Okay, good morning. We'll continue with the next session. I'm Paul Choi, and I cover this midcap biotechnology sector here at the firm, and it's my pleasure to welcome NGM. Joining us from management, to my left, immediate left is David Woodhouse, CEO, and to my far left, Siobhan Nolan Mangini, CFO. What we'll do is a little bit of Q&A. If any audience members along the way have any questions, please raise your hand and we can get a microphone to you. Otherwise, we'll just go ahead and start with David and Siobhan. So maybe, you know, perhaps most topical is people's interest in Geographic Atrophy, just given the news and events of the past few quarters here. Can you maybe, you know, frame for us how you think about the market opportunity in GA, how you think about the competitive landscape and how, you know, maybe some of the, you know, key things that investors focus on like, the complement pathway and its various, aspects, C3 and C5 and so forth are playing out? Multi-part question here, but how your lead asset in this area, 621 potentially could fit in here and be differentiated? Yeah, sure. Why don't I kick it off, and then Siobhan can expand on how we see the market growing. You know, we got interested in Geographic Atrophy because it's a completely unmet medical need. I think everybody's aware that while there are effective treatments for wet AMD, dry AMD and Geographic Atrophy as an advanced form of that is completely untreated. Our biologists got interested in complement C3 because the genome-wide association studies and the complement system generally, as well as some histopathological evidence. Our approach has been to develop this very high affinity antibody for complement C3. In the midst of doing that, I think the whole industry has been benefited by a few important clinical data sets that really seem to support the idea that inhibiting complement system has a positive effect in slowing the progression of disease. We're, you know, thrilled. It's been a while since we've seen something work in GA, and so we really think the targets are effective to go after. Enter our approach with a high affinity antibody. We think there are advantages that potentially could flow across safety, efficacy and convenience, and that's what we're looking to demonstrate. Siobhan, you should comment about how we see this market expanding over time. Yeah. Just to build off of what David was saying, you know, tremendous unmet need. Over 1 million patients in North America right now, over 5 million worldwide. Because of the aging demographics of the population, it's a relatively high growth area and no approved therapies to date. When we look to the evolution of the wet AMD market, we think of very similar dynamics of what's happening right now with Geographic Atrophy. What you saw there was, you know, through initial players, there began to be market formation. This is like 20 years ago. Then eventually, Lucentis come into market where there was really a step shift in terms of efficacy and safety. Then Eylea ultimately really differentiating off of convenience and dosing, every other month dosing. That really dovetails into exactly what David was just saying of our approach and how we think about, you know, coming into a market where we could differentiate on efficacy, safety and convenience of dosing similarly. I think one key thing, there's the patients and the unmet need, but the retina specialists are also very rapid adopters and are really looking for a solution. You know, in our work, we've seen that they are eager to see this differentiation, particularly on dimensions like safety and convenience of dosing. Okay, great. You know, perhaps, you know, one of the things that, you know, investors focus on most is just, you know, some of the competitive data in the category. I guess from your perspective and your scientific and clinical team's perspective, you know, what surprised you the most, I guess, in the Apellis DERBY and OAKS data thus far? You know, where do you see, I guess, the room for potential differentiation, maybe to, you know, follow up on my earlier question a little more granularly with regard to 621's, you know, what space is there, I guess, for 621 to play in relative to the Apellis data we've seen so far? Yeah, I mean, I think, OAKS in particular, but OAKS and DERBY together now at 18 months really validates complement C3 as an effective target to go after. The mixed data were a little surprising, I think, for all of us between the trials, but like I said, now that they've gone out further, it certainly seems to us that it's an approvable package from what we can see. I think that's really exciting, as I was mentioning earlier, for the space in terms of getting finally something on the market to work with and in physicians' hands. You know, I think the room we see around that, though, is pretty substantial because the bar is fairly low from an efficacy point of view. There was less efficacy demonstrated in the phase 3 trials. There's also room around safety in that we think this finding of exudative disease for both Apellis and Iveric's molecule relates to the fact that they have to pegylate their molecules to maintain presence in the eye for a period of time, at least a month or every other month. Because we're an antibody and by virtue of the size of an antibody, it stays in the eye naturally longer, we don't have to pegylate, and we think that could avoid that finding in those studies. The final one is area of differentiation is of course around convenience, which takes very little time to explain when you're talking about an intravitreal injection. The fewer, the better, no question. We are testing monthly and every other month dosing in our trial. Our hope is that we'll be able to show equivalent effect with both, suggesting we can use an every other month approach. I think generally the trial we have ongoing, CATALINA, our phase II, is intended to provide an opportunity to demonstrate these areas of differentiation clinically. Maybe just on a related note, how do you think about maybe two factors in the market? First, you know, potentially being, you know, second or later to market versus a competitor. To your point on potentially every other month dosing, ophthalmologists currently in the wet AMD space are obviously a sort of a volume-based reimbursement model. W hat does your research, I guess, suggest on those two factors? Yeah, I think Siobhan was touching on it earlier, which is, judging by the wet AMD space, and this happens in many different therapeutic areas, you know, the initial entrant is a big step forward, but often you have incremental improvements that actually build the market on the back of that. Certainly this disease area is large enough that I think we all expect multiple therapies to be available, and then it'll be a matter of the differentiating profile and the circumstances in which it's used that divides up market share from there. We're pretty far from the market to really get into the kind of payer reimbursement piece of it at this point, but it's certainly something we'll be paying attention to. Of course, we'll have to rely on whatever the first product that enters the market determines. They're probably the most foundation setting from kind of a payer interaction point of view. Maybe just something to add is that this demographic is relatively elderly, so this is something that is Medicare primarily in terms of reimbursement as we think about the payer component. Maybe just one piece on the volume that's been just interesting is, to your point, retina specialists are very data-driven. You can see that even as new programs have come onto market for the wet AMD spaces, they're gonna look at the data, see what effectively is best for patients, and are willing to adjust their kind of preferences based off of that data. We've seen that now play through four or five times i n the wet AMD market. Okay, great. David, you obviously brought up an important data point for NGM coming up here, which is the CATALINA study. Assuming the study's positive, I guess after that, what would potentially be next steps for you? How would you think about it? You know, how would you know, and your team potentially envision what a phase III trial might look like based on the Catalina study? Yeah, we're really excited about CATALINA. It's coming up in the fourth quarter is when we expect to top line the data. It really is the, you know, the trial to determine where we head further with the program. I think it's important maybe to take a step back from your question and describe the Merck relationship because that influences the phase III design coordination. Siobhan. Sure. So this program falls under a collaboration we have with Merck. They've been great partners as we've been working through CATALINA, and they actually have an option after this study. As David alluded to, you know, CATALINA was designed to be a, you know, phase II, potentially phase III study. Merck will have an option to license the program about a quarter after the CATALINA data. If they proceed forward, they will be responsible for the phase III development of the program. We have been working very closely in terms of pre-phase III manufacturing and other areas, but they would be responsible for the design and the go forward. Before the initiation of phase III, though, NGM would then have an option of either participating in an up to 50/50 cost profit split, of which half of that or 25%, could be financed by Merck and paid for with future profits, or we could just do a milestone and tiered royalty, as well. I realize that's leading into the structure of the deal, but it does influence also what the phase III will look like. Sure. I guess maybe to ask the question a different way, you know, perhaps based on what you've seen with the Apellis pivotal data, does that influence your thinking about assuming, again, Catalina is positive, you know, how you'd wanna think about potential trial design, duration, inclusion, exclusion criteria, and so forth? I'm sure there are a lot of subtleties, foveal, extrafoveal, and just sort of balancing those things out. How do you think about that potentially based on your learnings? Yeah, we think it's a huge advantage because we'll have the benefit of knowing if not the label for what Apellis will get approved on, you know, something pretty close to it just based on the data they've presented. Iveric's Zimura phase three data should be available. We'll have the context not only amongst what we have from Catalina to work with, but then where is the space, as you were asking earlier, to design a phase III to demonstrate differentiation. We think, you know, the timing's actually pretty good for us. I think there's an offshoot of what Siobhan was describing around this Merck option, which is, you know, for a market this size and for an opportunity that is fairly nascent, being paired with Merck potentially, we think is a real advantage. Not only to ultimately marketing the drug, but actually in designing a phase III that's probably of a bigger scope than we would contemplate on our own. You know, strategically, even if it's not Merck, if strategically they decide they don't want to go into ophthalmology, we do intend to likely find a partner for later stage development for that reason. Right. Yeah, that's a fair point also to bring up Iveric, which the firm doesn't cover, but also obviously will have late-stage data in the not too distant future as well, which will provide, I think, additional color on the landscape here in GA. You mentioned your collaboration with Merck, who, as Siobhan noted, has an option for NGM621 here. Maybe, you know, just for the benefit of the audience, you have a relationship with Merck that's been ongoing for years. Can you maybe just detail for us at a high level or provide for us at a high level, you know, just how the program and relationship works with them, the funding support for your R&D? Just potentially what other assets outside of NGM621 might be potentially collaborative on in terms of future programs? Sure. Sure, I'm happy to start with that. We did have an opportunity to restructure the collaboration to the benefit of both NGM as we've grown and Merck. We've been working with Merck since 2015, so many years. We focused the collaboration to ophthalmology. We've been talking quite a bit about 621. We're also working on two undisclosed preclinical retinal programs that, you know, could have the opportunity of being almost a bundle at that option point that we talked about. Could be maybe a franchise within ophthalmology. We also are focused in CVM and specifically heart failure. The option point there is much earlier than what we're talking about with CATALINA. Think about it, IND nomination. That is really the area of focus with Merck. What that has enabled NGM to have is then complete ownership of our oncology programs, which we will, I'm sure, talk about today. Those are all wholly owned by NGM as we're prosecuting them in the clinic. Everything that comes out of our discovery engine as well is now wholly owned. We shared a new program recently, a bispecific T-cell engager, wholly owned by NGM, as well as everything else that's coming out of our discovery engine. Okay, great. Obviously CATALINA and NGM is a near-term focus, just given the current environment we're here in biotech. You do obviously bring up a very important point, which is that you have a substantial oncology effort that's going on as well. Maybe, you know, the one that's furthest along is 120 at this point. How do your plans for clinical development, you know, develop, I guess, or think about after prior studies here in cachexia? You know, do you think about this drug being potentially prophylactic here or just sort of in terms of sort of an on-demand or treatment type opportunity for cachexia and that indication? Sure. Yeah. Just to maybe remind the audience, NGM120 is an antibody we created to block a receptor called GFRAL, which is the cognate receptor for a hormone called GDF15. The biologic rationale we're exploring in the clinic is twofold. One is an anti-cachectic effect, and the elevated levels of GDF15 in a whole variety of animal models cause significant weight loss. In cachectic patients, cancer cachectic patients, they tend to have elevated levels of GDF15. There's evidence, circumstantial evidence there that this could be playing a role there. Separately, though, the biology also suggests that there could be a direct anti-cancer effect. Elevated GDF15 leads to immunosuppression through a broad vagal stimulation process. When we entered the clinic, we were interested in designing a trial that we could look at both. Our initial work after we got through phase 1a in a variety of solid tumors was to go into metastatic pancreatic cancer, which I think is fairly well known as many patients suffer from developing cachexia. We went frontline trying to avoid the development of cachexia. What we've seen so far in our phase 1b study is some encouraging anti-cancer effects, for which the regulatory path is much more straightforward compared to cachexia. We're biasing our development more now going forward towards looking following this anti-tumor effect. In doing so, we're actually going beyond just pancreatic cancer. We're actually opening up a cohort in prostate cancer shortly, which happens to be the tumor type in which you see the highest elevations of GDF15. We also know from our phase 1a, we have a gentleman on monotherapy who responded very well. We have N of 1 patient. I'm not that kind of guy to raise a flag on it, but I think in the context of the biology, it actually is pretty interesting and worth opening the expansion cohort. We are still tracking cachexia endpoints, but we're much more likely to follow the anti-cancer. Okay. Yeah, I guess, as you know, the thinking on the asset has evolved over time, and as you think about the pancreatic cancer indication. Obviously, survival is well known to be very, very short here. I guess as you think about it, even though it's early stage, would even a small survival benefit here, I guess, you know, in your mind suggest a decent regulatory pathway or some visibility on that? How do you think about that? Yeah, that's the plan. I mean, in these very, tragically, tough tumor types, the bar is obviously pretty low to showing incremental effect. We are layering NGM120 on top of standard of care chemotherapy, which is gemcitabine and nab-paclitaxel. There's a very large historical database of response rates there. We feel like we'll have good information coming out of the phase II we're running right now to make a decision whether we wanna follow that signal in pancreatic or in prostate. I should have mentioned in prostate, the other thing that attracts us to developing in this area is PSA is such a powerful biomarker for that tumor type. We should be able to see effects fairly shortly in that cohort as well based on biomarker data. Okay, great. Maybe turning to another asset in your oncology portfolio, which is 707, your ILT2/4. Can you maybe help us understand, you know, where the developmental landscape is? Merck, I believe, has an asset here. They've shown some early-stage data, and maybe starting with that. Sure. Yeah. These receptors that we're inhibiting, ILT2 and ILT4, and I just wanna enunciate the T very clearly. This is not IL-2, ILT2. And it's companion receptor, ILT4. These are both, we think, very powerful myeloid checkpoint inhibitors. We're not alone in thinking that, in that, you can see a number of other biotechs and pharmas in the industry have jumped on to this area because it's a really interesting orthogonal play to the T-cell checkpoint area. The concept here is you have myeloid cells present in the tumor, so like macrophages and dendritic cells, that are, while present, suppressing the immune attack, even if you have a T-cell checkpoint inhibitor on board. These receptors, we think, are key to doing that. We, Merck, a number of other pharmas, particularly those that are protecting or building an anti-PD-1 franchise, have jumped on this as an area of actually helping more patients respond or respond better in combination with T-cell checkpoint inhibitors. We, of course, developed mono-specific antibodies against ILT-2, ILT-4. We actually have one against ILT-3. Our strategy is to inhibit both of these for the following reason, which is these receptors represent a relatively recent chromosomal duplication that occurred between non-human primates and humans. And we think and they're very structurally similar. They bind the same ligands. They're expressed in very high degree of overlapping cells in the myeloid compartment. We think there's a redundancy aspect here. Separately, ILT2 is actually expressed on some important effector cells as well. In both settings, we believe it's a suppressive signal. By blocking them, our intent is to release the brakes these receptors cause. We're benefiting now because Merck has shared a couple of years ago now, monospecific anti-ILT4 data that suggests sort of exactly what you'd wanna see, which is in pembro-refractory patients in particular, you see regained response to an anti-PD-1 or pembro. We think it's really encouraging that by only inhibiting one of these related receptors, we're seeing a response. Our hope is that by inhibiting both, we either can drive a deeper response or patients probably arrive at that resistant state either by elevating one or the other or both. We won't have to sort of pre-select or identify in advance patients that may need a release on one or the other. We're the most advanced dual antagonist, we're the only one in the clinic, and we're really excited to progress this further. It's in phase 1b at the moment. Maybe on that study, you said you are examining it already. How do you think about, I guess, its role as a monotherapy and potentially, to your earlier point, you know, a lot of companies with PD-1 franchises are trying to or who have one or are trying to build one, are thinking about combination approaches here. I guess my question is, you know, how do you think about the cadence of data that might come out for 707. Both as a monotherapy and then in combination with the lead PD-1 that you're focused on, which is pembrolizumab, over the next, call it 12-18 months? What we've guided towards is sharing in the second half of this year at a medical meeting data from our phase 1a portion, which is the monotherapy dose escalation. We have an R&D day that we split up into four different modules. We just released the one on NGM707. Let me plug the NGM621 one, which will come in about a month or so, just for those that wanna pay attention to that. For NGM707, we've gone through six different monotherapy dose escalation levels of seven we plan to do. We've progressed to the phase 1b, which is three dose cohorts in combination with pembro. The data we'll be sharing in the second half is from that 1a. I think it's important to put this in context, which is I know the monotherapy response has been elevated to something you really wanna see. I think it's important to look at the biology here, which is when you're layering on another T-cell checkpoint inhibitor, for instance, whether it's TIGIT or LAG-3 or, you know, the list of incremental T-cell checkpoint inhibitors. If you've already have a resistance to that approach, it's unlikely you'll see monotherapy activity on its own. We think myeloid cells by themselves may not be able to drive enough of an inflammatory response to see monotherapy. Merck's anti-ILT4 data would suggest that. We're, of course, hopeful, but we're not gating the program on seeing any sort of monotherapy activity, particularly given we're trying to move as quickly as possible to the expansion cohorts, race through the phase 1a, 1b, and then get to those, expansion cohorts in specific tumor types where we can really let the drug show us what it can do. Right. No, I think that's fair context just given to your point, what we've seen with other assets in the IO space targeting other targets with monotherapy responses. I think to your point, its potential and you know, can only be kinda clarified by expansion cohorts and/or you know, early-stage combinations. I guess on the combination side, I guess you know, when do you think I guess that you talked about the monotherapy dose escalation cohort coming before year-end, and maybe on the combination side, how do you think about that cadence, potentially? Yeah. It will follow fairly shortly thereafter. We've already started dosing that first cohort we announced as part of this Explorer Series R&D Day module that I mentioned. There are three dose levels, so we expect to progress as quickly as possible. We haven't guided on timing yet for that. It won't be this year, but we are obviously racing as quickly as possible to get to those expansion cohorts. Okay, great. Maybe looking at other things in the pipeline, turning to NGM438, you know, how do you think about its clinical development? Or, I guess, is the right way to maybe think about it focusing on traditional large tumor IO indications, is that the right way? Or thinking about expanding into sort of these white spaces that are out there in the immuno-oncology landscape where, you know, we haven't really seen great results from either PD-1s or other sort of early-stage monotherapy assets. Yeah. Maybe just to give some context around NGM831 and NGM438, both of which are in the clinic now. Both of these compounds represent what we consider our stromal checkpoints. Also myeloid checkpoint inhibitors, but specifically around biology, which we think is driven by these high desmoplastic tumor types that have a lot of extracellular matrix composed within the tumor. That has been known for a while that that's an indicator of poor prognosis for a patient. We're going after two receptor types that also are associated with poor prognosis for patients when overexpressed. It turns out the receptor ligand pairing makes a lot of sense. In the case of NGM438, we're blocking a receptor called LAIR1, for which the cognate ligand is collagen. Obviously, a big portion of extracellular matrix. Similarly with ILT3, we actually at NGM made a discovery that fibronectin is a cognate ligand of ILT3. That's important because there are other ILT3 antibodies in development, but some of them don't block that interaction because it wasn't known at the time they were blocking the receptor or developing the program. To your question, Paul, we are thinking about these as fairly broad applications, or at least it's worthy of exploring a signal in that regard. We obviously will think about tumor types that tend to have that dense extracellular matrix associated with them as pretty natural places to go. They also tend to be, as I referenced earlier, quite significant opportunities to help patients because they tend to be poor prognostic indicated tumor types. Our strategy will be very similar to NGM-707 in terms of clinical development. Phase 1a monotherapy dose escalation, a 1b that is in combination with pembrolizumab. We have supply agreements with Merck for free pembro across all of these. Get into the expansion tumors. We'll be looking for signals that we can follow. I do expect there's a possibility of finding signals for all three of these programs in accelerated approval potential pathways, of which we would probably run as quickly as possible. It's also possible for all of these that it may be such a broad application that we may want or need to seek large pharma partnership in order to do the heavy lifting to go broad. We'll be paying attention for all these programs to see what makes sense. David, as we think about the history of the company, when you and I initially met years ago, the focus obviously was on NASH metabolic diseases. Now you have a mid-stage, you know, ophthalmology asset, a few oncology assets in the clinic as well here. Is it fair to say that, you know, the cadence of INDs, you know, or maybe the sense of urgency at NGM has changed? You know, is this sort of the pace, I guess, you want to, you know, message to investors where you're just gonna be pushing into the clinic at this sort of sort of rate that you've been doing over the past year or two, which is suggested an acceleration? Yeah, the discovery engine from which all these molecules we've been talking about is really the foundation of the company, and it's been really productive for us. I think it's important to point out that it's also helped support the company because we're able to get business development funding through this innovation engine. In reference to the Merck deal that Siobhan was describing, which, we've received quite a bit of funding for the program. We view it as a real asset, a core strategic asset for the company. Our challenge becomes, from a portfolio management point of view and resource allocation point of view, how hot we stoke that engine. We don't intend to accelerate the productivity out of the engine. We have a really high bar right now about what the next one will be. Actually, Siobhan mentioned this T-cell engager that we've announced, but we don't plan to immediately put it into development in the interest of making sure we can turn over the cards on all the programs we've been talking about. It's certainly still operating. We think it's actually a source of revenue for the company ultimately. Don't think of it as INDs that will go into development necessarily on our dollar, but more again, developing assets that can be used for business development. Okay. Maybe for either you, David or Siobhan. You know, how do you think about, you know, on this point of business development and capital allocation going forward here, you know, is there a need for additional capital from your perspective? You know, or will the sources of capital primarily be business development as you've cited here? Sure. Sure. David alluded to this, but in our history, about half of our funding has actually come from business development, over $500 million, through BD partnerships, Merck being one, but there have been several others throughout NGM's history. It is a key component of, you know, how we operate the business, how we think about our portfolio. It's been really fun actually with the restructuring of the Merck collaboration to really have these programs for us to explore, NGM936, which is the T-cell engager being one of them that David was talking about. Looking for sources of non-dilutive capital is really core to our strategy. Also just supplementing our operations, given we have so many programs in the pipeline that we're prosecuting right now, it's really important to have that avenue. We happen to be in a fortunate position. We have $330 million of cash as of the first quarter of this year, cash into the first half of 2024. I think to your question, BD and really being open for the BD, again, has been a really key piece of, our activities internally at NGM. Okay, great. If there are any questions in the audience, please feel free to raise your hand and we can get a mic to you. In the interim, I was gonna ask, you know, you guys haven't completely moved away from NASH. You do still have a study going on here, which is ALPINE 4. You know, maybe with respect to that particular population and the mechanism and how do you think about, I guess, you know, potential success there, if you do see a positive result with ALPINE 4, you know, I guess, you know, how would you think about prioritizing your, you know, future NASH development or investment in that opportunity? Yeah, ALPINE 4 is our study with aldafermin, which is an analog of FGF19 that we are running in the cirrhotic NASH population or the F4 NASH population, thus the 4 on ALPINE 4. We have it fully enrolled at this point. We expect to report out data in the first half of next year. We made some important modifications though based on some learnings from our ALPINE 2/3 study, which was a reminder, I think to us and many that biopsy is an imperfect way to measure disease in NASH. In the setting of F4 or cirrhotic NASH patients, the FDA has a regulatory path that is outcomes-based, not surrogate approval on biopsy, either NASH resolution or fibrosis improvement. The reason that's important is the modification we made to ALPINE 4 was actually to elevate ELF as a biomarker that's the primary endpoint, so changes in ELF. ELF has now been approved as a diagnostic for NASH. It's just to be clear, not a regulatory endpoint yet, but the reason we selected it is there's a really good natural history database out there now of ELF changes correlating to outcomes. We think the power of the study to demonstrate ELF changes is greater because it's a continuous variable versus an ordinal one with fibrosis change. Of course we'll be measuring everything else, but we think that will be the clearest path if we were to show a meaningful effect on ELF to then have discussions with a partner to do the late stage NASH trial in cirrhotic NASH. It's a huge unmet need. We think the urgency of treating NASH is greater in the cirrhotic population. We've sensed from the strategic landscape and the discussions we've had over the last many years that that makes more sense to that group in terms of where you'd wanna start. We think it's a good setting. We'll have to demonstrate the data and potentially have partnering discussions on the basis of it. Okay, great. We're coming up on time here, so I'm asking this question of each of my companies at the end, which is you guys like some other companies, you know, have a multi-year cash runway, so funding is not a near-term issue in any way. But I guess in this, what has obviously been a very challenging biotech tape for the better part of a year and a half now, I guess what would you know, tell investors that you're prioritizing or any aspect of your strategy that you think is just, you know, in the context again of what is a very tough tape that investors may be missing here? Yeah, it's, I mean it forces, I think, as a management team because of our productivity of our engine, we're actually pretty comfortable with this which is portfolio decisions are so important in this context. It forces us, and I think all companies to come up with sort of the Sophie's Choice issue which is you have lots of children which one are you going to select in the case of the bad news scenario. Naturally we go through those exercises. We feel really like we're well-positioned because we'll have clinical data to make those decisions off of. That will be occurring within the timeframe that we have runway which is, very important. That combined with what we were talking earlier which is business development is a key tool for us. We're just spending a bunch of energy in that direction, just to be prepared. Siobhan, would you add anything to that? No. I think a lot of time on portfolio management and strategic optionality and exactly what we were just saying, walking through the decision tree around making really data-driven decisions. Great. We've run out of time so my thanks to David and Siobhan for joining us and we'll conclude on that note. Thank you very much. Thank you. Thank you.