All right. Good afternoon, everyone. Thanks for being here. We are very excited to have Jennifer and James from Trevi here with us for this session of the Morgan Stanley Global Healthcare Conference. I am just going to get through a quick disclosure. For important disclosures, please visit www.morganstanley.com/researchdisclosures. With any questions, contact your institutional salesperson. I am Judah Frommer, one of the mid-biotech analysts here, and like I said, we are very excited to have Trevi with us for this session. Maybe we will start off, it has been a year of significant progress for Trevi. Before we dive in, maybe give the audience an intro to the company and your chronic cough programs from a high level. Sure. First of all, thank you for having us. We appreciate it, and thank you for those of you that have hung around till the end of the day to hear us. Trevi is a simple story. We are a single-asset company focused in chronic cough indications. Three indications, idiopathic pulmonary fibrosis cough, other interstitial lung disease cough, and refractory chronic cough. There has been a lot of sort of movement on the competitive landscape around that. We have aligned with the FDA on our path forward and our lead indication of IPF cough. We have started those trials. We can get into more detail. We are in phase III, looking for a lot of data to start reading out some later this year and then second half of next year. It has been an exciting time to be in it. I am joined by Jim Casella, who is our Chief Development Officer, so he has had a very busy summer sort of getting all this off the ground. Great. Before we jump into the asset, maybe let us start with unmet need in chronic cough. Get us situated on the epidemiology, how patients are managed currently, and what the potential opportunity is here for Trevi. Yeah. Chronic cough has been an area that Big Pharma has been interested in for a while. Very big market. Just to orient you, just to kind of take each of the slices, idiopathic pulmonary fibrosis has a prevalence of about 140,000. 85% of them have cough. Two-thirds of them have uncontrolled cough. You can think about 100,000 patients. It is one of the number one complaints of these patients. We all know there has been a lot of work in IPF. Those are antifibrotics, slowing down disease. I think what our program brings to these patients is actually helping to manage their quality of life and day-to-day living. The other interstitial lung diseases, IPF is an interstitial lung disease, it is about half that market. You essentially double that whole opportunity. A lot of leverage in that market overall, with probably an additional clinical trial. Refractory chronic cough is a very big opportunity. That is sort of 2 million to 3 million patients. A little bit blows up the specialty model we are in. The reality is, there has been, I think, 20 drugs tried in RCC, all of which have failed, and we should probably talk a little bit about why we think we are different. We are approaching that market. We are not going to change our specialty sort of focus there. We are going to go after the most refractory patients and maintain our pricing there. Each of these indications is quite large, and as I mentioned up front, we are alone left in these cough indications, so really exciting commercially. Final point on that is, maybe you are going to get to this later, but respiratory has been an area very manageable commercial-wise by biotech. We are excited about the situation we are in. Okay, great. We will get into refractory chronic cough specifically, but maybe just starting with some history around nalbuphine. How is it differentiated from other cough mechanisms that have been explored? Yeah, that's sort of the crux. When we got into this space, there was probably 20 programs going on, and most of the programs were dealing with cough through peripheral mechanisms in the lung, which sort of makes intuitive sense. I'm one of the two co-founders of the company, and my co-founder's a neurologist, and he had been sort of kvetching at me for a while that neurological cough is not a lung problem, it's a brain problem. It's a response to, if you think about IPF, it's essentially fibrosis of the lungs, and your brain's sending this signal acknowledging this fibrosis. Tom was convinced that whatever drug you treated this with, it had to be neurologically active. What's interesting about our mechanism, we work peripherally in the lung, but we also work centrally in the brain, so along that whole cough reflex arc. I think as our data's rolled out, it's had a very big effect in almost everyone who's come on early. I think over time, these other mechanisms have failed. We're sort of left, and I think what we all take away from that is managing cough centrally is important. Okay. I guess within the context of opioids, how does abuse potential compare to other opioids? How well has that been characterized? We'll get a question out of the way up front that typically we'd save till later, but potential for scheduling risk in your mind. Yeah. I'll touch on it. Jim, you add any color. I know you're going to get into a lot of trials, so. Yeah You will be chatting away for a while. Nalbuphine is an opioid, but as I like to explain to people, not all opioids are the same. There are four opioid receptors. When people hear the word opioid, they think of morphine, fentanyl. Those are all mu agonists. There is a class of drugs that are called mixed agonist-antagonists that were designed to get away from drug addiction. Our drug, nalbuphine, actually blocks that mu receptor and works at kappa. The experiment we were running is kappa helpful? That is kind of where we started off. The drug has been around as a subcutaneous injection for decades, so it has been unscheduled. We had to do some work. We did some human abuse potential work. We have done some respiratory depression work. All of that has been clean. We believe this drug is going to stay unscheduled. We picked this drug intentionally, because we thought we could get away from a lot of the baggage that has plagued opioids. Okay. Great. You mentioned that it is an older drug. Just on patents and IP more generally. You have been proactive on patent strategy. Maybe talk a bit about the protection for Haduvio. Is there anything we should be looking out for on this front going forward as well? Yeah. It is an old drug, so no composition of matter. We have method of use patent issued that is quite broad in our IPF cough program. Basically covers chronic cough and IPF with nalbuphine, so broad claims. We have spent a lot of time and energy in the company over the last sort of year filing additional claims around the label. A lot of clinical work that has been done. We will continue to expand that. Issued patent goes through 2039, so we will have a good 10 years of protection. What we are now trying to do is build around the label and extend that out to 2046, 2047. A lot of room to move here. There had not been a lot of work done in cough. There was a lot of unknowns, so we feel we have got a lot of opportunity to patent. Okay, great. Maybe just transitioning to your lead indication, like you said, IPF-related chronic cough. At a high level, maybe help summarize the data we've seen thus far, safety and efficacy from the phase II studies. Maybe loop in you had a presence at ERS recently, so what were key takeaways there as well? I can. Sure. We have good experience with our IPF population. We have run two studies to date that were enabling us to start the phase III program. The first was a crossover study of the CANAL study. We learned a lot from that study. We did some dose ranging. The real important study that we ran was the CORAL study, which we reported out. This was a parallel arm study. We did some dose exploration in there. We were able to really determine our effect size. We were able to figure out the best optimal dose to bring forward. What that did for us is we picked a 54 milligram twice-daily dose. We brought that to the FDA, had a discussion with them about our dose ranging, about the efficacy that we saw there. In our CORAL study, we did see about a 36% differential from the placebo control arm. We saw optimal dosing there. We had a 108 milligram twice-daily dose that was also included in that trial, but the 54 milligram dose was really the sweet spot dose. We saw really the optimal efficacy. We saw no additional benefit from the 108 dose, so it was easy to make the decision to bring that forward. I think on the safety side, what we saw was a very well-behaved and well-characterized safety profile that we have seen throughout our cough program, but also with the history of the drug that existed before we even got into the cough space. We see typically CNS and GI-type side effects. These are typically transient. These are typically mild in severity, and I think that was the package that we brought to the FDA to get us to the End of phase II meeting and into the phase III program. Okay, great. Maybe just getting into the phase III, maybe let's talk a bit about design of these studies, and you've initiated the first study. Any update on status of the second study as well? The design really follows from the CORAL study. That was a really important study on a number of different dimensions, but it had a two-week titration period and a four weeks fixed dose period. So what we brought forward was the 54 milligram dose versus placebo. Now we're looking at a longer duration trial with the same primary endpoint, which is 24-hour objective cough monitoring. We did exploration and confirmation of PRO data from the CORAL study. We brought that into the phase III program. The End of phase II meeting was a really great meeting for us in that we got agreement with the FDA that we were looking at our primary endpoint the same as what we saw in the CORAL study and the secondary endpoints that we wanted to bring forward. On the PRO side, they agreed that those were important endpoints to bring forward. The differentiation now is really where we see the duration of the trial, what the FDA is looking for in terms of long-term safety, and what they're looking for in terms of showing durability of effect in terms of efficacy. With that, we are running as our OCEAN-1 study, our long duration study, 52 weeks of placebo-controlled safety data with our primary efficacy endpoint at 24 weeks of fixed dosing. So with a two-week titration, then 24 weeks of fixed dosing. So that's where we'll get our primary efficacy read with 52 weeks of long safety data. Our OCEAN-2 trial, just to sort of fill in what we came out of the End of phase II meeting with, is really a confirmatory on the efficacy endpoint where the FDA was not as strict in terms of looking at the duration of the trial. We came to agreement that a 12-week primary efficacy endpoint for the OCEAN-2 trial would be sufficient for showing confirmation of the effect on cough, and we're powering that trial for our primary efficacy endpoint as well as our key secondary endpoint. The OCEAN-1 trial, which is the longer duration trial, we have a number of key secondary endpoints, and we're powered. That's a 300-patient trial. We're powered for all the key secondary endpoints. With OCEAN-2, the shorter duration trial, we are powered for the key secondary and the primary endpoint. That's a 200-patient trial. Okay. That comprises the bulk of the data we need for efficacy and long-term safety. And timing, Judah, you asked about. OCEAN-1's running. OCEAN-2 will start this quarter. Yeah. Okay. So. Great. Then maybe just back to dosing in the phase III. Like you said, you tested the 108 in phase II. I guess maybe just a little more detail on the 54 mg dose selection. What did you see at 108 that convinced you that 54 is the right dose, or was 54 just good enough? What we saw was a modest increase in the effect on cough frequency through the cough monitor with the 108 dose. But as we looked at very important parameters on the patient-reported outcome side, the secondary endpoints, when we looked at things like patient-reported cough severity, patient-reported cough frequency, we saw no added benefit with the 108 dose. Just in terms of risk benefit, we saw the highest benefit really when you look at all the data together with the 54 milligram dose, with no added benefit from the 108. Right. Okay, great. Then maybe just a little more color on the titration strategy for the phase III. You've characterized the AEs with the Haduvio as being early, transient, mostly mild. So what have you learned from prior studies that helped you to optimize the titration here? We did a really careful analysis of the adverse events that occurred both in our RIVER program in the RCC space and also in the IPF space. And one of the things that is true across both patient populations is that we have the very similar type of adverse events, CNS and GI in nature. And what we see is in those two very different populations- we see the same type of adverse event profile. Right. But importantly, what we see in the analysis of when do those adverse events come on, they come on early. They come on with the initial dosing, with in titration, the 27 milligram dose trend. We also see a very similar duration of the adverse events with the CNS and GI, slightly varying between some of the specific adverse events of interest. So what we saw there was a characteristic sort of shorter duration, usually coming on with the onset of dosing. So what we did for the p hase III program in IPF is we increased our titration period, where we look at QD dosing with the 27 milligram dose. We did that before, and we started off with that in the CORAL study. But instead of a couple of days, we made it a week of QD dosing. The idea there being that maybe we can mitigate some of these adverse events of CNS and even some of the nausea and potentially vomiting. With nighttime QD dosing for one week Yeah we mitigate those, and then we go into a 27 BID for another week. So that came out of our analysis of the onset of the adverse events and sort of the nature of the duration of these things. We think the titration is going to be very useful in mitigating some of the effects that we saw even in CORAL, some of the effects that we saw in RIVER, where we can maybe get rid of some of those effects while the patients are sleeping. Okay, great. Like you said, OCEAN 1 evaluating the primary endpoint in 24 weeks and 12 weeks for OCEAN 2. The phase II-b, CORAL, you evaluated at four weeks of fixed dosing there. Talk to us a little bit about confidence that cough reductions you observed at that four-week time point will translate to longer time points. Any data with nalbuphine or the mechanism that kind of adds comfort on this? Yeah. I think there's two ways to look at that. We have data from our previous trials when we were looking in prurigo nodularis, where we had run a study that was a year long. In that, we saw full maintenance of effect, so no loss of the durability of the response. We have data with itch. There's previous data that was captured in pain. I think underlying these things that these are mechanisms or indications that have maybe a common underlying mechanism leads to this concept of sensitization. We have not seen empirical data that suggested that we would see any kind of loss of durability of response or tachyphylaxis in that time period. Also, I think there's a possibility that the mu antagonism that we have inherent with our pharmacology, different than the mu agonism that you see with the morphines and the fentanyls of the world. I think that switch from agonism to antagonism mechanistically can help prevent the tachyphylaxis that can occur at the receptor level as well. I think the empirical data with our itch studies tell us that there can be some confidence there. Of course, the data will be coming out of the OCEAN 1 study primarily, which is a longer study. We do not expect to see any kind of tachyphylaxis. Okay, that is helpful. Then maybe just touching on some operational aspects of the study. First, on the objective cough monitor that you are using. You have leveraged it in prior studies. There is some regulatory history with that device. So maybe for those who are not as familiar, give us a little bit on how the device works and how it was validated. We can thank Merck for a lot of the heavy lifting on the validation of that. I mean, they learned the hard way that they needed to do a little bit more validation work with the gefapixant studies. They did all that work. I think Vitalograph, the company, benefited, and I think as an industry, we benefited from all the analysis and from the hard work that was put in there. So that set the stage for us where some things were learned during the whole Merck program. Now, in our case, we did work out an agreement with the FDA that once we did the CORAL study, as others have to do, there is a validation study that goes on after the fact. Actually, we reported out the results of our validation study when we had our investor day. What we showed there was that when you look at the compression algorithm that is used specifically for this system where they have human raters, and they actually score. It is a chest sensor which picks up acoustic signal, and there is also an audio monitor. They are scored. The raters can hear the cough, and they count them in a compressed algorithm. So we had to validate the algorithm from the uncompressed to the compressed. I think that was one of the initial issues. We showed that there was extremely high reliability going from the uncompressed to the compressed, and also the inter-rater reliability. These are people that are highly trained to listen for cough sounds and count them. We did inter-rater reliability with three different raters, and we had very, very high relationship, high correlations between each of the three raters. In the world of validation, we feel very comfortable that this was adequate and sufficient to satisfy the needs that we have in the IPF program. It further enhanced the validation that was done previously by other companies. We feel very comfortable. That's a very different kind of- experience now with Vitalograph system versus the early days when there were some issues around that. Okay. Some good background. Then maybe just talk about site selection for the phase III program a bit. How many of these sites do you have experience with, and how many have participated in other phase III programs? I think we had a great experience with our CORAL study. We have a lot of those sites that are still involved. The beauty of what we're doing here in the U.S. is that we're working with a lot of the specialty centers that are part of the Pulmonary Fibrosis Foundation network. There's 80 to 90 sites there. We have tapped into a vast majority of those sites between OCEAN-1 and OCEAN-2. That's where the bulk of ILD patients, IPF and non-IPF patients, go for their care. So we really are tapping into centers that have the patients, well-characterized patients, and a lot of those centers have cough experience. Okay, great. Maybe we should've done this earlier on, but maybe we characterize standard of care for IPF cough. There are some off-label treatments. There are no approved therapies. With that in mind, how do we think about clinically meaningful outcome on the primary endpoint in phase III? While we're there, maybe help us with assumptions around power. Yeah. That's a good question. We can Yeah tackle this a bit if you want, Jim. So standard of care, they try all the things you try when you have a long viral cold. Tessalon Perles, codeine cough syrup. They will try some gabapentin. None of it really works. It has been a frustrating aspect of the disease. There have been publications put out that 30% reduction in cough is clinically meaningful. We have also had patient boards where we have consistently heard, "Any level of cough reduction is helpful to me." I think the real answer here from our trial perspective is we did a lot of work about what is important to patients and their patient-reported outcomes, and frequency is definitely important, but cough severity is equally important to them, so how severe they cough. That is our key secondary endpoint. I think hitting our primary and reducing cough and then reducing cough severity is clearly clinically meaningful. As far as powering and happy just at a high level, we have assumed a 30% effect size on reduction in objective cough. In our phase IIb trial, we saw 36% reduction, so I think we have been appropriately conservative here. So we feel good about that. Okay, great. What would be supportive of a win or positive data with respect to the secondary endpoints? How important are those from a regulatory and commercial perspective? Obviously, it sounds like the PRO aspects are important. I will comment on commercial. You can comment. Yeah on regulatory. Jim mentioned our bigger OCEAN-1 study's powered down through seven endpoints. We really only probably need the primary and key secondary for regulatory approval. In those other secondaries, I mentioned to you that the antifibrotics really don't treat what bothers the patient day to day. Their complaints are cough, breathlessness, and fatigue. We are looking at different variants on that. We are looking at breathlessness. We hit that in our phase IIb. We are looking at responder analysis. We are looking at clinically meaningful change in cough severity. The hope would be that we can get a nice robust label coming out of that. That will set us up nicely for payer discussions. Regulatory wise, Jim, I will let you comment. Yeah, we had a great discussion at the End of phase II meeting on the patient-reported outcome, so cough severity, NRS, is our key secondary endpoint. FDA is very comfortable with significant change from baseline as being what's needed there for our approval. Okay or for a meaningful result. I think that's really the key here is that we have that. As Jen mentioned, we also have other PROs in our hierarchy there. The other PRO that is important is the patient perception of cough frequency. Besides the objective cough count, we also have the patient perception, and we saw positive results there as well in the CORAL study. One other dimension from a patient-reported perspective, which is also in our key secondary endpoint, is that patients reported that they had improved breathlessness. We know that that's a very important aspect of the patient journey here. FDA agreed that that would be a meaningful key secondary endpoint as well. Okay, great. I want to fast-forward to potential approval and commercialization, so maybe broad strategy for a launch. What segments or centers would you be focused on, and how would you describe ability to reach patients? Yeah. Our first indication, hopefully, to get approval will be IPF. As Jim mentioned, just like clinically, we're out in all these IPF/ILD care centers. There's 90 of them in the U.S., so we're working with all them clinically. That'll also be our target commercially. Beyond that, there's community pulmonologists who obviously write these scripts, too. About 10,000 targets there. With about 50 to 100 reps, you can very effectively target this population. The nice thing about the other ILDs, it's the exact same call point. There's just a lot of synergy you can get at this entire market, IPF and ILD, with that same 50 to 100 reps. Okay. RCC sort of changes that dynamic a bit. Okay, great. There is a good portion of the IPF population not treated with antifibrotics. Maybe talk about the potential strategy to reach those patients. Maybe they failed, maybe they're not on drug yet. It's somewhat Judah relevant to us. Yeah because what these IPF docs talk about is when a patient gets diagnosed with IPF, ILD, they'll treat their fibrosis with an antifibrotic. Many patients drop because there's a lot of side effects. Yeah. But they'll treat their cough. That's sort of a separate notion. Right. So I think sort of on an antifibrotic, not on an antifibrotic, we've already shown our drug works the same across all the different antifibrotics. So for us, we're all about treating cough for that patient. Okay, great. I know you talked about this at the analyst day, but we continue to get the question. I guess, cough being a side effect of some of these next-gen antifibrotics, how do you think about that in terms of the addressable population maybe changing or not? Yeah, no, it's a good question. I mean, specifically, you're referring to tapentadol. Which has had a cough problem. I think first of all, it's not approved now, so it won't be in our study. We've carved it out specifically in case there's any overlap. It'll probably be something at some point, either we'll run the experiment or investigators will. Yeah. Because we have heard from KOLs that can be difficult to keep patients on. There's some hypothesis that because our drug will settle down hypersensitivity, maybe they'll be able to tolerate the drug better. I think at the right time, when that drug gets out and into the market, we'll do some separate work around seeing if maybe it's helpful in that arena. Okay, great. From your market research and early discussions, what were initial thoughts on how payers see the potential value of Haduvio? How could that translate into pricing? Yeah. That's the nice thing about having IPF lead our strategy. It's a specialty strategy. Antifibrotics are priced quite high here, sort of $200,000 to 300,000. It's because it's a rare population, 140,000, and it's terminal. Most of them live three to five years. The reality is payers are pretty clear it's a category they do not particularly manage. We price tested off of our phase II data, $75,000 to 125,000 a year. Got really no pushback. There will be some step edits in there, just like there are Yeah for antifibrotics. You will manage it through a hub model. But I think we have a lot of room to move there on pricing. Okay, great. I want to make sure we touch on the other indications. Like you said, other ILDs beyond IPF. Maybe just talk about the biologic rationale in those patients, how similar or different is the chronic cough in those other ILDs? Yeah. We've had a lot of discussions with the KOL pulmonologists in this space, and basically the conclusion was that it's the underlying lung fibrosis that seems to be driving the cough. The difference between the populations is IPF is a little bit more pure as a respiratory disease. Yeah. The other part of the population has other comorbidities associated with it. But the underlying assumption, which makes the trial relatively straightforward, is that you have underlying lung fibrosis, and that has been the underlying cause for the cough, and that's how we're going to treat the population. We'll be looking at that and not really slicing and dicing beyond that. Okay, makes sense. You have an upcoming meeting with FDA. Maybe just talk to us a bit about key questions you'll be discussing with FDA in terms of phase IIb/III design at your upcoming meeting. I think the key there is we're going to be talking about a protocol. We're going to try to be as aggressive as possible. We'll discuss the options of that 2/3 or push it harder to see if we can get away with a single phase III, relying on the information that we generated with IPF and the discussions we've had with them. I think the nature of the trial design, the one trial, the duration, the endpoints are all going to be aligned with the IPF program. Obviously there's going to be difference in the inclusion criteria, but not much in terms of we're going to rely on the fibrosis and cough. I think that's part of it and probably the bulk of it. We also need to talk about what is the path to approval here. This is going to be on top of and following the IPF lead. Right. These are nicely synergistic. We can gain a lot of information on safety and efficacy from IPF that will directly feed into this. What's it going to take to get approval here in terms of the size of the safety database and other things that are related to the approvability? That's really the focus of it. Okay, great. We'll look forward to it. Like you referenced upfront, RCC, very large opportunity. We saw GSK's program fail recently, making you certainly the leading program within chronic cough. Any potential read-throughs from the failure for your program with potentially having the first FDA-approved therapy in your hands? Has your thinking on commercial strategy changed at all given that failure? Yeah, no, it's a good question. It's a huge opportunity. We're sort of the only ones left here. It's hard to tell if there's read-through because GSK really hasn't put out the data yet. Yeah. We have sort of confirmed through investigator channels that placebo wasn't an issue. Which I think is important for us. That was really the only piece of data that would have probably sort of we would've had to think twice about. Commercially, I would say that that doesn't impact our strategy because we're going to be this IPF specialty led. Yeah company. The only caveat to that is Jim's going to be doing some formal dose ranging. Depending on where this dose ends up, there is a world where we end up in much lower doses in RCC, and that's a hypothesis. Yeah. That's what we'll sort out in this next study. If we can end up in a low enough dose range, then we might have room to price per milligram and be able to maybe sort of get this therapy to a broader set of patients in RCC. Okay. No, I would say nothing there. I think both Merck, to what Jim said, and GSK/AstraZeneca, they left behind good learning. Yeah. We're sort of in that great fast follower mode where you get to not make all the same mistakes and hopefully get it over the finish line. Okay, great. Maybe just a couple on your RCC trial. You initiated the phase IIb there. Maybe just remind us of study design. Does the philosophy for trial design in RCC differ in any meaningful way from IPF? A key question we get on this program, just that sample size re-estimation that's expected in the fourth quarter, just maybe walk us through that quickly. Sure. The trial design, you remember the RIVER study, which led us here, was a crossover design, which is very common for that first study. This is really CORAL. Yeah. This is our parallel arm study. Jen mentioned that we have three different active arms and placebo. We have a two-week titration period and a four-week fixed doses. That's where we are. That's very similar to what we had with CORAL. In the RCC world, coming in prior, obviously, to the GSK news, there was this concern about how to manage placebo response. Maybe that still is a concern. One of the things we learned from the KOLs is that it's important to put in some very important guardrails. We have RCC that has to be diagnosed for a year for the patient. We're really watching carefully over the inclusion criteria for making sure we have the right RCC patient. Also, one of the strategies that was proposed and actually used in the BELLA/GSK design was a placebo run-in period. We incorporated a placebo run-in period. This is really to mitigate individuals who may have a more variable cough where they fall out. We have an entry criteria of 10 coughs per hour. We will look at that at screening for eligibility and make sure that they still are above that at the end of the placebo run-in period. Those are the things that we are trying to do. Maybe that was effective if we learn more about the actual GSK data. But those are the things that the KOLs were really guiding us towards as we brought that program forward. The sample size- Yeah. Are you going to go there? Yeah. Sorry, I thought you were. You were welcome. No, we get that question all the time, too. Yeah. Essentially, we use it to make sure we can dial in the N. We made certain assumptions. We assumed a 30% effect size. Again, we saw 56% in our IIa, we saw 36% in IPF. Yep. We think we've been appropriately conservative. That's 100 patients, 25 per arm. We do allow when half the patients finish dosing, an unblinded statistician outside of Trevi rechecks our powering assumptions, and we get one of three answers back. Either your powering assumptions are fine, continue on. Yep. We're in this conditional power range where there might be a relative upsize here, which could go up to an additional 50 patients. That's just about dialing in the N, or you're below this 40% power rate, and we've deemed that futile for our experiment. Right. It's a really good look halfway through the study to make sure. In the olden days, we used to overpower all these studies and not worry about missing it by a few patients. Right. Now you can use some of these statistical tools Yeah to sort of dial in on that. Okay, great. Maybe just to round out the discussion, remind us of cash runway, what that covers within the operations that we've discussed today. Yeah. We have $306 million as of the last balance sheet date. We had a nice raise in April, thanks to our Morgan Stanley bankers. We are sitting in good shape. That will get us through an IPF approval. It will get us through all of our ILD work, that is good. It will get us through this RCC study we are talking about. It does not fund the phase III trial in RCC. We will have to sort out what that looks like. It funds pre-commercial work, but does not fund any kind of commercial launch. We guide into early 2030, but it gets us through all these data readouts. Okay, great with that. We are just about out of time. Thank you again for being here, guys. This was great. Thank you. Thanks. Great.