Good afternoon, ladies and gentlemen, and welcome to the Ventyx Biosciences first quarter 2024 earnings conference call. At this time, all parties have been placed in a listen-only mode, and the floor will be open for your questions following the presentation. If you would like to ask a question at that time, please press star one on your telephone keypad. If at any point your question has been answered, you may remove yourself from the queue by pressing star two. So others can hear your questions clearly, we ask that you pick up your handset for best sound quality. Lastly, should you require operator assistance, please press star zero. As a reminder, this conference call is being recorded. I would now like to turn the call over to Dr. Marty Auster, Ventyx's Chief Financial Officer. Please begin. Thank you, Operator. Good afternoon to everyone joining us today. Welcome to Ventyx Biosciences conference call webcast, where we'll be discussing our first quarter 2024 financial results and providing a corporate update. Before we begin, I would like to remind everyone that today's presentations will include forward-looking statements. These statements are subject to risks and uncertainties that may cause actual results to differ materially from those projected. A description of these risks can be found in our Form 10-Q for the quarter ended March 31, 2024, which was just recently filed this afternoon. Any forward-looking statements are made only as of today's date, and we assume no obligation to update any forward-looking statements made on today's call. With that, I'll hand the call over now to Dr. Raju Mohan, Ventyx's Founder and CEO. Raju, please go ahead. Yeah, thanks, Marty. And thank you, everyone, for joining us for our First Quarter 2024 Earnings Call and corporate update. As we recently provided a full pipeline and strategic update at our March Investor Day, I will be brief with my remarks today. Let me take a few minutes to provide some high-level comments on the status of our pipeline programs, and then I'll hand the call back to Marty to review our First Quarter financial results. We'll then open the floor to Q&A, where I'll be again joined by Marty and also with John Nuss, our Chief Scientific Officer. So I'll begin with our portfolio of potential best-in-class NLRP3 inhibitors. In March, we announced positive top-line results from a phase I single and multiple ascending dose trial of VTX3232, our novel CNS-penetrant NLRP3 inhibitor, in adult healthy volunteers. As you may remember, repeat VTX3232 doses as low as 3 milligrams once daily achieved steady-state IL-1 beta IC50 coverage in both plasma and the CSF, and repeat doses of 20 milligrams all the way up to 40 milligrams q.d. well exceeded IL-1 beta IC90 coverage in both plasma and CSF. Based on these data and our dose projection modeling, we estimate that VTX3232 doses as low as 12 milligrams once daily may be adequate to achieve IL-1 beta IC90 target coverage in the CSF and in plasma. We also observed robust dose-dependent pharmacodynamic or PD effects in a whole blood ex vivo IL-1 beta stimulation assay, and VTX3232 also showed an excellent tolerability profile in this phase I study. We thus believe that these data establish VTX3232 as a potential best-in-class drug candidate for the treatment of neuroinflammatory diseases and conditions. This includes excellent target coverage in plasma and CSF, favorable safety profile, and a convenient once-daily oral dosing regimen with our tablet formulation. VTX3232 is a phase II ready compound. As we also communicated in March, we plan to rapidly advance VTX3232 into phase II trials in high-value indications with substantial unmet need, beginning with a phase II-A trial of VTX3232 in patients with early Parkinson's disease, which we will initiate in the second half of this year. As we discussed, a growing body of preclinical evidence has implicated NLRP3-mediated information as a key driver of Parkinson's disease pathology by impacting neuronal death and degeneration. We therefore believe that NLRP3 inhibition represents a promising, potentially disease-modifying therapeutic approach in this devastating neurodegenerative condition. More recently, NLRP3 has also created much buzz and discussion as a potentially important target for obesity and obesity-related metabolic diseases, much of it due to data published last February showing central NLRP3-mediated weight loss in obese mice. We have initiated our own studies with VTX3232 in murine models of diet-induced obesity, similar to the published model we just talked about. In addition to assessing weight loss induced by VTX3232 and with the GLP-1 agonist semaglutide in a monotherapy study, we're also evaluating VTX3232 in combination with semaglutide. These are exciting studies, and we look forward to providing an update on these studies later in the second quarter. So now moving from mice to humans, we plan to initiate a phase II trial of VTX3232 during the second half of 2024 in obese participants with certain additional cardiovascular risk factors. Now moving on to VTX2735, our peripherally restricted NLRP3 inhibitor. In March, we announced positive top-line results from a phase II trial of VTX2735 in patients with Cryopyrin-associated periodic syndromes or CAPS. In this trial, VTX2735 demonstrated efficacy comparable to that observed with IL-1 biologics, the current standard of care. VTX2735 also demonstrated consistent and robust reductions in inflammatory biomarkers such as hsCRP, high-sensitivity CRP, IL-6, Serum Amyloid A, and fibrinogen. There was also a mean reduction of 85% in the key symptom score for these CAPS patients during the initial treatment period with a very favorable safety profile with all treatment-related adverse events graded as mild. These phase II data in CAPS patients is therefore a compelling proof of mechanism for VTX2735, for our peripheral inhibitor, and for systemic inhibition of NLRP3 and NLRP3-related biomarkers in general, including hsCRP and IL-6. As we communicated in March, we plan to evaluate VTX2735 for future development in cardiovascular and potentially other indications, with an initial focus on recurrent pericarditis and also in the secondary prevention of major adverse cardiovascular events or MACE. Both recurrent pericarditis, RP, and MACE prevention represent indications with large addressable markets and substantial unmet medical need. We thus plan to update or provide an update on our cardiovascular development plans later in this year. Beyond our NLRP3 inhibitor portfolio, the team continues to make progress advancing our IBD assets, including VTX002, our potential best-in-class S1P1 receptor modulator for ulcerative colitis, and VTX958, our allosteric TYK2 inhibitor in phase II development for the treatment of Crohn's disease. For VTX002, you recall that we announced positive phase II data in October of 2023, demonstrating what we believe is a potential best-in-disease profile for an oral agent in ulcerative colitis. This includes a highly differentiated rate of complete endoscopic remission and a potential best-in-class safety profile. At the March event, we also showed preliminary data from the open-label extension part of the phase II trial, further reinforcing the endoscopic remission data and the differentiated profile. We anticipate that the data from the 52-week long-term extension part of this phase II study will continue to show sustained or perhaps even improved data for endoscopic remission from that observed in the 13-week induction period. This program is fully phase III ready, and our teams continue to make preparations for a pivotal phase III trial that is ongoing. Last month, we completed a productive end-of-phase II meeting with the FDA, and we expect to conduct a scientific advice meeting with the EMA later this quarter. We continue to have confidence that our completed phase II trial may be sufficient to support approval of VTX002 with successful completion of a second pivotal 52-week trial in ulcerative colitis. as we have previously indicated, efforts are underway to identify a partner or other source of non-dilutive financing to support this pivotal phase III trial. Finally, our phase II trial of VTX958, our allosteric TYK2 inhibitor in moderately to severe active Crohn's disease, continues to progress. As we've mentioned, in the first quarter of this year, we implemented a protocol amendment to streamline detection of a potential efficacy signal in this trial. As a result of the protocol amendment, target enrollment was revised from approximately 132 patients to approximately 93 patients, and the trial's sole primary endpoint is now the change from baseline in the main Crohn's disease activity index, or CDAI, score at week 12. We have completed enrollment in the trial in March, and we look forward to reporting top-line results in early second half of 2024. In conclusion, I would like to again thank all of our Ventyx team members for their continued efforts and contributions across the pipeline, to our investigators and collaborators, and of course, all the patients that enroll in our trials. We are very much looking forward to a productive year for Ventyx and to continue to provide these exciting updates. I'll now hand the call back to Marty for a brief review of our first quarter financial results. Marty? Yeah, thank you, Raju. Our financial results for the first quarter ended March 31, 2024. They are presented in our press release issued at market close, and I'll briefly summarize those results here now. R&D expenses in the quarter were $33.7 million compared to $35.4 million in the first quarter of 2023. G&A expenses in the first quarter of 2024 were $8 million compared to $7.1 million for the first quarter of 2023, and our net loss in the first quarter of 2024 was $38.6 million compared to a $38.9 million net loss in the first quarter of 2023. Our cash equivalent and marketable securities balance was $302.6 million as of March 31, 2024. Net cash used in operating activities during the first quarter of $47.6 million was higher than the reported operating expenses of $41.8 million and is primarily due to an increase in prepaid expenses and a decrease in accrued expenses during the quarter. We expect both our operating expenses and our operating cash flows on a quarterly basis to decrease as we get into second quarter of 2024 and remain lower for the rest of 2024 as we complete the wind-down activities related to our phase II trial programs in psoriasis and psoriatic arthritis for VTX958. We continue to believe that our current cash equivalents and marketable securities are sufficient to support our planned operations into at least the second half of 2026. This concludes our prepared remarks for this afternoon's call, and I'll now turn the call back to the operator to begin the Q&A session. On the Q&A session, I'll be joined by Dr. Raju Mohan, as well as our Chief Scientific Officer, John Nuss. Operator, please go ahead. Thank you. If you would like to ask a question, press star one on your telephone keypad at this time. It is star one if you would like to ask a question. To remove yourself from the queue, you may press star two. Our first question today comes from Michael Yee with Jefferies. Hey guys, thanks for the question. This is Kyle from Michael. So on the CNS and NLRP3 program, what do you think is promising for a 28-day study in humans for an oral like this, and what do you think is the bar, and how do you think it stacks up other injectables and oral options under investigation? And a quick one on your mouse data, where do you think you're going to present the data? Is it going to be in the format of a press release, or are you going to report it at a conference? Thank you. Yeah. Well, thanks. So let me address the second question first. So now, as I mentioned before, we plan to report this data in the late second quarter, and we're in the process of compiling the data. And once we have all that together, we'll decide what's the right forum for presenting it, so just stay tuned. In terms of your questions about sort of what we expect to see in 28 days, I think there's plenty of studies out there, not just with GLP-1 agonists, but other modalities as well, showing measurable weight loss in 28 days in human trials, anywhere from single digits, 2%, to higher weight loss. So again, it remains to be seen what the competitor data will show, if and when that data are put out. In our mind, we have two things happening. One is obviously we've done we're repeating the study that was published in diet-induced obese mice. As we mentioned, it's a monotherapy study with compound in a control, and it's a combination study with semaglutide. And we're looking forward to reporting these results. We also, as we've said, committed to doing our own trial, a 28-day trial in patients. And we think there's biology out there now that certainly links NLRP3 activation in addition to hypothalamic control of obesity parameters or mechanisms, such as feeding behavior. And I think that body of evidence will continue to grow as folks try to link the dots, just like it's been happening for Parkinson's disease. So we're committed to doing this trial. We look forward to seeing the data from the competitor, if and when it's put out there. Our own path here is planned, which is, again, put out the mouse data and then planning for our phase II-A study in obese patients later half of the year. All right. Thanks. Thank you. Our next question comes from Yasmeen Rahimi with Piper Sandler. Hi, this is Liam Heaster on for Yas. So I guess my first question is related to what's the current talk package available for VTX3232? And then when moving on to the expected phase II trials, what work still needs to be done in order to initiate in obese patients with additional CV risk? And then moving to 2735, with those phase II trials, what are the rate-limiting steps in initiating a MACE or a recurrent pericarditis trial there? All right. So let me start with the first one. So our first study is a 28-day study in obese patients. It's a similar study we are planning, a 28-day study in early Parkinson's disease. And then we will initiate the longer-term studies, particularly the obesity study, if that merits the phase II in the latter half of the year. So right now, the tox package will support a 28-day study, and then we'll have the tox coverage to do chronic studies in the latter half of the year. Second question was on briefly, if you don't mind repeating the second one. Oh, yeah. So I guess for the VTX2735 asset, what are the rate-limiting steps for the initiation of the phase II MACE trials and recurrent pericarditis? There's no rate. Every trial has to have its own individual planning. The teams have to get together. The protocols have to be written, and the contracting has to be done. We've laid out our timelines for the Parkinson's obesity trial, and we'll lay out the timelines for the cardiovascular trials once those have been firmed up. There's no rate-limiting step. It's just a part of the planning process from going from a phase I study to a phase II study. So it's just a standard process that we have here. But we're pretty excited about the cardiovascular opportunities for 2735, both in recurrent pericarditis and also in the secondary prevention of MACE. Great. And then actually, just one more question. So with VTX002, just wondering if you could provide any more detail on the level of partnership interest, and then also any details from the end-of-phase II meeting. Yeah. So on the end-of-phase II meeting, we had a really good meeting with the FDA, and we laid our justification for a phase III trial with a single dose. We believe this should serve as a pivotal trial, as should the first one. We'll continue to have the discussion with the agency as the trial progresses. So, in our mind, a very successful meeting with the FDA. In terms of partnerships, we're not going to get into the specifics. We think this compound continues to show a very strong endoscopic remission, as we showed from the open-label. We believe the long-term extension data will continue to support both the durability of this and perhaps even improve scores, such as the precedent with S1P1 modulators. As we said, we are aggressively in the midst of getting interest from pharma partners across a wide range of folks. Stay tuned, and we'll update you guys once those things progress to something that we can talk about. Thank you. Our next question comes from Emily Bodnar with H.C. Wainwright. Hi. Thanks for taking the question. For Parkinson's disease, I'm curious if you can comment on what kind of neurodegenerative markers you're planning to evaluate, and if you're looking at any disease rating scores or kind of impacts on motor symptoms. And maybe if you could provide a bit more on study design for obesity in terms of how many patients you're planning to evaluate, and are you planning to exclude diabetes patients in that study? Thanks. Yeah. Good questions. So again, on specifics of the trial, and we're not trying to be cagey here. We don't necessarily disclose every aspect of this trial. Once we have it, it'll be on clinicaltrials.gov. But again, just to bring it in context, you saw the competitor's 28-day trial with an NLRP3 compound a few months back. They published a biomarker trial. We are planning not just a biomarker trial, but we also have an imaging component to this trial to see effects of this molecule on glial content and activation, as it translates into eventual effects on astrocytes and eventually neural death. Don't expect much effect on motor symptoms in these short trials, but we certainly expect to see effects on, number one, the NLRP3-related biomarkers, such as IL-1 beta, hsCRP, IL-6, fibrinogen. We've shown them now convincingly in multiple trials. Even in early phase I, we've seen some movement in these markers, even in healthy volunteers. We certainly showed a robust response of an NLRP3 compound, albeit the peripheral one, in hsCRP and, again, IL-1 beta and IL-6. And in the phase I trial with 3232, we also showed effects on these biomarkers, even in healthy volunteers and in the CSF, right? So those are NLRP3-related biomarkers. And then you have the other side of neurodegenerative markers, in particular in Parkinson's patients, such as neurofilament light chain and others. And again, thoughtfully explore a range of biomarkers. There is nothing that precludes us from having a much broader set in our measuring strategy. But again, we're not setting any expectation of seeing any sort of meaningful effects in this short trial. That's why we have a longer trial that we are contemplating towards the end of the year, which will be much more in line with what you've seen recently or published for much longer treatment in Parkinson's patients. These are 12 months or longer trials. Okay. That makes sense. Thank you. Thank you. We will take our next question from Vikram Purohit with Morgan Stanley. Hi, everyone. This is Gospel from Vikram. We have one question regarding your CD program. What is the hurdle for continuing VTX958 in Crohn's disease based on the data expected in the second half of the year? Yeah. Thanks, Vikram. Perhaps I'll let Marty address this. Marty? Yeah. Thanks for the question, Gospel. So for that trial, the primary endpoint is a change in CDAI score, and then we're looking at key secondary endpoints that include endoscopic response and things like that. If you look across sort of approved drugs in the Crohn's disease space, you're looking at some of the biologics as well as more recently developed products like deucravacitinib. You'll see CDAI changes in the phase II in the range of the upper double digits to kind of low hundreds as sort of kind of a meaningful type of response on that marker. We're adequately powered to sort of detect specific events at that type of response. And then on the endoscopic side, that's a secondary endpoint given the size of the trial. But we'd be looking to see sort of, again, something competitive there would be in the high teens to low 20s endoscopic response relative to delta versus placebo. So that's sort of kind of, I think, where the bar is for recently approved drugs to be attractive in this setting. So we're looking forward to reporting those results out to you in the next several months. Thank you very much. Thank you. We will take our next question from Alex Thompson with Stifel. Hey, great. Thanks for taking my questions. I guess first one on 3232 to follow up a little bit on the DIO mouse experiment. Can you talk a little bit about sort of the human dose equivalents you're going to be testing relative to what you're looking for in the phase II and what you want to see in both the monotherapy and combo studies to get more confident in the human trial? And then for 2735, just curious your thoughts on peripheral NLRP3 inhibition in the context of what we saw from lutikizumab and at AAD and whether you would consider an indication like HS in the future. Thanks. Yeah. So first, on human dose equivalent in the mouse study. So we don't do these studies in rodents, whether it's for NLRP3 or anything else. It's really a proof of concept, and you appropriately dose the animals based on the profile of the compound in mice, for example, right? So the exposure in mice, the potency of the compound in, for example, against mouse NLRP3. And that's the goal. It's not to determine the human dose. Remember, we've done a phase I trial with biomarkers in plasma and in CSF. We've calibrated that trial with what we expect to have the exposure to cover IL-1 beta IC50, IL-1 beta IC90. And if IL-1 beta is the driver or IL-18, but IL-1 beta and IL-18 are the drivers of the disease pathologies, then that's the calibration. So what doses do we need in humans to have complete aggregation or complete inhibition of the IL-1 beta produced by NLRP3 in periphery or in the CNS? And the CSF is a good surrogate. So just to make it clear, the mouse studies are not meant to find doses for the obesity trial or for Parkinson's trial or any other phase II trial. So in terms of mice, again, the doses are now set to make sure that we have adequate coverage in the mice to see effects on weight loss, to see effects on other endpoints. And again, it depends on the compound. So we don't take any sort of guidelines from the competitor dosing paradigm, in which case it was three times a day in mice. We have our own dosing regimen, and that's what we've done in both trials, the monotherapy and the combo therapy. I think the expectation that you have the question you had is, what do we expect to see in a combination trial? First of all, this whole trial, the old study - I shouldn't call it a trial - in mice was really to have our own calibration of our compound, which is a really well-behaved CNS drug, I think the best-behaved CNS-penetrant compound out there in the NLRP3 class. And so our goal was to set our own calibration in terms of these mice models, which we believe are in different parameters predictive of human disease. So it's not a one-to-one mouse model as a human model. It's different aspects and different readouts from this study recapitulate what you expect in human studies, right, in this case, obesity. So having no expectation but having the competitor data, we designed this trial with our compound, with a semaglutide control, with adequate controls, with a placebo. First thing is to see whether you see any weight loss with our compound. Obviously, have weight loss from semaglutide. That's been published many times. It was published in the competitor compound data that you saw. Next thing is to understand effect of weight loss, effect of food intake. And then once the study is completed, what happens to other parameters, lipid parameters, what happens to diabetes parameters like glucose, insulin, OGTT, HOMA-IR, what's happening to steatosis? So as we know, obesity or reduction in obesity results in benefit on a number of parameters. So we look for that. In the combo study, obviously, we would look for not just effects of monotherapy, but what is the effect of NLRP3 inhibition on weight loss vis-à-vis semaglutide alone or a GLP agonist alone? Is it additive? Is it synergistic? Eventually, we'd like to understand that this mechanism is orthogonal. So again, the mouse studies are really a way to build, like the in vitro studies, a lot of links in understanding this pathway, right? So we've done some work in the microglial cells. We'll get data from the mouse studies. And then obviously, we're committed to doing the human study. But it's a pretty exciting stage in this part of the NLRP3 pathway. So I've always been interested in Parkinson's, but this has opened a whole new area. I think we're sort of in the forefront of this with our molecule to be able to sort of connect the dots. And I'm looking forward to sharing the mouse data with you guys in a few weeks, end of the second quarter. I think your third question was. Potential for 2735 in HS. Potential for 2735 in HS. Yeah. So we think there's clear potential for a 2735 mechanism in HS. I just caution you that the results from the AbbVie study were very, very encouraging. But there isn't a real one-to-one correspondence between an IL-1 beta antibody such as canakinumab and an NLRP3 mechanism versus the AbbVie. It's an IL-1 alpha beta antibody as well as, for example, an IL-1 alpha beta trap such as rilonacept, right? So there's a little bit of an area there that has to be explored. But yeah, certainly, there is enough rationale for looking at NLRP3 molecule in HS. Thank you. We will take our next question from Derek Archila with Wells Fargo. Hey, Derek. Thanks for taking our questions. I guess just a couple on 2735. Given what you've seen in your phase I data in NodThera's NT-0796 positive outcome in their phase I-B, II-A, do you think getting to a phase IIb trial is now at deep risk? And then also, do you expect 3232 to differentiate from NT-0796 in Parkinson's? Yeah. Sorry, you were fading a little bit. So your question was, has the data from NodThera in their Parkinson's phase II-A de-risked our trial? Is that what the question? Yeah. So let me assume that's a question. So it's always good to see yeah, it's always good to see data from any drug in the class where there hasn't been a lot of data out there showing effects on biomarkers in the study, right? But again, for us, we believe from our phase I study, everything we've seen, this is an extremely well-behaved compound. It's suitable for QD dosing at low doses. We expect to have coverage of IC90 at doses starting at 10 to 12 milligrams. And it's a real clean single-order kinetics dosing profile. So we're looking forward to this 28-day study and generate our own data. Like I said, I don't have any doubts that we'll see effects on IL-1 beta downstream markers, NLRP3, again, IL-1 beta, IL-6, hsCRP. We'll establish our own biomarker profile both in blood and in CSF with respect to things like neurofilament light chain and other biomarkers as well. Now, there was some data from NodThera. But our compound is so well-behaved, we hit the target so hard that we'll have to set our own calibration for the phase IIa before we go into a longer phase II study. Thank you. We will take our next question from Sam Slutsky with LifeSci. Hey, good afternoon, everyone. I hopped on the call late, so if you answered any of my questions previously, just let me know. On the obesity preclinical study with 3232, just kind of generally speaking, how similar or different is the methodology to what NodThera did in their preclinical study? And then do you anticipate that there'll be any bigger conclusions that can be drawn from it other than just kind of the binary of it looks good or not on weight loss? Yeah. Good to hear from you, Sam, and happy to repeat the answers for you. I don't think I've ever in my 30 years spent so much time talking about mice studies, but happy to do so. So there's really no learnings from the mouse study that the competitor did. Again, it was a pretty standard DIO study. So you have obese mice. In olden days, you had to generate these mice by feeding them a high-fat diet for 15 weeks or longer. Nowadays, these are off the shelf. You can buy obese mice, diet-induced obese mice. In terms of so we have done these trials before, perhaps looking at different endpoints. In this case, the primary endpoint, obviously, is weight loss. And we look at secondary endpoints that I mentioned before, like effects on liver weight, body weight, body scan. We're also doing DEXA in this study. We look at lipids. We look at liver steatosis. We do staining in the liver. So everything that you would want to read out post the weight loss there as well. Really, again, like I said before, you need to look at individual readings from this study to understand how it translates or potentially translates into what you expect in humans. It's not a one-to-one correlation, right? These models are used for a number of things. You'll see them being used for developing drugs for diabetes. They've been used for DPP-4 inhibitors. They've been used for SGLT2. They've been used for GLP-1 agonist. Now, we're looking at NLRP3. So it's really a broad model. And you can take individual pieces from this model and then reconstruct what you would want to see in a human study, right? And again, we're excited about not just this model. This model is just a path for us to go into the humans. So we'll complete the models. We'll get you the data in a few weeks and then onto the human study. In the meantime, our biologists are actively trying to link the dots and understanding hypothalamic interaction with NLRP3 and effects on downstream. So just try to build a picture. Okay. That's helpful. And just real quick on 2735, on the potential prevention of MACE and pericarditis study. As you think about that landscape, unmet need, current treatment paradigm, where do you see the profile of 2735 kind of best slotting in? Yeah. Let me have Marty. We've thought a lot about it, but let him articulate this for you. Marty? Yeah. Sure, Sam. So obviously, there's some evolution in some of the management of cardiovascular disease. And so that'll sort of mature over the time course that we're developing 2735. I think on the recurrent pericarditis side, you have a pretty classic sort of niche orphan indication with limited therapeutic options. Currently, rilonacept's really sort of your go-to for difficult-to-manage refractory patients. It's obviously maybe less than perfect for some patients due to its nature. It's an injectable therapeutic. It's also a very expensive therapeutic. So there's some opportunities, certainly, to, I think, put forth an oral option for patients who are suffering with recurrent pericarditis symptoms. And I think that disease is often managed now with sort of a bit more of a scattered approach without necessarily a lot of consistency in treatment guidelines. And people use things like aspirin and steroids and colchicine and things like that. I think a very nice targeted NLRP3 inhibitor such as 2735 could play an important role. Obviously, the clinical pathway is heavily de-risked by the success of IL-1-driven biologics in this setting. Excited to kind of develop that and find the right slotting for that in the treatment paradigm. Got it. All right. Thanks, everyone. Thank you. We have no further questions at this time. I now turn the presentation back over to Dr. Raju Mohan for any additional or closing remarks. Yeah. Yeah. Thank you, everybody. Thank you to all on the call. So thank you for your continued interest in Ventyx. Obviously, a very exciting period for us. We look forward to connecting with you at the investor conference in the coming months, connecting with you on the mice data. We're looking forward to talking about our efforts with VTX002 partnerships, moving towards the phase III trial, and then hopefully reporting on and coming back and reporting on the ongoing Crohn's trial. So a lot to talk about. But again, for today, thank you all, and thank you to the team.