Good morning, everyone. Welcome again to day two of our conference. I'm excited to be hosting Merus for our session here. I've got with me Dr. Bill Lundberg, who is the CEO of the company. Bill, thank you so much for being here today. Perhaps if you'd like to just kick us off with some opening remarks and priorities for the company for this year, and then we can dive into Q&A. Happy to. I mean, thanks to you and the entire team, and really appreciate the working relationship we've had for now a long time. Appreciate the longstanding support from your entire organization. Merus is an oncology-focused company with multiple clinical stage assets of our own and those with our licensees and partners. We'll probably spend most of the time talking about petosemtamab. We could take a few minutes for other assets if that's helpful. We've been innovators in the field of multispecific antibodies for more than a decade. Yes, there are many different platforms and approaches, but let me just give you a few points on ours in particular and why I think that ours is so special. It's really given us meaningful clinical activity with zenocutuzumab, our HER2-HER3 bispecific, already approved by the FDA, and petosemtamab, our EGFR-LGR5 bispecific, which we'll talk about, and the strong data we have in head and neck cancer. We also have MCLA-129, our EGFR-MET bispecific, which is similar to Janssen's amivantamab. We don't talk about it very much, but it is also a very active molecule. We are looking forward to seeing data from our partner, Betta Pharmaceuticals, on MCLA-129 at AACR this year. I think our success comes in large part from our ability to make bispecific antibodies or multispecifics, essentially like monoclonal antibodies, relying on the tried-and-true methods and approaches that have given us so many really good medicines in monoclonal antibodies. All of this allows us to stand on approaches that are very well established and not take in unnecessary risk in our program. This includes high-throughput screens, manufacturability, large-scale production from single-producer cell lines, global access to manufacturing capabilities. All of this is with a fully human IgG1 molecule, a reliable structure that has predictable in vivo behavior, low immunogenicity, and consistent half-life, and can have all the Fc domain engineering of fully intact IgG molecules like ADCC enhancement or stealth silencing for T cell engagers. Making great molecules by following the monoclonal antibody playbook is a powerful approach. While it does not necessarily guarantee success in the clinic, we think it improves the chances. What we have seen is really active molecules that we have been able to bring into the clinic and with Bizengri get approved. Given recent events over the past week, let me just take a minute to talk about a couple of thoughts. One is with respect to the changes at the FDA. We, like everyone else, are following closely. At the same time, we're fortunate enough to have already passed through our major negotiations with the regulators. We're really in a phase of being head-down focused on enrollment of our two phase three trials in recurrent metastatic head and neck cancer. That's really what our efforts are focused on. With that, I'm happy to dive right into the questions. Okay, great. Thank you, Bill. Just as a quick reminder to our listeners, if you'd like to send over a question to me, feel free to send it over through the dashboard. Let's talk about petosemtamab. Perhaps you can just start with a quick overview of the data that you've presented for the product in first and second-line head and neck cancer, and then we can digress into, or we can actually move into kind of the first-line data that you will be presenting soon at a medical meeting. Yeah, absolutely. There is a lot of data. Let me start with the second-line data sets. petosemtamab is a bispecific that targets EGFR, which is a well-established cancer antigen, and LGR5, which is a cancer stem cell antigen in the Wnt pathway. It has been reported to be upregulated in a number of cancer types, including head and neck, colorectal, and other cancers. We discovered this bispecific antibody by screening a large library of our bispecific antibodies against, or looking at an array of tumor targets. In these assays, we cast the net wide with our screen to increase the chances of identifying unique molecules with specific anti-cancer activities. The result was selecting petosemtamab, which showed the most potent growth inhibitory activity of a tumor form of the model as opposed to a normal cell form of the model, particularly as compared to cetuximab or EGFR antibody envisioned. In terms of clinical data in the second-line setting, we just recently, December of last year, presented data at ESMO Asia, where we showed an overall response rate of our drug alone in second-line plus recurrent metastatic head and neck cancer that held up in 75 patients of 36%. We are continuing to see responses across all different subsets, including HPV-positive disease, as well as a deepening of responses over time. The median duration response was 6.2 months, and overall survival was around 11 and a half months. This is a data set that compares very favorably to what patients could otherwise receive. Patients with previously treated or second-line recurrent metastatic head and neck cancer typically have a response rate in the teens to single-agent chemotherapy or cetuximab, and an average survival of only around five to eight months, depending on the study. This clearly is substantially better than those historical controls. Our drug continues to be well tolerated with a manageable safety profile. This did garner BTD or breakthrough therapy designation, which is important because it is a recognition from the FDA that even the FDA believes that this could provide really meaningful activity above what patients could otherwise receive. In the first-line setting, the standard of care for most patients is pembrolizumab or Keytruda alone. That can provide a 19%-25% response rate and an average survival of around 12.3 months in one study and 17 months in another study. We shared clinical data of us combining our drug with pembrolizumab in 24 patients. This was at ASCO last year. In this efficacy population, we saw not a 19%-25% response rate, but a 67% response rate. Many of these patients, 14 out of 16 of the responders, were still on drug at the time of the presentation. The responses occurred across all subgroups, again, importantly, across the CPS 1-19 or 20 and greater levels of PD-L1 expression, and also HPV status, where three out of the four HPV-positive cancers responded. It was too early to get a sense of any time to event endpoints. We really couldn't speak to the durability there on that data. Many of those patients were continuing on treatment in response. The drug was very well tolerated with no significant overlapping toxicities from these two therapies. Infusion-related reactions were well managed. They can occur in almost about a third of patients with a single-digit rate of grade three and no greater grade four or grade five. We have guided to a clinical update of this data set. We believe that petosemtamab really has the ability and the potential to become both first-in-class and best-in-class and a new chemo-free standard in recurrent metastatic head and neck cancer. At a medical meeting at some point soon, you'll be presenting data from this first-line study. I presume it also will include data set from your dose-ranging work that you've done under Project Optimus. What we've provided previously is the Project Optimus work. Part of any clinical drug development effort these days is the FDA often asks for a comparison of different dose levels to make sure you're developing your drug at the proper dose level. We had done that work and discussed with the FDA and aligned around our current dose. We are set with that work. We presented the dose comparison data, which was all done in monotherapy at ESMO Asia in December, just a few months ago. We now have established the dose at 1,500 milligrams every two weeks. We do not need to redo any Project Optimus work now that we're developing our drug also in combination. We are already all set with the dose. The presentation will only focus on this cohort of 45 patients. Okay. What would be the duration of follow-up for this cohort? I think the last time you presented data at ASCO, I think the cutoff was sometime in March of last year. At least March is, we've already sort of crossed into April. I would imagine there would be at least one additional year. Can you maybe comment what would be the duration of follow-up at that point and what would be the endpoints that you'd be reporting on? That's generally the right perspective. As of the presentation at ASCO last year, we described all 45 patients in terms of their background, their demographics, because all 45 patients had been dosed by the March 6, 2024 data cutoff date. It's these patients that are being followed further and continuing on therapy that we'll provide a clinical update for. Okay. Obviously, there is sort of a debate around what is the right data set to look at in terms of thinking about how the Peto/Pembro combo compares with a lot of other drugs that are in development and in first-line head and neck. Maybe if you could sort of talk, put in perspective the response rate data that we've seen before and also the other data set that you'd be reporting on, which is the overall survival data percentage at perhaps one year and PFS. Maybe kind of put in context what is the right data point to kind of pay attention to. Sure. We should pay attention to all the efficacy data points, which, as you said, were overall response rate, progression-free survival or PFS, and overall survival. To be clear, the efficacy endpoints in our registration trial are overall response rate and overall survival. People do not really debate much about our overall response rate. We have shown a 67% response rate in combination where the monotherapy or the control arm has a historical 19%-25% response rate. It is not really even taking up much conversation there. In terms of overall survival, what I have talked about there is hopefully we have not reached a median. Hopefully, there is really good survival with our drug in combination with Pembro. The first time you can really start to see a separation of the curves, the survival curve is around 12 months. The 12-month rate of how many patients are still alive at 12 months is a really important number. We also have this debate about what's going to predict survival the best. Is it response rate? Is it PFS? The way I answer that question is let's use survival to predict survival. I actually think of all these data points, the 12-month OS rate is probably the best number we have regarding predicting survival. PFS or progression-free survival is also important because it's a way to look at the duration that patients are on therapy. While it won't directly impact the approval of our drug, it does impact how people think about the duration patients are on treatment for, for their economic models of the opportunity here. There's an important distinction between what's reported as a median PFS, the middle value, which is often what's shorter than the average duration of PFS or average duration of treatment, which is the number that needs to go into these economic models. I would say in addition, there are two single-arm data sets that have suggested PFS numbers from competitor molecules that are just worth paying attention to as well. I'm sure we'll get back to that in a minute. Yeah. Does ORR or PFS predict OS? Probably not very good. OS predicts OS. Okay. Perhaps if you could, this is a good time to lay out what is the bogey for the overall survival rate at one year, and with the standard of care being Pembro, Mono, and first-line, maybe lay out for us what you'd be looking to sort of compare that data set to. Here's where there's a lot of data where one can look at any one of a number of different published studies in solid tumor oncology or even head and neck cancer and ask how good is the 12-month OS rate and how much better does an experimental arm need to be for the trial to really win. In terms of the historical controls, the comparators of our control arm, Keytruda has had a 50% in one trial and 59% 12-month survival rate, which is the important control arm metric in those two historical studies. There have been studies that have failed, and those have had a 0% and 4% increase above that 12-month mark. Those trials failed. Keytruda in head and neck cancer in the CPS 1 or greater population had a 7% improvement, and that trial was successful. Now is the use of Keytruda alone in that setting. A really good result is the 16% increase in 12-month survival rate of Padcev Keytruda as compared to chemotherapy in bladder cancer. That led to a doubling of survival for those patients. That is a really good number. Okay. That gives us a good way to think about measuring kind of the improvement. Now, can we look at the response rate data that we've seen for Pembro, Peto compared to Pembro alone? Not in a direct trial, but just across trials. Does that give us any insight into whether we will see an improvement in the survival rate at one year? I mean, again, I think ORR may suggest a survival benefit and clearly a dramatic difference like we see 67% versus 19%-25% in overall response rate may suggest a longer overall survival. Progression-free survival has not been as good a predictor in head and neck cancer across a whole host of studies to predict overall survival. Ultimately, the early data on overall survival probably tells you how you are tracking in a really important way. Just an overall response rate, I mean, we feel really good about it. A delta of 67% we have shown with our drug in combination as compared to a historical 19%-25%. That is a really confidence-building, feel-good difference. Okay. I want to talk about kind of the HPV-positive patients. There's been a lot of investor sort of questions around what activity are we seeing for the drug, and are we really seeing something that is different from what we've seen with isatuximab, which hasn't really worked in HPV-positive patients. Can you talk about the types of patients that were enrolled in the study so far that you've reported on? Also regarding the HPV-positive patients, is there kind of a difference in efficacy between smokers and non-smokers? Do HPV-positive patients who smoke tend to have a similar sort of genetic profile as HPV-negative patients? I think those are some of the questions that have percolated on this topic. Yeah. What we've shown to date is in the second-line setting, petosemtamab alone has a 13% response rate in HPV-positive recurrent metastatic head and neck cancer. In the first-line setting, it has a 75% response rate in combination with Keytruda. These numbers are substantially different than what cetuximab has shown in this setting. I think it's really encouraging. In the second-line setting, the results are similar to what patients could otherwise receive. In the first-line setting, it clearly appears to be substantially better than Pembro or Keytruda alone. The notion of carving out HPV subsets is a relatively new thing. The historical registration trials in head and neck cancer have all taken all-comers or all-comers with CPS, one or greater, PD-L1 one or greater. The precedent that we're following is these five prior registration trials in the first and second-line setting. To take only HPV-negative population is a brand new thing. There isn't a lot of precedence around doing this, either for benchmarking how good will the data be or for regulatory path. It is different from where historical clinical drug development has been in head and neck cancer. As we've moved forward with our program in all the patients, positive and negative, as we've moved forward with our clinical development plans, our discussions with regulatory authorities, our phase three clinical trial plans, having received breakthrough therapy in the first-line setting and in the second-line setting, the discussion has always been around the entire patient population. The HPV subsetting has never come up as an issue or a question in those settings. Generally, I think that unless you're absolutely compelled to do it, to subset, it's not that helpful to subset a population because it implies that you're taking less of the commercial opportunity where, at least in the U.S., it can be a third of the patients or more. You're now needing to develop a diagnostic test, which isn't impossible, but it is headwinds in both approval and commercialization. Let me also say that as we think about different scenarios of what the rates of response could be, because I think the underlying question is, what if those good numbers you've shown already suddenly go south? With our registration trials, we do a lot of scenario planning and modeling. What if this subset performs worse? What if that subset performs worse? To ensure that we have enough patients to have enough power to succeed even if some of these subsets cut the wrong way. I can move on to the smoking question if you want, but do you have a follow-up question for this? Just a quick follow-up on that. As you've thought about the enrollment of your registration trial, is there sort of a representation of HPV positive and negative that you're sort of solving for pre-specified in the trial? Historically, the response rates in the second-line trials, multiple trials, have been around 25%, and the first-line trials have been around 21%, 22%. It is very different by geography. Much higher in the U.S., much higher in occasional other spots elsewhere, medium in Europe, and lower in Asia. Depending on where your trial enrolls, where you choose to enroll your trial, you can influence substantially the proportion of HPV patients. Now, when the trial is ultimately read out, people will look at the overall population and HPV subsets as among many different factors to ensure that there's consistency among many different subsets in the clinical trial. Historically, all of these trials have run clinical development programs in the broader population. That's fair. Okay. I guess my question was also to understand how have you powered the trial to manage the risk around the response rate or the durability in the HPV-positive patients being less than what we've seen in the trial so far. That's right. To be fair, in the first-line setting, we don't actually have—we haven't historically had durability data for our drug, petosemtamab, in the first-line setting. We have some data on the second-line setting. We've needed to analog around a wide range of potential outcomes for HPV-positive and negative and a relatively wide range around proportion of patients with HPV-positive disease to ensure that across all of those ranges, we're still confident that our trial has the power to succeed across all of those. That's been important. Okay. We can Okay. We can continue to smoke. Take on the HPV-positive disease and is it influenced by smoking question. There's been one particular KOL who's been advocating that smoking may change the responsiveness of head and neck cancer to cetuximab and EGFR-directed antibodies, including potentially petosemtamab. That's just not supported by the data. Now, the clinician may have his own anecdotal couple of patients, but across many clinical studies, many published clinical studies where cetuximab has been the control arm across hundreds and hundreds and hundreds of patients, smoking does not increase the response rate to cetuximab in HPV-positive disease. The cetuximab response rate in HPV-positive disease is zero. It doesn't matter if a population or a patient smokes or not. In these studies, 77% of the patients are smokers. It doesn't change the zero number to any other number. It's consistently zero across study after study after study. Okay. Yeah, that's helpful. Let's maybe talk a little bit about some of the competitors that are also pursuing the space. Let's start with Bicara. They're studying their drug in combination with Pembro, which demonstrated about 64% overall response rate in first-line HPV-positive patients. That seemed very comparable to the Peto plus Pembro response rate of about 65%, again, in first-line HPV-negative patients. Now, given that the efficacy so far looks comparable, how do you see Peto compete in this patient population? Yeah. Let me frame out first, in terms of the landscape competition, there are three trials competing in the first-line setting of the entire patient population, which is our drug, zanzalintinib from Exelixis, and the Akeso Summit drug, ivonescimab, which is actually in clinical development in head and neck cancer in China with a different experimental drug, which makes it probably not a viable approach in the U.S. There is one in the subset of patients only with HPV-negative disease, which is Bicara's BCA101. In this competitive landscape, I think with Zanza, which is the other overall population drug, we do not have any prior data with Zanza. We have data only with the prior drug, cabozantinib, and Cabo has shown data in head and neck cancer in a single-arm investigator-sponsored trial. The registration trial is a phase two/three registration trial, and we should see by the end of the year, does it pass from phase two into phase three. Zanza is a multikinase inhibitor that is like Lenva. Lenva itself failed in head and neck cancer because of toxicity. Zanza may be a little bit better tolerated, but we'll really have to see. In the HPV-negative patient population subset, Bicara's BCA101 or ficerafusp is an antibody that is cetuximab on one arm and a TGF-β trap molecule on the other. They reported out in a series of presentations a set of numbers that people do look at as reference, which, of course, they should. There is a publication of cetuximab with pembrolizumab, the Sacco 2021 paper, which also has very similar data. I think both drugs have around a 45%-46% response rate in all comers in the entire population in this first-line recurrent metastatic head and neck cancer setting. What we see now is that they're retrospectively selecting a population of patients with HPV-negative disease and use that to choose to move into the phase three trial. In this process, retrospectively looking at data to find where your best data are is what we all do. It's totally fine. It makes it difficult to really know what the response rate or what the numbers would be in a prospective setting because your eyes are naturally gravitated towards the most attractive retrospectively called data. It's a little hard to know what the real numbers would be if we ran a prospective trial with this as the intended endpoints. I think there are a couple of things just to note about the data as well. One is that, and this is true for our data set too, by the way, we have a combination therapy in a single-arm data set with no concurrent control. One of the criticisms of this type of setup is maybe pembrolizumab is just giving us an outside result, just an amazing, amazing result, and we're being deceived by thinking that it's the combination when we compare to historical response rates. A third issue that I would point to is no single agent activity in this indication for ficerafusp. These are generally three flags that it's harder for drugs with these three issues. Drugs with these three issues generally haven't done well in development. I think we just have to see the data and keep these issues in mind. Okay. That's really helpful context. Maybe I wanted to ask also about evorpacept, which is by ALX Oncology, which demonstrated promising data in phase 1b with a 12-month overall survival percentage of about a little over 87% in first line and 80% in second line. Their phase 2 data is expected in the second quarter of this year. Will that product be relevant? How do you think about that as you compare it to the Peto/Pembro combo? I'm actually quite curious to see the evorpacept phase I B two data. I think it will be interesting. Many of us had real big hopes for the CD47 SIRP alpha pathway and mechanism. I think just across a number of different assets, it hasn't held up well in subsequent studies, and that's been pretty disappointing. I think we just have to see. It's really hard to handicap and know how that's going to play out. Okay. All right. Maybe a last one on the competitive landscape. One of the other therapies that's mentioned by KOLs is Versamune, which is HPV by PDS Biotech. Any thoughts there? Their HPV-positive only subpopulation study showed about 35% overall response rate in both first and second-line patients with an overall survival of 30 months, which obviously is intriguing. What are your thoughts there? Yeah, this one is interesting too. I think it's clear that HPV vaccine Gardasil can prevent the subsequent infection and consequences of HPV. That's going to be an incredibly important impact on public health over the next 15, 20, 30 years. In multiple studies, it's been much harder to vaccinate against an already established infection or tumor. I think with this drug and with a couple of other efforts in the HPV vaccination setting, we haven't yet seen the really compelling data. We've seen a couple of data sets that haven't quite been as strong. I think this one, we have to see. Here too, we're seeing a combination. This is also with some of the issues that we've seen with the ficerafusp data set. I haven't seen any data of this drug in monotherapy to really know, are we just boosting the immune system with Pembra, with Keytruda, and how much is the vaccine really adding? Okay. Maybe perhaps just to sort of close on the head and neck conversation, I'd like to just sort of understand from here on, how do you see the paths to approval, what's the regulatory strategy, and maybe recap what your discussions with the FDA have been on that? Yeah. For both the first-line recurrent metastatic head and neck cancer and second-line, second, third-line recurrent metastatic head and neck cancer trials, those phase three trials are ongoing. We are pushing hard to get up and running as quickly as we can and get enrolled as quickly as we can. You can look on clinicaltrials.gov to see our site activation progress. I'm really pleased to be able to say, even though we started both trials in the third quarter of last year, the first-line trial has more than 100 sites open, and the second, third-line trial has more than 90 sites open. We're really happy with the progress we're making. We've been very clear that we believe in both trials. There's an opportunity for accelerated approval based on an early endpoint such as ORR with confirmation of that benefit coming from survival in both trials. We have also shared that we expect both trials to be substantially enrolled by the end of this year. We are really pushing hard. We feel like we have a very solid regulatory strategy, and time is of the essence. It is really important for us to execute in a timely manner and execute well. Just a quick follow-up there. For accelerated approval, you need kind of the overall response rate data. Do you need to have some sort of a look on overall survival or any other durability endpoint? Yes, that is likely. The FDA has been very clear in terms of this type of approach, which is a project front-runner approach. They're very motivated to get companies to look at an accelerated approval model in the context of a randomized phase three trial with an early endpoint like overall response rate. The two additional components to that, one is when the FDA says response rate, what they mean is a RECIST 1.1 response, which is confirmed, and that that has some durability. Historically, the FDA's accelerated approvals have had durability of six months or more. There is also some trend in another statistic like overall survival, certainly to know that it's not headed the wrong way, but hopefully to know that it's headed the right way to give the FDA some comfort that the likelihood of the ultimate approval is good. They have been very clear about that. I would also point to the first program that received accelerated approval in the context of Project Front-Runner, which is the Breakwater trial, which was recently approved in an accelerated approval way based on the first 110 patients per arm, which was ORR with some durability. I'm sure, I'm not sure, I would imagine that there was the opportunity to ensure that the survival was trending the right way too. Is the survival that percent surviving at six months or one year? The FDA hasn't taken a formal position on what the statistic is or what type of look or anything like that. There isn't a guidance document that will just tell you. We're all relatively early in this process with the agency. Okay. All right. We've got a couple of minutes left, and I certainly want to hit on CRC. Perhaps maybe talk to us about kind of the rationale that convinced you to study Peto in this indication. You are studying it in all three lines. Perhaps maybe also lay out, you're going to be reporting data on that later this year. What is it in terms of the response rate that you would expect to see across the three lines of treatment that would convince you to continue to develop it further? A lot of questions in one because we've got very little time. The signal for me to talk faster. Yeah. The mechanism of LGR5 being involved in tissue homeostasis and cancer growth and metastases is best worked out in colorectal cancer. A wide number of studies have now shown this in a variety of different academic publications. We are really interested in the potential for petosemtamab, which targets LGR5, to have a real impact in colorectal cancer disease. Balancing the really very strong rationale is an earlier data set that we have shown in dose escalation where 10 patients were treated at the top three dose levels, and we did not see any responses. One of the issues we have in looking back at those data is that it was a phase one setting, very heavily pretreated patients. Many patients' tumors had genetic mutations, making them unlikely to be able to respond to cetuximab and potentially also our drug. We view it as kind of uninformative now. Going back to colorectal cancer, we want to give it the best shot we can. We are now looking at patients with genetically wild-type tumors without any prior cetuximab in the first and second-line settings to give us the best chance to see a robust signal. In the third-line setting, also genetically wild-type tumors, but patients will have seen, almost certainly will have seen cetuximab in that setting. That really gives us the best chance to answer the question, is there a signal? Is there an opportunity for us in cetuximab—sorry, in colorectal cancer? Because on one hand, we have such strong rationale and preclinical data, very strong preclinical data. On the other hand, we have this 10-patient experience where we did not see signal. That is really how we think about the reason to pursue all three cohorts. Colon cancer is complicated. It depends a lot on the line of therapy in first-line, left-sided versus right-sided tumors, what we're comparing against, characteristics of the patient. There isn't just a bar, I can tell you, a number. It's not as easy as many other indications. One data set that people do point to and will look at is data that was recently shown for amivantamab in colorectal cancer, the Origami trial. That is a data set that we are likely to be compared to as we look at the clinical trial results. We have guided, we would provide the first look at the clinical data in the second half of this year. Okay. A quick follow-up, just in third-line patients, do a lot of patients have just wild-type? Do you mean do those patients with an originally wild-type tumor evolve to having multiple mutations? Yeah. How easy is it to find a third-line patient without multiple tumor mutations? It is not the most common fraction of colon cancer, to be sure, but there are many, many patients with colon cancer, unfortunately. We do not think it is going to be that rare or that small a population. Colon cancer overall is a much bigger opportunity than head and neck cancer. Okay. How would you sort of pursue, and I do not think you are studying it as monotherapy in all the lines, and maybe talk to us about kind of why a combination therapy versus a monotherapy? In the first two lines of colorectal cancer, its 5FU-based poly chemotherapy is standard. We're unable to, it would be unethical to deny patients standard chemotherapy as part of their treatment, right? Patients in the first-line setting almost certainly receive a biologic, either Avastin or cetuximab, us having shown in a variety of preclinical and clinical settings that our bispecific antibody that also targets EGFR like cetuximab has similar activity to or superior activity in some settings to cetuximab, gives us clinical and preclinical evidence to support the use of our biologic in that setting. We couldn't avoid offering patients the chemotherapy side of that as well. Okay. I think we are out of time. Thank you so much. I really appreciate you taking the time to be with us today and to our listeners for joining. Always a pleasure to chat. Thank you. Thank you.