Gubra A/S (GUBRA) Earnings Call Transcript & Summary

All right. So, it's 1:00 p.m., and we're ready to get started. So, good afternoon, everyone, and a very warm welcome to Gubra's first-ever Capital Markets event of this type. My name is Adam, Head of Investor Relations at Gubra. And, yes, on behalf of the entire team, we are very happy that you have decided to spend the next couple of hours with us, whether you're here in person or joining us virtually. Today is, of course, a great opportunity for Gubra to share more about the company, our pipeline and the ambitions for the years ahead. I think probably many of you have seen the press release that we issued this morning, outlining some of the key messages that we intend to discuss in further detail during the presentations today. Just a very quick reminder that, of course, today, we will be talking about the company's 2030 strategy. So, we will be making forward-looking statements that are subject to risks and uncertainties. Just a few key words on the agenda for today. We will start with our CEO, Markus Rohrwild, who will walk us through Gubra's strategy and ambitions towards 2030. We'll then move into our biotech business unit, including a presentation on our drug discovery platform and overview of the pipeline. And then we will have an external perspective from Professor Juleen Zierath on the importance of skeletal muscle health, both in an obesity setting, but also more broadly. And then we'll do a deep dive on Gubra's lead proprietary program, GUB-UCN2. After the biotech presentations, we'll do our first Q&A session, followed by a 30-minute-ish break. And then in the second half, we'll cover Gubra Ventures, our CRO business and capital allocation strategy. And we'll then wrap up with another round of Q&A and some concluding remarks. And of course, for those of you here in person, we hope that many of you are able to stay afterwards for the reception, where I think there should be a good opportunity to also continue the discussions more informally. All right. So just a brief intro to our first speaker for today. Markus joined Gubra in September last year, bringing more than 25 years of experience in the pharmaceutical and biotech industries. Before joining Gubra, he held senior global leadership positions at Novartis, including as Head of the Cardiometabolic and Ophthalmology business franchises. He has also served as CEO of several biotech ventures within the Roivant Group. Markus holds a PhD in biological and biomedical sciences from Harvard University. And with that, I will hand it over to Markus to get us started.

Thank you, Adam. Welcome to our R&D event in rainy London. I'm really excited about today's event because Gubra is at an inflection point, and we have set ourselves a new ambition. So we would like our investors to understand where the company is today, where we aim to be in 2030 and why we are confident that we have a credible path to get there. For the ones maybe also on the webcast who do not know Gubra so well, here are a couple of facts. Gubra is a revenue-generating clinical-stage bioscience company founded in 2008, almost 20 years of scientific expertise in metabolic diseases and peptide therapeutics. We have a validated discovery platform validated through clinical assets and validated through major partnerships with big pharma and biotech. And we also run a very successful growing CRO. Since the IPO in 2023, the company really has shown strong execution the IPO primarily on the basis of our CRO equity story. Today, we have really demonstrated great potential on the biotech pipeline side. Today, we have 4 assets in clinical development. We have 6 active partnerships with pharma and biotech. Our CRO serves 17 out of the top 20 pharma companies. And in the last 2 years alone, we have received over $400 million in upfronts and milestone payments from our existing partnership. So that's a great foundation for a new ambition. And I would like to point out our new ambition is based on a very, very solid foundation, and we are evolving and scaling a successful model. Now, where do we want to go? By 2030, we would like to have 8 to 10 assets in clinical development. We like to bring forward 1 to 2 drug development candidates from our own discovery unit every year. We will be active in 3 therapeutic areas. Of course, metabolic diseases will still play a major role, but we will venture into age-related functional decline, and we will also establish a presence in immunology and inflammation. By 2030, we will also operate 2 to 3 ventures and create additional value through our growing and successful CRO. What makes Gubra unique? Gubra's business model is unique. We are working with 3 synergistic business units. We have biotech, our key value driver, which discovers and develops novel peptide therapeutics towards clinical proof of concept. We have our venture unit, which is investing capabilities in great science adjacent to our core therapeutic areas. And we have our CRO, serving external customers but at the same time enabling our internal innovation infrastructure. So, a unique model, but actually quite simple. We serve a single customer. It's the pharmaceutical industry, and we serve a single industry need. It's a need for new innovative medicines. So, how do we do that? We basically focus between drug discovery and clinical proof of concept; that is a sweet spot for Gubra. Our CRO provides scientific expertise, competitive advantage, and cash flow to Gubra. Our biotech unit creates new peptide therapeutics, which we partner with pharma companies in return for milestone payments and royalties. And our ventures augment our pipeline via new structures in collaboration with financial investors but also strategic investors. So a point to make, we have multiple ways to create and realize value. In terms of the foundation of our new ambition, I'd like to point out that our platform, our discovery and development platform, is fully validated. Multiple assets have made it into the clinic. We have made very substantial deals, including our deal with AbbVie last year. And we can rely on this platform to bring new innovative molecules into clinical development. Our pipeline today already has multiple high-value assets, and we will continue to grow that pipeline. Today, you will hear a lot about GUB-UCN2, our new long-acting urocortin-2 analog. It's a great example of a high-value asset, and Thomas will go into that. We have also assembled an excellent leadership team, and I'm excited that you will hear from all of them today. And another point I'd like to make is the strategic optionality we have today in the company to decide whether we want to bring forward assets a little bit longer towards clinical proof of concept. Strategic partnering is still a very important aspect. But today, we have more optionality. So this is our leadership team. Let me introduce our speakers today. We have Louise here, our Chief Scientific Officer, an expert in peptide therapeutics. We have Thomas, a leader in translational medicine and early clinical development. We have Zoe, our Head of Gubra Ventures, a distinguished scientist and company builder. We have Kristian here, our CFO, my right hand, making sure we allocate capital in the right way. And last but not least, we have Trine here today, who has led our CRO business very successfully for many years. Now translating this into strategic priorities, our key priority is to build a broader pipeline, more key assets in our pipeline, driving value for the company. GUB-UCN2 is certainly our next big thing. Then we will multiply our growth engines. Obesity has been a real fantastic growth engine for us. We have 3 clinical assets in the pipeline just on obesity. But we want to apply peptide therapeutics to other areas where there's a high medical need and high commercial opportunity. And we believe age-related functional decline is an excellent space we would like to venture in, and we will also establish a presence in immunology and inflammation. On top of that, advancing our technology remains on our forefront. Longer-acting peptides, oral delivery, macrocyclic peptides, and also continuing our great progress in terms of automation, robotics, and use of AI, all with maintaining a high flexibility and optionality in terms of our strategic progress and investment. A quick word on technology because you'll hear more about this later in the talk by Louise, but also on Trine, and maybe you have seen the great images in the other room about brain and muscle imaging. We have been using AI-enabled peptide design for many years. And this is an important part of how fast we can deliver new drug development candidates next to our in-house in vivo capabilities. 3D imaging in our CRO is really cutting edge. It's amazing what we can do today in whole-brain imaging and on muscle imaging in conjunction with AI analysis. And you can probably imagine a company like us here creating tremendous amounts of data sets, and to distill insights out of that, AI is helpful. So we will -- we are actually an early adopter of AI across the company and certainly something where we are standing out. I'd like to emphasize that our R&D platform is disease-agnostic. We have been very successful in metabolic diseases, but peptides can be applied in multiple areas of biology and indications. We've done a solid analysis on which spaces we feel we can add a lot of value as Gubra and with the capabilities of Gubra, and age-related functional decline seems like a future space of opportunity. And we do have an opportunity to venture in the space today with GUB-UCN2 because the biology allows us to also address muscle health, sarcopenia, for example, right? On top of that is a broad space of immunology where peptides can add value. And here, we are currently evaluating multiple assets for business development and licensing, and those could be good ones for our first ventures. I'm very excited about UCN2. This biology will build a new therapeutic space. It's a multi-indication asset. It will go way beyond obesity, and it's a major opportunity for Gubra. We invest substantially behind our clinical program, which has just started. You will hear more about this, but also through a very compelling preclinical program, which will make clear that this asset has multiple indications and the potential to become a major, major asset for the company. Now a new ambition also needs capital. And you probably know from Gubra that we have always been very disciplined in capital allocation, and that essentially will not change. We invest behind evidence. We are really focused around value inflection points in the context of Gubra; that means clinical proof of concept. Reaching this stage and partnering our assets will create substantial value. An example of that is the long-acting amylin we have partnered with AbbVie, and Thomas and also Kristian will talk about that. Now, we are in a good solid financial situation. Our current cash position is complemented by the proceeds out of our CRO as well as by the milestone payments coming in the next years from our existing and future partnerships. So all of this together will make our ambition possible. Keep in mind, the area we are focusing on, discovery to clinical proof of concept, does not require major capital allocation. We don't invest in expensive Phase IIb or Phase III. That's usually what our partners contribute. So our goal of creating 8 to 10 assets in clinical development, including our proprietary, venture, and partnered assets, is not outside our reach, and it's financeable. Also the fact that we want to have 1 to 2 drug development candidates every year from our own drug discovery is within reach. We just have doubled our R&D capacity in Horsholm with a new building this year. And I'm confident that we will continue to bring out new exciting medicines, adding value with 2 or 3 ventures launched and operated in lean asset-centric companies by 2030. And of course, I believe our CRO, our preclinical specialist CRO, is differentiated. We focus on high-value areas to add value for our pharma and biotech clients, and that will continue to grow and will remain very profitable for us. And with this, I will hand over to Louise.

Thank you, Markus. My name is Louise, and I will take you through the biotech unit. And the biotech unit is Gubra's core value driver. This is where we take innovative ideas, turn them into differentiated peptide therapeutics and take them to clinical proof of concept. Fulfilling the pipeline is a core focus for all pharma and biotech companies globally, and many rely on sourcing external innovation. Gubra is part of the solution. Over the years, we have built a strong pipeline of differentiated assets. At the center is an AI-driven drug discovery platform, streaMLine. The strength of the platform has consistently been validated through multiple clinical assets and partnerships with leading pharma and biotech companies. At Gubra, we are peptide experts. All the work we do is done using an in-house developed AI-driven drug discovery platform, streaMLine. A core advantage is that the platform combines AI-driven design and data analysis with high-throughput wet-lab screening of multiple peptide libraries, thousands of peptides. We use multiparameter optimization. So, this means that we don't just optimize 1 parameter at a time; we optimize all parameters simultaneously. In the end, this will enable us to save time and identify better molecules at speed. Over the years, streaMLine has repeatedly generated multiple peptide assets with blockbuster potential. Beyond streaMLine, continued platform innovation is key to make sure that Gubra remains at the forefront of peptide therapeutics. So the current toolbox that we have today already provides a strong foundation for pipeline expansion. We have streaMLine at the center, complemented with capabilities within de novo design, multi-agonism, and peptide-peptide conjugates. And we continue to innovate towards 2030. Technologies of particular interest to us are long-acting technologies to enable less frequent dosing, but also macrocyclic peptides, which could be an important enabler and a first step towards oral delivery of peptides. Collectively, this will support a 2030 strategic ambition of building a broader late-stage clinical pipeline and increase the number of development candidates that we can generate every year. So, many companies have a drug discovery platform, but the core strength of the platform is measured by the quality of the output and whether these assets can repeatedly go into the clinic. Our platform has consistently generated differentiated peptide therapeutics that have advanced into clinical development. This is evident from the pipeline shown here. This pipeline is a direct result of the power and efficiency of our drug discovery platform. It covers both our internal proprietary assets that are not yet partnered and our partnered assets that have been progressed through strong partnerships. Starting with our internal proprietary assets. The most advanced internal asset is the long-acting UCN2 analog currently in Phase I for the treatment of obesity. And you will learn much more about that later from Thomas. And at the same time, we continue to advance the next wave of future opportunities for Gubra, including new assets within obesity, but also beyond obesity, for example, sarcopenia and cachexia. Turning to the partnered programs. The 2 most advanced programs are the Phase II partnerships within obesity with AbbVie and Boehringer Ingelheim. Beyond obesity, we also have other highly interesting programs in collaboration with leading biotech companies. We have the Hemab, the Amylyx and the Camurus collaborations, and they truly illustrate the platform's versatility and opportunity to go beyond obesity and consistently generate differentiated peptide therapeutics across a broad range of therapeutic areas. But now let's take a closer look into some of these assets. Starting with obesity. At Gubra, we have been dedicated to treating and understanding obesity since the company's inception. And over the years, we have built deep scientific expertise all the way from discovery to clinical translation. And today, we'll take a closer look at some of these assets, each designed with a differentiated profile compared to current standard of care and with blockbuster potential. But before getting into the data, let's just take a step back and take a closer look at the overall obesity treatment landscape and where the field is heading. Because it's no secret that obesity continues to be a growing global health care challenge, and there is a well-acknowledged need for novel treatment approaches. By 2035, it's estimated that more than half of the global population will be living with overweight and obesity. And at the same time, treatment penetration is really low with less than 2% receiving active treatment. So there is a huge unmet medical need here. And one of the core issues is that today we're actually treating obesity as if it's 1 disease, but it's not. Obesity is a complex heterogeneous disorder. Different patients have different biologies and different needs. So we need more tools in the toolbox if we want to treat all patients efficiently. For the past decades, a core question with obesity treatment has been, can we make patients lose weight? This was the focus for the first generation of obesity treatments really spearheaded by the first generation of incretin therapeutics, the GLP-1s. The focus for the current wave has been to maximize efficacy and improve tolerability. Here, we've seen the introduction of alternative and complementary modes of action. We've seen amylins, dual and triple agonistic concepts emerging, and there has been amazing progress. But it's also well acknowledged that body weight reduction is not just fat mass. Lean mass actually accounts for 25% to 40% of the weight loss. And lean mass is muscles, it's bones, it's internal organs. So it's basically all the tissue that we would ideally like to preserve when we're trying to lose weight. Therefore, we believe that the next wave of obesity treatment will increasingly focus on the quality and not just the quantity. So in other words, improve body composition by maximizing fat mass loss and improve muscle mass and function. That is where the field is going, and Gubra's pipeline is strategically positioned to meet these emerging trends. So across our proprietary and partnered portfolio, we now have 3 clinical-stage assets in our pipeline, each addressing obesity from a different biological angle to address important unmet medical needs in the growing obesity treatment landscape. We have ABBV-295 by engaging with the amylin receptor biology. We have the triple agonist by engaging with 3 complementary modes of action involved in body weight reduction. And finally, we have an internal long-acting proprietary UCN2 analog building on a completely novel concept of improving body composition and muscle health. Now let's take a closer look at some of these assets. Starting with the triple agonist. This is a long-acting first-in-class triple agonist, and it targets the GLP-1, GIP, and Y2 receptors to engage in 3 complementary modes of action involved in body weight reduction. From a biological perspective, this is highly attractive. GLP-1 and GIP are 2 well-known incretin receptors with well-established effect on glucose and body weight regulation. Adding the Y2 component introduces a non-incretin mode of action, and the Y2 receptor is an important regulator of hunger. So the underlying scientific hypothesis is that by engaging with these 3 complementary modes of action, we can achieve better body weight control compared to engaging with each receptor individually. So the program was discovered in collaboration with Boehringer Ingelheim, and they're now responsible for advancing it through the clinic. And after seeing positive Phase I data showing a favorable safety profile and a body weight reduction, they have now initiated the Phase II study. The study will enroll 300 participants, and the primary endpoint is body weight reduction after 42 weeks of treatment. We see this as further validation of the asset's potential and of Gubra's discovery capabilities. Now let's turn to amylin. Amylin offers an attractive alternative to current standard of care. Amylin is an antagonist peptide hormone released from the pancreatic beta cells, and it has a well-established role in glucose and energy regulation. And importantly, amylin is not an incretin. It activates a different set of receptors and mediates the effect by a distinct and complementary mode of action compared to GLP-1s. So this means that amylin can be used as a stand-alone treatment or in combination with an incretin. So the class of amylin have repeatedly shown to deliver competitive body weight reduction with a favorable tolerability profile. This is evident from these 2 clinical data sets. On the first set here, you see the Phase II data from the Phase II trial with eloralintide. Here, you can see that eloralintide can produce a competitive body weight reduction. On the other slide, we have the Phase III data with cagrilintide. Here, you can see that cagrilintide can deliver body weight reduction that is clinically relevant with a favorable safety profile. So, you can say that's exactly the type of biology we're talking about when we're talking about expanding the toolbox for patients living with obesity and why we find it so compelling in context of 295. 295 is a differentiated amylin analog discovered at Gubra, out-licensed to AbbVie. It has a balanced receptor profile on the amylin and calcitonin receptors just like native amylin, and it has a very long half-life of 11 to 12 days. This means that there is the potential to go with every second weekly dosing or even monthly dosing. In addition, it has a delayed time to Cmax. So this means that there's an almost built-in titration in the molecule, which could potentially explain the favorable tolerability profile. Across the comprehensive Phase I studies, 295 has consistently demonstrated competitive clinical data. Early signs of body weight reduction were seen in the SAD study. Here, 1 injection with 295 led to a body weight reduction. This was further substantiated in the 6-week MAD study, where 6 weeks of treatment with 295 led to an almost 8% reduction in body weight. And finally, in the 12/13-week MAD study, 295 delivered almost 10% reduction in body weight. Across all studies, 295 was well tolerated, AEs were predominantly mild GI-related and transient. So there's another Phase 1b study ongoing right now with ABBV-295. This study will include a bigger proportion of female participants and a higher BMI range, and this is to generate data in a more representative patient population. But now let's take a detailed look at data from the 12- plus 13-week MAD study. This slide shows detailed data from the Phase I study presented recently by AbbVie at EASD. What you can see is that 295 delivers a competitive body weight reduction, dose-dependent, of almost 10%. I also want you to pay attention to 2 of the dose cohorts here, the yellow one and the green one. Here, we see competitive body weight reduction with every second weekly dosing or even monthly dosing. And remember that this is in a patient population being predominantly male with a lower BMI range. So key highlights here is that 295 delivers meaningful body weight reduction of almost 10%. It has a favorable safety profile, and the pharmacokinetics supports every second weekly or even monthly dosing. So, based on these encouraging data, AbbVie has now initiated the Phase II study. This is a comprehensive study enrolling 360 participants, 6 active treatment groups, and the primary endpoint is body weight reduction after 32 weeks of treatment. This is to get timely data for a potential Phase III study, while treatment will continue through Week 52. So to summarize here, the class of amylin provides an attractive treatment alternative compared to current standard of care. 295 is a differentiated amylin analog that has the potential to become an important tool in the obesity treatment toolbox. It also exemplifies the Gubra Biotech operating model, where we take a differentiated peptide, take it to clinical proof of concept, and generate further value through strong partners. Beyond obesity, we also have 3 highly interesting programs in collaboration with leading biotech companies. The Hemab collaboration centers around the long-acting plasmin inhibitor that we have discovered in collaboration with Hemab for treatment of bleeding disorders. Hemab has now initiated the Phase I study with this asset. Next, we have the long-acting GLP-1 receptor antagonist discovered in collaboration with Amylyx for treatment of post-bariatric hypoglycemia. Amylyx is now running the IND-enabling activities with this asset. And finally, we have the PTH analog that is being formulated in Camurus' FluidCrystal technology to generate long-acting treatments for patients with hypoparathyroidism. So, collectively, these programs demonstrate the versatility of our drug discovery platform to repeatedly generate differentiated peptide assets across multiple disease areas. And you can say that's exactly the versatility that gives us the opportunity to think beyond obesity and to go into new therapeutic areas in the future. So, to summarize, the biotech is Gubra's core value driver. This is where we take innovative ideas, turn them into differentiated peptide therapeutics, and take them to clinical proof of concept. Over the years, we have built a strong pipeline enabled by AI-driven drug discovery platform, streaMLine. The strength of the platform has consistently been validated through multiple clinical-stage assets and partnerships with leading pharma and biotech companies. We have a competitive obesity pipeline. Across our internal and partner portfolio, we now have 3 clinical-stage assets, each addressing obesity from a different biological angle to address important unmet medical needs in the growing obesity market. Beyond obesity, we also have 3 other highly interesting programs with strong partners. These programs demonstrate the versatility of our drug discovery platform and the opportunity to go beyond obesity. And that's exactly what we want to do, use the same underlying discovery capabilities to repeatedly generate differentiated peptide therapeutics and build a much broader clinical-stage pipeline with time. And with that, thank you for your attention, and I'm happy to turn over to Juleen, who will talk about the importance of skeletal muscle health.

All right. Thanks a lot, Louise. All right. So my background over the years really is on skeletal muscle health. And I think my role here is to do some frame setting and to give you some of the physiology and maybe the molecular biology on why muscle health is important to think about. And muscle is really one of your largest organs in your whole body, and it's incredibly important for maintaining metabolic health. So it's a major site of glucose disposal and insulin sensitivity. It's a key organ in regulating substrate metabolic homeostasis. And it communicates with other tissues through muscle-derived signals. And I'll mention some later, but they're called myokines. And so it's a real communicator to the whole body. Muscle is really important for physical function. It's important for locomotion. It provides strength and power for everyday movements. It's critical for mobility, for balance, for independence for people throughout the lifespan. And impaired muscle function is associated with poor physical performance. Now if we think about sort of the lifespan, muscle mass and strength is important and declines with aging. So we see this in the clinic. And if you can maintain muscle mass and muscle function, that promotes resilience and independence in individuals as they're aging. We also see that there's a rising incidence of obesity, and muscle function and muscle health is really compromised with obesity. So muscle health extends well beyond preserving lean mass. And I'm just going to give you some examples about what is muscle health. So if you look at sort of a cross-section of the thigh, you can see the muscle in the pink colors, you see the bone, you see the fat surrounding the leg. We try to analyze muscle for its quality. So how much muscle is in that leg, and we can do that by measuring the mass of muscle through noninvasive techniques, DEXA, for example. We can look at the quality of muscle, not only the mass, but the quality, what's the condition of the muscle. And we look at the architecture, and we can do that again through noninvasive tools, and we can look at something called myosteatosis, how much fat is, kind of, coming into the muscle itself. How many fibrosis molecules are around the muscle that compromise its quality. And we also measure muscle function. What can the muscle do? And that can be measured physiologically by looking at strength and physical performance. And this is done by looking at gait speed, grip strength, and other tests that we can do. So it's not just about the amount of muscle we have. It's about the quality and the function of muscle. And these are important things to think about when we think about targeting muscle. Now when we look at obesity and aging, both of those factors can compromise muscle health. And again, muscle is your largest organ in your body. It's really important. And with obesity, 1 in 4 people globally are going to be expected to be living with obesity. And I mentioned already this myosteatosis. As people have increased visceral adiposity, they also have an infiltration of fat into their muscle that compromises the function of muscle. It impairs the muscle metabolism. It impairs insulin sensitivity, and it leads to this cardiometabolic syndrome. And it reduces the quality of muscle and the function, the performance that people have based on their reduced muscle quality. With aging, we see that 1 in 6 people globally are aged. They're going to be either equal to or more than 60 by 2035, which is, I'm already 60, so I'm in that category now. And what we worry about with aging is something called sarcopenia. With aging, there's a progressive loss of muscle mass. There's a decline that we all feel in strength and power as we age, and there's reduced physical function and resilience. So both of those aspects are really important when we think about muscle health. And with the weight loss that we're seeing, muscle health may be already impaired before significant weight loss. So let me dial into some of this weight loss. It's been a revolution in the field to see the therapeutics that have been helping people with obesity lose weight. They lose a lot of weight. But weight loss is not always fat loss. And that's one of the concerns that we have in the clinic. People have been able to lose between 60% and 75% of fat mass, which is extraordinary. But at the same time, they're losing 25% to 40% of lean mass. And that is a cause for concern. What we in the clinic want to try to do is preserve lean mass, and that is the muscle, the body water, the organs, and other lean tissues. So it's a balance. Not all of weight loss is going to be the kind of weight loss we want to achieve. We want to lose the fat mass. We want to preserve the lean mass. And here are some examples. So I just got back from the EASD meeting, and this slide was everywhere. Everybody is talking about the weight loss we see with the incretins. This is some data from the SURMOUNT-4 study with tirzepatide. You've all seen this curve. It's remarkable. People are losing 20% of body mass. And as long as they stay on the drug, they do quite well, and they keep the body mass down. But we're seeing that if people come off the drug, and this is only after 36 weeks of treatment, people come off the drug and they stop treatment, they start to gain back body mass. And 2/3 of the weight loss is regained within a year. And the cause for concern is that if you look over here, the weight loss, 67% loss of fat mass, 33% loss of lean mass. The cause for concern is that when individuals are regaining weight, they're gaining disproportionately, the more fat mass is gained. So when they come off the drug, they gain mass, the mass they gain is fat mass, and they're not gaining back the lean mass, a cause for concern. So the long-term studies in older individuals also suggest that the fat may be regained more readily than the lean tissue. So how can we put a brake on that? So 2 big questions in the field are, with the weight loss therapies, can we further improve the quality of weight loss, and can improvements in muscle health translate into meaningful functional benefits? And we want to lose the fat mass, but we want to preserve the lean mass or maybe even build the lean mass. All right. So there's multiple biological approaches that are being explored today, and I'll give you some kind of outlines about some of these approaches. And in the next slide, I'll kind of go into some of the molecular mechanisms for what some of these approaches are trying to achieve. And so we've heard a lot about myostatin, which is a myokine. It's something that's released from muscle and it talks to muscle. And its normal job is to promote muscle -- its important job is to really function on muscle growth and regulation. And myostatin inhibitors can really relieve the inhibitory signals on muscle growth. They can increase muscle mass, they can reduce fat mass. But today, it's not been consistently translated into improvements in physical function and better physical outcomes on the muscle function. Another approach is inhibin beta E signaling, and this primarily works on the fat tissue. It's called a hepatokine. It's something secreted from the liver. It talks to the fat. And this approach can release a break on adipose tissue lipolysis. It can reduce fat while preserving lean mass. But also like the myostatin inhibitors, this approach has not shown efficacy in improving physical function today. The other approach we've heard a little bit from Louise is urocortin or the UCN analogs. And this is a strategy to improve muscle protein turnover, so you can promote protein synthesis, you can reduce protein breakdown, and this is one way to maintain muscle mass. There's a potential to preserve or increase muscle mass. And this has been shown to improve muscle function, and it's also been shown to have some cardiorenal benefits, and I'll show you some data for that. So these emerging approaches can improve body composition through many different mechanisms. And if we look at the myostatin approach, I mentioned this is something that's called a myokine. It's released from muscle. It acts on muscle. And normally, what it does, its normal job is to decrease muscle protein synthesis and increase protein degradation. And this approach is to use antibodies to block myostatin -- to block the myostatin molecule, and it inhibits the receptor binding and it alters the signaling. And what it will then do is increase muscle protein synthesis and decrease protein degradation. And it's a way in which one can maintain muscle mass. And there are some clinical approaches already out there, myostatin inhibitors, where bimagrumab is a molecule already been tested in clinical trials, a 48-week trial, where this therapy has been shown to lead to a modest reduction in body weight, a 25% loss in total fat mass. And at the same time, there's a very modest improvement in lean mass, and this is the blue bars. And if you compare that to sema, you can see that it's very much equal in terms of its body weight loss and its effect on weight loss, fat mass loss, but sema causes a loss in total lean mass. So the idea here is that the bima is one approach to be able to lose fat mass and at the same time, have a weight neutral for lean mass. And I think what's very intriguing is that when individuals are getting a combination dose of bima and sema together, they have a pretty striking change in body weight. They have an even more robust change in total fat mass, but they do not have a change in lean mass. So it's one way in which one can dial down fat mass and dial up potentially or maintain lean mass. So body composition can be improved. But in this case, the functional benefits on the preservation of muscle mass have not been convincingly demonstrated. The other approach I mentioned earlier is this inhibin beta E, which is a molecule that is secreted from the liver and it talks to the fat cells. So it's a way of communicating between liver and fat cells. And its normal job then is to be released from the liver, talk to the receptors on the fat cells. And normally, what it does is it downregulates lipolysis and it increases fat storage. And the approach here would be to block the production of inhibin beta E, block it in the liver so that it cannot talk to the fat cell. And it would put a brake on the fat cells to increase lipolysis and decrease fat storage. So it's a way in which one can then target weight management independent of body food intake. And so -- and this is an experiment where there's been an siRNA approach that targets the liver that can silence the production of inhibin beta E. And what it does then in a time-dependent analysis where it's 1 dose treatment, you've got 3 months and 6 months treatment, and it's been shown to lead to a reduction in visceral fat mass, and this is the fat mass that really one wants to target in the clinic, the body fat. There's a reduction in total fat mass, and there is an increase in lean mass, and they're body weight neutral. That's because you're losing fat and you're increasing lean mass. And so this is one approach to improve body composition, but the effects again on physical function remain to be established. So these are 2 approaches that are already being tested. Now urocortin analogs are unique in that they target not only one organ, they can target muscle and fat. And these peptides are physiologically produced from multiple organs in the body. And this approach with these analogs is to target both muscle and fat. And targeting muscle, the receptors are highly expressed in the muscle cells. They promote anabolic or growth-promoting effects in muscles, and they improve metabolic signaling. And there's preclinical evidence in animal models for preserved or even increased muscle mass, and there's preclinical evidence for improved muscle function. And that is something we don't see with the other approaches. So it really does something more, and it affects the adipose tissue. So the urocortin analogs can regulate the fat metabolism. They promote lipolysis. They basically burn fat out of the fat cells. They lead to energy mobilization, and there's preclinical evidence for a preferential fat mass reduction. And as I mentioned earlier, this is a tissue effect that goes beyond appetite regulation. So this approach is interesting because it holds promise for fat loss with preserved or even increased muscle mass. And I'll give you some examples. So these are preclinical studies. They're all done in rodents. And the first 2 panels, the left and the middle, are a study actually from my lab, and they're in a mouse model where the mice have been fed with a high-fat diet for weeks. So they become obese and they become insulin resistant. And these mice are either sedentary or they are given wheels and they can run in a cage. And we found that when we treat the animal with the UCN peptides, they reduce their fat mass. And in the middle panel, we take out a muscle from the animal and we weigh it, we can show that with the UCN treatment, they have an increase in muscle mass. In a study where we've done some casting where we've immobilized animals and their muscles atrophy, we can show that there is a loss of muscle mass in the blue bars. If we immobilize -- sorry, if we immobilize the animal in the green and treat them with this vehicle, they have an atrophy in the muscle. And if we treat them with the UCN peptides, they maintain their muscle mass even though they're immobilized. So this would have some implications for bed rest or sarcopenia that UCN2 peptides could preserve muscle force with immobilization. So the other thing that this approach has beyond the myostatin inhibitors and the inhibin beta E is that they have cardiorenal protective qualities to them. And there's preclinical and clinical studies that provide evidence to suggest this. So if we look at the cardiovascular effects, this has been demonstrated in humans. There's been effects on cardiac output, left ventricle ejection fraction effect, and there's reduced systemic and peripheral vascular resistance, and this has been seen in even healthy people and people with heart failure. And the renal effects have been shown in preclinical models where there's improved creatinine clearance, reduced renal injury and inflammation. And these effects may be both direct and they have -- because of the hemodynamics that we can see. And I'll dial into some of the primary data that supports these assertions. So this is the cardiovascular parameters. It's a study in humans where people have been infused with urocortin-2 analogs, and you've got the control in the blue and the dark is the urocortin-2 analog that's been infused into these people, and it shows that it improves cardiac output. It shows it improves blood pressure. And in an ovine model, it's been shown that there is an improvement in urine sodium excretion and also kidney markers of inflammation, fibrosis are also improved by these relatively short-term exposures to urocortin-2 analogs. So just the take-home message here is that, first of all, muscle health is incredibly important for physical function and healthy aging. Weight loss, it's not all the same. Chronic weight management should extend beyond weight loss per se, and we should focus on preservation of lean body mass, looking for healthier body composition and function. And the urocortin biology offers potential across not only body composition, muscle function, but also the cardiorenal health parameters. So that's a little bit of the science behind the molecules. And with that, I'm going to turn over to Thomas, and you will probably dive deep into your portfolio here.

Thank you, Juleen. So my name is Thomas. I'm Chief Medical and Development Officer at Gubra, and I would like to discuss our development program, GUB-UCN2. And I would also like to highlight why we believe that GUB-UCN2 could be the next potential value driver for the company. So we have just heard obesity treatment is really entering a new era. Incretin therapeutics have demonstrated how much weight loss we can really achieve with pharmacotherapy. However, we do see a substantial reduction in fat mass, which is desired, but also a reduction in lean mass, including skeletal muscle mass, which is undesired. So the next opportunity is to improve what patients lose, what they keep and how they function. GUB-UCN2 has the potential to address exactly that gap by improving body composition and potentially also improving physical function. So today, I will explain you the preclinical data set supporting the value proposition. I will talk about how we intend to translate that into the clinic and how we view the broader indication expansion potential in order to maximize the value of GUB-UCN2. So the presentation will follow the 3 areas summarized on this slide. I will first briefly summarize the mechanism of action and walk you really through the preclinical data set. I will then talk about how we translate the findings into the clinic and how we test what parts of the biology really materialize in a clinical setting. And finally, I'll come back how we use this data set along with additional clinical and preclinical data to think about further indication expansion. So let's start off with the mechanism of action and the preclinical data set. So you have seen this slide before. Native urocortin-2 signals through a receptor called CRHR2 and the peripheral biology involves the target tissue that is really relevant for the therapeutic purpose we are developing GUB-UCN2 for. So specifically adipose tissue and muscle tissue. In the adipose tissue, UCN2 can reduce fat mass. In the muscle tissue, UCN2 can drive anabolic processes, inhibit catabolic processes and drive oxidative metabolism. And that together is the biological rationale for developing GUB-UCN2 in obesity with the purpose of improving body composition. The biology extends beyond adipose tissue and muscle into the heart and into the kidneys where we have seen that UCN2 can improve cardiac function, can drive natriuresis and diuresis in the kidney. And that in itself is the biological rationale for thinking about indication expansion opportunities into the cardiorenal space. So on the left-hand side of the slide, you see the key product characteristics of our UCN2 analog, which we are calling GUB-UCN2. It's a 38 amino acid peptide, which is highly potent and highly selective for the CRHR2 receptor, and it's formulated for a convenient once-weekly subcutaneous administration. So the development ambition is derived from the biology and from what we would like to achieve for the patients, driven by medical need. We would like to start off with looking at healthy body composition, right, with a question, can we really reduce fat mass and improve muscle mass. Improvement of muscle mass is a good thing to do. But the next question, of course, is does it translate into improved muscle function, right, and improved physical function and improved muscle strength. And that's the second aspect we are going to address. The third question is, how are we going to use GUB-UCN2 in the clinic? Is it going to be used as a monotherapy in combination with available obesity treatments or potentially as a follow-on treatment once patients have achieved substantial weight loss. This is what we are going to address both in the preclinical as well as in the clinical setting. And finally, I spoke about it briefly, how do we lift the full value of GUB-UCN2 by looking into indication expansion opportunities, right? And across all these indications, we are looking at once-weekly subcutaneous administration of GUB-UCN2. So now let me dive into the preclinical data set. So we have evaluated GUB-UCN2 in 2 species in mice and in rats, and we used obesity models based on high fat diets for both species. And what is really common across species, and I'll walk you through the data in a second, is that we can indeed improve body composition. We do see a substantial reduction of fat mass and preservation or increase of lean mass. So the first data set on this slide shows data in mice that were treated for 4 weeks with GUB-UCN2. And you do see on the left-hand side that we see a dose-dependent reduction in body weight. And you see in the middle graph that this body weight reduction is predominantly driven by a reduction in fat mass while we maintain lean mass in these animals. And body weight reduction and reduction of fat mass came with additional improvement of other metabolic parameters. So we have an improvement in glucose metabolism. You see on the left-hand side here, glucose-related hemoglobin A1c, and that goes down as does triglycerides and total cholesterol. So this is also a favorable metabolic profile that we are achieving with GUB-UCN2 treatment. So we have also evaluated GUB-UCN2 in rats, and this slide summarizes data from a 12-week treatment study. Monotherapy was evaluated and compared with treatment with semaglutide and the combination treatment. The mono treatment is depicted here by the green bars. And you can see in the middle and on the right-hand side that we do achieve a substantial reduction in fat mass, and we do see a substantial increase in lean mass. The overall effect was weight neutral with GUB-UCN2 as a monotherapy. If you look at semaglutide, which are the purple bars, we do see the expected weight reduction. But what we see in contrast to GUB-UCN2 is a reduction in fat mass, but also a slight reduction in lean mass. If we now combine both treatments, we can maintain the weight reduction that we have seen with semaglutide in the combination, but we can favorably modify the body composition by further decreasing fat mass and increasing lean mass. This is exactly the desired profile that we would be looking for. So we have now also thought about what are other potential combination partners for GUB-UCN2, and we specifically looked at tirzepatide and an amylin analog. And the next slide shows the data from a treatment experiment using tirzepatide as a comparator and as a combination partner. GUB-UCN2 monotherapy, again, is depicted by the green bars, where we see exactly the same effect here already after 4 weeks of treatment. And we do see that we have a substantial reduction in fat mass and increase in lean mass with a weight neutral effect. Tirzepatide behaves as expected. It reduces body mass. These are the aqua bars, but it also reduces beyond fat mass lean mass. And if you again combine and these are the dark blue bars, we do see that we can maintain body weight, but further reduce fat mass and increase muscle mass. Exactly the same pattern with an amylin. And cagrilintide was used in this specific experiment, again, a treatment period of 4 weeks with the same findings for GUB-UCN2 monotherapy. Amylin therapy alone resulted in the expected body weight reduction. And again, we did observe a reduction in fat mass and a reduction in lean mass. With the combination, we got a much better body composition and that we could further reduce the fat mass and increase the lean mass. So this basically tells us that GUB-UCN2 has a favorable effect on body composition, and it does so as monotherapy as well as a combination partner with available obesity treatments or those that are in development. So the next question, of course, is, and Juleen already touched on that, do we actually have an effect on muscle volume and muscle mass itself? The data I have shown you here are lean mass, of which skeletal muscle is only part of. So we use Gubra's 3D imaging technology to analyze the muscle volume in the hindlimb of these rats. And Trine will speak about the technology in a little bit more detail later on, but the processing involves a clearing of the tissue, a light sheet imaging, building of a hindlimb atlas and then AI-based analysis of the skeletal muscle volume of the hindlimb. And you can see on the right-hand side how the analysis looks like. And here, we very clearly demonstrate that, yes, muscle volume drives at least in part the increase in the lean mass that I have shown you on the previous slides. So we have now thought about how could GUB-UCN2 be used in the clinic, right? What happens if we discontinue semaglutide, for example, switch to UCN2 or add UCN2 at a later point in time in patients that have been pretreated. And the preclinical setting is reflected here on this slide. So we have conducted a 7-week study where we put obese animals on a monotherapy with GUB-UCN2. These are the green -- is the green line and with semaglutide, this is the purple line. Vehicle-treated animals are the gray line. These are basically the control groups for the experiment. And you can appreciate that with semaglutide, we did observe the expected body weight reduction, but it came really at the expense of a loss of lean mass. So we have now switched therapy after 3 weeks into the experiment. And this is what the vertical dotted line presents on the graphs. So first, we discontinued semaglutide. So as expected, we did observe an increase in body weight all the way back to vehicle-treated animals. And interestingly, that gain in body weight was almost exclusively driven by an increase in fat mass. You can very nicely see that in the middle graph. So if we are now switching from semaglutide to UCN2, that means we still continue -- discontinue semaglutide, put the animals on UCN2, we see exactly the same weight curve but the body composition is quite different. The body composition is now driven by a maintenance of the low fat mass that we have achieved in the first 3 weeks and the weight gain is almost exclusively driven by lean mass. So it's quite the contrary that then what we observed with discontinuation of semaglutide. So if we now add UCN2 to semaglutide at a later point in time, we observed the same favorable effect on body composition that we have observed when we initiate both treatments at the same time. We again see a further reduction in fat mass and a further increase in lean mass. And again, the same question is the increase in lean mass we are seeing in this experiment also driven by increase in muscle mass? The answer to that is yes. You see the absolute weight of the different muscles of a hindlimb of the animal, the EDL muscle, soleus and tibialis anterior and across all muscles, we did observe an increase in muscle mass. So with this preclinical data set, we have shown that GUB-UCN2 drives a favorable body composition with reduced fat mass, increase in lean mass. We have shown that increase in lean mass is at least in part driven by an increase in muscle mass, which is desired. We have demonstrated that it works as a monotherapy, that it works in conjunction with obesity treatments and that it works as a follow-on treatment. With that, we have now moved the program forward into clinical development. And we have now started a very comprehensive Phase I/IIa clinical trial to look at safety, tolerability, PK and also relevant pharmacodynamic endpoints. It's, as I said, a comprehensive trial. We are targeting an enrollment of approximately 188 participants. These will be either healthy participants in the SAD portion of the trial or participants with obesity in Part 2 and 3 of the trial. We will test GUB-UCN2 as a monotherapy and as an adjunct to an incretin-based therapy, and we will be looking at body composition and body function endpoints. So this is how the trial is phased. We are currently in the SAD portion of the trial in healthy participants. The key data set we are getting out of this is safety, tolerability and PK as well as the dose selection for the MAD portion of the trial. The data are expected to read out in the first half of '27. We are then moving on into an obese population in the MAD portion of the trial. Here, the participants will be treated for 6 weeks. And we are going to collect initial data on body composition in the MAD portion of the trial to understand if we get the directional changes that we have seen in preclinical species. And the data set from the MAD trial is expected end of '27, early '28. Subsequent to that, we will be moving into a 16-week treatment arm where we have multiple populations and multiple treatment regimens. And this will allow us to do a full assessment of the effect on body composition as well as muscle function endpoints. So how are we going to assess body composition and muscle function in the clinical trial? So we will be utilizing MRI imaging for body composition assessments. And Juleen has already pointed out multiple technologies that are available to actually do that. We have decided to go with an MRI because we can really distinguish between muscle volume and other components that are part of the lean mass and that are basically summarized in a lean mass readout with DEXA scan. So we will be looking at subcutaneous adipose tissue. We will be looking at visceral adipose tissue. We will be looking at fat-free tissue and at muscle volume. The muscle volume is given here by the red color. We then go one step deeper and also image the tie muscles. And Juleen also explained the reason for that because it's not only muscle volume that drives function, it's also muscle quality. And with an MRI technology, we can really look into intra and intramuscular fat and look at potential improvement of muscle quality as a contributor to a functional impact. The functional assessments will include 2 one bucket you might be familiar, is called a short physical performance battery, and that includes 3 tests that we are doing. It's gait speed, sit to stand and balance. And these are tests that look at very different domains, mostly related really to the lower body because that is very important for movement and independence, which includes mobility, lower limb function and static balance. And the second bucket will be a set of tests where we look at muscle strength, and we will be performing very standardized knee extension tests where we can evaluate lower limb static and dynamic strength. So this, all in all, will allow us to fully assess what biology from the preclinical species is translatable into the clinic. And it will also guide us in terms of further progressing the asset into other indications. As I indicated, obesity will be our entry point for UCN2. But we are interested in expanding the indication potential beyond obesity. And this slide, again, you have seen it before, puts GUB-UCN2 into the context of our therapeutic area strategy. It sits along with the partnered assets within the core obesity TA, but we really view that as a transition asset that based on functional muscle functional assessments will really allow us to determine if we can drive forward into conditions that are characterized by muscle-wasting and loss of muscle function. And one of those indications that we are very interested in is sarcopenia. And the rationale for sarcopenia really follows from the relationship between muscle decline and loss of independence. And as you can see here on the left-hand side of the slide, as we age, we lose muscle function and muscle mass declines by 10% per decade in individuals aged 50 and older. This is quite a lot. And at some point, we arrive at a threshold where daily activities become challenging and individuals also potentially lose independence. And this is what we would like to avoid. Demographics, as depicted in the middle of the slide, increases the need of the scale. And you see that by 2060, it's projected that we have 20% of the population in an age group that might actually be affected by sarcopenia. So we are really talking about a large population. But the population is already pretty large. Now if you look at the left-hand side -- on the right-hand side of the slide, where we have prevalence of 10% to 27% already now in individuals 60 years of age and older. And that extends well beyond obesity. We see that in individuals with a number of underlying diseases like chronic kidney disease, heart failure, COPD and cancer cachexia. So it's really a growing population and across multiple disease settings. And why is sarcopenia important? If you are looking at this slide, it nicely summarizes the meta-analysis across 35 studies looking at really the impact of sarcopenia on older individuals. So we have almost 99,000 older individuals that drive this analysis. And here, we see a 2.8x higher risk of disability with sarcopenia and an approximately 2x higher risk of falls, fractures and death. So there is quite a significant medical need. And this is basically the basis for the value proposition of GUB-UCN2 in sarcopenia, high unmet medical need associated with an aging population with an increasing and aging population and a therapeutic white space with no approved therapies currently, right? So we are looking at lifestyle management mainly in this population. So this slide puts GUB-UCN2 into the broader development vision we have for the asset. We start off with body composition, which is very relevant for obesity, either as a monotherapy or in conjunction with available obesity treatments. And clinical data demonstrating functional benefit would also enable us to move into muscle-wasting conditions such as sarcopenia, as I indicated before. We have also spoken about the general mechanism of action and the biology beyond adipose tissue and muscle, in particular, the cardiorenal space is of interest. And here, we could envision GUB-UCN2 playing a role in improving cardiac and renal function and also improving maladaptive remodeling that we do see in a number of underlying cardiorenal diseases. Long term, GUB-UCN2 could be utilized in the context of healthy aging to preserve mobility and prolonged independence. Each of these indications require their own clinical evidence and their own clinical development program. What is important for us now really is to focus on obesity, deliver the initial clinical data set, understand the translatability of the biology, and that will guide how we embark into indication expansion for GUB-UCN2. So let me leave you with 3 key messages. Number 1, we have a very compelling preclinical data set that demonstrates that GUB-UCN2 really has the desired impact on body composition in multiple relevant obesity models. Number 2, we have set up a comprehensive clinical program to test the question at hand, which is, do we see the same improvement in body composition with an effect on physical function in the clinic. And number 3, data from the clinical program will guide how we further think about the development of GUB-UCN2 beyond obesity and how we intend to realize the full commercial potential of the asset. So with that, I would like to thank you for your attention. I would like to hand it back over to Adam to moderate the Q&A session. Thank you.

Yes. So thanks a lot, Thomas. I'll now invite Markus, Louise and Juleen back on to the stage, and then we can open the floor for questions focusing on the biotech presentations. Of course, more than welcome also to ask questions of broader strategic character as addressed by Markus in the opening remarks. So please, if you have any questions, raise your hand. We have a handheld mic that we can pass along. So virtual attendees can also hear what we're saying. We'll start here with Thomas. Go ahead.

Thomas from SEB. So a few questions on UCN2 maybe. So first of all, we recently saw Roche also entering the space. So can you maybe highlight a bit on your understanding on your compound compared to the one from Hanmi? Receptor selectivity, PK, whatever we have of understanding here? And then maybe second question, Thomas, you just showed sort of a broad-based increase in muscle volume across the rat leg, I think it was. Do you have any data on cardiac muscle volume as well? So is there any, say, observation, any signs of cardiac hypertrophy, for example, here? So anything we should be concerned about? And also in addition to that, maybe you do highlight the potential in the cardiorenal setting. But does this maybe also highlight that there could potentially be a risk in cardiovascular risk for healthy CV? So just focusing on the weight loss, but in patients without any cardiorenal comorbidities. Can I ask another one?

Let's start with -- yes, I can maybe start off with addressing the questions, Thomas. So with regards to the Hanmi compound and competitor compounds, your first question, right? So I think, first of all, it really shows that there is really substantial interest, right, in the community and in the industry in the biology of UCN2. And we have heard about why that is. It's really a very interesting and very differentiated biology. So at this point in time, the data that are available are very limited, right, on all the different assets, and there are currently no clinical data available, right? We have multiple clinical programs ongoing, and we will really need to wait and compare the clinical readouts in order to determine, right, whether there is room for differentiation across the assets with the data that are available, this is a challenge. So then with regards to your questions around effects on the heart, we have very closely looked at effects at cardiac effects. And that included basically pharmacodynamic assessments in the relevant disease models and included assessments like the one that you were specifically asking for in our tox program. And from both perspectives, I can say that from a tox perspective, we have no concern with regards to cardiac hypertrophy. And the contrary is actually the case, right? If you are looking at disease models, for example, heart failure, ischemic heart failure due to LAD ligation, and we have spoken about the data before, then we actually do see an improvement in left ventricular function that is similar or even better than what can be achieved with standard of care. So there is really a case to be made to really develop GUB-UCN2 in cardiovascular indications. I think that addresses probably.

This is Romy from Kempen. I have 2 questions. The first is that there is some evidence out there of differences of acute and chronic effects of corticotropin-releasing hormone receptor 2 agonism potentially due to receptor desensitization. So I was wondering how you're thinking about the durability of effects on adipose tissue and the energy mobilization that you were talking about earlier with sustained UCN2 exposure. Have you also looked at potential desensitization preclinically? And then my next question on strategic -- on the 2030 strategy. So you mentioned you have strategic optionality there. So as you expand your preclinical pipeline, looking at 8 to 10 assets. So how do you envisage continuing to partner most programs around Phase II development? Or do you see Gubra retaining greater ownership maybe to capture more downstream value?

Thomas, let's start with the first 2 related question and perhaps Markus, you can...

Yes, I can start off, Louise, you might want to chime in. It's indeed correct, right, that there are effects that are different, right, if you compare chronic and acute administration, right, in particular, if you're looking at insulin sensitivity and glucose metabolism. And we have not really looked very specifically at receptor desensitization. However, we have compared really the effect of different treatment regimens and treatment duration -- if you compare that, we see that pharmacodynamics is building up with continued treatment duration, which may suggest that this effect is really realizable with chronic administration.

Yes. I think you covered it really, really nicely, Thomas. And you can say you can draw some parallels with regards to GIP receptor antagonism and agonism that also to some extent, can result in the same pharmacodynamic readout. As Thomas alluded to here, we have explored UCN2 treatment for many, many, many weeks in preclinical animal species and have seen consistent competitive results here.

And with regards to your second question, I think it will really depend on the asset -- for some assets, clinical proof of concept may be achieved with grade Ib assets while others will be Phase IIa. For some assets, we may believe we have all the capabilities to -- we need to drive it to such point. For some assets, a potential partner may be really valuable to take an asset earlier. So we will do those decisions asset specific, understanding what is our core contribution and how much value we can generate in-house and what's the best for Gubra. I don't want to generalize that we will develop all assets to make it Phase IIb ready. Because all different indications have specific Phase I programs in terms of how much patients would I need, how much capital do I need to invest, what's the risk benefit to this particular target and biology. So we'll make those trade-off decisions. But for the ones we can do it, we'll probably do it because then, of course, the value inflection, what I get at a partnering stage will be higher.

I think Rune has a hand over here.

Yes Rune from DNB Carnegie. So also on UCN2, first of all, obesity pricing has come down. UCN2 will be an add-on. What do you see the willingness to pay for UCN2 on top of GLP-1? And then back to potential partner discussions. With UCN2, you clearly have a road map for the opportunity. But in the past, you have partnered and then fully out-licensed the assets to the partner, and they decide what happens afterwards. So with this road map, should we be thinking that you would take a stake like a 50-50 partnership on UCN2? Or are you still willing to fully out-license and then maybe not get the potential that you're outlining here today?

Yes, those are 2 very good questions. I think pricing in a market which is more becoming a chronic market over time plays an important role. People will pay for outcomes, right? Obesity is a highly consumer-driven market, right? And people will pay for performance. In the combinations, if you look at other areas like cardiometabolic diseases, type 2 diabetes, respiratory, the prices have come down within the combination, right? That will probably also happen in an obesity context, but the innovation piece will always be priced at a level where you can still have substantial value. But that is a driver. And I think in terms of what will be the actual partnership depends on the partner, what does the partner bring? What can we still bring into the development piece where we can add value. Some of our partners we have on the triple agonist on the amylin are very good, right? AbbVie is an excellent partner, driving multiple programs, multiple ideas forward, exploring different combinations. They're all in on the asset, right? And I think I feel very comfortable that AbbVie is driving the program. Similar also on the BI side, very keen on driving the program forward as fast as possible because it's a unique triple, first-in-class triple. So I think for those 2 partners, I wouldn't worry, right? So if we find the right partner, I will probably continue to give them the control over the development program. It also depends on what stage of capabilities in later-stage development we are building over time. But I think at the point today, the deal structure, the partnership structure we have with AbbVie is probably a good blueprint within the time line of our strategic plan until 2030.

Yes. Morten, go ahead.

Morten Larsen, ABG Sundal Collier. First to Juleen, thanks for the presentation. Obesity is a super volatile and fast-moving market and UCN2 may be on the market in 5, 7 years. How would you see the role of a, let's say, a stand-alone project or monotherapy UCN2 in that market in 5 to 7 years? What combination products would you ultimately see this teamed up with?

Part of it, I think, depends on the staging of where people are in their journey of weight loss and maintenance. So I think it would be important to have it early. People are losing weight rapidly tend to be losing more lean mass and that, that you'd want to mitigate that as early as you could. So I'd probably want to have that early when you start to dial down the weight loss. I think females tend to lose a lot more lean mass. So you could think about the sex and also the age of the individual where they're in their weight loss journey. I know I'm not being very specific, and that's what you want. But I think it's going to be more of this precision health, but not to the actual individual, but maybe to classifications of individuals and phenotypes in that journey of weight loss. And I mean I'm a muscle physiologist. So my bias is that I think there's a big role for it, not only with obesity, but with cachexia, injury and aging along the way.

Okay. Second to Markus. You talked about 8 to 10 clinical stage assets. Just to clarify, that is the absolute number you're going to target. It's not the total number you're going to come in and if anyone drops off, right?

Sorry, maybe you clarify again the question.

Okay. 8 to 10 clinical assets by 2030. That's the total number in 2030. What happens if someone drops off or is pruned out?

Yes. This is a total number. Yes, it's a total number. Of course, some of those development programs, it's not sure that will continue. But I think this is why we're also giving a range of 8 to 10. We have 4 today, right? And with our productivity internally plus selective opportunities from the ventures side, I'm very confident that 8 to 10 is realistic.

Okay. Obesity, super volatile and fast-moving market. You already have 3 obesity assets out of those 8 to 10. You want to lean even more into obesity. But as you said, super volatile now with prices coming down half. Is this really the right way to go to be even more obesity focused long term?

Well, we talked a little bit about expanding our TA focus to age-related functional decline and immunology and inflammation. Those are markets which are rapidly developing. So there's great opportunity for us. Those 8 to 10 assets will certainly not be in obesity alone. But given we have 3 already, they will still have a substantial part of our value generation also by 2030. But we are diversifying our pipeline. And we're also lucky to have a disease-agnostic R&D platform, so we can diversify.

Rajan has a question.

It's Rajan Sharma from Goldman Sachs. So firstly, just on the use of MRI versus DEXA scan in the Phase I for UCN2. Has there been any -- I know it's quite early in the field, but has there been any discussion with regulators around that and some agreement there? Just wondering that as this field emerges, if regulatory bodies and potentially academia move towards DEXA scan versus MRI, are you kind of wrongfooted there? So just wanted to understand the level to which you've had those conversations. And then secondly, AbbVie running a combination trial of GUB-295, I guess is it ABBV-295 with lutikizumab in HS. Conscious it's not your trial and you won't be leading it, but you know Amylin pretty well. So I just wanted to understand your take on the rationale for running that trial. And then I've got a third, but maybe I'll do that afterwards, if that makes sense.

Let's start with the first 2. So perhaps, Thomas, I don't know if you can start with MRI versus DEXA and any regulatory input and then we can move afterwards to Louise on 295.

Yes. So it's a good question, right? And DEXA has been the tool of choice, right, for a long time to look at body composition, right, and look at fat mass, look at lean mass. The challenge is that we now have novel mechanisms that are being explored that target a very specific compartment within lean mass, right? And the assessment of lean mas in itself is not sufficient any longer to determine if we have the desired pharmacodynamic effect or not. So we need to move away from DEXA to methods that are more suitable to what we expect from a mechanistic perspective. MRI is the first step in that direction. You see that now more and more utilized across clinical trials, but the compounds that are using them are not far enough so that regulatory alignment did happen, right? This is an open discussion. Beyond MRI, there are other biomarkers that are being in development that might be much easier to implement in later programs. In currently and correlate with MRI imaging to understand what is really the best biomarker then to carry forward in the development program. For now, we think MRI is really the tool of choice relative to the mechanism of action and what we would like to show.

Good. And then the second question, just to reiterate, I think that was on AbbVie's communication around initiating Phase II trial with 295 and lutikizumab for HS. So perhaps I know it's limited what we can speculate, but perhaps we have some comments, Louise.

Yes. So definitely, you can say, again, it's up to AbbVie to comment on the specific rationale for entering this study. What we know is that a large patient population with HS also, to some extent, obese and overweight. So from that perspective, there is a huge rationale in also reducing body weight in such a study. You can also say that it really shows that AbbVie believes in the potential of 295, not just within obesity, but also beyond obesity. And that is a strong signal for them to be sending.

Okay. Perfect. And then last one was again on UCN2. Kind of hear the comments that you will explore beyond obesity. And I guess if you were to see a very, very strong signal on muscle strength, for example, and there was potential in maybe kind of neuromuscular disorders, would you consider maybe pausing the development in obesity just because thinking from an economic perspective, it's probably a little bit more attractive to be in rare muscular disorders, whether that's an add-on therapy. And I guess, what would you need to see in the Phase I to justify development outside of the obesity space?

Well, I guess that's highly speculative.

That's highly, highly speculative, right? I think we need to see what part of the biology is really translatable into the clinic, right, and really understand if we can have an impact on function. Function is driven by multiple aspects. It's not only the volume, it's the quality of the muscle, it's the capillarization, it's the neuromuscular coupling. There are multiple aspects that need to come together, right, in order to drive muscle function. And this is what we need to further understand, right? And if data are available, we can evaluate and then we can determine what is the right development pathway forward, right? For now, I think the focus is really on getting the data.

Thanks a lot. Any additional questions before we do a break? No, it doesn't seem to be the case. All right. I think please ignore the 3:30 p.m. reconvene. I think we should reconvene here at 3:10. So 10 minutes past 3. Let's do a 30 minutes break. Thanks a lot. [Break]

So good afternoon. Welcome back from the break to the audience online, but also here in front of me in London. My name is Zoe. I'm Head of Gubra Ventures. This is our third and most recently launched business unit at Gubra. And before the break, you heard about the strength of our scientific platform, our R&D capabilities and the progress we've made in advancing our internal pipeline. For the next 15 minutes or so, I'm going to tell you what Gubra Ventures is, why we've launched it now and how it fits into the broader Gubra organization. But before I do that, let me make it absolutely clear what Gubra Ventures is not. And Gubra Ventures is not a corporate venture fund. Instead, you can think of it as our external innovation arm of Gubra. And since we launched in March, we've reviewed over 150 opportunities. And what that's taught us is the pool of external innovation is large, and there is a lot of opportunity for Gubra to apply what we've learned and our expertise to those opportunities. However, to date, we have not yet launched a venture, and that's because we are applying the same high bar to Gubra Ventures that we apply to our internal pipeline progression decision-making. So what are we seeking? We're looking for credible science, derisked path to development and something where Gubra can really add an asymmetric upside to the opportunity. So how does Gubra Ventures sit within the broader Gubra model? Well, Gubra CRO is our value enabler, and you're going to hear about that shortly from Trine. You've already heard that Gubra Biotech is our value driver. Gubra Ventures is our value accelerator. And what do we mean by that? What we've built at Gubra over the last 2 decades is not just a peptide platform. We've built a proven R&D engine with all the capabilities spanning discovery, translational pharmacology, preclinical and clinical development, but also a proven partnering platform. Building new tech is a very high investment endeavor. And at Gubra, we don't believe that we need or want to build everything internally. Instead, we will bridge external innovation to use what we already have internally to drive further pipeline value. So what you can see is what we're going to do is broaden the innovation footprint at Gubra with limited capital risk. So why do we believe now is the right time to launch Gubra Ventures? Successful venture creation requires much more than credible science. Many early biotech companies need to build from scratch all the capabilities that we already have at Gubra today to advance an interesting scientific idea into the clinic. We already have discovery. We already have deep expertise in core therapeutic areas. We understand how to turn a molecule into something that's clinically developable. But importantly, we also have a very strong operational infrastructure. And that means we can focus incremental capital on experiments, decisions and the next milestones to create true value with what we already have today. And that's the core advantage of Gubra Ventures. So the strategic rationale has 4 parts. We will strengthen our innovation pipeline through external assets and venture creation. We will be able to expand into new disease areas and also new technology areas or modalities beyond our current biotech and CRO focus. We will generate financial returns that can then be reinvested to support future growth at Gubra. And we will build and advance assets using our existing innovation and development engine. Now selectivity is really central to this model. I've mentioned we've looked at 150-plus assets to date in the last 6 months, and we've got a very deliberately high rejection rate. We must have a clear and active role in creating future value and quality and strategic fit matter much more than transaction volume. So how do we translate strategy into an operating model? We intend to create lean asset-centric companies that leverage our integrated capabilities to really accelerate this value creation. And we will start by bringing in assets and using Gubra functions early. So we do not intend to build large structures around assets, but rather use what we already have today to develop those assets further. At the early stages, we expect this to be a low capital need and a rather straightforward governance with the Gubra majority. So we will concentrate that early capital on the advancement of the asset to the next milestone. Then when we approach the clinic in IND-enabling, we will add a dedicated team as evidence and capital needs increase, and that will really depend on the skills and capabilities that we need. We still intend at this stage to be a Gubra majority venture, but we will start the outreach to selected investor partners. Moving into the clinic, of course, the capital needs will step up as well the needs within the venture. And here, we expect to bring in more capabilities in the ventures, but also selected investor partners to share the capital and development risk as we progress those assets forward to the key clinical proof of concept. At that point, we then see several routes to value creation. So we can take the route that Gubra has traditionally done to date, that's partnering. It also includes strategic transactions. But of course, there is a possibility we will continue ownership of these assets and progress those further within Gubra itself. The principle is consistent. We will match capital, capabilities and ownership of the asset to the needs of that asset. So what is it that we're looking for at Gubra Ventures? We have 3 levers. There's the stage of development. We have the modalities that we can work with and there's also the therapeutic areas that we want to focus on. The aim of Gubra Ventures is to maximize the value opportunity by creating synergies between our existing strengths and the external innovation landscape across all 3 levers. In simple terms, we see 2 real routes to create value. The first is Discovery Ventures. This is complementary external tech paired with Gubra's scientific and peptide platform through partnerships to expand StreamLine beyond our core therapeutic areas. The second approach, and this is where we're focusing the majority of our efforts at the moment is asset-centric. This is where we're looking for opportunities from development candidate stage through to Phase I that already have some level of technical validation and are therefore, to some extent, derisked either through derisking of the modality, derisking of the target or derisking of what we know about that therapeutic area. The intention is that we will diversify but stay very close to our scientific and CRO advantages. So in other words, we will diversify without losing focus. We will look in our core therapeutic areas of metabolic and cardiorenal, but we're also expanding into immunology and inflammation. So how do we see this expansion into new therapeutic areas? You've already seen a version of this slide before, and this is how ventures fits into that. So obesity, cardiovascular and renal metabolic disease remains our therapeutic area of core. We have deep expertise in this space. It's the foundation on which Gubra is built and that we are recognized for. We have strong leadership in this area, and we will continue to look for opportunities here, potentially expanding beyond peptides. Age-related functional decline is the logical expansion for new ventures as we leverage our increasing expertise and leadership in this area, and we're actively looking at opportunities in this space. But I also want to talk a little bit about immunology and inflammation and why we see that as another frontier for us to expand into. Immunology and inflammation is a very large therapeutic area. And despite the advances that we've seen with biologics over the last couple of decades, there's still a huge unmet patient need. There are emerging opportunities in this space as we understand more and more about the biology and underlying pathophysiology in part thanks to those biologics that have already led the way. We also see increasing interest in peptides in immunology and inflammation. For example, last week, we saw an incredibly high-value deal where Gilead acquired a very early Phase I asset from a stealth biotech called PepStar, targeting IL-23 receptor, a very well-validated target in I&I. And this is a peptide asset acquired for over $1 billion. That tells us that there is an appetite for peptides in I&I, and we're only just starting. Therefore, we see an attractive venture profile for I&I. This is emerging biology, a high level of pharma interest and subsequently investor interest and multiple routes to eventual downstream value. And I'd like to finish with 3 messages. We are going to use ventures to expand into new therapeutic areas and new modalities to create differentiated value for Gubra. We are going to accelerate the development of those assets through using our integrated capabilities that already exist today. And then we are going to repeat a scalable engine to create more shots on goal and multiple paths to long stream value. We reviewed more than 150 opportunities by maintaining that same high bar for the selection of those opportunities, and we'll be working with selected investor partners as those assets mature and the clinical capital needs increase. And our ambition is to launch at least 2 ventures by 2030. And this is why we call Ventures Gubra's Accelerator. In practical terms, it's a way for us to broaden our pipeline, diversify our potential future growth and apply our scientific platform to more areas of high unmet need. So I thank you for your time, and I'll now hand over to Trine.

Thank you, Zoe. I'm very excited to be here today. My name is Trine. I'm Gubra's CRO. Yes. So we're leading in the metabolic and fibrotic preclinical CRO industry. We have a proven track record of delivering profitable growth above market average and substantial value to our customers. This is not by coincidence. This is by design. So today, our customers are facing substantial challenges. Speed and innovation, drug discovery is accelerating these years and companies are competing to progress their drug discovery projects as fast as possible with a high-quality data as possible. And this is where the CRO adds value. We are Gubra's core value enabler. We provide deep scientific and translational expertise, reproducible disease models and advanced technology platforms, and we combine it with reliable, high-quality data and execution. This is really our value proposition to our customers, with our internal customers, the Biotech and Ventures and our external customers. Gubra was founded as CRO back in 2008. We started out in diabetes and obesity, and we built our strong scientific platform on this foundation, and this is the legacy that we are building our future on today. So we invested in obesity even before it was recognized as a disease. We're also part of the early efforts characterizing liraglutide. And so we built a strong metabolic platform. And in 2014, we spotted a trend in the market. In dialogues with our customers, our network, conversations with academia, publications and conferences, we spotted a trend revolving around fibrosis in the liver. There was an unmet need in the market and no available treatment. So we decided to expand from our stronghold in the metabolic into fibrosis and MASH. And in the beginning, I said our success is not built on coincidence, it's by design. Let me use MASH as an example of how we have built a successful playbook for creating differentiated, high-quality services and created market leadership. So as I said, in NASH, we started -- we spotted the trend early, and we invested ahead of demand. We developed a clinically translatable GAN DIO-NASH model. And very importantly, we built it ready to scale from the offset. To enhance speed, precision and data quality, we use machine learning to go from manual scoring of liver sections to AI-assisted histopathology. Also here, we were ahead of the curve, building AI and machine learning directly into our service delivery. We were first in the market with this translational disease model for NASH, and we built early commercial leadership and loyal customer trust. In 2024, the LITMUS Consortium also recognized the MASH model for clinically top ranked for clinic translatability. And it is now considered a golden standard model in the market. So this is the element of the successful playbook that we have. We invest ahead of demand. We expand from our existing scientific platform, translational platform. We apply cutting-edge technologies, and we gained first-mover advantage in the market. And it is with this playbook close to heart that we've also expanded into other disease areas such as, for example, the kidney area, IPF, lung fibrosis and most recently, sarcopenia and women's health. And I think it will be hard to find a company in the industry working in obesity, in NASH, in kidney diseases that have not worked with us over the years. And our ambition is to continuously innovate and expand from our strongholds to be ahead of the curve. And this model is really amplified by us using cutting-edge technologies. So as we venture into new disease areas, we always -- it's always accompanied by our strong technology platform in 2D and 3D imaging. And this is an example of our 3D imaging platform. We invested early also ahead of the curve in 3D imaging in 2017. And this technology is really part of revolutionizing the understanding of disease progression and drug distribution. So we started in the brain where we can visualize the entire brain at a cellular resolution to understand the treatment effects. And this is really important for our customers when making drug discovery decisions. We can map the drug distribution throughout the brain to really evaluate delivery technologies such as the blood-brain barrier shuttles, and also, we use whole-brain c-Fos mapping to show which brain regions respond to treatment, which is also especially helpful in obesity research. And so we transform complex 3D images into quantitative insight through automated analysis and this interactive visualization. And as Thomas was talking about previously, we also have used the technology in other organs, such as, for example, the sarcopenic muscles that you see here where we can measure muscle volumes within an intact hindlimb here being which muscles respond to treatment. We can quantify vascularization, nerve density and fibrosis to better understand changes in the muscle tissue and we can enable direct measurement of skeletal muscle changes. So this helps customers across therapies aimed at preserving muscle during weight loss or sarcopenia. Also here, I hope you can appreciate the beautiful 3D imaging of an entire ovary in 3D. We can count the [ ovarian ] follicles and to really assess treatment effects without sectioning bias. This technology is what differentiates us also in the market. It's our competitive edge. And while technology is differentiating us at Gubra, automation, digitalization and robotization is really what makes this differentiation scalable. So automation allows us to increase throughput and consistency without scaling cost and headcount proportionally. This is also an example from our 3D imaging lab where we have high throughput light sheet microscopy. We can handle data from more than 800 brains per month and fully automated staining and sample handling. This robot that we've built, it can also handle hundreds of samples at one time. In this way, we invest heavily in increasing throughput, quality and consistency while reducing manual labor. And this is enhancing the value for our customers and also for profitability at Gubra. So the commercial value of our entire capabilities combined is really demonstrated by customers choosing to work with us. We've worked with 17 of the top 20 pharmas hundreds of biotechs globally. We have trusted long-term customer relationships, high Net Promoter Score of close to 70, and we have demonstrated a historic growth above market average. Our ambition towards 2030 is to continue to grow from our strongholds at around 10% towards 2030. This decision also -- the strength also become increasingly important in volatile market conditions as we have seen in the past 12 to 18 months. But the market is returning and we see it evolving in our direction as well. So the market for services in metabolic and fibrotic diseases is still growing. Biotech funding has rebounded. More preclinical R&D is being outsourced towards 2030 and beyond. And there's the growing scientific complexity is also increasing the value of highly specialized services. And this is where our value proposition is extremely clear. We provide deep scientific, translatable expertise, reproducible disease models and highly advanced cutting-edge technologies and high-quality, consistent data and execution. So we're well positioned to -- we believe, to capture the growth that we foresee in obesity, in NASH, in kidney diseases. And we also believe that we can -- that these areas in sarcopenia and women's health represent attractive opportunities for us in the future. Both areas fit our playbook very well. There's an unmet need in the market, no or few available treatments. There's a growing focus in drug discovery on these diseases and in academia as well, and we have invested ahead of demand. There's a strong fit with our scientific and translational platform and scientific expertise, and we can combine it with our leading 2D and 3D imaging capabilities. So this is why we expect to have an attractive first-mover advantage in these 2 disease areas. Our ambition towards 2030 is to remain a leader in this industry. We've shown that we can deliver profitable growth year-over-year above market average. We've shown that we have the guts and the brains to invest early ahead of the back demand. We have the capabilities. We have the customer trust, and we have the strategy to scale this competitive advantage towards 2030. Thank you for your attention. And now I will hand it over to Kristian.

Thank you, Trine, and it's a pleasure to talk about one of my favorite topics, capital allocation. My name is Kristian. I'm CFO in Gubra. So you heard my colleagues speaking about where we play and how do we win and our strategy towards 2030. Capital allocation is really how to turn this strategy into action to create long-term shareholder value. What assets we prioritize under what conditions, what activities we fund. So it's a real pleasure to be here to talk about that across Gubra. So if you look across Gubra and starting with the Biotech discovery business here, I've graded the different business activities in terms of capital intensity. This is significantly less capital intensive compared to biotech development. Our discovery engine is where we develop novel differentiated peptides. We invest to master new type of peptide technologies like Louise talked about, macrocyclic peptides, oral delivery, long-acting peptides to really stay at the top of the peptide field. When we have assets, of interest, we progress them and we make data-driven decision. I will come back to that shortly because when Louise delivers something to Thomas' organization, the Biotech development, all we know is that costs will rise. So it's so important to only progress those assets, which will have high potential and weighing risk and return. So we'd rather, as Zoe also said, progress few assets rather than striving to build a large pipeline. So very selective in our choices and data-driven decisions. The ventures is essentially an extension of the Biotech business. We want to have more shots on goal, more biotech assets in development. But importantly, the venture is a vehicle to progress assets but with limited capital at risk. So essentially, we can put an asset in an asset company, get external funding at the project level and have the ability to progress more assets without committing too much capital. The CRO business is a service business. So in terms of capital intensity is fundamentally different. There we invest to develop new service areas, new technology areas, as Trine talked about in the 3D imaging field, opening up new areas like sarcopenia, women's health, where Gubra invest ahead of everyone else. So we are willing -- when we have a conviction that we think an area where we can master and we think demand is there, we're willing to invest to broaden out our service catalog of offerings so we can remain the preclinical specialist and the go-to place for preclinical tests. The biotech business, everyone that has worked in the biotech business knows that the capital requirements increase alongside the development stages. So in order to drive the R&D efficiency, it's so important to make all development decisions based on rigorous data. So whenever we progress an asset, we also have a lot of assets that do not pass the bar. So we have this failing fast concept. So whenever we're looking at the assets at certain development stages, has some on whereas others will not progress because again, the capital commitment, the capital requirements increase significantly and especially as you approach and go into the clinic, it's so important to be selective. And as Markus talked about, we want to drive our assets to pre -- sorry, clinical proof of concept, and we want to make sure we have really strong assets that we enter when we enter the clinic. So you can think of us as an asset portfolio manager. We look at the assets and we choose the assets we want to fund and proceed. Of course, a really great example is the amylin asset. That project started in 2018 and starting working with the molecule and ensuring we had all the properties we would like from a peptide. In biotech, you need to have patience. So it takes years to progress the assets and the amylin made it through various development stages, whereas some other ideas did not because we have high bars and those assets will progress, they have the properties we would like to see from our peptides. We started the Phase III back in '23. And then a year later, we had the first clinical results. And just a few months after that, we made the landmark deal with AbbVie of USD 2.2 billion, including a very sizable upfront of USD 350 million. So here, we turned an investment of around USD 25 million into USD 2.2 billion. So quite a high return on invested capital. And we also returned funds to shareholders also last year in terms of an extraordinary dividend. So a very good blueprint case in how you should expect and how we want to develop our assets and that we are very selective among those we progress. The amylin, ABBV-295 is not the only strong asset we have partnered out. We also have the triple agonist as Louise and Thomas talked about, the Hemab collaboration, the Amylyx collaboration and the Camurus collaboration. So a number of recurring, hopefully, also in the future recurring revenue streams that provide us with good funding to fund the investments in new R&D assets. Just repeating a little bit what Zoe said on Gubra Ventures. So here, we have the ability to get really interesting science without taking too much risk. So we can in-license an asset, put it in an asset company, get external funding at the company, asset level, project level and then Gubra will contribute with capital, and we will also invite investors to that project. So it's really a way to accelerate our biotech business without taking too much risk. It's a way to get more shots on goal because we're very mindful of having capital discipline. And this is a vehicle that we can use to drive more assets in parallel without, again, taking too much risk and too much capital commitments. CRO business. As I said, in terms of capital requirements, it's fundamentally different compared to the other areas. This is a service business that ever since the start has been profitable and growing. So a very asset-light business and very high return on invested capital. So over the last 10 years, it has generated around 14% revenue growth. That's double up compared to the overall industry and profitable. And that's part of having high customer trust. We service 17 out of the top 20 largest pharma companies plus a vast number of biotech clients and they return to Gubra to get the preclinical results to make their next development decision. So we stand out with our quality and our speed. So Trine talked about Gubra investing ahead of the curve. We go into areas which we think we can master and we get the first-mover advantage. The fatty liver, the MASH field was one example, and we pioneered also in 3D imaging technologies. Now we are looking into women's health, sarcopenia, areas we think we can master and where we can build a strong position as a preclinical specialist provider, be provider to use for preclinical services. Just a few words on our solid financial foundation. So we have a strong balance sheet. At June 30 this year, we had around $140 million in cash. That is before the milestones from AbbVie, the $50 million and the $10 million (sic) [ EUR 10 million ] from Boehringer. So a very strong financial foundation. The CRO business continues to generate recurring cash flow over the years. So that's another source of funding or cash flow. We have the partner programs, the existing partner programs, and we also have the potential, of course, to enter into new partnership providing recurring revenue. So multiple revenue streams across the company that gives us financial flexibility to execute our strategy towards 2030. So summing up, it's really important that we invest where we have an edge, where we have a scientific competitive edge, that's where we prioritize our capital allocation. And we selectively choose assets to progress and fund them. And equally important, we deselect assets that doesn't live up to our bar. And we fund it progressively. Each and every asset in the biotech business needs to live up to our rigorous requirements to what we want to see in a peptide. And we also have the venture unit as a possible vehicle to accelerate our biotech business without taking too much capital at risk. With that, I leave the field open for questions.

Thanks a lot, Kristian. So yes, we will be joined by Zoe, Trine as well as Markus again. And yes, same as before, I'm very happy to address your questions. So please raise your hand if you would like to ask a question. We have a mic that we pass along here. I think perhaps we should start here with Theodora.