Conference Transcript - NMRA 2026-04-13

Ami Faria, Analyst — Needham

Good morning again, everyone. Thanks for joining the next session with Nomura Therapeutics. I'm Ami Faria, Biotech Analyst here at Needham. It's my pleasure to be hosting the team from Nomura. We've got Josh Pinto, who's the president of the company, along with Nick Brandon, Chief Scientific Officer, and Bill Arora, Chief Operating and Development Officer. Maybe if I could turn it over to you, Josh, for some opening remarks and maybe talk about the priorities for the company for this year.

Josh Pinto, CFO

Yeah, absolutely. Nami, thank you for having us today. Numura was founded to confront one of the greatest medical challenges of our generation, which is the global brain disease crisis. And our therapeutics pipeline has really matured where we've got four programs now in or entering the clinic, all that are going to make substantial progress this year. At the end of March, when we put out our 10K in annual release, we announced that Novacoprint had completed last patient in in the first quarter, and we will have data for Coastal 2 and Coastal 3, which is our Phase 3 studies of major depressive disorder in the second quarter of this year. So very excited for that upcoming catalyst. We've announced new data from NMRA 511 in patients with Alzheimer's disease agitation. We actually view some of this data as some of our most compelling around the mechanism. Really what this program is showing is that it can have a clinical effect size comparable to existing approved agents such as Rexalty, but with a much more tolerable safety profile. So we're really excited about moving this program forward. We'll be looking to dose higher as the safety and tolerability profile for NMRA 511 looked very clean, you know, and we'll complete a MAD extension this year and ultimately look to initiate a phase two study in 2027. We announced that with our M4 franchise, we are prioritizing NMRA 898. After completion of the SAD studies, it looks really fantastic. PK to support once daily dosing. We're seeing everything we'd want to out of a range of pharmacodynamic measures. and so that program will move forward. We'll complete the SADMAD studies in the third quarter and then look to move it into a phase 1b proof of concept study thereafter and then finally with our NMRA215 program, this is our NLRP3 inhibitor which we're moving forward for obesity. We announced data from our 12-week DIO study which validated the switch and maintenance paradigm as well as you know some tox data and so we'll be looking to move that program into the clinic early 2027 once we complete the repeat 13-week RAT talk study, as we announced. This is all supported, Ami, by a very strong and robust balance sheet. We ended the year with about $180 million on it, and that provides cash runway into the third quarter of 2027.

Ami Faria, Analyst — Needham

Great. Josh, you've got a multitude of very interesting assets. I feel like each alone can be meaningfully transformative for the company. Is there one that you guys are more excited about than the other?

Josh Pinto, CFO

Yeah, so we intentionally built the pipeline, Ami, so that we could have multiple shots on goal at any given point, and there wouldn't be any one program or the other. As we sit here right now, obviously, we're in a quarter. The second quarter, we're going to have major data and catalysts for NovakaPrint with Coastal 2 and 3 data coming out, so that's going to be very exciting. And then obviously, hopefully, some de-risking data as we move forward with 215 on the repeat 13-week RAT Talk study. So very exciting events from both of those programs, you know, coming up over the next number of quarters.

Ami Faria, Analyst — Needham

Yep, yep. So maybe if we could talk a little bit about Novacoprant. I wanted to understand the regulatory backdrop here. The FDA has talked about the potential for approving drugs based on a single pivotal study. And I don't know whether this may be quite relevant, given kind of where your program is with the coastal studies here and some of your plans to analyze the data for, you know, the patients across Coastal 2 and 3 that have been enrolled after the data reader from Coastal 1. So maybe put it in context for us, how important is that commentary from the FDA around their willingness to approve drugs on one pivotal study?

Bill Aurora, Other

Good morning, Ami. This is Bill. I'll be happy to take this question. As you said, with the recent FDA publications, including their commentary in the Newland Journal of Medicine, one positive study with supportive confirmatory evidence may be sufficient. If one of the two remaining coastal studies is positive, we do plan to move forward in requesting a pre-NDA meeting with the agency. We think there are a variety of permutations by which confirmatory evidence, supportive evidence is possible coming through these studies and more to come. But we think there's a clear path forward here with one of the two studies being positive. Of course, we're planning for both being positive at the moment.

Ami Faria, Analyst — Needham

So for that, either coastal two or three with the full intent to treat patient populations would be considered, right? Because I know that you've talked about doing a separate analysis for the over 450 patients that were enrolled post some of the adjustments that you made to the two studies. So help us think about what might be considered as kind of a data subset that would support going to the FDA and requesting a meeting.

Bill Aurora, Other

Sure. Seeing positive results on one of the two studies on the primary endpoint, along with supportive evidence, may be sufficient for the pre-NDA meeting and consistent with the FDA communications, including the publications that we've just referenced. So in that context, we will take a look at the totality of the evidence as these two studies read out, look at them individually, we'll be able to look at them across both studies, and make the determination on what the best path forward is. But we do believe that that body of evidence will help us with clear decision making with next steps.

Ami Faria, Analyst — Needham

Yeah, that makes sense. If you think about the mechanism of the drug, it really targets anhedonia as well, and that's likely certainly a differentiator in the real world setting. Have you had any discussions with the FDA or thought about the potential for approving or seeking approval of the drug for anhedonia based on the SHAPS score instead of just the traditional depression endpoint?

Bill Aurora, Other

Sure. As you know, the primary endpoint for each of these studies is the change from baseline to week six on the Modras. But the SHAPS is a key secondary endpoint to take a look at anhedonia. We know that 70% of individuals with MDD suffer from anhedonia. And we know that currently approved agents just do not adequately treat this really important symptom. It's been associated with a higher degree of disease severity, a poor prognosis, higher rates of suicide. And in that context, we believe this mechanism has high relevance in being able to treat that symptom. So as we move ahead, we think that this could be very important evidence as we move forward with the program. But simply winning on the primary endpoint is sufficient here for approval.

Josh Pinto, CFO

And as Bill's mentioned, you know, the primary endpoint here is the change from baseline to week six on the Madras scale. And as we know the Madras, about half of the questions underlying it are the Madras anhedonia factors. So we know anhedonia is captured very much within the Madras scale. That's why we elected to move to that scale for pivotal studies. And so we think with a well-controlled and appropriate patient population, the Madras should be a very great measure, not only for capturing the benefits on depressive symptoms, but also on antedonic symptoms as well.

Ami Faria, Analyst — Needham

Fair. I think that makes sense. If I try to think about the range of outcomes, and in a scenario where both CO2 and 3 do not meet the primary endpoint, but we see a meaningful change on the SHAP score, do you think that that leaves you with a path forward to maybe pivot in terms of the indication that you go after?

Josh Pinto, CFO

I think at this point, Ami, our studies have been set up to really test major depressive disorder. That's the indication and that's the end point. So I think with these studies, ultimately, we'll have to, you know, our goal is to see if we can hit statistical significance on one of these two. As Bill highlighted, we think that would be the basis for moving forward with the pre-NDA If we don't see that, but there's interesting or supportive data that would suggest another direction, we'll have to dig into that and look at that and the viability of a path forward in an alternate indication moving forward. As we know, up to this point, the FDA has not really registered any drugs for the treatment of anhedonia, so it's not necessarily an indication

Ami Faria, Analyst — Needham

that has a clear registrational path. Maybe before we move on to a different topic, I just wanted to close this segment with just sort of a review of the changes that you had made to Coastal 2 and 3, and with the enrollment numbers, you know, how are these studies powered for the primary endpoint of the Madras change?

Bill Aurora, Other

Sure. I mean, when we saw the results of the Coastal 1 program, we paused Coastal 2 and 3 and implemented a number of changes that we think really helped both of the ongoing studies. First, we work with Maurizio Fava, Mass General, CTNI, to implement the SAFER approach, where there is a MGH clinician involved in confirming the diagnosis, interviewing patients, and the alike. We believe that this has helped make sure that we're getting more appropriate patients in. They've partnered closely with our medical team that's been heavily involved with medical eligibility verification, and that has worked well for us with respect to some of the data that I'll reference in just a moment. Secondly, we added VCT or verified clinical trials as a screening database to identify those participants who may be attempting to participate in multiple clinical trials or perhaps just have come out of a TRD study. Again, patients that wouldn't be appropriate for inclusion in our particular study. And third, we pared back on the number of sites that were involved in Coastal 2 and 3 and focused on those that have the greatest degree of expertise and experience in conducting MDD studies. What we've seen as a consequence of some of these changes has been a higher rate of screen failure in Coastal 2 and 3 than what we saw in Coastal 1. This gives us confidence that the changes we've made are helping to screen out those patients that may have otherwise come into the trial, but they may not have been appropriate candidates. And then to address your question related to the powering, prior to the initiation of the coastal program, we estimated that approximately 332 patients was the appropriate sample size power at 90% to be able to show a 3.2 change, a placebo-adjusted change, on Modra's total score. And so that's how we designed those studies, and we've moved forward accordingly.

Ami Faria, Analyst — Needham

Got it. Okay, great. Maybe if we could move to NMRA 511 for AD agitation. Earlier this year, you disclosed promising phase 1b data for this asset, where you demonstrated compelling efficacy, especially in the elevated anxiety population. And recently, you disclosed some additional data analysis in the patients with NPI AA over 4, equal to or greater than 4. Could you help us understand what percent of the AD agitation patients have elevated anxiety versus what percent have the, you know, the ABIA over four? Is it mostly overlapping? And how should we think about that in the real world setting?

Bill Aurora, Other

Sure. So anxiety is really highly prevalent when we think about AD patients and AD agitation. Up to 70% of patients experience the anxiety, and oftentimes it presents early in the disease course, and it persists throughout the duration of the disease itself, of AD, and ends up being an underlying driver for some of the agitation, some of the aggression that one ends up seeing. When we think about our data from the Phase 1B study, the NPI AA of four or greater is not an inclusion criteria that we had put into place. We cast a broad net to take a look at a broader set of patients. We know some sponsors have actually used that as a part of the inclusion criteria, something that we would have the ability to do as we advance the program. In there, we saw 53 of the patients had an NPI AA of four or greater. And so, again, we are looking at high prevalence of anxiety, agitation. The anxiety is often an underlying symptom here in the disease.

Ami Faria, Analyst — Needham

How does this impact, you know, as you sort of looked at this data a couple of different ways, how are you thinking about designing your future trials? Is it just to continue to cast a broader net once you've identified the right dose? or does it make more sense to really narrow down on maybe the elevated anxiety patient population and try to differentiate on that?

Bill Aurora, Other

Jeremy, we are currently advancing the MAD extension study this year. We expect to have data in the second half of the year. And before we move to the phase two study in the first quarter of next year, we'll come back and share some of the details on the design, the elements for that program. We want to take a look at a higher dose, as you know, In the Phase I-B study, we saw nice, robust efficacy, particularly in the elevated anxiety population, in the population of an NPI AA of four or greater, again, really robust results. We have the opportunity, we think, to potentially pick up an even greater degree of clinical response by being able to push the dose. These MAD cohorts will help us assess a higher dose, higher doses, and see if we can preserve the pristine tolerability profile. So more to come with respect to the phase two design, which will be further informed by the MAD cohorts that we'll be running and concluding this year.

Ami Faria, Analyst — Needham

Certainly, and I think that as you finalize your dose, you'll have a better sense of the clinical profile across this patient population. From a regulatory standpoint, should we, you know, is it possible for you to still get a broader label, even if you study the drug in maybe a subset of the patient population? Should you decide to do that?

Bill Aurora, Other

Sure. So when we think about what precedent is with the FDA thus far, we do know that at least with the one approved agent, they did have an inclusion criteria that was NPIAA, a four or greater, and that preserved a broad label. We know another sponsor has submitted some more dynamic with the NPIAA. So right now, from what we know, having that as an inclusion criteria does preserve the broad label. And certainly the precedent does suggest that that could be a viable approach as well.

Josh Pinto, CFO

Yeah, no, I mean, as you think about it, I think you could assume that could be our base case moving forward, which is looking to preserve the broad label. With the new data we put out with our 10K, it shows that in that comparable population, Our clinical effect size, you know, is just as good, if not better than Rexalty when you parse out some of the subscales. And so I think in our view, we'll be able to move the program forward, preserve the broad label with our inclusion exclusion criteria. And then we'll be able to first and foremost, stratify patients based on baseline anxiety to ensure that we don't have an imbalance like we did in the 1B, where you had patients on placebo that had a much higher baseline RAID score. So we'll be able to make sure they're balanced, but also we'll be able to enrich for that in different ways, similar to how we're ensuring we get, you know, patients with elevated anhedonia into the coastal studies without having a clear cutoff. And so we feel really good about the data and our ability to go broad, but also, you know, target patients that we think could respond to this drug.

Ami Faria, Analyst — Needham

um how should uh maybe another question on on the data that you've shown so far uh we we saw slight reduction in the um sort of the absolute placebo adjusted change um from week six to week eight should we perceive that as maybe just being noise as being a function of the size of the cohort, or is this something that we need to read into more in terms of how data could evolve with studying the treatment over a longer duration?

Bill Aurora, Other

Jeremy, just importantly, I'll highlight the fact that over the eight weeks, we continued to see accrual of clinical response on NMRA 511. So whether it be on CMAI total or a range of the other scales, we didn't see a plateauing of benefit on active. And in fact, if anything, one could argue that going a bit longer might allow for even a greater accrual of a clinical response. We didn't institute some of the placebo controlled compliance elements that one might put into place with later phases of development in a signal seeking phase 1b study. So for example, in our MDD program, we've done things that, like a placebo control reminder script, we've looked at AI care as a way to confirm compliance. Those are things that typically one wouldn't do in a phase 1B signal-seeking study, but has the opportunity we do to implement those as we're moving the program forward, helping to mitigate some of those placebo responses, et cetera, while ACTIVE continues to accrue responses it did over the eight weeks and potentially longer.

Ami Faria, Analyst — Needham

Yeah. Yeah. What is the appropriate duration to study the drug on? Is there sort of a regulatory view on whether the primary endpoint should be measured at week five, which we've seen in the case of ovality? And with Rixalti, we've seen it being measured at week 12. I guess just from a mechanistic perspective, do you think that there's an appropriate timeframe frame to be able to capture the efficacy and if there is a view from the FDA on what is the appropriate time frame that they would like the endpoint to be measured at. Sure, I mean, as you

Bill Aurora, Other

reference, there's a range with the study duration that different sponsors have taken, and in part that may be determined by if there required titration, a whole host of other factors that come into play, as well as how long it may take to accrue clinical benefit. We've seen everything from five weeks to 12 weeks, and we'll learn more with the application that's currently in front of the agency with a five-week trial. For our particular phase 1B study, it was an eight-week study. We continued to see a cruel response through that eight-week time period on active. We'll come back and share more details on the duration of the study for our phase two, but certainly you can think about that range being a reasonable one for how we might bring something forward with the design in phase two. We want to make sure we give the 5.11 asset an opportunity, the greatest opportunity to show benefit, and we'll come back with the appropriate

Ami Faria, Analyst — Needham

time duration for that phase two. Maybe just sort of stepping back, I mean, you know, the AD agitation space is just about evolving. The only drug that's approved certainly has a black box spawning and obelity certainly has a cleaner profile on the safety side of things. And we're expecting that maybe they'll get approval soon. How do you see the treatment landscape evolving with additional treatment options that may become available over time? And how do you see your asset, you know, can you just sort of impact that paradigm? Absolutely. I mean, so as

Josh Pinto, CFO

we look at the treatment paradigm and based on our market research, what we've really seen is physicians want a product to be moving forward that has two components. One, they do want the efficacy. And so as they look at the effect size, they want to see products that have a clinical effect comparable to Rex salty. And so they are looking for that robust effect size within this patient population. And so that is where we feel good about 5.11 and ultimately the profile we've shown in the broad NPIA greater than 4, as well as the elevated anxiety population. The other thing is, and this is from physicians, but also from caregivers, they want products that aren't going to derive potential side effect profile issues or risks. Obviously with Rexalty, the black box warning, that's a big one. So we think about other programs and products such as Avelity, another side effect that we in our market research suggested could be challenging is sedation. As you think about the elderly population with the potential for falls, that is also something physicians and caregivers are looking to avoid. And so given the fact that we did not see any sedation in the phase 1B product, being able to come forward with a product that doesn't really have any sedating properties could be quite compelling with this effect size. And so we really view that 5.11 could be in a class of its own, just as you think about the benefit risk profile that could bring forward with the efficacy profile comparable to, or even potentially better than Rex salty and a side effect profile that up to this point looks much more tolerable than the competitor data that's out there. And so we feel good about the product profile. And then with the anxiety component coming in and anxiety being one of the symptoms that first presents, we feel like this will give us an opportunity to treat patients early in the diagnosis and hopefully stay with them, you know, through the disease course. So it could ultimately allow us to get in there early

Ami Faria, Analyst — Needham

as well. Okay. All right. Let's switch gears to NMRA215. Could you provide an overview on the asset? How is it differentiated compared to some of the other NRP3 inhibitors in development?

Nicholas Brandon, Other

Hi, Amir. I'll take this one. Just as a reminder, NRA215 was developed in-house, and it was really optimized around potency and selectivity for the target. But most importantly, it was optimized around CNS penetration, and it's really on that feature where we do think it differentiates from other sponsors' compounds. and that's just really important as we think about the main indication we're looking at here in terms of obesity from the pre-clinical models it's clear you need high cns penetration to see weight loss in these dio models so that's you know that's one of the critical pieces uh one thing about the compound 215 it does bind to this so-called knack domain and that's where most of the direct nlp3 inhibitors bind including the ventix or eli lily compounds uh it does it Obviously, BioAge has a distinct binding site and obviously is very different from the next seven approaches. We do think there are some differences in terms of how it binds up in that domain, which I think in future we may see some of that, it may explain some of its improved properties.

Ami Faria, Analyst — Needham

Okay. You recently disclosed that there were some AEs in the 13-week talk study in rats that were found. And I think you're redoing some of the work there and indicated that a lot of companies have reported a similar issue. issue, can you maybe provide any more color on what type of issue it is or what might be causing that and what helped you get comfortable that this is something that can be addressed by repeating

Nicholas Brandon, Other

the study? Sure. Yeah, Josh mentioned a little bit earlier, but what we did see was a number of unexpected adverse events in the 13-week rat study. I think there's a number of features around those findings, which still give us a great deal of confidence in NMI 215. So importantly, these findings were not dose-dependent. They're not attributed to anything we know about the molecule or the target. Importantly, we've seen nothing like that in any of our other studies, and that includes 28-day rat and dog studies and a 13-week dog study. So all of that, and then combined with the fact that these events were sort of coincident with what we believe are procedure-related issues, that has allowed us to initiate a full-cause audit, which is ongoing. So they're the details we're providing right now while the audit is ongoing and maybe later in the year we may be able to come back with more details. But that really drove us to think that we should be repeating the study as soon as we could. So that was obviously with discussions with our key consultants and KOL. So that's ongoing now. So that will read out in the middle of the year. And again, I think Josh has said this before, we really see this as just a delay in time. And we still have great confidence in the molecule.

Ami Faria, Analyst — Needham

Great. Maybe just sort of stepping back and trying to think about the mechanism and the impact on the weight loss. And I think different companies have taken this mechanism into different directions, whether it's cardiometabolic or obesity. And obviously, these are very closely interlinked. Um, can you maybe talk about what might be different about the mechanism of your asset that, um, sort of positions it better for obesity, uh, compared to what some of the other drugs, such as the Ventex drug have done or BioAge?

Nicholas Brandon, Other

Yeah, no, absolutely. And, you know, it's, it's clear that people are sort of diverging, but we are very committed, you know, to the obesity indication. and that's because of what we believe is best in class cns penetration from all of the pre-clinical studies today it's very clear you know that you need high levels of nlp3 inhibition in the brain we believe presumably in the hypothalamus to cause you know impact on the sort of eating circuits and decreases in food intake and we think that may cause a divergence other molecules may just not have those optimal cns properties we also think though uh we also get good peripheral exposure so the sort of more cardiovascular peripheral cardiometabolic effects we'll also see we almost see those as table stakes for any good compound but with a compound like 215 you'll also get these weight loss food intake reduction properties as well yeah and ami i think you have

Josh Pinto, CFO

to remember, you know, NMRA215 was originally developed with CNS optimization in mind as a neuroscience company that's always at the forefront. That's what Nick and our chemistry team are some of the best, you know, in the business at generating. And we initially thought some neurodegenerative conditions could be the initial indication. I think that's what's given us the leg up now that we've realized that highly CNS penetrant molecules could be the key to unlocking obesity. And that's what's setting 215 apart from other companies that may have started more as inflammatory companies, not as, you know, pure neuroscience companies. And so I think that's really what's going to give us the opportunity, hopefully, to show the benefit in weight loss

Ami Faria, Analyst — Needham

once we can get the program into the clinic. Maybe last question on this. Obviously, you've focused on optimizing the CNS penetration. How do we measure that it's adequate to achieve what you need to see on weight loss. How much of IC90 do you need to see and what's the relevance of that with regards to achieving the weight loss benefit? Absolutely, Ami. And so as we've shown

Josh Pinto, CFO

in our DIO data, you know, maximizing the weight loss potential for NMRA215 is achieved by getting to those IC90 concentrations in the brain. We've also seen that from other sponsors such as Tenvi, And so we believe that it is fairly well established that you do need IC90 concentrations in the brain to drive weight loss. As we think about moving forward, that'll obviously be a key translational measure that we'll look at in early clinical studies, and we'll want to look to confirm that, you know, we do have, you know, CSF concentrations, you know, would support IC90 dosing levels. And so that will be a critical translational measure to look for as we get into early clinical studies.

Ami Faria, Analyst — Needham

Okay. So maybe just to close this topic, maybe lay down for us the timelines of what we should expect to see next. And as you redo the talk studies, what would you like to see? What would be a good outcome in terms of, on the efficacy side of things, assuming that you don't see the AEs that you saw in this one in order to move forward with the program?

Josh Pinto, CFO

Yeah, absolutely. And so, Ami, what we've announced at the end of March with our 10K was that in the first quarter, we had initiated the repeat 13-week rat talk study. We haven't put any guidance out in terms of when we would expect to report results from the study, but you can fast forward the 13-week timing to look at that. And what we did announce is that we expect to get the program back into the clinic, you know, by the first quarter of 2027. And so once we have data from the repeat 13-week talks and have more concrete plans around the path forward, you know, we'll provide an update to the street. But, you know, you could assume that once we have more info, we'll be back out with it.

Ami Faria, Analyst — Needham

Okay. I would definitely want to talk about the masquerading program and the time that we have left. You obviously picked NMRA 898. Maybe talk about what gives you confidence that you've got the asset you need to move forward in the muscronic space. And what can we expect with regards to the next steps and data from this asset?

Nicholas Brandon, Other

Yeah, we're really excited to announce the prioritization of NMRA 898. And that really came from our initial data from from the sad study so i've really the first important feature was the half-life which is somewhere between 80 and 100 hours supporting the once a day dosing you know alongside that we saw really exquisite dose dependent exposures with really really low variability which other molecules in the field have have struggled with uh importantly we also what we believe saw really good signs of target engagement so that's by measuring heart rate so these sort of transient increases in heart rate, we believe, you know, are related to central engagement of the M4 target. So all of those in, you know, together, it really made 898 stand out. You know, as we look to the second half of the year, we're obviously going to be completing the SADMAD study, both in healthies and in stable schizophrenia patients. Some of the important data, which we'll get there, We'll get a CSF exposure of the drug, and there we'll really be looking to see what sort of fold elevations we are over the EC50 for the target, which we believe is going to be really important for efficacy. So, you know, we'll be reporting that data out in the second half of the year.

Ami Faria, Analyst — Needham

Okay. All right. Maybe just more broadly thinking about the muscarinic program, maybe stepping back, how are you thinking about any additional assets that you might consider? And this one is certainly for schizophrenia. How are you thinking about more holistically with regards to other indications that this class of drugs is being pursued for?

Josh Pinto, CFO

Yeah, absolutely. And I mean, we've always really characterized our muscarinic set of assets as a franchise because we do believe that there is a wide range of indications that these molecules ultimately could have potential for. As you've highlighted, we're going to focus on 898 in schizophrenia for the time being. But as we sit here today, we have 898, which has progressed to a really good point. We've gotten some initial clinical data out of 861. And ultimately, if we decide that there are other indications that would warrant a different product profile, if you think about alternate call points or potential neurodegenerative conditions or others, that might warrant bringing forward an alternate molecule. So as we think about indication expansion, you know, we'll talk about that as it relates to what to do with 898, as well as what we could want to do with a different molecule. But for the time being right now, we're just focused on progressing 898 through the SAD-MAD study this year, and then getting the acute schizophrenia study initiated

Ami Faria, Analyst — Needham

in early 27. Okay. All right. I think that covers it all. I really appreciate the time that you'll I've taken for this conversation and thank you for all our listeners for Great.

Josh Pinto, CFO

Thank you, Ami.