time because if you're 18 years old with a lymphatic malformation, you've been living with a lymphatic malformation for 18 years, right? There's a lower urgency to treat, but as you get into the school-aged children and importantly, the preschool-aged children, there is intense urgency to treat on behalf of the patients and their families, and so Jackie talked about a full backlog of prospective patients, you know, we'll be moving very quickly into evaluable patients at those younger age cohorts, and we're really excited to see if that single dose curative dose profile holds up as we expand that patient population. Because listen, this drug, because of its, or this program, because of its sort of modality, is in the vaccines division of the FDA, which by definition is oriented towards treating massive populations, not rare disease populations. We're excited to work with the vaccines division to sort of articulate why a program like this might benefit from some type of an accelerated approval. We don't want to make any promises. We don't want to claim that that's what our path will be. Right now, this is a phase two study, but it's pediatric, it's curative, and even the way that we measure complete response, which is through MRI, is a biomarker. You're sort of ticking all of the boxes of what Peter Marks at CBER defines as the appropriate elements of an accelerated approval. But again, we got to make sure we have the conversation with FDA. And anybody else? Of course, you know, getting the choline program, being in phase three with, you know, a PK-based approval endpoint, you know, we're excited to get that started as well. Perfect. Perfect. I know we've got about 40 seconds left here, so I'm going to just reach out to the audience if anyone has any questions. If not, thank you all for coming out, and thank you, team, for your presentation today. Thank you very much, everybody. Thank you.