Good. I think you can hear me. A warm welcome to Novo Nordisk Investor and Analyst event here at the ADA this year in San Diego, and also a warm welcome to those of you listening to the webcast. My name is Daniel, and I'm heading up Investor Relations here at Novo Nordisk. We'll start this session by a presentation, and then we'll have a Q&A afterwards. As always, I need to remind you that there might be forward-looking statements in what we're going through. This is our strategic aspirations we defined back in 2019, and we report on them on a quarterly basis. You see here the highlights for the Q1 of this year. We continue to make progress on all our aspirations within the purpose and sustainability, ESG. We made progress on all our aspirations, I will only highlight that we now treat more than 37 million people living with diabetes. That is also reflected in our diabetes value market share, which we increased, and we are now at more than 32%, in line with our tracking well on our aspiration of achieving more than a third of the diabetes market in 2025. Sales growth was really strong, 25% in the Q1, and operating profit growth of 28%, mainly driven by our strong portfolio of GLP-1 treatments within diabetes and obesity. It also led to us raising the guidance, so we are now guiding a 24%-30% for the full year 2023. The main reason for us being here today is, of course, to discuss what we call innovation and therapeutic focus. To do that, we will have these two gentlemen, Martin Holst Lange. Many of you are familiar with Martin. He joined Novo back in 2002, had various roles over the years of increasing complexity, and then in 2021, he became Executive Vice President of, and Head of Development. With me today is also Stephen Gough. Stephen joined Novo in 2015. In 2018, he became Global Chief Medical Officer and Senior Vice President. Previously, Stephen worked as a professor for diabetes at Oxford and was heading up the diabetes center for endocrinology and metabolism, also at Oxford. With that, Martin, over to you. Thanks very much, Daniel. We hopefully have put together a very exciting agenda for you. Obviously, starting a little bit with insulin. This is the ADA, Stephen will go through the IPERTEC program and the results from the IPERTEC program for you. We'll focus on GLP-1 in diabetes, first with CagriSema, and then with all sema obesity. Sorry, all sema in diabetes. We'll progress to GLP-1 in obesity. We'll focus on all GLP-1 in obesity, but also, hopefully exciting, showing you some data from the just finalized result from the HFpEF trial that we conducted in obesity. It's just gonna be a few highlights, primary endpoint, nothing more than that, because some of the data are still embargoed, but hopefully something that you will enjoy watching. I just give a brief highlight on what has happened in our pipeline and for our pipeline over the last year, since we last met at ADA. Just as a reminder, we have broadened and deepened our pipeline with focus on quite a number of therapy areas as we speak. We have phase III assets in eight therapy areas, obviously beyond diabetes and obesity, and a broader focus in the cardiometabolic space. We also have exciting, both obviously, pre-clinical assets in our pipeline, but also activities in all therapy areas in phases I and II, which is obviously interesting for us. I've been asked in this slide to only highlight three things. One is obviously, CagriSema phase III, initiated for the treatment of obesity. This is incredibly exciting for us. As you know, we've seen data from phase II suggesting that CagriSema has the potential to lead to an at least 25% weight loss in obesity. A little bit maybe reflecting that some of you heard me talk about, for me, a rule of thumb in terms of how exciting is this potential. I sort of draw a little bit on that from our ability to recruit. I am happy to tell you that the pivotal time for CagriSema is finalizing as we speak, so basically ahead of time in terms of recruiting into that trial. Obviously, if I use that rule of thumb, then it bodes well for the excitement that we should feel for CagriSema. At the same time, you've also heard us talk about we'll initiate phase III for type 2 diabetes later this year. I also wanna highlight Mim8, and I will use the same rule of thumb. We are currently recruiting into phase 3, and the phase 3 pivotal trial. Again, this trial is also ahead of schedule in terms of patient recruitment, speaking to the potential of what Mim8 can do in the space of hemophilia. Finally, maybe highlighting something very early, but something that actually makes me a little bit proud. You know, it's only a couple of years ago since the acquisition of Dicerna, and already now we have 2 molecules in clinical trials based on the siRNA technology. Both molecules are for the treatment of NASH. One is LXR, and the other one is called MAC1. Given the nature of the RNA-based technology, these are reasonably long studies due to the long sort duration of action of this intervention. Reasonably long phase I trials, but with a readout during the course of the next year. I'll leave the floor for Stephen and a very nice introduction to what insulin icodec can do. Thank you very much, Martin. It's a pleasure to be here. As Daniel said, I was previously Professor of Diabetes in Oxford, and I've been with Novo Nordisk now for just coming up for 8 years. This slide, which is just an introduction to diabetes, is sort of close to my heart because, having come from Oxford where UKPDS was done, prior to me, I have to say, it really set the scene for Type 2 diabetes, because prior to UKPDS, there were big questions about whether we should even be treating Type 2 diabetes. Were we doing harm by lowering glucose? UKPDS changed everything. It helped us understand the relationship between glycemic control and complications, whether it's microvascular or macrovascular complications. It also gave us the 7% target that we now stick to, and that we work to, and that's where it came from. This relationship between diabetes and complications was established, and there's been lots of studies, and you don't need me to tell you about all the CVOTs we've seen over the last few years. The other thing that UKPDS taught us was that Type 2 diabetes is a progressive condition. The bit in the middle here is important because treatments don't fail. Patients get worse. The beta cell declines. It's a progressive condition, ultimately, we know that somewhere around 50% of our patients will need insulin. I also know that's with Type 2 diabetes, I know as a clinician, that's then the hurdle, that's the barrier. Patients don't want to go onto insulin. They certainly don't want to go onto daily injections of insulin. There's fear of it, there's an apprehension. They delay going onto it. There's some statistics or some numbers here. Patients delay going onto insulin, and when they go onto it, they don't stay on it, or they miss injections. That's really the impetus for us to move into a once-weekly. What we wanted to achieve was: Can we achieve something once a week, that we've seen with once daily? The summary of this slide, I know you've seen probably all of the data on this slide, is that we can do once-weekly, what we've been doing with once daily. In fact, we can do it even better. If you look at what we set out to do in terms of comparing a once-weekly to a once-daily, not only did we achieve non-inferiority in every trial, but in most of our studies, and you can see four of them, we also achieved superiority in terms of A1C lowering. We can do what we need to do. The big fear was hypoglycemia, and Will you see more hypos? Will it be more prolonged? Will patients really struggle? What we've shown is hypoglycemia is not an issue. Some of you will say, "Yeah, numerically, we've seen more hypos with the once-weekly." What I can tell you is that our hypo rate is extremely low. In terms of patient years of exposure, it's less than one. What does it mean in terms of the difference between the once-weekly and the once-daily? What it means is that equates to one extra hypo every three years in patients who are insulin-naïve. Patients going on to once-daily, or sorry, once-weekly insulin will have one more hypo in three years. I think that was I don't know if any of you were at the symposium this morning on ultra-long-acting insulins, but that was a very clear message from our independent KOLs, that we can do with once-weekly what we could do with a once-daily. I think that's a testament to this program and to the molecule that we've developed. What I'd like to do is just take you through a couple of our ONWARDS trials. You'll have seen some of this data, but I hope not all of it. I doubt not all of it. I want to just say something about ONWARDS 1. I was really pleased to see that we're able to have a simultaneous publication in the New England Journal of Medicine when we announced this. This was about confirming the efficacy and safety of once-weekly insulin icodec in insulin-naive patients, obviously in type 2 diabetes. You can see here, it's a 52-week study with a 26-week extension. This is really important because what it tells us is it gives us data over 18 months. When we're talking about trying to improve glycemic control, what we're talking about is the persistence, because we're trying to avoid diabetes complications. When I was in clinic, yes, I was focused on numbers, but what I really wanted to do was avoid complications. To have data over 18 months is crucial. What we showed here, and I think you've seen these data, we know that we see this significant improvement in terms of A1C, an impressive drop, and that is maintained at 78 weeks. This change in A1C, which is important to patients, is maintained over the duration of the study. Then you could ask me about hypoglycemia. Well, just look at these numbers on the right-hand side of the slide. Once-weekly insulin icodec, Level 3 severe hypos, 1. In terms of 1 patient, in terms of once-daily insulin glargine, there were 6. In terms of the total number of patients who experienced Level 2 or Level 3 hypoglycemia, very similar, you will point out to me, "Yes, but there's more events with your once-weekly." What I can tell you, whether. What this means to you, it certainly means a lot to me, is that 3 patients contributed over 100 of those events. What this is really showing is low rates of hypoglycemia, and the difference between the two is small, and as I say, in insulin-naive patients, we're looking at 1 extra hypo over a 3-year period. What I'd also like to talk to you about is what's important to the patient. Because when I treat patients, and I try to get their A1C down, and I improve their glycemic control, they say, "That's fine, but I don't want a hypo." On the left-hand side of the slide, what we have here is the proportion of patients achieving an A1C of less than 7% without hypoglycemia. This is without Level 2 or Level 3 hypoglycemia. You can see for once-weekly insulin icodec, over 54% of patients achieve that target without hypoglycemia, compared to 46.4% in once-daily insulin glargine. We can get more patients to target without hypoglycemia. The other thing I want to talk to you about, which is on the right-hand side of this slide, and something I've been really impressed with at the ADA this year, is the increasing amount of CGM data and the use of CGM. Now, I started off by saying A1C is the gold standard. It's the thing that we judge glycemic control by, but I think increasingly, you're going to see the importance of people being in target range, because we know an A1C can cover a lot of... There's a lot it can cover with the highs and the lows. What's important is CGM or what's your blood sugars over a 24-hour period. If you look on the right-hand side of the slide, you can see with once-weekly insulin, we have a longer period of time in that target range. The international guidelines suggest 70% is what we should be aiming for. That's good for patients, and you can see that's what we've achieved with the once-weekly insulin, which is greater than what we see with once-daily insulin glargine. Also, the red bits, the bit below range, there's criteria for the international criteria for the really low levels, it has to be less than 1%, and for those below 54, below 70 mg/dl, less than 4%. We're well within international guidelines in terms of where we should be, in terms of time and range that we get from continuous glucose monitoring. I think this is also assuring, and I hope, and I think we will see over the next few years, that CGM will have a much greater prominence. I'm not saying it will replace A1C, but it will have a much greater prominence. I'd like to say something about ONWARDS 5, because ONWARDS 5 has 2 really important components to it. The first is that we were trying out a new app. This is a guidance app to help people, a digital tool to help them calculate their insulin dose. It wasn't just taking blood sugar values. It would also incorporate whether a patient had an episode of hypoglycemia, whether they were planning exercise. They didn't have to use this, but it was a guidance app that we evaluated in this trial. The other thing is that this trial was as close to real world as we can get. In fact, all clinical trials on insulin, you see patients every 2 weeks, every week. In this trial, we saw patients every 3 months. That's what it's like in normal clinic. When I do clinic, I can't see patients more frequently than every 3 months. The important thing with this trial was it was close to real world, and if you look at the inclusion criteria, we included just about everybody. The only people we didn't include were people who the investigator thought wouldn't complete the trial. This took all comers. It was as close to real world as we can get, and obviously compared once-weekly to once-daily insulin. We saw these great improvements in terms of A1C. We matched, and we were superior to once-daily. Again, you can see very low rates of hypoglycemia, both in terms of Level 2 and Level 3 hypoglycemia. We can do, as I say, with once-weekly, what we can do with once-daily, and this is as close to the real world as you will get. I think that's very reassuring when this goes out into clinical practice. The other thing that we did in this trial was we looked at patient-reported outcomes. If I'm telling you that patients don't want a once-daily insulin, what you want to know is, does quality of life improve? We used 2 standard tools here. We used the DTSQ, which is a health-related quality of life questionnaire. We also used the TRIM D, which is a compliance questionnaire. For the DTSQ, top score is 6, lowest score is 1, just to orientate you. In terms of TRIM D, top score is 100, lower is worse. What you can see here with the once-weekly insulin, is we have high at the end of trial, we have better quality of life in terms of the quality of life questionnaire, but also in terms of compliance. This is telling us that, yes, patients do prefer, which you would expect, but they do prefer a once-weekly insulin. One of the things that I tell you or that you've heard before, is the great thing about a once-weekly, is you go from 365 injections a year down to 52. Actually, that's not true. Because patients don't take their once-daily insulin 365 days of the year. Most of my patients would miss it at least once or twice. Actually, we haven't been telling you the right numbers, because most patients, as you can see here, it might be twice a week, they don't take their once-daily insulin. What that means is they don't get the best glycemic control, and they don't get the best outcomes. What we can say is that we are trying to get down from this high number, right down to 52, and this is really important to patients. The other thing I will just say is it's easy to use. I think that in our clinical trials, when you speak to patients, when you speak to investigators, it is easy. If you take insulin-naive patients or patients naive to insulin, it's a starting dose of 70 units. Once daily, it's 10. What do you do if you're on once a week? You just multiply by 7. It's as simple as that. The titration is exactly the same as it would be for once daily. If you're already on insulin, you need a slightly higher first dose, a loading dose, so that you don't have a glycemic lag for the first 6 weeks. You don't have to do that, but you can do that. Then you're back on to the normal 7 times. It's the same volume because it's the same volume because we have an increased concentration, so the volume that you give for once daily or once weekly is the same that you give for once daily. Takeaway messages from my point of view is that we've got lots of treatment options for type 2 diabetes. We know ultimately patients will require insulin. A high proportion of patients need to go onto insulin. We know it's a barrier, just going on to that once-daily. If we can reduce that's a benefit for patients. We've shown with insulin icodec that we can achieve what you achieve with once-daily, but we can actually do better. We can do better in terms of glycemic control with low rates of hypoglycemia. I think the way we see this is that we see this as a starter insulin, and this will be standard of care in the coming years. Why would you start a once-daily if you can start a once-weekly? I think that's what I was gonna say about insulin. You don't want me to steal your slides. Hello? Yeah. Okay, we'll change subject now. We'll go on to GLP-1. I'll just give you a little bit of background on GLP-1, because I know you know all about GLP-1, but we see GLP-1 still with a big future, but also as a backbone to what can we add to it? Martin will obviously talk quite a bit about CagriSema. The effects of GLP-1 receptor agonists are well proven in type 2 diabetes. We know about glycemic control and weight loss. It's interesting when you look at the literature and it says, "Oh, this was developed for glycemic control," and actually, you then happen to show weight loss. Lots of the efforts, and the mother of liraglutide hates that because she knew weight loss was there right from the start. We were looking for cardiovascular safety, and actually, we got cardiovascular benefit. What we also know is that, and I've taken the liberty of putting one of my recent papers here, where I propose that GLP-1 receptor agonists could be expanded to help the healthy lifespan. If you look at the diseases that GLP-1 receptor agonists can benefit, it's the diseases that develop as we get older, unfortunately. Chronic kidney disease, Alzheimer's, metabolic liver disease, and peripheral artery disease. Why is it doing this? We can speculate. We know there's a glycemic effect. We know there's a weight effect. There may be a lipid effect, a blood pressure effect, but there's also the X factor, which may well be inflammation. We know, and we saw today, data almost 60% reduction in high-sensitivity C-reactive protein. There are a multitude of effects of GLP-1 receptor agonists, which is why they're becoming increasingly used, and there's a focus on adding other incretin hormones into them. What I'm really pleased to see is that GLP-1 receptor agonists have really made their way to the top of the treatment algorithm. Again, I think we saw this today, that if you are trying to protect your organs, and from a sort of cardiorenal risk point of view, GLP-1 receptor agonists are right up there. Even in terms of glycemic control, where your A1Cs are high, this is where these come in early as well. It was great to see an update to standards of care, which we might want to talk about later. ADA standards of care now putting NASH in here, and also the role of GLP-1 receptor agonists in NASH. That was my background, Martin. Now I hand back to you. Thank you very much. We talked about the GLP-1s and the broader applicability of GLP-1. This is obviously about an effect, as Stephen talked about, on glycemic control, on weight loss, but also on what we could call markers of comorbidities, hypertension, dyslipidemia, but also inflammation. What we've seen with GLP-1s is impressive. Specifically for semaglutide or Ozempic, we've shown a 25% risk reduction when it comes to MACE in the SustAIN-6. That's impressive in and of itself. You heard us talk about CagriSema, the dramatic potential for weight loss with CagriSema in phase I/II. Based on phase I/II, we basically project a 25% plus weight loss in that space. We were actually a little bit uncertain what to expect when it came to type 2 diabetes and glycemic control. We were very gung ho on weight loss, but we didn't exactly know what to expect when it comes to glycemic control. The data on amylin are a little bit sparse, and the amylin analogs that are out there are short-acting. We had CagriSema, we had cagrilintide, and we wanted to investigate that for the treatment of type 2 diabetes before we went into phase 3. We designed a reasonably small study, 30 patients in each arm, comparing CagriSema to semaglutide, 2.4 milligram, and cagrilintide, 2.4 milligram. Type 2 diabetes patients with a reasonably high BMI, allowing us to do assessment on glycemic control, but also on body weight lowering. You heard us talk about the glycemic control data. We saw a substantial reduction in A1c with CagriSema. This was better than what we saw, obviously, for cagrilintide in monotherapy, but actually also with semaglutide in monotherapy, with a 0.4 percentage point difference between the two treatments. This is after 32 weeks, which is, in our eyes, impressive in and of itself. With the mode of action of CagriSema and the combination therapy, we would actually expect that difference to be more pronounced over time. Potentially, this could be even more in phase 3 longer term studies. What is also, I think, quite impressive, is the proportion of patients achieving an A1C below 7, 89%. This is to be compared to the 70% that we see with semaglutide, and obviously a lower proportion of approximately 35% with cagrilintide in monotherapy. Quite impressive data on glycemic control. That made us happy in and of itself, but it's being supported, as Stephen said, by something that is becoming more and more important in the way that we assess the clinical relevance of a diabetes intervention. When we look at time and range, we are looking at a staggering, almost 90% of the time, patients are in range. That is incredible. Even with semaglutide, we see 77% after treatment, and we actually don't see a bad number, with 72% for cagrilintide in monotherapy. 90% for cagrisema is obviously making us feeling quite confident in terms of what this molecule can do in chronic treatment for type 2 diabetes patients. We became even more excited when we looked at the weight data. There were a lot of discussions during some of the sessions today, also on why do GLP-1 or incretin therapy introduce a lower weight loss in type 2 diabetes as compared to non-diabetes? We're gonna have a lot of discussions on why that is. We have some theories, but we've never really seen an intervention that could sort of uncouple that weight loss resistance that we see with type 2 diabetes. I think we see that with CagriSema. In 32 weeks, patients lose almost 16% of body weight. That's to be compared with 5% and 8% for semaglutide and cagrilintide in monotherapy. If we extrapolate that to a year of treatment, our modelist tells us that would correspond to approximately 20% weight loss. Never seen that in type 2 diabetes. If we take the holistic approach on how we treat type 2 diabetes, not only the glycemic control, but also weight loss and also cardiovascular risk, and to Stephen's point, kidney risk, liver risk, and so on, this is truly impressive. This is a very holistic approach to the treatment of type 2 diabetes. Some of you attended the session where CagriSema was discussed on Friday. You saw data on blood pressure, also quite impressive in and of itself, and actually blood pressure lowering that almost suggested synergy and not additivity in this space. We had similar data on other cardiovascular biomarkers, including, obviously, markers of inflammation, but also lipids. All of them show a very impressive improvement with CagriSema as compared to the two monotherapies. We are very excited with CagriSema when it comes to efficacy. We're similarly excited when it comes to safety. Overall, if we look at adverse events, there's no difference between the three treatment arms. That basically means that we don't see more side effects numerically overall with CagriSema as compared to the two monotherapies, despite the difference in efficacy. Some of you will point out to me, and I agree to that there's a higher rate of gastrointestinal side effects. My personal bias is because we have more data, and you'll remember that both from obesity, but also with cagrilintide in monotherapy, that this is a matter of small numbers, because, again, the overall side effects is actually on par. Normally, when we see data with GLP-1s, it's higher because of the gastrointestinal side effects. We don't see that here. You'll also see that numerically, we see approximately 60% of patients with gastrointestinal side effects with CagriSema. That's actually what we normally see with the GLP-1s. Our current assessment is that we probably, with some likelihood, I still have to show that in phase 3, we'll have with the data that we have, both in obesity and diabetes, something that is very efficacious and not having to compromise on tolerability and safety. That basically means that we are very gung-ho also on initiating the diabetes phase 3 program. We'll start out with what we call REIMAGINE-2. That's the pivotal trial, that's the regulatory trial, comparing CagriSema to the two monotherapies and to placebo.... We also have a dedicated, reasonably small, placebo control trial in a fairly small setting. We have REIMAGINE 3, which is add-on to insulin. This is a diabetes program, and we want to have, in the label, the ability to add on to insulin. Obviously, the infamous REIMAGINE 4. A lot of you have asked about that. That's a head-to-head against tirzepatide. Based on everything that we've seen, both in terms of efficacy and certainly also in terms of safety, we believe that cagrilintide, CagriSema will have a good and strong profile, and we want to test that up against another good drug. That study will be initiated around the turn of the year. To answer a lot of questions I received over the last couple of months. Finally, I had to call out REDEFINE 3. You'll notice that it's a different name, and it's basically because REDEFINE 3 is the cardiovascular outcome trial that will serve both the obesity and the diabetes indication. In its base, it's 4,000 patients, designed as a non-inferiority study versus placebo. We have the option of expanding the study, so we're adding more patients, approximately 3,000 patients, to the trial, and then look for superiority. For regulatory purposes, approval purposes, the primary proportion of REDEFINE 3 will be a non-inferiority study based on 4,000 patients. With that, back to Stephen. Okay, thanks, Martin. What I'd now like to do is just cover two trials that I think those of you at the symposium between half past four and six this afternoon will have seen the data on. This is Pioneer Plus with oral semaglutide in people with type 2 diabetes. We know that with oral semaglutide, when we went up to 14 milligrams, we knew we had not maxed out. What we now want to do is to see whether we can gain additional benefit by moving to higher doses greater than 14 milligrams. In this study here, in the Pioneer Plus trial, we compared semaglutide 14 milligrams to two higher doses, the 25 and the 50 milligrams, to compare efficacy and safety in people with type 2 diabetes. This was a 68-week trial. Primary endpoint was at 52 weeks. It's the 52-week data that I will present to you this evening. Standard, fairly standard inclusion criteria. In terms of what did we see with this higher dose of oral semaglutide, you can see here in the purple line, the 14 milligrams of semaglutide, Rybelsus, with a 1.5% reduction in terms of A1c from a baseline A1c of 9%. When we go up to the 25 milligram, an A1c reduction of 1.9%, and at the 50 milligram, A1c reduction of 2.2%. Large reductions in A1c that are also clinically meaningful. What I'm also showing you on the right-hand side of the slide is the proportion of patients achieving a target A1c of less than 7%. Again, as a clinician, when I'm in clinic, what I want to know is if I'm going to put somebody on a medicine, I hope it's going to work, and that the majority of patients are going to benefit from it. What you can see here is up at the 50 milligrams of oral semaglutide, almost 75% of patients are achieving that target A1C of less than 7%. Even at the 25 milligram dose, you can see that almost 60% of patients are achieving an A1C of less than 7%. It's still pretty impressive with oral semaglutide 14 milligrams, but you can see so much, a much higher proportion of patients achieving a target A1C on these higher doses of 25 and 50 milligrams of oral semaglutide. What we also looked at, obviously, in addition to A1C, is also weight change. What weight loss could we see in these higher doses? Again, for the 14 milligram dose, 4.5% reduction in weight from a baseline weight of 96.4 kilograms. With a higher dose of 25, a 7% reduction in weight, with a 50 milligram dose, a 9.2% reduction in weight. Again, on the right-hand side of the slide, which is probably of great, well, not greater clinical relevance, but certainly of clinical importance, is the categorical weight loss. What proportion of patients achieve 5% or more loss in body weight? We know that to lose 5% of your body weight is clinically significant. That's clinically relevant in terms of the comorbidities that you develop with obesity. Additionally, if you then go above 10% weight loss, we know there's even greater clinical benefit. If we look at the proportion of patients achieving more than 5% body weight reduction, with a 50 milligram dose of oral semaglutide, it's over 75%. Similarly, if we look at achieving a 10% body weight reduction, it's almost 44%. These are high proportions of patients achieving clinically relevant weight loss that will impact in terms of comorbidities related to obesity. When we go up to these higher doses, what does it mean in terms of the safety profile? First of all, there were no new safety findings going up to these higher doses. You can see here, if we look at adverse events, they're similar across these doses, slightly higher for the 50 milligram oral semaglutide dose, but similar numbers in terms of adverse events. This is driven, as you would expect, by gastrointestinal adverse events. A low rate of serious adverse events. Again, if you look at the adverse events leading to drug withdrawal, they're also low. We haven't seen anything here we wouldn't expect. The majority of adverse events are gastrointestinal. They usually occur, they tend to occur, as we've seen with semaglutide and other GLP-1 receptor agonists, during the escalation period. Once you get over that escalation period, the gastrointestinal side effects or adverse events settle. We would say that based on these data, in addition to our efficacy in terms of A1C and weight, in terms of safety, the 25 and 50 milligram doses are well-tolerated. In terms of diabetes and some then GLP-1 takeaway messages, sort of combining what Martin has said with what I've said, we know that there are benefits with GLP-1 receptor agonists. We've seen them being elevated higher up in terms of the treatment algorithms, and as I say, we've even seen, I think it was today, the update on the standards of care of the ADA, now including NASH as well, and there... Also a role for GLP-1 receptor agonists. The phase two data in CagriSema, in diabetes, is really encouraging, that's encouraged us to go into a phase three program. In terms of CagriSema, it certainly seems to be safe and well-tolerated. Also based on the efficacy profile in PIONEER PLUS, we think that the 25 and 50 milligram dose will give people that extra option. If you need to go to more than 14 milligrams, you now have the opportunity, or we hope you will have the opportunity, to go up to those higher doses if needed, both in terms of glycemic control, but also weight loss. If we now move from diabetes, and we move into GLP-1 and obesity, I think this is still with me, Martin. Again, you will have heard this afternoon, OASIS 1, just remind myself to say that both of these studies simultaneously appeared in The Lancet today. Those of you at the session will have seen that. This is now looking at the 50 mg dose of semaglutide, so obviously a much higher dose in people with overweight or obesity. This was a study of over 600 patients. It was a 68-week study, and in addition to either placebo or oral semaglutide, patients got a lifestyle intervention, as with all of our obesity trials, both in terms of exercise, but also, reduction in calories. The co-primary endpoints were the percentage change in body weight from baseline to week 68, and the achievement of more than 5% weight loss from baseline at week 68. What did we see? Those of you at the session will have seen this afternoon. You can see a 17.4% weight loss with a 50 mg dose of oral semaglutide, compared to 1.8% with placebo from a baseline body weight of 105 kg. Again, importantly, if we look at the right-hand side of the slide, where we're looking at categorical weight loss, you can see that the proportion of patients achieving more than 5% weight loss with 50 mg of semaglutide is almost 90%. This is clinically significant. This is clinically relevant. You can see high proportions achieving more than 10%, 15%, and even 20% weight loss. This is, I wouldn't say staggering, but it's, it's really impressive weight loss, and to think that almost 40% of patients on 50 mg of semaglutide can achieve that magnitude of weight loss. Safety profile. I've just got a summary of the safety. We can talk more about this. In terms of adverse events, similar between, well, slightly higher between oral semaglutide and placebo, again, driven by gastrointestinal adverse events, with a low rate of serious adverse events and a low rate of adverse events leading to withdrawal. As I've said, the major adverse events are gastrointestinal, and they, again, tend to occur during titration or escalation. I think in summary, we have seen impressive results with 50 milligrams of semaglutide in terms of weight loss, but also in terms of its safety profile and its tolerability. In terms of where are we with the development program for this, we've now completed OASIS 1 with a 50 mg dose. Our plans are to submit in the US and the EU later this year in 2023. We have a pretty full program in terms of OASIS 2, 3, and 4 in East Asia, in China, and also looking at the 25 mg dose, because it may well be that patients don't need to go up, they don't need the full 50 mg dose. We're gonna be looking at 25 mg as well in OASIS 4, and that will also read out in 2024. When I see the picture of that man, I know I hand over to Martin. Thank you very much. Thank you. All right, I hope that's not me, at least not the comorbidities. I think you know this, obviously, we all know that the association between obesity and the number of comorbidities, both in the mental, the mechanical, the metabolic, are staggering. This also leads to detrimental outcomes. I still think a lot about if you have BMI of 35 to 40, your chances of reaching the age of 70 is dramatically reduced, and that's obviously driven by these comorbidities. We focused a lot on specifically the cardiovascular comorbidities in some of the trials that we're conducting as we speak. You asked me a lot about SELECT, you asked me a lot about SOUL. We also had the FLOW trial looking at kidney disease. Obviously, we have ESSENCE looking at liver disease. We have peripheral artery disease. One of the studies that we've not discussed a lot because it was not an outcomes trial, was our studies in HFpEF, so Heart Failure with preserved Ejection Fraction. We conducted two studies, one in obesity and one in diabetes. Both are required for regulatory submission, specifically in the U.S., and we today have the results from the obesity study. We are still awaiting the results from the diabetes study that will read out later this year. Heart Failure with preserved Ejection Fraction is a serious and actually quite common disease. Heart failure, as such, is afflicting 64 million patients globally. Approximately half of these have Heart Failure with preserved Ejection Fraction. It's a serious disease associated with increase, obviously, in mortality, but also in terms of higher risk of hospitalization and a very high impact on patients' everyday life and ability to perform. We wanted to conduct a study to look at the impact of semaglutide versus placebo on functionality in patients with obesity and established heart failure. It was a really reasonably small and focused study. Slightly more than 500 people being randomized to either semaglutide or placebo. Approximately a year of treatment, slightly lower than a year of treatment. A co-primary endpoint of a questionnaire, Kansas City Cardiomyopathy Questionnaire, KCCQ, between friends, and change in body weight. Also important is obviously looking at biomarkers, not only for heart failure, but also for outcomes from heart failure, as well as the 6-minute walking test and a broader composite endpoint. Out of respect for our investigators who wants to publish this data and wants to communicate them in a broader setting, I'm not gonna show anything but the primary endpoint today, but obviously, we are very excited by the data. Just maybe two words on the Kansas City Cardiomyopathy Questionnaire. It is actually consisting of several domains covering both symptoms, functionality, and quality of life. There's a sub part called the Clinical Summary Score, which is consisting, in part, symptoms and in part, assessment of functionality. That's sort of the standard, also in a regulatory framework to look at these domains. What we see is a dramatic difference between semaglutide and placebo in this space. Just to put this into perspective, an approximate 10% change is considered moderate to large, and it's actually from a, sort of, broader epidemiological perspective, correlated to improved outcomes. Obviously, we are super excited about this data, also because, even though I can't show the data, they are actually largely followed by the 6-minute walk test and other secondary endpoints. A very, very positive study overall, suggesting a fundamental effect of semaglutide in the, in the functionality of patients suffering from heart failure. Not surprising, we also see a body weight loss. It's moderate in this study, approximately 13%, and the safety profile. Whoops! Sorry. Similar to what you've seen or show 2 times today. Sorry about that. We're now waiting for the type 2 diabetes study that will read out, as I said, later this year. It's in design and in size comparable to the obesity study, and we are, from a regulatory perspective, submit the sum of the two. Basically, we had to await this study before we can do the regulatory submission for having an update of the obesity label, also including these functionality benefits in heart failure. Key takeaways from obesity. We're obviously super excited about the data from OASIS 1, suggesting that we, with an oral offering, can provide the same efficacy, the same safety to patients with obesity as we have done with the subcutaneous offering. We are also very excited by the fact that semaglutide has shown to be beneficial in patients with heart failure. These patients have a fundamental, big unmet need in terms of their outcomes, both in terms of mortality, but also risk of hospitalization, as well as impact on their everyday life in terms of functionality. With the current STEP-HFpEF study, we have showed an improvement in the functionality of patients, which actually, again, from a broader perspective, correlates to improved outcomes. Really exciting data. To sum up, we are on track to fulfilling our 2025 aspirations. Looking at our four quadrants, we've obviously focused on the R&D quadrant today. We are looking into a very exciting next year, obviously the data of SELECT coming quite soon. We'll also see the results from the icosemap program within the next couple of years. We'll see SOUL, well, sorry, within the next couple of months. We'll see SOUL, we'll see FLOW. Very, very interesting times in terms of our outcome trials, but also in terms of the phase 3 programs that we are currently running. I mentioned Mim8. I also want to point out the now three outcome studies that we are gonna conduct with ciltapecimab, our anti-inflammatory compound. Very exciting times, and at the same time, when we look at our purpose and sustainability, both when it comes to our societal, our environmental, but also our responsibility as an employer, we are clearly on track. I think I don't have to mention our commercial execution and our finances. These are really exciting times, and we are well in track to achieving our aspirations. With that, I think it's over to Q&A. We are ready to Q&A, and please state your name and your institution, and limit yourselves to 1, maximum 2 questions, so we'll have a chance to get a lot of questions. Let's start off with Richard Vosser. Hi. Thanks. Richard Vosser from J.P. Morgan. Just a question on CagriSema. First of all, the data showed an imbalance, I think, in the duration of diabetes, and just wanted your view on how that might have skewed the ease with which the blood glucose was changed or improved with Cagri relative to semaglutide. The curves looked like they skewed up for semaglutide. What's going on there? That's the first one. I've got one more. In terms of the imbalance, in terms of duration of diabetes, based on everything that we know also from other studies, that's probably not driving a lot with this kind of intervention. In terms of the lines, obviously that was a focus for me as well. I take a lot of comfort in two things. One is the time and range, the CGM data that we just showed, which are clearly suggesting that CagriSema has one up on both semaglutide, but certainly also cagrilintide. Again, with this mode of action, we would expect maybe an even more profound effect on glycemic control over time. The other thing is obviously looking at the individual patient profile, we look at spaghetti plots, and again, here we see a very consistent trend, that's clearly suggesting that it's. What we see is very consistent with CagriSema. Some of you have also asked whether 5% weight loss with semaglutide is a bit on the low side. Again, I remind you, these are diabetes patients, what we typically see, Stephen actually also showed the data just now, with semaglutide in type 2 diabetes, we see an 8-10% weight loss, and if you extrapolate our, or these 5.1% from 32 weeks to a full year of treatment, you're actually getting into that range. I think it's I mean, again, it's a reasonably small study, 30%, 30 patients in each arm, but I actually think from an efficacy perspective, reasonably robust data. thanks, Martin. The second question is just on benign neoplasms. I think there was an imbalance called out in the OASIS 1 data. Just across everything that you've seen, across all your trials, for semaglutide, either oral or higher doses, are you seeing anything on benign neoplasms? You're basically providing the answer. Is it okay I take that? Because that was exactly the purpose of both PIONEER PLUS and the OASIS, that these are reasonably small studies, you heard me talk about the importance of having semaglutide pharmacology exposure similar to that what we see with subcutaneous, because the requirement is to bridge back to the data that we're talking about, the big databases, where we have basically from clinical trials, several thousand patients exposed, but from market also, millions patients exposed, and in those data, we don't see any imbalance. This we have to see as a study abnormality. I don't want to call it an abnormality, but I mean, on balance, we haven't seen anything. Good. Thanks, Richard, and let's move to Michael Novod next up. Thank you, Michael Novod from Nordea. Two questions. First of all, Martin, can you try to explain what is sort of the key advantages of an oral peptide in obesity and type 2 diabetes, when you also have a small molecule likely coming to market, that can potentially mimic? Is it safety that's gonna be the key advantage, or is it familiarity with semaglutide, or how are you sort of gonna position this if competing non-small molecules come to market? I think it's the sum of a lot of things. You have to think about efficacy, obviously. We've seen some data during this ADA that is suggesting that even the small molecules will provide good efficacy, so I don't want to belittle that. I still want to see a strong safety profile as well. Obviously, we have that with semaglutide, and that's gonna be even further expanded in the next couple of years, while we are still waiting for the small molecules to come. Obviously, there is the ability to scale and the ability to manufacture. I don't wanna talk about the small molecules, but they're not that small, and they're not that simple. While we are actually investing to be able to scale semaglutide also in the oral version, we had to await and see how it goes for the smaller molecules. The final thing we may want to point out is obviously the added benefits that we've established with semaglutide, as we just discussed. We'll see the SOUL data readout next year. I think we already now see the impact of having a cardiovascular benefit established with Ozempic, 26% risk reduction in MACE. That's in the US label. I think it's a substantial driver of Ozempic preference and focus. We will have the ability, potentially to bridge the cardiovascular benefit, maybe the HFpEF benefit, and potentially also other, it could be, the renal, the hepatic, but also potentially, again, the Alzheimer's benefits in all of this. From a data perspective, we'll have a very holistic package, going beyond just weight loss or glycemic control, with the oral version. It will take some years for smaller molecules to establish a similar package. Thanks. The second one, non-ADA related, but more on all the safety. There's been a couple of days now, we've been talking about the thyroid cancer, and we've seen the request from EMA. Maybe you can just address this, because we've had tons of questions. Also secondly to that is, has the FDA requested the same thing? Maybe to answer the other question first, no, the FDA has not requested the same thing. There was a paper out a couple of months ago suggesting that there could be a risk with broad GLP-1, not specific to any GLP-1, but broader GLP-1 modalities and the potential risk for thyroid cancer. As per normal pharmacovigilance standard, that calls for the European authorities to open safety signals. Any regulatory authority will do that as a matter of course, and we can actually also do that ourselves. We do continuous safety monitoring for all of our drugs as well. Standard is, the signal is opened, data is provided to the regulatory authority. In this specific case, it's all GLP-1 sponsors, required to deliver data to the European authorities. In vast majority of cases, the safety signal is closed, and not being substantiated. If a signal is substantiated, typically that will lead to a safety, update in the label. In this specific case, if we look at the totality of our data, we've now had GLP-1 therapy on the market for, almost 15 years, with millions of patients exposed, and obviously some strong also RCT data, with strong control. We don't see any, substantiation of a correlation between GLP-1 therapy and thyroid cancer. Our expectation is that, as per normal routine, EMA is opening this signal because they see something that they want to investigate, and based on the data that they will receive from us and other sponsors, we expect them to close the signal in due course. Let's move to the front row here. Thank you. It's Mark Purcell from Morgan Stanley. Two questions. First one is, fresh off the press, the heart failure data, where do you envisage some are fitting in with SO2s and interest there, and other things it'd be interesting to know your view. Secondly, just to ensure you get the most out of Cagri, can you help us understand how you'll monitor in phase 3 for the kidney and other organ benefits, you know, looking at postprandial glucose, where there seems to be some differentiation? Can you assure us you're gonna be aggressive and up from Cagri, given there's a number of competitors, you know, biting your heels in some of the dosing that is? Yep. Starting with CagriSema, yes, I can assure you we'll be aggressive. We're starting out with obesity and diabetes. I also talked a lot about the other markers that we've been privy to. All of them are suggesting that the broader benefits that we see with semaglutide will be even more pronounced with CagriSema. That basically means that we have a quite aggressive plan in terms of how we intend to roll out into adjacent disease areas. Maybe even investigating disease areas that we've not investigated with semaglutide, because this has shown to be very promising and quite impressive in terms of, at least from a biomarker perspective, what we have seen so far. On the heart failure side, I have to acknowledge, I don't think neither I or Stephen are cardiovascular experts, but I've obviously talked to a lot of cardiovascular experts. Again, not being able to share the rest of the data set, I can maybe allow myself to quote one of the investigators, who is also a key opinion leader, saying that these are if he assumed that this is corresponding to phase 2 data, these are some of the most impressive data that he's seen in this space. Obviously, from that perspective, we're super happy with what this bodes for semaglutide, we could also imagine that we would see ourselves go into the space with cagrilintide. Let's take Florent next. Thank you. Florent Cespedes from Société Générale. Two quick questions on the insulin icodec. When you said on the level two hypoglycemia, that three patients were responsible for 100-ish events. If you adjust from these three patients, would you have a more balanced profile? If you... I can't remember the exact numbers, but if you looked at the number of events that we had, I think it was something just over 200 versus 100. Those additional 100 events, and you can argue whether it's the right thing to do, but those additional 100 events in 3 patients almost make up the difference between the two arms. Thank you. A follow-up, on the insulin icodec. On the injection site reaction, do you have any data? On the publication, it seems that there is a little bit more with icodec versus the comparator, 8% versus 4%. Is it something that is, you have observed across the different clinical trials? I mean, obviously, we've looked at this because this is an insulin injection. We've not seen anything, any consistent difference between once daily and once weekly. As I said, when I was talking, it's also the same volume, so there's not a volume thing in terms of whether you would raise an area of elevation. In terms of skin reactions, in terms of antibody development, There's nothing that we've seen with insulin icodec. Thank you. Let's move to Emily next. Next, sir. Hi. Thanks. Emily Field from Barclays. Two from me. The first one, just if you could go into more details on the skin sensation adverse event that was discussed in the presentation this afternoon, and, you know, if you see that being a limitation in clinical practice. Secondly, just, you know, growing anecdotal reports of evidence of, you know, potential semaglutide on, things like alcohol use disorder. Are these any, you know, ancillary indications that you would expect to explore in clinical trials? I'll let Martin take the second. In terms of the first, there's a small number of patients have developed this change in skin sensation that you mentioned. It's a small number of patients. It's not something we've seen in other trials. It's not something we've noticed. We don't have a full explanation for it. What we do know is that it's mild, and it's transient. I think, as you heard this afternoon, most of the cases, they're developed within the first 20 weeks, and developed and settled within the first 20 weeks. I can't really say more than that at the moment. Martin, I don't know if you have anything to add. No, I mean, just to speak to the mildness, we had one patient out of the 60 events that we saw withdrawing from the trial, and in 56 patients, I believe it was, to Stephen's points, it was transient. But we have no clear explanation for what it is. On the abuse thing, we've seen and we've heard that as well. There is a reasonable sort of understanding of a potential mode of action. We don't necessarily intend to pursue this from an indication perspective, but Stephen and his team are actually working with potential investigator-sponsored trials for semaglutide. We are actually also evaluating the potential for cagrilintide again. Martin Takai, CB. First, a question about nausea rates. We saw at the SURMOUNT-2 symposium Friday, that they made this cross-trial comparison, also looked at nausea rates for tirzepatide versus the go in the STEP trials. As I understand it, Lilly have motivated people to use nausea-reducing medication. Are you doing similar tricks in phase three on cagrilintide to, you know, artificially pull down the nausea rates, also maybe with respect to number of visits? That was the first question. We never do anything artificial in our trials. No, jokes aside, I think you also indicate that there's something about the number of visits that could drive this. It goes without saying that if you have 20 visits in a trial and you ask the patient 20 times, you get 20 responses. If you have 10 visits in the same duration trial, you get 10 responses. That can actually drive a little bit of rate when and also patient proportion when it comes to adverse events. That's actually why I am ever concerned about doing these cross-trial comparisons. If we are to really have an objective assessment of efficacy and safety between drugs, we need to do head-to-head comparisons. That is specifically what we do, for example, with REIMAGINE 4. The second question, we also saw on the in the cagrilintide phase 2 diabetes trial, you know, that the the ameliorate actually performed quite well on weight. What are your plans on doing a phase 3 on that and maybe, ... giving patients the options to do a loose combination instead of, you know, dependent on CagriSema? It's a really good question, and we don't have a very clear answer right now, because obviously, we also act on the data, and we were positively impressed by what we saw for cagrilintide in monotherapy, in Type 2 diabetes. What we're doing right now is basically evaluating the potential of this also as a monotherapy, in diabetes, but also potentially in obesity. Good. Let's go to Mike. Thanks. Mike Nedelcovych from TD Cowen. 2 questions. The first is on Wegovy. We've spoken to at least 1 KOL, who indicated that some of her patients would like to titrate down from the maintenance dose of 2.4 mg after achieving target weight loss, but that coverage actually is a barrier to that strategy. Do you plan to develop any data in that area that might support that kind of strategy? I'll actually give you the same answer I just gave Martin. Obviously, I've heard the same request, and obviously, we'll be evaluating our options there. Second question's on icodec. You showed some very nice time and range data from your trial. Lilly insists that its once-weekly insulin BIF has a PK profile with lower peaks and higher troughs that might actually deliver superior time and range data. If the phase 3 data end up supporting that claim, do you think that that's a meaningful differentiating factor that would affect treatment decisions between icodec and BIF? I think, as you say, it's early, too early to say what we're going to see with Lilly's insulin. I think with our own insulin, we're confident that we have really good time and range. We have, as you've seen from the data that I presented, we have good A1C reduction, not just non-inferiority, but also superiority in 4 of our trials. On top of that, we have really good CGM data. You can speculate on what others might develop, but in terms of our own data, we're pretty confident. Let's move to, Simon Baker. Thank you. Simon Baker from Redburn. I've got two questions as well. Firstly, on icodec. Despite the higher hypo instance in Type 1 diabetes, there seemed, in a number of the presentation today, to be quite a lot of enthusiasm and appetite to use icodec in that patient group, but a need for more data. I just wonder if you could update us on what the plan is going forward on icodec in Type 1. A general question on semaglutide and weight loss across the various presentations. You've given us categoric weight loss, but unlike Lilly, you've not given us waterfall plots for any of the studies. I just wonder if you, going forward, if you plan to do so, to give us a better feel for exactly what the distribution is. Given the likely range of outcomes, I just again wanted an update on, are we closer to identifying any biomarkers of response, or are there no biomarkers and the variability of response is simply down to diet? Thanks so much. If you want to take, semo, but certainly in terms of Type 1, our submission to the regulators is for Type 1 and Type 2 diabetes. We see that, as I mentioned, certainly in terms of Type 2 diabetes, we see this as a starter insulin, and we see this becoming standard of care. Why would you want to have a once-daily if you can have a once-weekly? In terms of Type 1 diabetes, there are more hypos in Type 1 diabetes, but we also know there's a large proportion of patients who gain the benefit and still have a positive benefit risk in terms of the use of once-weekly. Of course, in Type 1 diabetes, there are other options. As we move forward over the next 5 to 10 years, we're going to see an increased use of pumps, artificial pancreases, closed loops. There will still be some patients who we know will benefit from this, and we've seen those patients in our clinical trials. As I say, in terms of our regulatory submission, we have put in for both Type 1 and Type 2 diabetes. Martin, if you want to say anything about semaglutide? Sure. You were asking about markers of response. With present data available to us, the best marker of response is weight loss during the first four weeks of treatment, which is sort of a simple measure, but correlates reasonably well to the broader response. I think we have the ambition of also being able to predict response before initiating treatment. This is specifically where we have high aspirations for the SELECT trial, where we're doing a lot of assessments on both pheno and genotype typing patients, looking at proteomics, genomics, metabolomics, in order to be able to potentially predict responders to treatment, but also predict who are at risk of having comorbidities. For us, SELECT serves a purpose of not only obviously establishing a benefit of intervention with cardiovascular disease, but also potentially informing us on how we better treat these patients and identify responders and patients at risk. Let's move all the way to the back. Laura Hindley, Berenberg. Well, you reiterated your target of CagriSema hitting 25% weight loss in obese patients. I'm just wondering, you've got more assets earlier in your pipeline, is there a target number that Novo ultimately wants to hit? Is there a ceiling, and what can you achieve versus what the patients actually want to achieve? That's a complex question. Thank you for that. We have assets in our preclinical pipeline that holds a potential of possibly going beyond the 25%. I think it goes without saying that a plus 25% weight loss is not gonna be for everyone. We would be looking at patients who are either with very high BMI and substantial need for weight loss. Again, if you just use the example, for example, of patients with BMI 40, which is not a rare occurrence in the Western Hemisphere, losing 25% of body weight, you would still be in the obesity realm. Therefore, a bigger body weight loss may be required and may be advantageous. That sort of talks into our broader strategy of delivering options to more categories of patients. Right now, we're treating obesity as 1 disease. We did the same thing with type 2 diabetes, where basically everyone got metformin, they still do. With the advent of more differentiated treatment, we could also do more differentiated approaches towards the patients. I think we will focus on high efficacy in terms of high weight loss, but we will also have to focus innovation on innovation. Sorry, innovation in terms of maintenance of weight loss, and potentially also what we would call the healthy weight loss, preservation of lean mass while losing fat mass. I think you also asked a little bit about where's the sort of patients' sort of limit. I don't think there's, I mean, you can't lose 100% of your body weight, but in terms of the applicability and the safety of body weight loss, I think we also had to look at the speed of a weight loss. We don't have a big ambition of accruing a big weight loss in a very short period of time. We'd rather do it over a longer period of time, which is also why you see us not being very aggressive on titration. We would rather, again, have a reasonable weight loss, but then a sustainable weight loss over time. Thanks. Let's take Peter, and then after that, we have room for one final question, I believe. Peter Welford, Jefferies. Two questions, sticking with the trend. First one, CagriSema. Should we understand then, is the REDEFINE 3 then, is that the limiting factor to understand, to file both diabetes and obesity together when the REDEFINE 3 trial finishes? Similarly, just on the dose, and I guess this comes back to Mark's question, are you confident that the dosing you're using in the CagriSema trials is as high as you need to go? Or I guess, what is the limiting factor that is limiting? I mean, is this a manufacturing sort of dosing thing, or what would... Given obviously, again, the competitive environment. Then just the second question is just on the SELECT study, and this is not the people you need to admit. What I'm actually wondering on the SELECT study is, can you tell me a little bit about what do you think, presumably we're gonna have an average of, let's say, 3 years roughly treatment. There was comments made about how the body weight loss, how we made in prior trials, we've seen that vary over time. Are you assuming in the SELECT study, can you talk about what are you envisaging seeing with sema with regards to the sustained effect, potentially during the maintenance phase of the weight effect in the trial? I'm not looking at Daniel, but I can feel him, and he's counting three questions there. Just on the SELECT trial, we have data from STEP 5, which is a two-year study, and after two years of treatment, we see a very nice and flat and sustainable weight loss, at around 15%-17%. I have no reason to think otherwise around SELECT, but obviously, we are super excited to see the data. What we've seen so far is a sustainable 15%-17% weight loss that for now lasts at least two years. On CagriSema, as you know, we tested the 2.4 mg of Wegovy together with up to 4.5 mg of cagrilintide, and did not see a substantial up in terms of efficacy. Therefore, we decided on the 2.4 and the 2.4. That being said, I don't think you'll ever hear a categorical statement from me that we are absolutely confident that we hit it right, because we are, and I have to acknowledge that, also testing 7.2 mg of semaglutide as we speak in phase III, because we do believe we can actually see more weight loss with that high doses. That would actually also be informative of the potential for CagriSema. When we have those data, and as I said, the study is ongoing, then we speak again. The final question, REDEFINE 3 is not rate limiting. It is a requirement but from a timing perspective, we actually intend that REDEFINE 3 will provide data in a timely fashion. It is required for type 2 diabetes and obesity, respectively in Europe and U.S. Good. Let's take the final question. Thank you. Alana Lelo from Guggenheim. Two questions on 2 pipeline assets. For the once weekly GLP-2 agonist, you completed phase I with the subcu and oral formulations on initiating phase II with the subcu. Any plans for an oral formulation to advance into phase II? Anything you can share with how this GLP-1 is differentiated from Sema, and why we might not have seen results we might have wanted with the fixed dose combination that was halted? With the emicreutin, when we can expect to see that data and our plans to still roll directly into phase III with that asset. On timing on emicreutin, I, again, I'm not looking at Daniel, but I can only say second half of this year. Otherwise, I'll have some explaining to do. On the GLP-1 GIP, the bioavailability was there, but it was not in a place where we would take it directly into phase II. We're focusing on the subcutaneous, because obviously we also have to think about scalability. We saw some efficacy safety data that was so convincing that we would like to progress this. At the same time, obviously, we are working with the oral formulation, because that is still an attractive offering. Good. That concludes our call here. Martin, I don't know if you want to say any final words? Well, first of all, thank you for your attention. I hope you will agree that we have presented some interesting data not only during this ADA, but also over the last 12 months. We are certainly looking forward to what we're gonna do over the next 12 months with a lot of interest in readouts. At the same time, we continue to see nice progress on our commercial, but also on our financials. Enjoy the rest of your ADA, and see you next year.