Ventyx Biosciences Inc (VTYX) 2022 Q3 法說會逐字稿

Good afternoon, ladies and gentlemen, and welcome to the Ventix Biosciences Third Quarter 2022 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, Fintex Chief Financial Officer. You may begin.

Thank you, and good afternoon, everyone. Welcome to Ventyx's conference call and webcast where we'll be discussing our third quarter 2022 financial results and providing a business update. As a reminder, the company's most recent investor presentation can be found on our website at www.ventyxbio.com and the Investors tab in the News & Events section. Before we begin today, I would like to remind everyone that this conference call and webcast will contain forward-looking statements about the company, including without limitation, statements about the anticipated timing of commencement, enrollment and completion of clinical trials for our product candidates, the anticipated timing of release of clinical trial data, the market opportunity for our product candidates and the expected time frame for funding operations with current cash, equivalents and marketable securities. These statements are subject to risks and uncertainties that could cause actual results to differ. Factors that could cause actual results or outcomes to differ materially from those expressed in or implied by such forward-looking statements are discussed in greater detail in our most recent parodic reports filed with the SEC. Please note that these forward-looking statements reflect our opinions only as of the date of this call, and we undertake no obligation to revise or publicly release the results of any revisions to these forward-looking statements in light of new information or future events. With that, I'll hand the call over to Dr. Raju Mohan, Centex's Founder and CEO. Raju, please go ahead.

Yes. Thanks, Martin and thanks, everyone, for joining our call this afternoon. So just to start, let me briefly run through the agenda for this afternoon. So I'll provide a high-level business update and review recent highlights, and then I'll hand the call over to our President and Chief Medical Officer, Bill Sandborn, and Bill will provide updates across our pipeline programs, a more detailed update across various programs. And then I'll turn the call back to Martin for a brief overview of our third quarter financial results before we open the call up for Q&A. So it's been just over a year since our IPO last October, October 2021, and I couldn't be prouder of what the Ventyx team has accomplished over the last year, and there is a lot more to come. So let me first start with this quarter. So we presented positive top line results from our allosteric TYK2 inhibitor, VTX-958 Phase I results. And as we've disclosed, we believe these data demonstrate a potential best-in-class safety profile, and this may drive clinical differentiation in relevant disease populations by allowing us to target levels of TYK2 inhibition comparable to currently prescribed biologics. We also believe greater TYK2 suppression and greater suppression of TYK2 mediated pathways has the potential to yield improved efficacy in indications such as psoriasis and psoriatic arthritis than previously shown by deucravacitinib or so TYK2. For indications where greater levels of cytokine inhibitions are required, such as for Crohn's disease, we believe VTX-958 may demonstrate greater efficacy than less selective TYK2. inhibitors, and Bill will provide additional details and commentary during his remarks. During the third quarter, we were also pleased to see the FDA grant approval of Bristol-Myers 2 inhibitor Sotyktu as the first approved TYK2 inhibitor. Notably, the drug label is quite different from other oral anti-inflammatory classes such as JAK inhibitors and contained no black box warning. This, we believe, this lack of black box warning we believe will support long-term physician and patient uptake of this important neo therapeutic class. We believe the $20 billion-plus global psoriasis market is ripe for disruption as new competitive agents emerge, and we believe that the TYK2 inhibitor class is well positioned to be a key driver of this change, again, with VTX-958 positioned as a potentially best-in-class drug. Finally, in mid-September, we completed a successful private placement of common stock that yielded gross proceeds to Ventyx of $176.6 million, extending our capital runway to do well over 2 years into 2025. This strong cash position is expected to provide us with resources to generate meaningful Phase II proof-of-concept data across our portfolio of oral immunology drug candidates and allow us to seamlessly prepare for future Phase III trials. Before I turn it over to Bill to highlight and more detailed progress across our portfolio, I do want to remind the audience today that Ventix at its core is much more than VTX-958 or any other single drug candidate in our portfolio. At our core, we are driven by our passion to discover and develop innovative medicines that have a meaningful impact on the lives of patients. So to that end, I am very happy to announce we are planning a science-focused R&D Day on January 26th of next year in New York City. And at this event, we will provide additional details on our internally discovered wholly owned pipeline of drug candidates, along with updates on our development plans for what is shaping up to be a very busy 2023. So with that, I'm going to hand you over to Bill.

Thank you, Raju, and good afternoon, everyone. While VTX-958 remains a central part of the Ventyx story, there is so much opportunity within our pipeline to improve therapeutic options for patients, and I'm excited to be providing an update on our clinical progress with you this afternoon. Let's start with VTX-958. We are very enthusiastic about the potential of this compound. Following our successful Phase I results, we have been working to rapidly advance this program and product into Phase II, and we remain on track to initiate Phase II clinical trials in psoriasis, Crohn's disease and psoriatic arthritis during this quarter. We expect the first Phase II trial to be in moderate to severe plaque psoriasis patients, we intend to explore the dose response of VTX-958 as pathway inhibition is increased. We will dose VTX-958 to achieve exposures in our Phase II trial across the range that includes IL-12 and IL-23 target coverage that approximates Sotyktu exposure levels that we at the approved dose of 6 milligrams QD, which would provide IC50 coverage for approximately 9 hours as well as doses that would achieve exposure levels that we anticipate would provide trough coverage of TYK2 around the IC90 level. In psoriatic arthritis and Crohn's disease trials, we will emphasize robust target coverage. As Raju mentioned, we will be hosting an R&D Day in January, and we look forward to sharing more specific details on trial design for all 3 of these Phase II trials at that time. I should also add that launching 3 Phase II trials with VTX-958 this quarter is a substantial undertaking. In the last several quarters, we have assembled a truly talented and dedicated group of individuals who have come together to form an amazing team. While we're gearing up for the 3 planned Phase II trials, we have been conducting preclinical evaluations of an extended release formulations of VTX-958 that can approximate the duration of TYK2 coverage that we demonstrated in our Phase I trial with convenient once-daily oral dosing. We expect to evaluate our extended release formulations in human relative bioavailability studies in early 2023 and to be in a position to provide an update in the first half of 2023. Our goal is to have an extended release formulation of VTX-958 ready for use in Phase III trials, which we expect could begin in 2024. Now let's turn our attention to VTX002, our selective S1P modulator, which is in an ongoing Phase II induction trial for the treatment of moderate to severe ulcerative colitis. This trial is designed to enroll approximately 180 patients across 3 cohorts, low dose and high dose arms of VTX002 and a placebo group. The trial's primary efficacy endpoint is clinical remission at 13 weeks using the 3-component modified Mayo score. We believe that VTX002 has the potential to improve upon other S1P1 receptor modulators, zeoposia and etrasimod in patients with ulcerative colitis through rapid and greater lymphocyte reduction, which, if achieved, may correlate with higher rates of clinical remission and improvement in other clinical response measures. We have been guiding for top line data in 2023, and we remain comfortable with that guidance. Recent enrollment trends have been strong. And based on the current trajectory, we estimate Phase II enrollment to be complete by mid-2023. Next, let's look at VTX2735 our peripheral NLRP3 inhibitor compound. NLRP3 remains a very exciting target with potential to impact a broad range of dermatologic, rheumatologic and cardiovascular diseases. We released Phase I data for VTX 2735 in the second quarter, which demonstrated a safe and well-tolerated profile in addition to strong evidence of target engagement and pharmacodynamic effect, including substantial impact on key markers of inflammation such as high-sensitivity C-reactive protein. We plan to initiate a trial in an ultrarare disease resulting from gain-of-function mutations in the NLRP3 gene known as CAPS in the fourth quarter. We believe that this small study will confirm clinical proof of mechanism while providing incremental safety data and evidence of target engagement in a patient disease setting. Meanwhile, we have been actively narrowing down the large list of potential indications in the disease areas that I mentioned earlier, and we intend to provide an update on the selection of an additional Phase II indication during our R&D event in January. This indication will be focused on a larger commercial opportunity. Our fourth pipeline candidate is our CNS penetrant NLRP3 inhibitor compound VTX3232. We remain on track to initiate a Phase I trial in the first quarter of 2023. We are very excited about this novel drug candidate, which we believe has the potential to be a first mover among truly CNS penetrant in NLRP3 inhibitors and may have the therapeutic utility and a number of neuroinflammatory diseases with high unmet need, including Parkinson's disease and Alzheimer's disease, among others. We believe that it also has potent peripheral NLRP3 inhibition. This concludes our pipeline update for now. In summary, we continue to make great progress across our wholly owned, internally discovered portfolio of drug candidates. I'm so proud of the team's efforts, and we look forward to sharing more with you during our R&D Day in January. Before we move to Q&A, I'd like to hand the call back to Martin for a brief discussion of our financial results.

Thanks, Bill. I'll briefly summarize our financial results for the third quarter now. R&D expenses were 25.5 million in the third quarter of 2022 compared to 10.5 million in the third quarter of 2021, reflecting advancement of our pipeline into later stages of clinical testing. We continue to expect that our R&D expenses will trend upwards over the balance of the year in 2023 as we launched the 3 Phase II trials for VTX-958 and continue to build out our clinical pipeline, as Bill alluded to earlier. G&A expenses in the quarter were $6 million compared to 2.2 million for the third quarter of 2021 and net loss in the third quarter was 30.5 million compared to 12.8 million in the third quarter of 2021. Approximately 4.2 million of this net loss in the third quarter of 2022 represents noncash stock compensation expense. Cash, cash equivalents and marketable securities were 412.4 million as of September 30th, 2022, and we believe our current cash equivalents and marketable securities are sufficient to fund planned operations into 2025. This concludes the prepared remarks from this afternoon's call, and I'll now turn the call back to the operator to commence the Q&A session, where I'll be rejoined by our CEO, Dr. Raju Mohan; and President and CMO, Dr. Bill Sandborn. Operator?

Thank you. The floor is now open for questions. (Operator Instructions) Our first question comes from Michael Yee of Jefferies.

Hi, good afternoon. This is Janine for Michael Yee on the line. Maybe 2 questions for me. We're aware that a competitor will be reporting Phase II top line data for their TYK2 programs pretty soon. So could you comment on, first of all, your differentiation for your molecule? And then Bill maybe comment on how you would interpret the read-through of the results and how should market view it for Ventyx? And second, for the S1P program, I understand you're guiding data in 2023. So could you comment on what do you want to see in the study and your expectations?

Great. Yes, thank you. So let me take the first question, and then I'll have Bill address the S1P1 question. So in terms of how we differentiate from competitor compounds and we've shown the differentiation on a molecular basis with docravacitinib. So we've shown extremely high selectivity of 4,000 fold more selective for the tick to Alisteric domain. We've shown how this translates into selectivity for TYK2 pathway. So we hit all pathways robustly, 1223 and interferon alpha. We have no interaction with JAK1 pathways. We have no interaction with no innovation of IL-10, IL-10 22, 4, 6 and if you're on gamma. So we've shown the molecular differentiation with (inaudible). More importantly, we've shown clinical differentiation in terms of target coverage as well as the safety, which is the key to achieve meaningful coverage of IC50 AND IC90 and Bill during the Phase I data dissemination actually compared with Decrava and the competitor compound in terms of what has been seen across head-to-head trials in Phase I in terms of significant effects on dermatological effects as well as other hematological effects as well. So we believe with our profile that we've demonstrated again on a molecular basis against Sotyktu and more importantly, on a clinical basis for what data is publicly available, remember, for the cravacitinib and the competitor compound that you just mentioned, we have shown meaningful differentiation, target coverage but more importantly, ability to cover the target IC50 and IC90 for 22 to 24 hours without any significant impact on being able to dose escalate given the profile of TX-958. Now in terms of how we position ourselves with respect to this competitive data, I think it all depends what the data are and how the data are in terms of efficacy versus safety of this compound. But what we can position ourselves is what we've seen thus far, which is, again, the safety manifestations of safety events that have shown up for these compounds to Crave and the competitor versus what we have seen, which is a very well-tolerated program or molecule all the way up to the highest dose in MAD, our ability to cover the target IC90 for 22 to 24 hours and few to mild events that Bill had shown compared to what competitors have shown in head-to-head trials. So I think any more follow-up question follow up question on that, otherwise, I'll hand it over to Bill.

All right. So with regard to the our S1P modulator, VTX002, this is a relatively short half-life drug with a 20-hour half-life. That compares to about 30 hours for etrasimod and many days for the dominant long-acting metabolite with ozanimod symposia. So the short half-life allows the drug to act quickly. The design of our trial is a 1-week dose titration period to address the first dose heart rate reduction effects that you see with this class and we very carefully worked that out in Phase I. And then a full 12 weeks of target dosing with the 2 active doses. The primary endpoint is remission and some of the key secondary endpoints include things like endoscopic improvement, so pretty typical. If you look at other S1P modulators, there are 4 approved in the multiple sclerosis arena. There's fingolimod or Gilenya and ponesimod, Ponvory and Siponimod or Mayzent in addition to ozanimod or zyposia. The other 3 drugs, besides symposia in the multiple sclerosis setting are dosed to have lymphocyte reductions in the sort of 65 up to high 70, 78, 79% range from baseline. By contrast, you see about 45 to 50% reduction with symposia, and you saw a reduction in the 40s with etrasimod in Phase II and Phase III trials. So it's really considerably lower lymphocyte reduction. And there are hints that as you get up to that greater lymphocyte reduction in multiple sclerosis that you see greater degrees of efficacy. So our clinical trials or trial is really designed to have the top dose be up in that higher range of lymphocyte reduction, which has not yet been tested in ulcerative colitis. And we believe, based on the multiple sclerosis experience that, that could lead to incremental efficacy over the efficacy that's been observed with both symposia and etrasimod. Operator

We'll take our next question from Yasmeen Rahim of Piper Sandler.

Hi, this is (inaudible) it's just 2 for us. One is, can you provide a little bit of more color on how are you thinking about the different in doses for Crohn's versus the psoriasis study? And then the second part is like what are some of the steps that are remaining in order to initiate the Phase II studies in this quarter?

Yes. So let me have Bill address both of those. Bill, why don't you take it.

Yes. I think from the dosing, what we had in our earlier prepared remarks is that we will look across the range of doses that really for all of the drugs that at the top end, allow for exposures that would cover IC90 for much of a majority of the day. And we think that, that is very different from the doses that have been achieved with other competitor product or the target coverage that has been achieved with other competitor products and particularly in the context of dermatologic adverse event, off-target tolerability. For Crohn's disease, we sort of think of but it's equally true actually for psoriasis. You have IC75 and 90 and 100 rates with psoriasis that are considerably higher with anti-IL-23 antibodies, where we believe that IC90 coverage for IL-23 would be 24 hours. And there's a delta between what you see with the approved TYK2 inhibitor for those outcome measures and what you can see with monoclonal antibodies. So it's that difference in target coverage that we think will give differentiated efficacy in psoriasis. But that's also what makes it possible to see efficacy in Crohn's disease. So we think that it's essential to have IL-23 IC90 coverage for most or all of the day to see robust efficacy in Crohn's disease and our dose range in the Crohn's trial will encompass exposures up to that level. Yes. Sonal, in terms of what remains to be done, we've publicly stated we will start all 3 Phase II this year. It's November. It's a lot of work as the 3 trials just all the work that goes into prep, but everything is on track and we're planning to initiate all 3 trials in less than 2 months, right? Stay tuned.

Thank you.

Thank you. Again, [Opperaator Instructions) our next question comes from Sam Slutsky of LifeSci Capital.

Hi, thanks for the update. Got a few questions from my end. So first, given that there's proof of concept with deucravacitinib and lupus at this point, just curious on how you're thinking about that indication for 958. And then when might be the right time to expand development there, if you want to go that route?

Yes. Again, thanks, Sam. And obviously, we've talked a lot about this since the deucravacitinib data came out at EULAR but let me have Bill give you some color on our thoughts. And obviously, we'll talk a lot more about this in our R&D Day, but for now, let me have Bill address this.

Yes. I think we saw the ducravacitinib data that presented at EULAR as robust evidence of efficacy in lupus. And so there's every reason to believe that, that Phase II data with ducravasitinib reads through to other TYK2 inhibitors who would have similar or greater interferon alpha target coverage in the IC50 and IC90 levels. So we certainly will have coverage that meets and exceeds the coverage that demonstrated efficacy with ducavocitinib in lupus. We're still considering the options about whether we would trigger a program in lupus or not. So we haven't made a decision about that. But we believe that all the translational medicine data indicate strongly that the efficacy that we're seeing with dupavacitinib reads through to our compound.

Got it. Okay. Next one I have is just there's some interesting data recently from Janssen, where the combined an IL-23 inhibitor with a TNF inhibitor for UC and they saw a higher remission rates compared to either therapy alone. So I guess given your pipeline , I'm curious on how you're thinking about the potential for combination approaches overall? And then what it makes sense to do a tip to S1P1 combo at some point in the future or some other kind of combination approach?

Let me just say that at a high level, I think, and I think our company thinks that combination therapy is very interesting and will play a role in the future therapy of inflammatory bowel disease and potentially other autoimmune diseases. That Janssen data in ulcerative colitis with the combination of an anti-TNF and anti-IL-23 is very interesting. It essentially doubled the remission rates, really, with the way that we plan to dose VTX-958 at the higher end, we think we have very close to anti-IL-23 antibody target coverage for the target. And so you could even imagine something more simple and straightforward than what you were posing, which is to mix VTX-958 with the TNF blocker, we need to sort out the safety and efficacy and dose response first with the clinical trials. So as monotherapy, and that's our focus right now. But the potentials there for the future. I think mixing a TYK2 inhibitor with an S1P modulator is interesting, it would require a lot of thought and diligence around what you anticipate the benefit to be on one hand and any risk on the other. So it's a great question, something we will think through in the months to come and years to come, but it's not the focus of our current development plan.

Got it. Okay. And just last one for me. Just on the new formulation of VTX-958 the QD1, I realize it will be in the clinic, but just anything more you're able to say on kind of the animal data you have to date and translatability historically of that?

Yes. So the beauty of the approach we have is that we build and test our ER formulations protypes in a human setting right from get-go. And so really optimizing the prototype in a sort of build and test model from human data, right? And so we lay out a plan with a clear target product profile, which is to achieve the QD dose, the unmatched coverage we see, which is IC90 for 20 to 24 hours. And then we have a number of methods where we validate this ER tablet and its exposure profile for QD dosing to have this target coverage, which is part of the TPP and then we'll take it into a human PK study and then rapid iterations once we get the first read to the target profile. So really optimizing from a base camp all the way to our target peak and as Bill said, we hope to wrap that up in the first half of the year, and we'll happy to show and share that data on the QD tablet. So all on track, all good. Stay tuned.

Okay, thanks.

We'll take our next question from Emily Bodnar of HC Wainwright

Hi, two for me. First, do you anticipate that you'd have any data from either of the Phase II studies that you're planning to initiate for 958 in 2023 or one is kind of the earliest that we should be looking for results. And for VTX002, do you expect to initiate any studies for other indications besides ulcerative colitis like Crohn's disease or atopic dermatitis, thanks.

Yes. So on data from Phase II, so our first trial to kick off is our trial in moderate to severe plaque psoriasis. All 3 will start this year, but we expect the psoriasis data to read out in 2023. So you will see Phase II data for the Phase II trial in moderate to severe patients with 958 in 2023. On the second question, Bill why don't you just address that about other indications for 002 that we might consider.

Yes. Other products in that field that are being evaluated have indications that include Crohn's disease. There's a trial in eosinophilic esophagitis and a trial in atopic dermatitis so those are all possibilities. I think we're watching the landscape play out. We're a little busy at the moment for all the reasons we've been discussing this half hour, but we do see the interesting potential in some of these other indications, and other possibilities are certainly in our mind.

Got it, thank you.

Thank you .(Operator Instructions) We'll take our next question from Alex Thompson of Stifel

I guess I wanted to follow up again on upcoming data from NIMBUS. I guess, in the Phase III for Ducera at 12 weeks, they showed about a placebo adjustment at 75 around 40%. And I do wonder if assuming there's no safety issues in the NIMBUS trial, if they don't succeed in getting a better past 75 rates than that, how much confidence can we have in this better exposure efficacy hypothesis for TYK2 inhibition? Thanks

So we are positioned to have the best-in-class coverage. We have the best-in-class coverage for IC90 and there is limited data on coverage, but there is data from the Phase II trial, in particular for Ducray, where they had higher coverage for IC50 for 16 to 18 hours at the 12-milligram dose and about 9 hours for the 6-milligram dose. So there is data out there that suggest you can get meaningful incremental differences in passing 75 and even passing 90 as you get higher coverage. And so while IC90 doesn't exist right now for efficacy for oral TYK2, we have enough precedence from biologics to get biologic-like efficacy, you need biologic-like coverage. And so obviously, we'll wait and see what NIMBUS's data look like, right? So in terms of but there's clearly a data set out there from biologics on coverage and also from (inaudible) across not just the psoriasis travel, but that dose efficacy response available for psoriatic arthritis as well. Bill, you want to add anything to that.

Yes. Just to reframe what you said slightly. If you think about dose finding, as Raju said, that with ducravositinib in various trials, we've seen 3 milligrams BID and 6 milligrams once a day and then 6 milligrams BID and 12 milligrams once a day. And the difference between 3 BID or 6 ones a day and then stepping up to 6 BID or 12 ones a day, you improve by as much as 70, 80% the IC50 coverage going from 8 or 9 hours to maybe 15 hours, but the IC90 coverage is not hit at all in any of those doses. And recall in Phase I with ducravacitinib as you went up to 12 BID, you had 78% of patients having skin adverse events. So that product is really locked in by the off-target adverse event in the skin manifestations. So yes, there's dose finding with ducravacitenib, but the whole range of doses are not really leading to the exposure range that is an interesting experiment because it's limited by the therapeutic window. So as other competitor data reads out and you see different doses and whether there's dose response and what the maximum PASI75, and 90 and 100 responses are, you want to ask yourself whether the real exposure response for IC90 coverage of IL-12/23 was done. And if the doses and the resulting exposures are not getting to most of the day coverage of IC90, then the question hasn't really been addressed.

Okay, I appreciate it.

Thanks, Alex.

We'll take our next question from Jeff Jones of Oppenheimer.

Thanks guys and I appreciate. On the S1P front, Pfizer talked a little bit more about etrasimod on their earnings call. And I guess in that context, they talked about being no complex dose titration. So interested in your thoughts on the dose titration versus not in adoption and use as well as the population they studied in being the bio-naive JAK naive population and the population you're using for your ongoing Phase II, thank you?

Yes. Let me have the S1P1 expert address it.

Well, I think defining a dose titration regimen as complex is an overstatement of the facts. It's a blister pack and you have pills that you push out of the blister every day it's not a big deal. So I don't think that, that is an important limitation. In terms of patient populations, etrasimod recruited patients with moderate to severe ulcerative colitis and there was a mixture of biologic or advanced therapy naive and advanced therapy failure patients. As I recall, it was something like a 60-40 split of naive to failure. And our trial is still running different countries coming on at different times. So you don't know what the final mix will be until the trial is fully recruited, but we are recruiting a mixture of advanced therapy naive and failure patients similar to other drugs in the class.

Okay, thank you.

Thanks Jeff.

We'll take our next question from Tiago Fauth of Credit Suisse.

Hi guys, it's John on for Tiago. On VTX002, can you just talk about the significance of its selectivity for S1P receptor 1 specifically and the implications of avoiding receptors 2 through 5. What are the potential trade-offs, if any, in terms of efficacy or safety for having a more selective approach, thanks.

Yes, great question. So there's a plethora of data for effectively for S1P1 and let's not just limit ourselves to (inaudible) data across multiple MS trials and the biology of S1P1 class, the biology of how S1P1 class of drugs mediates its efficacy primarily through lymphocyte equestration. It's really S1P1 receptor or S1P1 modulation that drives that efficacy. So as a class, you see compounds that are selective for S1P1, most of these drugs crossed over to some extent, into S1P5, even though they're highly selective SMP1. Really not a consequence to us. P5 is primarily expressed in the CNS and was eventually a thought to be a consequence for MS. Our drug, let me remind you, is a non CNS-penetrant compound, so that P5 activity is really inconsequential in driving efficacy driven through S1P1. Now we've seen reference to S1P4 with one particular compound I think was sorry with etrasimod in particular. And from our point of view, first of all, there's not an update on S1P4 class of drugs. But just as a biology, S1P4 is primarily involved in denditric cell trafficking. So again, no real relevance to S1P1 and its role in IBD or UC or the mechanism. So not having S1P4 is, again, a highly selective drug no nonselective nonrelevant crossover. So again, a highly selective compound and unlike (inaudible) it doesn't even hit S1P4. And there's only positive consequences to being selective for a drug.

Got it, thank you so much.

You're welcome.

Thank you. I would now like to turn the call back to Dr. Raju Mohan for some closing remarks.

Yes. Well, thank you all. Thanks to the team here. We're really pleased to present our accomplishments for this quarter to highlight attributes of 958 or 2 in our LRP portfolio. And so really, I'd like to welcome you all to our R&D Day in New York, January 26 marked the date and we'll be sending out more details on that event in the near term. So I'll look forward to seeing you all there and answering questions in person. So thank you all again.

This concludes today's Fintech Biosciences Third Quarter 2022 Earnings Conference Call. Please disconnect your line at this time, and have a wonderful day.