Hi, good morning, everybody. I'm Serge Belanger, one of the healthcare analysts at Needham. I want to welcome you to our 24th annual healthcare conference. For our next fireside chat, we have Trevi Therapeutics with us, the company's President and CEO, Jennifer Good, and the company's Chief Commercial Officer, Farrell Simon. I think Jennifer has a few slides for us, and then we'll proceed to, I guess, the fireside chat portion. For those listening in online, you do have the option to submit questions via the portal that you're watching this on. As they come in, we'll be asking them. I'll hand it over to Jennifer. Thank you, Serge, and thank you for including us in your conference. We appreciate it. I just wanted to show just a few slides on Trevi. It's been a data-rich period for us, and fortunately, we're three for three at this point with one more data readout coming. I thought I'd just show a snapshot of that. The company is focused in chronic cough conditions, two in particular, chronic cough and idiopathic pulmonary fibrosis, which we have signaled that we'll report phase II B data in the second quarter of this year, and refractory chronic cough data, which we just reported in the first quarter of this year. I'll show you what that looks like, both very meaningful readouts. The backbone of Trevi's story really is about the mechanism of action. I think what's unique, there's been a lot of drug development work done in cough, probably some of you are aware of that, been a lot of failures. I think what's unique about our proposition here is our drug works not only peripherally in the lung, but centrally in the brain. Cough is mediated at the brainstem. We work broadly across the whole cough reflex arc. When you look at a lot of the development work that had been to date, it had all been in sort of single peripheral receptors, and it had had a challenge being able to deal with sort of cough broadly. We went at this, not only does our drug work in the lung, but also at the brainstem. I think you'll see from our data, we think is an important aspect of treating these neurological chronic cough conditions. This is a snapshot of our phase II A IPF cough data, which was the first cough data we reported out. This was a couple of years ago now. I think you'll see remarkable consistency with the RCC data we just reported. The upper left is the mean change, which is the primary endpoint here using a VitaloJAK cough counter. You can see 75% reduction with our drug, 23% placebo for a very large placebo-adjusted change. The bottom left shows you we also had a very rapid onset of effect. This is a patient-reported outcome about how frequently they cough. You can see it not only mirrors the cough monitor, but is happening quite quickly across the dose range, which you can see across the bottom here. We did force titrate people up across our entire dose range in this trial. You'll see when I show you this study design for the II B, we're just finishing up, we did drop this high dose. We didn't appear we needed it. The upper right's a responder analysis in this 30% bucket, which is clinically meaningful. Every patient but one responded to this, which I think links back to the mechanism as well. Some of the KOLs have done work around cough bouts, linking that to damage in the lungs. You can see highly statistically significant as well. The efficacy data here was very strong. I didn't put the AE data here because I'm going to show it to you in RCC, and it's virtually the same table. I will get to sort of the other side of this coin. Right now, we're in the middle of our CORAL trial. It's 160 patients. It's a proper dose-ranging trial. As I mentioned, we dropped the high-dose arm. We have 27, 54, 108 versus placebo. Same primary endpoint of this VitaloJAK cough monitor, you can see in the bottom left. We had our last patient enrolled at the end of February, and we do expect to report top-line data in the second quarter. Excited about this. I would mention one more thing, and Serge, maybe you're going to ask me more about it, but we did do a sample size re-estimation at the 50% mark. That SSRE was positive and confirmed our initial powering assumptions. There was no upsize required. At least at the halfway point, we got some good assurances this trial was on track. This is the RCC study data that we just reported out in the first quarter. That call is probably still up on our website. It was a crossover design. You're going to see this data looks very similar to the IPF data I just showed you. Very large placebo-adjusted change, 57%, which is significant. We also had broken this out between moderate and severe coughers because a lot of the trials that had had success here had sorted out that they really only worked in the most severe coughers of greater than 20 per hour. We felt because of our central mechanism that wouldn't be the case with our drug, and indeed it wasn't. You can see here a nice consistent effect. Upper right, you can see again a really strong responder analysis here on this data. It's working essentially in a big way in a lot of people across all baseline cough counts. Importantly, the bottom right's a key finding here. We had a rapid onset of action. Our first measurement was day seven at the lowest dose. You can see it was already highly statistically significant. As we move forward, we're going to have to do a II B dose range study. Probably we'll need to bring in one lower dose and sort this out as we move forward. This is the AE chart from this study. You can see the typical AEs here tend to be GI and CNS side effects, so constipation, somnolence, dizziness, nausea. The important thing about the AEs in this trial, they tend to be more tolerability. They happen upon initiation of therapy, but after a few days, they dissipate and really go away. We just need to, we figured out ways to help the patient manage through that. The last slide, and then we'll go to Q&A, but chronic cough has a big unmet need and disease burden across both IPF and RCC. I think importantly, we are the first company that had positive results in both of those indications. We do have this upcoming, our lead indication in IPF will report out this quarter. We have a nice strong balance sheet, $108 million in cash and runway into the second half of 2026. We can talk more later about what that does and does not cover. That is just a snapshot of Trevi and happy to get into questions. Thanks, Jennifer. Great overview. Let's start with the RCC since it's so recent. I think heading into the RIVER trial readout, at least personally, I thought this had a good chance of reading out positively, but we just didn't know how large of an efficacy level we would see just given that this has been a difficult indication. Obviously, it was surprising to see Haduvio outperform what we saw in IPF cough. Just curious, you know, what kind of feedback you've gotten since then on the data? It's a good question. I'd be lying if I didn't say we weren't also surprised. We thought it would work, and we thought it'd work in a bigger, better way than what you'd seen out of these peripheral-only agents. I think we were surprised at how consistently it worked across cough counts and everything else. The KOLs have been interesting because we had always heard that IPF was a higher bar than RCC. RCC is an idiopathic type cough. IPF, you've got these diseased lungs that's progressive and getting worse. People had always said, "Look, if it works in IPF, it's going to work in RCC." We just didn't know exactly what that meant. I think KOLs now are thinking about treating this space as more of a hypersensitization disorder and that this central mechanism is truly important in treating these patients. I think it's been really important science for the field to look at sort of all the things that have failed peripherally and understand that this probably is more of a central mechanism. Have you had a chance to dig a little more into the data and some of the subsets and by dose? I am just curious if there is anything you can unveil now or we will have to wait until upcoming medical meetings. They did get it last week, Serge, and our MDs and Jim were going through it. None of that's trickled to Farrell or me yet, but I think at ATS, we're going to do an investor event. I'm going to try to share some of the key analysis people have been asking for. We will put it out. I haven't yet seen any of that, though. They're digging into it. Okay. We talked about, like you said, the IPF cough was seen more of a higher hurdle typically than RCC. Maybe just highlight the pathology of RCC and how it differs from IPF cough. Yep. Farrell, why don't you go ahead? Yeah. I'm Serge. Good to see you. You know, when you look at cough and refractory chronic cough, it's really thought to be this hypersensitivity, as Jennifer said, and it's really along this entire cough reflex arc. That could be thought of as different from IPF. IPF has these diseased fibrotic lungs that may or may not be sending signals from the lungs. It may be just centrally mediated. In RCC, there's definitely a central brain component, brainstem, cortical areas of the brain that are playing a role here. I think that really goes back to the differentiation within our mechanism and why we work across that entire cough reflex arc and maybe shown the rapid effect that we show, but also the broad and kind of magnitude of effect. Farrell, maybe as Chief Commercial Officer, I'm sure you have a good handle on what the market opportunity looks like in RCC. Just maybe highlight where it's at and the unmet needs that need to be addressed. Yeah, I mean, there's a large remaining unmet need within this category. Just to start off, there's no approved therapies in the U.S., right? This is something where off-label therapies are being used, and those carry a lot of baggage in different ways. When you look at where the development landscape is progressing, RCC is a category, I'd say, split in two. There are these high-frequency coughers, which we showed benefit in, as well as the P2X3s, but that only makes up about a quarter of the market. When you get into a clinical environment, physicians aren't going to put a cough monitor on people. It's going to be hard to really monitor these individuals and understand where they are in their baseline cough frequency. The other 50% of the market, or close to 50%, are these moderate-frequency coughers. That's where the P2X3s have not shown a benefit. When you look at the overall opportunity, you know, I'd say there's about 2-3 million RCC patients. About a third of those are seen by, call it a subset of specialists, those pulmonologists and allergists. We would be well-positioned after a P2X3 failures in these high-frequency coughers, which is about, call it 40-50% of those, and then really this moderate space where nothing has shown to work. It opens up the market, and we believe our addressable market is about 1 million patients in the United States. Like you said, their treatment paradigm is more or less not established here just because there's no approved product. What are physicians using to allay the symptoms? Some of the most common therapies, right, if you go back to what RCC is caused by in the primary underlying disease, asthma, gastroesophageal reflux disease, as well as upper airway cough syndrome or postnasal drip. They're using a lot of therapies to first control the underlying condition, inhaled corticosteroids, PPIs, right, the proton pump inhibitors to control the acid, antihistamines. When it gets down to this cough hypersensitivity disorder and it's refractory to those, you're seeing usage of Tessalon Perles. You're seeing usage of codeine and morphine in some situations. These therapies are kind of off-label therapies being used, but also some of those codeine, morphine can carry a schedule two, schedule three kind of scheduling with it, which carries a level of addiction as well. We talked about earlier that RCC has been a difficult indication. There's been a lot of development failures. Just curious if you think it's the mechanism of action or the clinical development approach that was taken that's at fault for these misses. I would say I think it's been both, Serge. I think the peripheral-only agents just make it very difficult to tease out this mean change. You have to be in this enriched group. You have to have enough patients that you can tease out a stat-sig trial. The placebo-adjusted change is always probably going to skate around right on the edge, which is what you saw with Merck. Ultimately, one of their trials fell out of stat-sig. You know, I think even the GSK program runs at risk to some extent. I think when you have a big efficacy effect, it certainly helps. I do think, though, there were unique things to learn from a clinical development perspective that both Merck and Bellus did a great service to this patient group about learning. One is making sure you get RCC patients in the study and that their underlying conditions, Farrell mentioned, are truly treated. If someone has active asthma, you're not going to be able to get rid of their cough if that's not appropriately treated. I think adjudicating sort of that diagnosis, making sure you're getting the right patients. The other thing that's plagued this space is a big placebo effect, which I do think is linked to getting the wrong patients in the study, but particularly Bellus built in this placebo run-in to get out any patients who had big placebo effects. I think both of those have been really helpful just to make sure that if you're seeing a drug effect, you're able to show it in the study and not get overwhelmed by the placebo response. Okay. Actually, we learned a lot from the River Trial in terms of potential dosing, the onset of the drug. Curious how you're thinking of those things as you start planning the next development step and whether that's another phase II or phase III trial. Yeah. It is a high-class problem. We have a huge effect at the lowest dose, right? There are development questions you still need to answer around that. I think the most important one is making sure you know what your dose range is. We will go into a phase II B dose ranging study. We will design that to look like a pivotal study. Because RCC is our second indication, this will be an sNDA for us. You are required to only have one pivotal study. We plan for this development program as a proper dose ranging study and one pivotal study. Now, whether you can consolidate that or have a quicker path through, those will be conversations we will have along the way. I think that the team is analyzing the data now, but we likely are going to have to find a dose lower than 27 milligrams b.i.d. Whether that's QD or a lower dose, they're sort of sorting through that, the 27 and the 54. I think probably 108 goes away. We are excited to see the coral data because that's a proper parallel arm design. Although different disease, I think we'll learn some things from that as well. Team's just going through all the data and sort of waiting on our coral results to figure out which doses we take into the II B. In that II B, what patient population do you plan on recruiting? I think Farrell mentioned kind of targeting the maybe P2X3 failures. How do you evaluate those types of patients in the phase II B? Yeah, probably by the time we start this II B, there won't be an approved P2X3. We won't be able to do that. We'll have a documented treatment failure. All of them have that. I mean, I think the average time to diagnosis of RCC is what, six to eight years, Farrell? They've all been through most of those sort of tier one therapies. We'll make sure and document there's been a treatment failure. The good news for us is we're done with this moderate versus severe conversation. This will be an all-comers trial. You'll have to have a minimum level of cough, which will be somewhere roughly 8-10. Other than that, we can just enroll this study and move forward because we didn't see any difference. I would say the population will look a lot like our II A study, you know, just a bigger overall population. Okay. Looking forward to ATS to see the additional data. Yep. Maybe, you know, as we transition to the IPF cough program, what you learned in the River Trial that gives you confidence for the IPF cough trial readout that we're going to see soon? I mean, my biggest source of comfort came not only from the II A data being so strong, but when we did the sample size re-estimation and confirmed the powering assumptions, because that's, you know, that's a hard thing to do in an area where nothing's worked. We didn't have a lot of information around placebo effect and what parallel arm design drug effects look like. I was always nervous about that. Confirming the fact that we had at least our 80% power or better for me was probably the most telling. I know we haven't changed anything in the second half of the patient group. Really, we should be able to replicate that. I think the RCC data is just icing on the cake. The data was so strong. There was nothing that was surprising there. I think it just probably gives us all more comfort that the mechanism is working where it needs to work. Yeah, I think we all left that feeling good about the readout. Every indication's different. Every trial's different. We never take it for granted, for sure. Sure. Maybe it's worth it to go over the design of the CORAL trial and give us a little overview of its powering and what we could expect for the readout that's, I think, expected in late Q2. Yep. We said second half Q2, so you're right. This is a parallel arm phase 2B dose ranging study. Important to note that the phase II A data I showed you as well in IPF as well as in RCC, those were both crossover designs. There's a lot of advantages of crossover designs, but they do minimize the placebo effect. You get rid of variability. You know, we've seen in the RCC world where companies have had a hard time going from that crossover design into parallel arm design. You know, it's an important step for us. I think we've got the three different doses, so hopefully we can sort out a dose through this. It's a little longer study. Our prior study was three weeks. This is two weeks of titration plus four weeks of fixed dosing. It's a lot bigger. It's 160 people versus the 40 we showed you in the phase II A trial. It's 10 countries, 60 sites, so a lot more sort of diversity. Now, our first study wasn't small. It was 14 different sites across a couple of countries. You know, but still, it is all scaling. I would say generally when you're sort of going through that, managing placebo effect can be more challenging. The helpful thing here is placebo has not been a major problem in IPF, I think, because people truly have disease long. It's not sort of that idiopathic response you're seeing in RCC, but we'll see. There has never been a phase II B or parallel arm design in IPF cough that's worked. It's a telling study for us. Okay. I think in the CANAL trial, if I remember correctly, you were slightly above a 50% placebo-adjusted cough reduction. Yep. Is that kind of the bar for this trial? And if, you know, what is clinically meaningful on that endpoint? There have been papers published that clinical meaningfulness here is 20-30%. We powered this study with a 36% placebo-adjusted change. That was a 66% drug effect, 30% placebo effect. It was at 80% power. Our sample size re-estimation we touched on confirmed that we were at 80% power halfway through the study. Presumably we are at that effect size or better. The information we did not get out of the SSRE is if we are running better than that. We did not get the option to make the trial smaller. We will wait and see. That was the powering assumptions here. I think importantly, you know, you were around, Serge. You were getting a lot of questions from investors in RCC. What does this need to look like to move it ahead? Because we did have someone ahead of us in GSK. We had sort of laid out some parameters for ourselves. I think the difference in IPF is there is nothing here. All these patients have are these antifibrotics, which have not translated into day-to-day benefit for the patient. If this trial's positive, we are moving forward. I think anytime you're affecting that hypersensitization and giving these patients a better quality of life, it's meaningful here. Unlike RCC, where I think we had our eye on competition, this feels wide open for us and also a desperate end-of-life patient group. Okay. As you mentioned, the SSRE took place last December. We thought it was a significant de-risking event for this trial, but just curious your takeaway from that exercise. You mentioned recruiting a smaller patient number was not an option, but it sounds like it could have been a potential one if it had not been an option. Yeah. I mean, I was very happy. I had joked, the only thing I want from Santa is a positive SSRE because, you know, these patients are hard to find. It's a rare condition. If you have to upsize by 100 patients, that's no small task here. Internally, I think we were all very happy that, you know, our drug seems to be performing well in this parallel arm design. Yeah. It was a great holiday gift to get here, I think, feeling positive about moving forward and that the drug's behaving as we thought it would. Okay. As you start thinking about a potential phase III program, the next step here for IPF cough and the results you got from RCC, I mean, how do you start thinking about what that trial could look like in terms of the doses being evaluated for IPF cough? Yeah. So we're hoping that this trial's positive. We'll be able to select our doses from this study. Then we would look to do an end-of-phase two meeting with the FDA, hopefully by year-end. We all know what's going on at the agency. So, you know, we'll have to sort of play along with their timelines. We are already internally preparing for two pivotal studies that we intend to run largely in parallel, probably a little bit of a staggered start. The nice thing is those studies aren't much bigger than what we're running now because we'll probably drop at least one dose. So it's probably roughly 150-200 patients per study. We just ran that. We recruited it in a year. We'll double our number of sites and hopefully go run these in parallel. The primary endpoint will be the same. We'll probably have an efficacy read at the three-month mark, you know, which you need for chronic dosing. Fortunately, here, there's been a lot of work done in IPF and refractory chronic cough, so we can pull from the agency's guidance here and be pretty clear about what our pivotal program's going to look like. The one thing here, we will need one-year safety data. We've got a lot of safety data on our drug because we've been studying it for 10 years. It's been in over 1,000 people, but we're going to need one-year data in the IPF patients. We are assuming roughly a year to recruit and then a year to get to the long-term safety data. We hope that's it. We hope that's the rest of our program. Okay. I know in the past you've talked about since the Haduvio was delivering such a large placebo-adjusted reduction in cough, there was potential to impact disease progression or the overall pathology. You know, how would you measure that? Is that something that would be observed within three months in a phase 3 trial, or you'd have to go much longer to see anything of that kind of impact? Yeah. There's been speculation here. This isn't just Trevi speculating, and Farrell can probably give more of the color on it. There's been, Farrell, you want to comment on the paper written and how it links to disease, and then I can talk about our plans. Yeah. There is a large registry database out of the U.S., approximately 1,500 patients, that just showed a worsening cough leads to worse health outcomes. By that meaning, worse respiratory hospitalizations, mortality, and transplant risk. To supplement that, right, mechanistically, how would that even be linked? Just the stress on the lungs. We had somebody in our IPF trial cough 1,500 times in a day. We had someone in our RCC trial actually cough 3,500 times in a day. IPF specifically, when you look at the stretch fibers, the increased stress there has led to increases in TGF-β, and TGF-β we know is a known marker. We do not expect to see that in a short trial like what we have in a phase II B, but we can monitor that. It really doesn't change many of the commercial dynamics that we look at and the ability to help these patients in need. I think, Serge, just to follow on where you were heading, our primary endpoint's going to be cough because that's a tried-and-true path. We don't want to reinvent the regulatory pathway. I think we will, though, look at hospitalizations and FVC, which is the endpoint that's being used in antifibrotic trials, exacerbations, things like that. You know, whether three months is long enough is a good question, but because we have to do one-year safety trials, we will probably do some kind of efficacy read at the end of that year just to try to see how things have progressed. That's certainly long enough to try to document some of these factors. Okay. Farrell, maybe just highlight what the market obviously looks like in IPF cough, just some numbers around the opportunity. Yeah. So right now, you know, the IPF market as a whole is about 150,000 patients in the U.S. You know, from our own research, we know about two-thirds of those have uncontrolled chronic cough requiring additional treatment, meaning they've probably failed other therapies and they're still not controlled. So that brings you about 100,000 patient population within the U.S. We've recently dug in a little bit more and looked at this is a growing market. We have 150,000 patients today, but by the time we get to launch, this could be a market of close to 200,000 patients. It is growing. These additional antifibrotics are just going to prolong, right, that life of these patients in need. I think really help grow this market. This is a large opportunity, and it's very focused in terms of supporting it from a commercial standpoint. Eighty-eight centers of excellence here in the U.S., pulmonologist call point, which is a small specialty, enables us to really cover this as a, you know, a small biotech company. These are patients that have no treatment options to address the cough. They're simply on antifibrotics, and those normally have an impact on cough? No, there have been multiple studies of antifibrotics, you know, and none of them have supported, you know, many, not even on a subjective basis, have supported a benefit of cough. None of them have been run objectively on whether or not it changes the cough in these patients. They continue, even those on antifibrotics, to search. They have a high unmet need for additional therapies. Looking forward to seeing that data coming soon. Now that you've shown solid proof of concept in both RCC and IPF cough, can we start thinking of Haduvio as having a broad cough role? How does that influence the development path for this program going forward? Yeah. This is something, Serge, we've been thinking deep about. I think, first of all, just to kind of frame this world, we are focused on cough that's neurological cough. We do not want to get involved in any kind of productive cough of clearing the lungs. That would obviously be a problem. Fortunately, there's a lot of conditions that have neurological cough associated with them. Because we're a small company, though, we've decided we're really going to put down three legs of the stool here. The lead indication, as Farrell mentioned, is our IPF chronic cough program. IPF is about half of an interstitial lung disease market. This other half, all these other ILDs, and Farrell, there's what, like 150 of them or some crazy number, about 60-70% of those diseases have this neurological cough going on. In the antifibrotic world, there's sort of a path here where you can run one phase 3 basket trial and add that onto your label. That gives us an ability to double that market. As a matter of fact, with a positive IPF trial, we're hoping to announce that we're going to try to start that phase II A and these other basket indications later this year so that we can get data out next year and tie that together. Those are each, I mean, $1 billion-$3 billion opportunities, each of those. Very big opportunities. You take RCC, as Farrell mentioned, and even playing in this most refractory space, that's up to, you know, 1 million patients. Also several billion dollar opportunities. We're going to stay home. We're not going to keep wandering and pursuing other things. We're going to try to drive these three across the finish line. Big unmet needs, a lot of opportunity here. Would these phase II A take the form of the similar crossover trial design that you've used in the past and been successful with? Yeah. We're doing some work. What we're trying to learn there, IPF is that there's a clear diagnosis of IPF. You can do a chest X-ray. These ILDs have a whole lot of different things going on. Some of them have productive cough. Some of them have neurological cough. Farrell's working with our Chief Development Officer, Jim, to try to identify sort of inclusion-exclusion criteria, if you will, of who's appropriate for this study. I think that'll be what we learn through this. Is there anything unique about this group? Interestingly, we got several comments back from the KOLs or the investigators running our IPF trial saying, "You guys should run an ILD trial. It's the same cough. It'd be easy to enroll." From our perspective, it's the same centers, same investigators. They either have IPF or they have ILDs with cough. Which trial you're in. So it's a very easy add-on for us operationally. Okay. That's great. On the human abuse liability study, you reported results last fall. Just curious, what changes now that we've seen additional data from the RIVER trial and, like you said earlier, efficacy at the lowest dose? Does that change anything regarding the next steps with FDA? I mean, low dose has always helped the risk-benefit equation, right? It is always a good thing. I would say just for people maybe listening that are not as attuned to this issue, our drug now, Haduvio, is broadly in the opioid class, but it is in a subcategory of what is called mixed agonist antagonist. It actually blocks the mu receptor and agonizes at kappa. Because of that, the drug has been unscheduled for decades. Unless we learn something new here that raised red flags, this drug is probably not getting scheduled. DEA actually just looked at it again three weeks ago and left it unscheduled. That is all really helpful. Serge is right. We reported out results on our human abuse potential study, which is just bringing it up to current-day standards, which is why we had to do that. In the clinical doses we're working in, we statistically, highly statistically separated from the comparator, which is all helpful. If you remember, Serge, there's this guidance that you have to study 3X your marketed dose. 3X, call it the 54, which looks like it would be the highest doses within those first couple of doses. I think there's a lot of reasons all this data plays into our favor, but we'll put that together and discuss it all with the agency. We're feeling good about it. Okay. Maybe you can just give us an overview of the IP around Haduvio. Yeah. So old molecules, so no composition of matter, which, you know, I'm one of the two co-founders of the company. I think the first dollar we spent was with a patent attorney to start working on patenting. The core of the IP is our method of treatment patent. So the indication with our drug, we have an issued patent in IPF that goes to 2039, and we're in late stages of hopefully getting our RCC patent under the same description. So feel good about that IP. It's broad claims, covers a lot of ground. Somebody would have to come in and invalidate that, which is not easy to do because there wasn't work being done here. There are some formulation patents. Those start to expire on the earlier end, 2029. We're also, as we complete our clinical development, filing IP around basically things in the label, how you dose in the elderly, how you dose in hepatically impaired patients. We just had a patent issue in the last month in the hepatic impaired patient population that extends those patents to 2041. We'll continue to do that as we complete the development work. I think we'll end up with this method of treatment with these other sort of dosing and label things around it. On financials, I think a topic that's becoming increasingly relevant given our current markets, but can you just give us a picture of the cash balance and runway? Yeah. Fortunately, we have a strong balance sheet. Your bankers advised us well, Serge. In December, we took a bit of money off the table, which put us in a strong position of not wanting or needing to raise money off the positive RCC data, which was great. We have $108 million on the balance sheet at December 31. We have guided that that takes us into the second half of 2026. To be clear what that covers and does not cover. It covers all the work we are finishing now, the phase II B. It will cover the next RCC trial. What it will not cover is the full both phase threes for IPF. We can get started, but it will not get us all the way through. Somewhere around the IPF program, we will need to raise money again. We're still working the numbers, but we estimate each of those trials is roughly $40 million-$45 million each. You know, very doable for us. All right. To wrap up, anything you feel is still misunderstood or underappreciated about Haduvio or the overall Trevi story? I would say, and Farrell, I want you to give your views as well. I would say people get too hung up in the opioid thing. You know, they hear the word and they think they don't even understand it. They just assume all opioids are the same. It's just not true. DEA certainly understands that. It's why they've left it unscheduled. I think the strength of this story and this compound is in the fact that it's the opioid mechanism, which is very active in the body, and they've had great efficacy. I think people should spend the time to understand that piece of the story because it's not as scary as it sounds. Farrell, anything you'd add? I think the only commercial piece that we commonly get asked is the transition from IPF into RCC and how we make that work commercially. You know, IPF will be our lead indication. We recently did market research and tested, you know, WAC price points of list prices of $60,000-$80,000 per year, which was favorable. It's very inelastic pricing, especially at the efficacy levels that we're showing in these trials. Making that transition, going to RCC and later call it treatment failure patients within RCC, taking the restrictions from payers, whether that be prior authorization of label, whether that be reauthorization, those will enable us to maintain the IPF/ILD specialty pricing, right, and be able to access that market in a meaningful way, not only just helping patients, but helping build the value of the company. Thank you for your time. I think we've seen some exciting data over the last few months, and it sounds like we're set up to see more in the coming months. Exciting times for Trevi. Thanks. Thank you for your participation. Thank you, Serge. Thanks, Serge.