Welcome to Citi's Biopharma Back to School Summit, for 2026. We are very pleased to be introducing our next company, Lexicon Pharmaceuticals. We have Mike Exton, CEO. Welcome. Good day, Yigal. Craig Granowitz, CMO, and Scott Coiante, the CFO. Welcome, all of you. Thank you so much. I am Yigal Nochomovitz, cover the company for a long time. Well, since before COVID, I think. Anyway, so maybe, Mike, you want to just start us off with the quick overview of where things are with sotagliflozin. Of course, you have a very important phase III readout coming up in a critical area of cardiology. So why don't you start there? Yeah, no, great. Thanks, Yigal. Perhaps before diving into SOTA, I can give you a little bit of where we're at as a company. Over the last couple of years, really, we focused on driving our R&D programs on establishing financial flexibility and completing a number of partnerships that have gotten us to, I think, a really good state, particularly with SOTA, but across the board. Now we're on the precipice of a very important data readout in HCM, hypertrophic cardiomyopathy, with SOTA. We expect data in Q1 of next year. Really that is the North Star for the company. As we sort of execute that, all of the data into the trial, in parallel to that, we start to think around what the commercial opportunity is for us in this pretty important space. We recently just promoted Rachel Martens in our company to Chief Commercial Officer. Rachel's been leading our BD&L and partnership strategy, and was the driver behind our partnership with Novo Nordisk. Really pleased to have her in that position. She ran the insulin businesses for Sanofi and has worked in biotech. We're going to form a very small but very mighty commercial team. We now have a head of marketing and on the precipice of bringing in a market access person, who are really going to do all the pre-launch preparation in HCM because that is our number one commercial opportunity. Beyond that, of course, we're very soon to resubmit sotagliflozin for T1D. In addition to that, we have pilavapadin, which is a phase III-ready program in DPNP. Of course, our program with Novo Nordisk, which is in phase I, LX9851 for obesity. A lot of things over the next six months where, if you think at the end of Q1 of next year, we could be in a situation where we have data from SONATA-HCM, a potential launch in T1D, have started a phase III program in DPNP, and Novo starting the phase II program in weight management for LX9851. Really important time for the company. Lots of things happening, but with a clear focus for us in HCM. Okay. Let's start with SONATA-HCM, as the study is called. The primary endpoint is this something called this KCCQ measurement. Maybe Craig, you could just review exactly what that is so people understand. You're looking for, what I understand, is a four- to five-point improvement there. But you've also over-enrolled and you've exceeded your target. Just frame how should we think about having an over-enrolled in terms of probabilities of success. Overall, even without the over-enrollment, how do you think about the hitting on that target? Yeah. Thank you, Yigal. Important questions you are asking. The primary endpoint that has been identified by health authorities is improvement in feeling and function. Since we have a long history with the molecule sotagliflozin in heart failure, and not only have improvement in symptoms in heart failure, but also improvement in cardiac mortality and reduction in heart failure events. Outside the U.S., our partner has gotten approval also for use to reduce stroke and MI with the agent. FDA and we agreed and have, before we started the study, that the primary endpoint would be in this KCCQ score, and the secondary endpoint would be in the New York Heart Association score. Change in those scores, placebo controlled and adjusted. That is consistent with HCM. The regulatory hurdle is to improve patient functionality and feeling. There are no long-term outcome studies. The CMIs that have been approved do not have long-term outcomes associated with that agent. In part, they needed a dual endpoint because these are unproven agents that have never been on the market. I think there was a concern that KCCQ score alone would not be enough, and that is why they have a co-primary endpoint, particularly outside the U.S., for a physical function benefit of peak VO2. In our trial design, and I hope as we go to market, we have really tried to take a very broad and pragmatic approach and really think about being first and only in mechanism, and complementary in use no matter what the agent. The trial design really takes those criteria into account. We have the broadest range of ejection fraction included. We have the broadest range of baseline medications, including CMIs in the trial. Not requiring all of the physical testing like peak VO2 or exercise testing, it also allowed more centers to enroll more patients more rapidly. That was the philosophy behind the trial. I think the result of that is we enrolled the trial quickly at relatively modest cost compared to some of these other trials. As you have already pointed out, we actually over-enrolled the study. Maybe if I just add on to that, Yigal, because you mentioned a four or five-point delta versus placebo. The study was certainly powered for that, and having an over-enrollment improves that powering, obviously. What our expectation for success is has really been set by the marketplace. A delta placebo adjusted at three points that is statistically significant, we think given the benefit risk profile of SOTA would be a home run for us commercially, and anything above and beyond that is obviously upside for us. We think we have a great chance of this being a very important part of the armamentarium in HCM. Okay, let's just dig a little deeper in terms of the components. You are obviously enrolling the obstructive and the non-obstructive groups. The argument you have made many times is the mechanism is general to the cardiac energetics as opposed to being a mechanical MOA where you may see a benefit more in one subset versus the other. Without directly me answering the question, maybe go into a little more detail there as to how to think about the non-obstructive versus the obstructive, and then also just when you present the data, how are we going to see it? Are we going to see the groups? Are we going to see everything together? Just frame that part of it for us. Yigal, you are doing such a good job answering the question, I just wanted you to continue. But the trial is designed for the combined group together to be analyzed as one. So all of the 500+ patients as one primary group. As we have mentioned, the trial is stratified based on baseline obstructive or non-obstructive, but as you have already pointed out so elegantly, the mechanism really is going to be independent of the underlying mechanism. I think there is an expectation in the field, which may or may not be borne out, that the obstructive group is less heterogeneous than the non-obstructive group. The non-obstructive group seems to probably be an amalgamation of different diseases. Certainly, the sarcomeric mutations is going to be a more severe and a relatively more pure form of the disease. It might be more prevalent having these identified underlying genetic mutations primarily in the energy molecules, the energy proteins of the muscle cell, but not uniquely dependent on them. I think particularly in a non-obstructive group, perhaps one of the reasons why the cardiac myosin inhibitors have not been as effective on a relative basis is that the disease itself is more heterogeneous. And one of the advantages we believe with SOTA is its breadth of mechanism. So you are not only getting a number of benefits on the cardiac cell itself with the SGLT1, and as you have already pointed out, you are looking at calcium flux, sodium flux, inflammatory markers, energetics. There is a broad range of activities that have been demonstrated for SOTA and only SOTA because there are only SGLT1 receptors on the heart, not SGLT2 receptors. But you are also getting all of the benefits of SGLT2 inhibition on improving the cardiorenal function, which remember, we are enrolling only patients with symptomatic disease, so they all have elements of congestion, and SGLT2 inhibitors are very good at reducing congestion. As I have said before, I think the idea is to be first and only in mechanism and complementary in use, that we believe that if the profile that Mike laid out bears out, that we would be very high in the use categorization of agents. But at the same time, it is not going to be necessarily exclusive because we have enrolled patients on a cardiac myosin inhibitor in the trial. Can you speak to the relative split on the populations, or you can't get into that yet in terms of the percent that are HCM versus non-HCM and the percent that are on CMIs? Or just based on the general guidelines and knowing the marketplace, what would be expected there? Well, again, we designed the trial pragmatically, and I think with very strong encouragement from our steering committee. We did not cap at a hard number one or the other. Yeah. I think we enrolled more non-obstructive patients than obstructive. We've been public on that. We have not provided numbers because we haven't finished cleaning all the baseline demographics yet, and we will be presenting that data at an upcoming medical meeting, probably in the early part of 2027. But I think we went where the need is. I think where the centers are right now is there's a greater need and more patients available for clinical trials with non-obstructive disease. Again, we try to model what would be what most people see more closely in clinical practice than having a very rigid clinical trial. Okay. To the second part of your question around CMIs, we haven't said the exact number. In fact, we don't know the exact number yet, but it's relatively small but significant enough that you can take some data and some questions and some understanding from that. We've got a cohort, and really this will be the only trial that has a cohort of patients on both a CMI and SOTA. It's going to be really fascinating data to see how the two work in tandem. But the other take-home from that very point is that patients on a CMI still have the propensity to be symptomatic which sort of underscores this original point you made, Yigal, that the underlying disease truly becomes the energetics of the disease and diastolic dysfunction. Despite improving the obstruction, these patients still remain symptomatic. There's something much more at play here than just the obstruction, and we'll see that from this data. Yeah. I think, to Mike's point, some of the artificialness of how people think about the disease is a reflection of the trial designs that were done. If you think about obstruction, it's a continuum, and I think there's this belief, and again, it's totally understandable, that by running obstructive trials and non-obstructive trials that they're like these two different things. When you think about a patient, a lot of the issue around obstruction or non-obstruction is how much effort did the person do with their Valsalva? There's a lot of very qualitative factors. We faced a similar issue when we studied HFrEF and HFpEF together in a population. By being able to study the entire continuum, in this case of outflow tract obstruction, and looking at results across a continuum as opposed to this artificial line, I think it's going to be far more informative to the medical and investor audience about the effectiveness of sotagliflozin in this indication. Plus you'll also, I just thought about it. Plus you'll also get, I don't think it's stratified by CMI use, right? No. But nonetheless, you are going to get some data on CMI plus SOTA versus CMI plus placebo. That is right. That you can put interestingly and analyze, even though that is not stratified, that is not the main thrust of the study, but there is some very interesting data there, potentially. Yeah. To that point, presumably every patient that was on a CMI, when they were placed on the CMI, because they just need to be on a stable dose. So that means they have been on a CMI six months because that was the entry criteria. So they were all on CAMZYOS because aficamten was not commercially available in that timeframe. We didn't stratify or hold them accountable to a certain baseline outflow tract obstruction. I can tell you there's going to be a continuum of outflow tract obstructions, some of which would be considered classically obstructive, and some would be at the baseline non-obstructive. To Mike's point, there is not a great correlation between obstruction and symptoms, and we have all of those flavors in the trial. Yeah. It's always dangerous when you try to create two categorical variables out of what's a continuous variable. We'd love to do it. Yeah You're right. It is fraught with danger and misinterpretation. Yeah. Okay. By the way, we should talk, too, about some of the secondary endpoints, please. What are the ones that are most important in the study? Well, I think the ones, and you saw some of that data presented at ESC from the aficamten study from ACACIA. There's really, beyond the New York Heart, which is basically the provider assessment of patient functionality, so sort of the mirror image. The patient with KCCQ is rating themselves. New York Heart is the healthcare provider sort of making an external assessment to the patient. But in general, they're very highly correlated over time. There's really a lot of parameters. I would put them in the function and feeling, so those are the primary and secondary endpoint. There's a lot of secondary endpoints, the enzymes, and then really looking at a lot of the echo parameters. I think the echo parameters are really important. I think to me, one of the key takeaways from ESC is that a lot of the benefits, I would say, and the speaker on the podium said, these benefits are modest and reversible. That to me is an important element, not just looking at it in the enzymes, because I think the enzymes are not very reflective, at least with CMIs, on benefit, because the biggest benefit is on cardiac enzymes, but there's no correlation of that to anything. I think looking at things like left atrial volume is going to be really important because that's a real reflection of left ventricular function. The less functional the left ventricle is, the more you generally get a large left atrium. We're going to look at left wall thickness. We're going to look at the speed of the contraction. There's a lot of echo parameters that are going to be looked at as either secondary or exploratory endpoints. Okay. I imagine if you hit presumably on the first, on the primary endpoint, that you would expect to see these secondary endpoints track accordingly if the patients are reflecting a better feeling, better quality of life, right? I have a high degree of confidence in that, Yigal, because again, we've got this massive database of heart failure outcome studies, and like in HFpEF, the primary endpoint of the trial, we've talked about that SOTA-P-CARDIA was left ventricular wall thickness, and that was a primary endpoint and was achieved. KCCQ score was beneficial, and six-minute walk, and a number of other parameters. So I have a high degree of confidence just based on our prior experience in heart failure, that you're going to see benefit across a range of these parameters. Did you want to say anything else about ACACIA-HCM read-through, or any other comments there in terms of thinking about your study? I just think they're complementary mechanisms. Yeah. The fact is we're going to have patients on a CMI in our trial. I think that's going to give people comfort around relative safety and tolerability of that in a way, to Mike's point, that you're probably not going to see otherwise because it's in a placebo-controlled large multicenter trial. Now you mentioned the promotion to Chief Commercial Officer of one of your BD people. So what are you learning or have learned recently in terms of the marketplace that will help you with launching the drug. Yeah. We'll likely be more elaborate as we get into Q3 earnings to talk about some of the specific research. But listening in to some of these conversations with KOLs and payers is clearly in non-obstructive HCM, there's a huge opportunity, and the profile of SOTA as presented is, in layman's terms, a no-brainer given the lack of other options, given the relative low bar that's been set for us to be successful there. What has been interesting is that there's still quite a lot of enthusiasm in obstructive HCM as well for various reasons. One, because despite alleviating obstruction, there's still a high degree of symptomology. Of course, dependent on how the drug functions in obstructive HCM, the safety and the tolerability of the drug still lends itself either as an add-on to a CMI in those particular cases, or even in first-line use because of the ease of use of that particular drug. It's been very encouraging so far, and we'll present a lot more specific information on that at earnings. Okay. Just one thing, so the data is 1Q 2027, but given you now know you're done with the enrollment, can't you be a little more granular with the timing in 1Q, or are you still just going to keep it open to in 1Q? Or do you have a sense as to where in the quarter we might get the data? That's a good question. Look, I think it's probably still a little bit early. Closing a trial it actually involves a lot of work. So you've got to get all the data in. You've got to make sure it's clean. Clearly, you do the analyses, et cetera. I think we'll be more confident to give a more specific guidance at the start of next year. Okay. All right. Fair enough. All right, let's make sure we talk about some other things. We still have to talk about SOTA, but in a different area. So type one, where I remember being at that AdCom many, many years ago. So things have progressed a long way since then. So tell us what we're waiting for. I know there's this very important natural history study which is being conducted over in Denmark, I believe. So tell us what the significance of that is, this Steno-2-1, why that's so important, and then just sort of thinking about what the FDA wants to see and the resubmission path. Yeah, maybe let me start Okay, sure. Craig can dive into some of the details. The FDA in the history of SOTA in T1D has really asked for a couple of things the whole time. This time around, we feel very confident, in fact, having very good engagement with the FDA that we can deliver that. Those two things are we want a new prospective study, not a retrospective look at the data, cutting it in a different way. We need to see from that study a certain amount of exposure on SOTA and to see a DKA level that's acceptable. Until now as a company, we've never really known what those expectations are. What we have now is we have that prospective study, Steno-2-1, that you're saying is running in Denmark. We have agreement from the FDA that that study is sufficient and will gather sufficient exposure, which they've given us the exact number. In fact, we achieved that exposure at the end of August. The data is done. Now we just are in the throes of preparing it and getting ready to submit. We have a DKA level that is less than what we saw in the inTandem program. All of those three aspects have been fulfilled. We're in constant engagement with the FDA to prepare this resubmission. They are the things that are different this time around. We are highly confident that we can finally bring this drug to patients with T1D. That sounds like some new information there, the fact that you've reached that exposure target at the end of August. Right. Okay. Hot off the press, just for you. Thank you. In terms of the DKA rates, is the point that those rates now are more in line with what would be expected in the T1D population, or are they more because the Steno-2-1 trial, it is not just SOTA, right? It is a whole bunch of things, if I am not mistaken. How are those DKA rates comparing to all those other cohorts that are being studied? Because I think it is, was not it like 2,000 patients or something? It is big. Yeah. You are exactly right, Yigal, it is a 2,000-patient study, and it is a treatment algorithm study. What that means is patients were randomized by study site, either have a standard of care treatment, which was optimized lipids, optimized A1C, and then continue with the standard of care, or an enhanced treatment regimen that the added treatment would be according to their baseline demographics. The three options were either a SOTA group, a semaglutide group, or a finerenone group. As patients went through in that enhanced treatment group, the clinicians could add other medications onto that within that mix, depending upon their clinical judgment and the background patient characteristics. But there is a period of time when they are on one of those three. You have got 1,000 patients that are in this enhanced treatment group. A significant fraction of that 1,000 is on SOTA, and that speaks to Mike's point. It was just a matter of fully enrolling that 1,000-patient cohort, the percentage of those patients that are on SOTA, and then the accumulated exposure that met the threshold that we, and agreed with the FDA, which was roughly the total SOTA exposure in the inTandem registration program. Okay. The comparisons we can make are we can make a DKA comparison of the SOTA group in Steno-2-1 compared to the standard of care group in Steno-2-1, and the rate achieved with SOTA with DKA in the SOTA group in Steno-2-1 compared to the historic rate achieved or realized with sotagliflozin in inTandem. The primary metric that FDA set was comparing yourself to inTandem, because in their communications with us, some of which I think was in the end of review meeting that has been made public, is they accepted the efficacy. Okay. The only thing they wanted to get was a risk-benefit, right? They said, "If you get a prospective group of patients where that DKA rate is lower than that in inTandem, then the risk-benefit will be favorable and the drug approvable." Just to be sure, we want to have both a rate compared to inTandem, but also the rate compared to the standard of care, and I think we've publicly disclosed this at earnings, that the rate that we've observed is similar to that of the standard of care in the Steno-2 trial. You've sort of achieved, if I'm not mistaken, sort of a higher bar than even what the FDA was stipulating, a little bit maybe. I think it's just supportive. I think it's supportive from we've certainly achieved the expectation that FDA has given us, and we've got a number of different angles that support the same conclusion. Yeah. Okay. Now just very quickly, what are the gating factors now to get this? This just happened a few days ago, the exposure target, so when is the submission timeline? I mean, all that. It's been more than a nine-month process we've been working with Steno-2 and the FDA on this, and we've had repeated meetings with the FDA. We've had ongoing, almost daily dialogue with Steno-2. We're at the point now of collecting all the data in the database that they use, all of the relevant metrics that FDA wanted to see. Steno-2 is in the process of cleaning that data adequately for us to then take that database, put the final analyses together, and submit to the FDA. That is the ongoing process, literally as we speak, is that they are collecting the data, cleaning it to make sure that it is accurate, providing us all of that raw data in a database, and we've already covered all of the issues around patient privacy and all these other things, which again, is a long process knowing the data privacy laws between the U.S. and Europe. Then we're in the process now of putting that in the final format for submission of what FDA wants. At this point, you're not quite ready to give a timeline on that. No, we've said Q4. Oh, yeah. It's going to be this year. Okay. As we march forward over the coming months, we may be able to provide a bit more granularity at earnings. Okay. Very good. Let's just switch over then to the DPNP program. There, you had some very strong data in the phase II, and you determined a dose. You've been talking about a partner, but I guess just update us there because the emphasis on that seems to a little bit deprioritized perhaps. No, absolutely, Yigal. A number of things have transpired in the earlier part of this year. That means we continue to progress that particular asset, but HCM has risen to the top of our focus, both from our resourcing as well as our investor engagement, et cetera, and where the nearest stage opportunity, large opportunity is. Nevertheless, one of the things that we said when we were, at that time, engaging with potential partners as well as publicly, is this mechanism, AAK1, has a lot of promise well beyond DPNP. We wanted to ensure that they saw that value they could realize well beyond just neuropathic pain. We do not have the data ready for prime time yet, but later this year we will present data, preclinical data, admittedly, but again, with pilavapadin, the lead asset that we use in DPNP, that shows really remarkable results in a number of new indications. We want to bundle all of that up as we look to progress pilavapadin generally, and for DPNP specifically. Okay. You want to give any teasers there in terms of what O ther indications? Nice try. All right. You'll hear it first, mate, along with everyone else. Okay, fair enough. Okay. All right. I think it's fair to say these are broadly also aligned with where we are as a company in the cardiometabolic space. In areas of high interest. Can I ask this? I gather, or maybe I'm interpreting, that some of the partners were saying, "We'd be interested in X, Y and Z," and then you did some of these preclinical experiments to get a little clue or this wasn't like that? No. Look, we, and Craig really instigated this early last year, I'd say, that we have, as you know, through Genome5000, a pretty significant database of lots of different studies, preclinical studies across lots of indications for many, many mechanisms. We went back and did a huge review of that. We kickstarted that work before we were really getting serious with the conversations with partners. Those conversations with partners and some of this preclinical work were ongoing in parallel, but certainly those conversations helped reinforce the idea that really, let's make sure we capture the full value that this mechanism potentially brings well beyond what is a significant opportunity in DPNP, but we want to make sure that we're not missing any value by leaving potential high-value indications on the table. Yeah. I think the other element, and again, I really thank you, Mike and Scott, for this, is that by raising other source of capital, we were able to do the capital raise, the deal with Novo. We took some of the pressure off of having to do a deal to finance, in part finance the company. We thought that there's a much better value proposition of trying to get additional data and really validating AAK1 as a pathway. Just like we validated sotagliflozin as a pathway, we validated LX9851 as a pathway, as we've shared with you, not only in obesity, but also in MASH, and potentially in looking at lipids and cardiac plaque to maximize the value proposition. These are really interesting pathways where we're first, and in many cases only. I think doing the additional work to have a disproportionate impact on value is what has been afforded with being able to find other ways to finance a company. Okay. That's a perfectly sensible way to go. Last one, the Novo partnership. I remember at the R&D day in New York many years ago, you showcased the initial mouse data there, which looked pretty interesting. ACSL5, obesity is obviously super competitive space and dominated by the heavyweights. No pun intended. Tell us why ACSL5 and what do you sort of expect Novo to do with this drug? Yeah. Again, maybe I'll speak generally, and Craig, you can speak about ACSL5. This was really one of the first things we did in my tenure as we looked to focus the company and focus our resources. We knew that we had in LX9851 a very powerful, as you mentioned, the results are pretty incredible on weight loss, either as monotherapy or combination on top of semaglutide. Yet we had a number of other things that were later stage where we wanted to focus our resources, and this would be best served in one of the heavyweight's hands. We had discussions with a number of companies, and Novo really rose to the top because of a few things. Of course, the financial aspect, and this was a very lucrative deal for a preclinical asset, I think. But really, they were very enthusiastic about the mechanism. Craig can talk about that in a second. The other very compelling part of Novo taking this on is that, as you know, all of our medicines are once a day orally dosed. We had the feeling/knew that this would move to an oral-based therapy program like many cardiometabolic diseases, where you use different mechanisms of action pills in combination. That's indeed where Novo thinks they're going, and they're putting this right at the top of their mission critical status and are moving at a speed of knots. Yeah, the ACSL5 mechanism is very important. Early gate in triglyceride metabolism, both biosynthesis, and degradation. That's why it's expressed in the organs where triglycerides are most actively managed and packaged in the body, which is in the gut and in the liver. Now, triglycerides are really important in a number of major diseases. It's the major energy source for the body is triglyceride, and how the body moves triglyceride from the gut to the liver to the muscles and the other tissues is via these particles, lipoprotein particles, that are primarily triglyceride. Having a mechanism that impacts triglyceride metabolism has massive benefit, potentially in obesity, in MASH, which again is the mismanaging of lipids, primarily triglyceride in the liver, and then also in plaque, because as you've seen with all these LDL and HDL and Lp(a), these are all packaging addresses of these lipoproteins that go through the bloodstream, and if they're not packaged correctly, they get deposited in the bloodstream, which leads to development of plaque and cardiac arrest and in stroke. So I think that's why Novo has been so interested. While the primary focus is on obesity, there are these other potential benefits. Just to put a point on what Mike said. They only highlight a few of their early-stage assets. Every time now, this is one of the assets that they highlight in their public statements, in their corporate deck, so we are really pleased with having them as a partner. Okay. Great. One more, just because we are asking everyone about AI, very quickly, if anyone wanted to throw in their two cents on how are you using AI internally. Yeah. So, at the moment, we are evaluating AI for what I think could be a pretty transformational program for the company. It is interesting, we have never talked about this, but it is not necessarily material yet to the company. But as you can imagine, the Genome5000 database is a huge data set across both structured and non-structured data that was collected over the span of a decade or so. Researching and extracting information from that database is very complex. It was set up 30 years ago. We are now looking to how do we overlay an AI engine over the top of that where we can make search queries automatic, to enable not only work on our current core programs. But if partners are interested in oncology, for example, we do not even really touch the oncology space of Genome5000. We have the potential to interrogate that database in a very automated, fast, and systematic way. Systematic way, I should say. Just to remind everyone, that was something that was started, I think, in 1995. Correct Something like that. Yeah. Your memory is good. That was where you basically serially knocked out every gene in the mouse and tried to interrogate the phenotype, yes? Is that what it was? 5,000 genes. Right. Okay. Yeah. Across 60 or 70 different sort of therapeutic trials, preclinical trials across oncology, metabolism, cardiovascular disease, immunology, et cetera. Okay All of the targets that Craig and I have discussed today came out of that program. All of our medicines are internal. We haven't in-licensed anything. It shows you the power of that Genome5000. But really, given the sort of dating on it, there's untapped potential that we're not necessarily taking advantage of completely, and we think AI will provide us the tool to do that. Okay. Very interesting. Okay, well, we'll have to wrap it up there, but thank you all very much. We appreciate you. Thank you. Thanks, Yigal. Sure. All right, great. Thank you