All right, welcome, everyone. Let's go ahead and get started. This is a fireside chat with Ventyx Biosciences. Thank you all for joining. My name is Vikram Purohit. I'm one of the biotech analysts with the research team. I need to read a brief disclosure statement before we get started. For important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. With that, happy to join the discussion with Raju Mohan, CEO, and Mark Forman, CMO of Ventyx. Thank you both for joining us. Yeah, thank you. Thank you. Before we get into pipeline specifics, Raju, do you want to just recap for us kind of where Ventyx is right now, kind of in its pipeline journey, and what some of the key, key inflection points you think have been this year, and where you're headed over the coming, call it, twelve months or so? Yeah, thank you. Thanks, Vikram, and thanks for having us here. I think as a company and as a pipeline, we've evolved. You know, some people use words like morphed or pivoted. I think it's more a growth of the company. In some way, the growth takes you back to an earlier stage. We always have growth as being vertical, but in our case, we were an immunology company, primarily, in the world of, you know. On the view of the world, we were a TYK2 company, right? With an S1P1 portfolio and a NLRP3 portfolio. The microscope was on TYK2 a couple of years ago, as were other companies that, you know, you were tracking and the investors were tracking. We, at the end of last year, we had both of our trials in phase II, S1P1 for UC readout first, and then we had the TYK2 program for psoriasis readout. I want to first commend the team because both trials were flawlessly executed. Both trials met their primary endpoints. In the case of psoriasis, we just felt the data were not competitive, and, you know, we can talk about why we think that happened. The data were not competitive with other TYK2 compounds, especially deucravacitinib and the Takeda molecule, and we decided to stop the trial. We did continue on the Crohn's trial, and I'll talk about that, but the other readout was S1P1, and there we met both endpoints, and data were extremely competitive, probably best in class and best in therapy. You know, there, because stage of the compound and way the UC field has evolved, we've decided to find a partner to take it on to phase III, as opposed to us going to phase III, which was the intent with the psoriasis molecule. Besides the fact that there's always discussion with parties, but at least we were committing to do a phase III trial there. The company has now evolved from those two trials and an immunology company based on TYK2 and S1P1 to what I would call a broader immunology company. I would say also a CNS immunology company and a biology shifting from TYK2 pathway, which was really an IL-23 oral path, to now a novel oral small molecule that is going after the IL-1 path, in particular IL-1 beta path, right? That's sort of the evolution of the company. I think we have the best compounds in NLRP3. For us, NLRP3 has grown in its interest across. You know, when I started the when we started the company on NLRP3, people used to confuse it with NPR. Literally, they would say, you know, "NPR," and I'd say, "That's a different, different entity." It's really evolved, and you can see the buzz around IL-1 beta. You see the buzz around cardiovascular effects of this drug. That's the evolution of the portfolio. The company view evolved. You know, obviously, we have a new CMO, in Mark Forman. Strong, strong translational background, strong background in neurology, neuroinflammation, neurodegeneration. We've added a chief operating officer. We've got a whole new energy to the company, because we now have a different platform, and I would say, in fairness, it is the NLRP3 platform that we are now exploring, and we can talk about where this has taken us, but that's where we are as a company. Got it. That's helpful. I do want to spend a good amount of time on the NLRP3 portfolio, but just before we go there, I did want to touch on VTX-002. You mentioned that you're interested in finding a partner there. Just taking a step back, though, from the phase II data you've seen and reported so far, what were some of the key slivers of the data set that kind of gave you conviction that this is a differentiated asset within the- Yeah, absolutely. Safety is, is, you know, people sort of don't minimize that, but in this case, you know, our, our compound was designed to be a non-brain penetrant compound. Also, we have a titration regimen in, by which we mitigate the class effect of cardiovascular activity, be it on the bradycardia side or on AV block, which is the conductance side, right? By doing that, we have literally no concern with any significant changes in heart rate or, or any, any chance of a, of a AV block. This allowed us to dose higher because we didn't have a ceiling because of the cardiovascular, which is exactly which is where Arena, Pfizer now and Receptos, BMS were. They couldn't dose higher, they were boxed in. Able to dose higher, get deeper penetration of the drug through the lymphocyte lowering, and what we showed on objective endpoint, which is really what physicians and clinicians want, is the response on endoscopic remission. Right? And we had a close to 20%, I think it was 27%, if I'm right, placebo-adjusted. Actually, it was 22% placebo-adjusted endoscopic remission, which is unmatched with an ES of zero, so endoscopic score of zero, right? Which is complete healing in the mucosa, unmatched by any other drug out there other than Rinvoq, right? Which is a JAK inhibitor from AbbVie, and we know the issues with that molecule. Not even S1P1, I'm talking about the entire class of compounds, the TL1As, the alpha-4 beta-7s, the IL-23s, the JAK inhibitors unmatched there, right? That's the thesis we have now and what we saw in the induction phase. We hope to see that when the entire analysis is done of the fifty-two weeks, because with S1P 1s, what you see on induction, the durability is unmatched. In some cases, you actually see improvement in the endoscopic score, in this case, the endoscopic remission. That is a differentiated asset. I think people recognize that, right? The challenge is, it is behind sort of the negative cloud on the other two S1P1 s. Ozanimod, siponimod, really not a factor. Etrasimod, Velsipity, which is now in Pfizer's hands, had a very slow start, although I believe they will put muscle behind it. You know, they've had some successes. That is where we are with that, and we hope to convince partners that this is a drug that belongs in phase III. This is a drug that's gonna be a differentiated asset, but reality is behind and that's sort of the headwinds we face on that side. Got it. Got it. That's helpful. How much engagement have you had with the FDA on what the pivotal program for VTX002 should look like? We've had a nice dialogue with end of phase II with both the FDA and the EMA, right? The EMA is... The FDA is, I'm not gonna get too much into detail- Sure ... but needless to say, that we will have a single phase III with a single dose, so they have not asked for a dose-ranging trial. Other than that, the FDA will not give you a categorical yes or no on exactly what the box has to be checked for registration. It's always gonna be on review, and that's sort of the canned line they will give you. The good thing is they didn't push back and say, "You cannot use the highest dose here, you cannot do this." They agreed to that, obviously with all the caveats that come back to us with the data, and we'll take a look at it. In a similar vein from the EMA, EMA as well. I would say they were very productive meetings with the outcome that we know with the FDA, which is to say it'll be on review. Got it. Got it. Final question from my side on VTX002 then. What would a strong partnership look like? What would you be looking to gain from, from seeing a partnership? I think it's having conviction from a partner, which really is a conviction from the commercial side, because we know the clinicians within these companies really believe this is differentiated, right? Having that kind of input from them, input meaning a partnership, really brings the commercial people into it, and that bodes well because this drug will... I hate to say will, but, you know, the drug will work, right? It's a well-established pathway, and we've seen success with other drugs in there. We know what deep remission does. We know what deep penetration does in terms of getting a clearly differentiated response. If you see endo- lymphocytes in that range we've showed, which is the 65% and higher, relative to the sort of the 50% floor that we've seen with both of the drugs. Right. Right. Okay. That's helpful. We should probably pivot now to the NLRP3 portfolio. Just to level set, in case not everyone's been following Ventyx in a great level of detail recently, where do VTX2735, VTX3232. Just remind us kind of where do they sit right now in their respective development programs? VTX2735 was our first molecule. It's a peripheral NLRP3 inhibitor. It completed phase I studies, it was a couple of years back, right? We announced the data towards the end of, I think, July timeframe in 2022. We then decided to move the or discover a CNS penetrant compound. As you know, our CNS penetrant compound is not a descendant of the peripheral compound. It's a standalone chemotype, which is designed to be brain penetrant, right? We decided to bring that into the similar stage as VTX2735. We committed to the market that we would announce indications for the portfolio as our phase II programs were coming to a close last year. We've taken VTX3232 through phase I. We announced phase I data earlier this year. That was a larger phase I, where we looked at exposure in the periphery in blood. We looked at exposure in the CSF, a dose-ranging trial, looked at food effects of the drug. We had a DDI component to it, and finally, we had a solid oral tablet that we had made that we also profiled in this study for food effects and showed that there was almost 100% bioavailability and no food effects. Both compounds were now in completed phase I. In the case of VTX2735, last year, we started a CAPS study in CAPS patients. The reason for doing that was there's really nothing out there with any sort of proof of mechanism of a NLRP3 mediated disease. In this case, it is a direct effect of gain-of-function mutation of NLRP3, and albeit a smaller population, it's about 250 people in the U.S., patients in the U.S. It's a familial disease, and we conducted an impeccable trial with seven patients, which is a lot, if you think of how many—there's 200 people, 200 patients in the country. Seven, seven folks, showing a treatment arm washout period, which is rechallenge and treat, and showed efficacy both on the symptomatic endpoints. This is sort of well-being scores and very well calibrated in terms of headaches and fever and chills and joints, as well as objective scores, which is lowering in—the inflammatory state on these patients, which is primarily hs-CRP, was IL-1 beta, but which drives then IL-6, which then drives hs-CRP and other factors, right? Phase one completed, proof of mechanism, first time showing effects of biological relevance of this compound in patients. VTX3232 finished the phase I, and so VTX2735, yes, has done a proof of mechanism, but you can assume that for the VTX3232 as well. VTX3232 by being CNS, is also a peripheral compound. In essence, both compounds now stand or stood on the periphery, on the verge of being phase II-ready earlier this year when we talked about the R&D day we had. We disclosed our plan for moving these compounds forward. The plans have been and then Mark, of course, came on board. Happy to say that he did his diligence and he, you know, has embraced our approach, and because he's gonna be at the helm of this, he'll be carrying the baton, and so it was important for him to... I would say the only difference that, that's happened is that we have changed our- we've added- we've categorically, you know, taken RP as our, you know, as our, recurrent pericarditis as the one of two that we had said. We had said we are gonna-- going into two RP, recurrent pericarditis, or a biomarker trial in the secondary prevention of MACE, and so we picked RP as our first trial with VTX2735. The other difference is that we had talked about a biomarker study with our VTX3232 compound in patients with early Parkinson's disease. That is where we are, so that nothing has changed in that sense. The only difference is we had a obesity cardiovascular study, which was supposed to be 28 days, and based on external data, internal discussions, that study has now... and the fact that we have tox coverage for a longer study, that study has now changed to a 12-week study, which is gonna be a study that will start end of the year. We have, we have guided, internally and externally to what we said we would do. We've committed to our RP trial. We have initiated the biomarker trial this morning. We put out a press release that our first patient was dosed in a, in a biomarker/imaging trial. Very excited about that. Of course, the third one is going to be the... Second and third are going to be the RP and the obesity, cardiovascular, metabolic, broader probing of the mechanism in a, in subjects where we can actually look at not just obesity, but a broad range of metabolic, cardiovascular, hepatic, renal dysfunction as a result of abnormal inflammatory signaling through IL-1 beta. Understood. Understood. Before we move on to the clinical programs, one foundational question for you. How have both molecules been designed to be differentiated from other NLRP3 agents in this space? Yeah, good question. The first one is, is a sulfonylurea, right? And the genesis of those compounds is somebody at Pfizer, discovered that internally, a compound, a Pfizer compound, it was a glipizide, for diabetes. His name was Chris Gabel. And Chris discovered this compound in, in some assays for, for inflammasomes, right? NLRP3, NLRP4, and he found that this was a NLRP3 inhibitor. Wasn't super selective. And so Chris left Pfizer and Matt Cooper, just to give you the history, who was with a company called Inflazome, poached this compound, named it after himself, called MCC950. And Chris started, started NodThera, right? Ironically, he was at NodThera, which is a company that's been in, in, you know, in the news. That was... Everybody started taking the sulfonylurea. It became a privileged scaffold, just like TZDs are, or benzodiazepines are. It's called a privileged scaffold, put their own spinach on either end, right? That came, IFM Therapeutics, Ventyx, NodThera, us- Not Ventyx. We all had sulfonylureas, but we designed a compound that was outside of any of the patents. We, we, typically, what we do is not cowboys. We design chemistry that's not easily tractable, right? So it's like doing a yoga pose. I can't do it, but, you know, when you take your hands and you try to go around and catch the other hand, that's how we build these compounds. That, you know, very hard for most people to design and execute, especially on a commercial scale, right? Yeah. That became VTX2735. We have an issued patent. Unlike a lot of these companies that were sort of all over the place, suing each other, because, you know, when you design something in eighteen months, you have a black, you know, it's a, you know, have a black box, right? VTX3232 was designed to be a brain penetrant compound. And the clear instructions, at least from my end, was, you know, don't go after a sulfonylurea, because you're not gonna get it into the brain. It's a polar charged compound. Go find a scaffold that's brain penetrant and build the NLRP3 sort of backwards, right? Pick a benzodiazepine, pick an imidazopyridine, which is Ambien, pick something else, and screen the library of those guys. Something will hit, and once it hits, take that as a lead, optimize it, and that's the VTX3232. All right, understood. We've got a published patent there. I'm very confident of the IP space, and it's, it's a, it's a really, the chemists have, and the team have done an amazing job. It's, it's a beautifully brain-penetrant, balanced compound. The problem with it is you also don't want something that never leaves the brain. A lot of these compounds make it in the brain, and either because they are sort of phospholipid type, they just don't leave the brain, right? That can be a problem on a repeat dosing. You don't see it on a single dose. Once you repeat doses, you accumulate in the brain, there's a lot of issues. This compound has no accumulation. Like I said, it's, it's, it's well absorbed, reaches the CSF, and now it's in, you know, in his hands to demonstrate all the different aspects that we talked about. Got it. Got it. That's helpful. So diving into VTX3232 then, Parkinson's disease, obesity, just remind us, where those programs currently stand and what people should think about for kinda timelines to initial data. Yeah, I'm gonna maybe I'll let Matt, or Mark, sorry— Yes. Mark, jump in now. Let's-- VTX3232. We have the Parkinson's-- we-- we're doing... We started, as you, Raju mentioned today, we started this biomarker study in Parkinson's disease, and this is really focused on... It was limited to 28 days because of the tox coverage we had, so it's really focused on a proof of principle, right? Can we modulate the inflammatory pathway, both the systemic inflammation, which is sort of the low-hanging fruit, but also sort of can we modulate the inflammation in the brain? And really, that's in the... We're using that with a series of biomarkers that are, you know, indicative of microglial activation in the brain, astrocytosis in the brain with GFAP, neurodegeneration in the brain with neurofilament, and some advanced imaging techniques, TSPO PET, with one of the newer tracers that can really look at microglial activation in the brain. That study is really sort of a proof of principle to show that our CNS penetrant compound can really modulate inflammation within the CNS, which we haven't done in the—you know, we did a little bit of that in the first in human looking at, like, IL-6 levels, but this gets us a much more robust look at that. Obviously, it opens up a... That study is started now. The expectation is we'll have data readout from that in the first half of next year, and it would really sort of set up a pathway for, for additional studies in Parkinson's disease, but actually opens up a world of CNS disease that we can then explore based on medical need and commercial evaluation, et cetera. The cardiometabolic study, and I'm gonna specifically call it a cardiometabolic study rather than obesity study, is the idea is of looking at the role of inflammation in cardiometabolic disease, using obesity as, as that platform, where we're gonna look at, patients who have obese—individuals with obesity, but also evidence of inflammation. We are doing that both as a monotherapy and on top of semaglutide, based on our preclinical data, showing that we can get additive effects on not only weight loss in animal models, but as well as in promotion of lean body mass, but also an array of biomarkers of lipid profiles, glycemic changes, hepatic function, renal function. This study is designed as monotherapy and add-on to semaglutide for twelve weeks, looking at weight, yes, weight loss, of course, but an array of other parameters that will give us a sense of what the potential mechanisms that we can really sort of go after, whether it is a weight loss program or some of these other things. I think there is a lot of opportunities there. That study should be, we'll be getting started by the end of the year, the expectation that we'll have data sort of in the early second half of next year. That's for, that's for the cardiometabolics? Yeah. Got it. Got it. Okay. So I mean, assuming both of these trials, maybe let's just focus on cardiometabolic first. If they hit the threshold that you kind of have in mind that you just laid out, what do next steps look like from there? A lot of that's gonna be a data-driven sort of decision, you know, decision. What the expectation is that we're gonna be doing is a lot of scenario planning in the next few months, so that when the data comes out, we're ready to run with it. I mean, it could... Obviously, if we, if we see an effect of, of weight loss, particularly on top of semaglutide with, with preservation of lean body mass, that's, you know, the study's powered to see that. That's sort of a, you know, from our end, that's a, that's a big win. There are a whole other, other areas that we can look at. We can look at studies in liver, liver, fatty liver disease or NASH. We can look at areas of renal dis- chronic renal disease. We can look at other glycemic studies. I think it's gonna be a little bit driven by the data 'cause we've done these studies in mice, what's gonna happen in human is really very much an unknown. We're sort of at the cutting edge here. We're gonna, you know, really let it be a data-driven decision as to how we develop these based on what we see coming out of the study. Got it. Got Got it. Sort of relatively new. I don't know, Raju, if you may add a— No, I think, no, I think that's absolutely spot on, right? Which is, treat the mono and combo as really an exploration of the effects of the compound itself, but more and more important on standard of care, especially in the sense of metabolic and cardiovascular. As you know, there's going to be label on GLPs now already, right? In terms of metabolic and cardiovascular events. You know, there was a label on statins as well. It didn't prevent other companies from coming in with novel modalities. We think this is an opportunity to look at what we've seen in a mouse, not get hung up on whether a human is a mouse or not, but look at individual modules of the data that we saw, whether it was on weight loss, as you said, on lipids, on cardiovascular, on renal, on hepatic, on preservation of lean mass, and take each of these now in one model. This model now is a human with the BMI obesity index, and see if this recapitulates again, each of these modules, right? What happens on-- Again, don't forget, there is a reminder that number-- there's a sizable number of folks that don't respond to GLPs, right? The question is what happens with a compound such as this on top of a GLP? These people are not genotyped, they just do not respond to GLP, so they have, you know, intolerable side effects, as you know. There is a lot to be done, and we will internally look at scenario planning, and a lot of it will depend on the data that starts to come out as we start to see it, plan for that. I think it is similar on the Parkinson's side. You know, it would be too sort of cowboy to say we are going to go on a full-blown trial, but the data are compelling. We think the strategics recognize the role of this pathway there, and there might be a mutual, you know, meeting of the minds in that case. There are other things we could do. I know Mark's a big, fan of Alzheimer's and the link of these, this pathway there as well, and maybe this trial opens up that, that angle. There's potentially other ways to look at those diseases here as well. Right now, it's, it's about thoughtful execution of, of biology. In old days, we call it reverse endocrinology. It's not quite that, but it's having a good compound, a drug, not even a tool compound, and just see what it, what happens while we build the internal scenarios and strategy for what we would do, right? Planning for success, obviously. Sure, sure. As we go into the CNS disease- Yeah. One of the key things that we really have to think through is the population that's most likely to derive benefit. I mean, we've learned a lot from the Parkinson's disease, from failures in Parkinson's disease, from failures in the Alzheimer's disease space, about how to conduct these trials. I think making sure that we apply those learnings in a very tactical way so that we're actually studying that population, those ear... I mean, what our biomarker studies in early stage disease, and making sure that we're really focusing on that population, because by the time patients progress, unfortunately, for these sort of disease-modifying approaches that we're targeting, we've learned that that's a population that's very, very hard to reach. You have to, I mean, that's why these fields in general, yet for these both, for Parkinson's, you need to focus both on symptomatic treatments as well as disease modifying, because there's different populations that are gonna benefit from different approaches. We're really focusing on the disease modifying, so really got to get in using biomarkers and tools, really identify those patients that are most likely to benefit. There's a lot of work that's been done on that space over the last decade or so, and we're certainly gonna leverage that in the future. Go forward, assuming that we see positive data from the study that we just got off the ground. Got it. Got it. Any questions from the audience on VTX3232, Parkinson's or obesity? Okay, if not, we should keep moving forward then. VTX2735, I did want to ask you how you arrived at recurrent pericarditis, excuse me, as the best first indication to target here? Two, couple of reasons. One, certainly the biology has to be first, right? You, you do what the science takes you. And in both RP and, and the MACE prevention that we had outlined, there was biology coming from the biologics that had been used or, or the, or the, data coming from these studies. The MACE was a big catch-all CANTOS study, which was done thousands of patients, and the role of canakinumab, which is an IL-1 beta specific antibody, in, in really showing risk reduction in these patients, right? And, with or without statins, it was an amazing outcome in the trial. Sort of not that dissimilar to what we're doing in this, certainly in this obese cardiovascular, really probing effects to see where does it hit, right? What stood out when you did all the algorithms was risk reduction, cardiovascular ASCVD, right? Atherosclerotic cardiovascular disease. That was one angle. The RP is more opportunistic because of what's been shown with not just IL-1 beta drugs, canakinumab and anakinra, also with an IL-1 alpha beta trap. It's a little different. This is a drug called rilonacept, and a company called Kiniksa, and they did a trial in recurrent pericarditis. It was a small trial, but the results from that small trial were so compelling and so clear that the FDA allowed them to go down to a single phase III and all the way to registration and approval and commercialize it. There, it's pretty obvious to us that, you know, there's an opportunity there with an oral drug that obviously has benefits across a number of, for a number of reasons and take that opportunity. It's a very tractable trial for us while we conduct these little more elaborate endpoints. And here's a case where you can actually have a speed to market approach. If the data are positive, we totally have the capabilities and optionally taking it all the way, or we'll have interest from folks out there, and we'll partner it. So really is, is, the secondary prevention of MACE would have been a smaller biomarker trial for us. It is always, "And then what?" Right? Because the outcome, large cardiovascular outcome trials really are not in a domain of a company like ours right now, unless we sort of shelved everything else and became a CV company. Right. I'm not ruling it out. I think that's, it's-- there's more data coming out from Novo on IL-6. Some of the-- much of this is, we talk about IL-1 beta, it's really IL-6 that's been studied, right? That's where we will see what happens with that data, but for now, I think RP is a very prudent choice. It gives us a real angle with this molecule and a clear line of sight to taking it all the way, assuming the data are positive, and that'll come out sometime in the second half of the year, next year. Got it. Got it. To remind us, what are the current treatment options right now for RP? It's colchicine, which is a broader, anti-inflammatory drug, a pretty dirty drug, but that's sort of the poor man's approach. There is rilonacept, Arcalyst, which has been marketed and, you know, a reasonable trajectory on their sales over the last two years. Pretty bullish about it. We see this as a clear positioning of our compound. It doesn't have to be rilonacept, it's a good drug. We have to be equivalent to that, close to that, with an oral drug that's safer and cleaner and directly targeting, you know, assuming the biology of this, which is an NLRP3. Got it. Right. Got it. Okay. I mean, taking a step back, does the experience you had with VTX958 in psoriasis and then Crohn's, does it provide any kind of reflections on future development programs, whether it's NLRP3 or- Honestly- S1P. Honestly, not. Because... Look, first of all, and this is no, no, I'm not being defensive or making excuses. Sure. You know this, right? Drug development is never easy. It's never for the faint-hearted. We've been doing it a long time. You know, you have successes, you have failures. I honestly don't think S1P1 or even the Crohn's disease, and we can talk about what are all failures. In the Crohn's, we missed, we missed the CDAI score, which is more subjective, but we nailed the endoscopic response, with a P value of, you know, less than 0.05%, in some cases, in one case, 0.001%, right? But psoriasis, I think the lessons we've learned is be humble. Biologics are biologics, and don't try to say, "I'll be in IL-23, or I'll be a certain charge," because that's sort of bravado, right? You know, oral drug is gonna be surpassed a biologic any day, so just, you know, let the data drive it, right? Do not put, do not put the prediction before the data. Honestly, if we had failed on execution, if the biology was off, I would say we should do things differently. At psoriasis, the game is, you know, it has moved on, I think, for all other companies as well. There are gonna be oral IL-23 peptides coming out, there will be other drugs coming out. I still believe the S1P, and we have the best compound, would not have done anything differently. Crohn's, we will see where the data ends up once the entire trial is complete. RP3, you know, it is, it is, it is... We are, we are now sort of pioneering the pathway. You know, what I want to say to investors who are really thoughtful, they get our approach, right? They get the fact that this year is going to be data-generating for us and going forward. There is a subset that got fixated on obesity and sort of said, "Weight loss," some competitor know. You know, I'd love to have those folks look at our plan, look at the data, look at how thoughtfully we've built this, and the trajectory we are on, right? That's our goal. Of course, we learn from experience. Of course, we all learn from experience, and we will adapt that, but nothing that we could have done, or, you know, I'm very proud of the team, and they did an incredible job, and they're going to transition into the newer programs. Fair points. In closing, could we just kind of recap your current cash balance, and where does that bring all these current programs? Where can you get to? Yeah. So, we disclosed end of second quarter, almost about $280 million at the end of June. Our burn will go down slightly, and then it'll go up again. I'm just gonna give you a quick answer here in a slightly different way, which is: these trials are not as complex or expensive as the UC Crohn's trials. There's not a lot of imaging and endoscopy. Our guidance is still well into 2026. Okay. We will reforecast end of the year as these things go, but stand behind the fact that the current cash, with all these trials reading out next year, still takes us into the end of 2026. Great. All right. With that, we'll close out. Raju, Mark, thank you so much for joining us. Yeah, thanks. Thanks, everyone. Thanks, Vikram.