Ventyx Biosciences, Inc. (NASDAQ:VTYX) Q1 2024 Earnings Call Transcript

Ventyx Biosciences, Inc. (NASDAQ:VTYX) Q1 2024 Earnings Call Transcript May 11, 2024

Ventyx Biosciences, Inc. isn’t one of the 30 most popular stocks among hedge funds at the end of the third quarter (see the details here).

Operator: Good afternoon, ladies and gentlemen and welcome to the Ventyx Biosciences First Quarter 2024 Earnings Conference Call. [Operator Instructions] As a reminder, this conference call is being recorded. I would now like to turn the call over to Dr. Martin Auster, Ventyx’ Chief Financial Officer. Please begin.

Martin Auster: Thank you, operator, and 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’ Founder and CEO. Raju, please go ahead.

Raju Mohan: Yes. 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 1 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 QD, well exceeded IL-1 beta IC90 coverage in both plasma and CSF. Based on these data on our dose projection modeling, we estimate that VTX3232 doses as low as 12-milligram 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 excellent – showed an excellent tolerability profile in this Phase 1 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 2-ready compound. As we also communicated in March, we plan to rapidly advance VTX3232 into Phase 2 trials in high-value indications with substantial unmet need, beginning with the Phase 2a 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 inflammation as a key driver of Parkinson’s disease pathology by impacting new 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 neuroi 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 2 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 our Phase 2 trial of VTX2735 in patients with cryoprin-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-sensitive 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 2 data in CAPS patients is, therefore, a compelling proof of mechanism for VTX2735 for our peripheral inhibitor and for systemic inhibition of NLRP3-treated-related biomarkers in general, including hsCRP and IL-6.

And 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 indication with large addressable markets and substantial unmet medical need. So 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, or allosteric TYK2 inhibitor in Phase 2 development for the treatment of Crohn’s disease.

For VTX002, you’ll recall that we announced positive Phase 2 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 2 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 2 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 3 ready, and our teams continue to make preparations for our pivotal Phase 3 trial is ongoing.

Last month, we completed a productive End of Phase 2 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 2 trial may be sufficient to support approval of VTX002 with successful completion of a second pivotal 52-week trial in ulcerative colitis. And as we have previously indicated, efforts are underway to identify a partner or other source of non-dilutive financing to support this pivotal Phase 3 trial. Finally, our Phase 2 trial of VTX958, our allosteric TYK2 inhibitor and 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 end point 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. So 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 across 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 financial – of our first quarter financial results. Marty?

Martin Auster: Yes. Thank you, Raju. Our financial results for the first quarter ended March 31, 2024, 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 ‘24 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, cash equivalents 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 2 trial programs in psoriasis and psoriatic arthritis for VTX958. We continue to believe that our current cash, 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.

Operator: Thank you. [Operator Instructions] And the first question today comes from Michael Yee with Jefferies.

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Q&A Session

Unidentified Analyst: Hi, guys. Thanks for the question. This is Kyle for Michael. So on the CNS NLRP3 program, what do you think is promising for a 28-day study in human or 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 the company? Thank you.

Raju Mohan: Well, thanks. So let me address the second question first. So we – 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 the right forum for presenting it, so just stay tuned. In terms of your question about sort of what we expect to see in 28 days, there was plenty of studies out there, not just with GLP-1 agonist, with 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 the data are put out. In our mind, we have two – there’s two things happening.

One is, obviously, we’ve done – we’re repeating the set study that was published in diet in these obese mice. As we mentioned, it’s a monotherapy study with compound under control, and it’s a combination study with semaglutide, and we’re looking forward to reporting these results. We’re also, as we’ve said, committed to doing our own trial, 20-day trial in patients, and we think there’s biology there now that certainly links NLRP3 and NLRP3 activation in addition to hypothalamic control of obesity parameters or mechanisms such as feeding behavior. And I think that, that body of evidence will continue to grow as folks try to link the dots just like it’s – linked 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. But our own path here is planned, which is, again, put out the mouse data and then driving for our Phase 2a study in obese patients latter half of the year.

Unidentified Analyst: Alright. Thanks.

Operator: Thank you. Our next question comes from Yasmeen Rahimi with Piper Sandler.

Liam Hiester: Hi, this is Liam Hiester on for Yas. So I guess my first question is related to what’s the current tox package available for VTX3232? And then when moving on to the expected Phase 2 trial, what work still needs to be done in order to initiate in obese patients with additional CD risk? And then moving to 2735 with those Phase 2 trials, what are the rate-limiting steps and initiating a MACE or recurrent pericarditis trial there?

Raju Mohan: Alright. So let me start with the first one. So our first study is a 28-day study. These patients, it’s a similar study. We are planning with 28-day study in early Parkinson’s disease. And then we will initiate the longer-term studies in particular the obesity study if that merits the Phase 2 in the latter half of the year. So right now, on the tox package, we’ll 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.

Liam Hiester: Yes. So I guess, like for the 2735 assay, what is the rate-limiting steps for the initiation of the Phase 2 MACE trials and recurrent pericarditis?

Raju Mohan: There’s no – 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 time lines for the Parkinson’s obesity trial, and we lay out the time lines for the cardiovascular trials. Once those have been firmed up, there’s still rate-limiting step. It’s just a part of the planning process of going from a Phase 1 study to a Phase 2 study. So it’s just 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.

Liam Hiester: Great. And then actually, just one more question. So with VTX002, just wondering if you could provide like any more detail on the level of partnership interest. And then also any details from the End of Phase 2 meeting?

Raju Mohan: Yes. So on the End of Phase 2 meeting, we had a really good meeting with the FDA, and we laid our justification for a Phase 3 trial with a single dose. And we believe this should serve as a pivotal trial as should the first one. And we’ll have – continue to have a 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 specifics. We think this compound continues to show a very strong endoscopic remission. As we’ve showed it 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 a precedent with S1P1 modulators. And as we said, we are aggressively in the midst of getting interest from pharma partners across wide range of folks and stay tuned. And we’ll update you guys once those things progress to something that we can talk about.

Operator: Thank you. Our next question comes from Emily Bodnar with H.C. Wainwright.

Emily Bodnar: 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 could impacts on motor symptoms. And maybe if you could provide a bit more on study design for obesity in terms of like how many patients you’re planning to evaluate? And are you planning to exclude diabetes patients in that study? Thanks.

Raju Mohan: Yes. Good question. So again, on specific of the trial, and we’re not trying to be cagey. We don’t – let’s say, disclose every aspect of this trial. Once we have it, it will 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 of this trial to see effects of this molecule on glial content and activation as it translates into eventual effects on astrocytes and eventually neuro 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 1, we’ve seen some movement in these trials – 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 1 trial with 3232, we also showed effects on these biomarkers even in healthy volunteers and in the CSF, right? So those are NLRP3-treated biomarkers. And then you have the other side of neurodegenerative markers in particular with – 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 an expectation of seeing any sort of meaningful effects of the short trial.

And 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. And these are 12 months or longer trials.

Emily Bodnar: That makes a lot of sense. Thank you.

Operator: Thank you. We will take our next question from Vikram Purohit with Morgan Stanley.

Gospel Enyindah-Asonye: Hi, everyone. This is Gospel on for Vikram. We have one question regarding your CD program. What is hard for continuing VTX958 in Crohn’s disease based on the data expected in the second half of the year?

Raju Mohan: Yes. Thanks, Vikram. And perhaps, I’ll let Marty address this. Marty?

Martin Auster: Yes. Thanks for the question, Gospel. So for that trial, the primary end point is a change in CDI score and then we’re looking at key secondary endpoints that include like 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 recent – more recently developed products like upadacitinib. You’ll see CDI changes in the Phase 2 in the range of the upper double digits to kind of low hundreds as sort of a kind of a meaningful type of response on that marker. We’re adequately powered to sort of detect statistical significance in 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 versus relative 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 here in the next several months.

Gospel Enyindah-Asonye: Thank you very much.

Operator: Thank you. We will take our next question from Alex Thompson with Stifel.

Alex Thompson: Great. Thanks for taking my question. I guess first one on 3232 to follow-up a little bit on the DIO mask 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 2? 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 at AAD and whether you would consider an indication like HS in the future? Thanks.

Raju Mohan: Yes. So, first on human dose equivalent in the mouse study, so the mouse – 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 have done a Phase 1 trial with biomarkers in plasma and in CSF. We have 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 a driver or IL-18, but IL-1 beta and IL-18 are the drivers of the disease pathologies, and that’s the calibration.

So, what doses do we need in humans to then have complete aggregation, a 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 of a Parkinson’s trial for any other Phase 2 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 losses, see effects on other endpoints, and it again 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 have 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, we – 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 is 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 is a human model, its 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 competitive data, we designed this trial with a compound with the sum of the tight control, with adequate controls with a placebo.

First thing 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 that 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 would 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 have built – we have done some work in the microbial cells, we will get data from the mouse studies. And then obviously, we are committed to doing the human study, but pretty exciting stage in this part of the NLRP3 pathways. Always been interested in Parkinson’s, but this has opened a whole new area. And I think we are sort of in the forefront of this with our molecule to be able to sort of connect the dots, and 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…

Martin Auster: Potential for 2735 in HS.

Raju Mohan: Potential for 2735 in HS, yes, so we think there is potential – clear potential for a 2735 mechanism in HS. I will 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 a IL-1 beta antibody such as canakinumab 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 is a little bit of area there that has to be explored. But yes, certainly, there is enough rationale for looking at analog PC molecule in HS.

Operator: Thank you. We will take our next question from Derek Archila with Wells Fargo.

Derek Archila: Hi there. [Technical Difficulty] Thanks for taking our questions. I guess just a couple on [Technical Difficulty]. Given what you have seen in your Phase 1 data in your NT-0796 positive outcome in their Phase 1b/2a, do you think getting to Phase 2b trial is now de-risked? And then also, do you expect 3232 to differentiate from NT-0796 in Parkinson’s?

Raju Mohan: Yes. So, if I – sorry, you were fading a little bit. So, your question was, has the data from NodThera in their Parkinson’s Phase 2a de-risked our trial, is that was the question. Yes, so let me assume that’s the question. So, 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 1 study, everything we have 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 milligrams to 12 milligrams. And it’s a real clean single-order kinetics dosing profile. So, we are looking forward to this 28-day study and generate our own data.

Like I said, I don’t have any doubts that we will see effects on IL-1 beta downstream markers NLRP3. Again, IL-1 beta, IL-6, hsCRP, and we will establish our own biomarker profile both in blood and in CSF, with respect to things like neurofilament light chain and other biomarkers as well. And there was some data from NodThera. But our compound is so well behaved because we hit the target so hard, that we will have to set our own calibration for the Phase 2a before we go into a longer Phase 2 study.

Operator: Thank you. We will take our next question from Sam Slutsky with Life Science.

Sam Slutsky: Hi. Good afternoon everyone. I hopped on a tad 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 will be any bigger conclusions that were drawn from it other than just kind of the binary of it looks good or not on weight loss?

Raju Mohan: Yes. Good to hear from you, Sam, and happy to repeat the answers for you. I don’t think I ever in my 30 years spent so much time talking about mice studies, but happy to do so. It’s – so there is really no learnings from the mouse study that the competitor did. Again, it was a pretty standard IL 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 in these 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 end points, as I mentioned before, the effects on liver weight, body weight, body skin.

We have – we are also doing dexa in the study to 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 the study to understand how it translates or potentially translates into what you expect in humans. It’s not a one-to-one correlation. These models are used for a number of things. You will see them being used for developing drugs for diabetes. They have been used for DPP-4 inhibitors. They have been used for SGLT2. They have been used for GLP-1 agonist. Now, we are looking at NLRP3. So, it’s really a broad model, and you can take individual pieces on this model and then reconstruct what you would want to see in a human study, right.

And again, we are excited about not just this model. This model is just a path for us to go into the humans. And so we will complete the models. We will get you the data in a few weeks and then on to the human study. And in the meantime, our biologists are actively trying to link the dots in understanding hypothalamic interaction with NLRP3 and effects on downstream, so just trying to build a picture.

Sam Slutsky: Okay. That’s helpful. And just real quick on 2735 on the potential prevention of MACE in pericarditis study, you think about just that landscape unmet need currently in paradigm, where do you see the profile of 2735 kind of best slotting in?

Raju Mohan: Yes. Let me have Marty. We have talked a lot about it. Let Marty articulate this for you. Marty?

Martin Auster: Yes, sure, Sam. So, obviously, there is some evolution in some of the management of cardiovascular disease. And so that will sort of mature over the time course that we are 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 your sort of your go-to for difficult to manage refractory patients. It’s obviously may be less than perfect for some patients due to its nature is an injectable therapeutic. It’s also a very expensive therapeutics. There is some opportunity 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 prednisolone [ph] and things like that. And I think a very nice targeted NLRP3 inhibitor, such as 2735 could play an important role. And obviously, the clinical pathway is heavily de-risked by the success of IL-1 driven biologics in the setting. So, excited to kind of develop that and find the right filing for that in the treatment paradigm.

Sam Slutsky: Got it. Alright. Thanks everyone.

Operator: Thank you. We have no further questions at this time. I will now turn the presentation back over to Dr. Raju Mohan for any additional or closing remarks.

Raju Mohan: Yes. Thank you everybody. Thank you to all on the call. So, we 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 are looking forward to talking about our efforts with 002 partnerships, moving towards the Phase 3 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.

Operator: Thank you everyone. This concludes today’s teleconference. We appreciate your participation. You may disconnect.