Alligator Bioscience is a clinical-stage, phase III-ready biotech company. Our lead asset, mitazalimab, is a best-in-class CD40 agonist that we are currently developing in first-line metastatic pancreatic cancer with some very encouraging data, especially long-term survival data. I'll show you that in just a second. Based on this data, we have established a clear path to approval in the indication, both in the U.S. and in Europe. In addition to this lead indication, we are building the clinical footprint and potential clinical benefit and commercial case for mitazalimab through a number of so-called IIT programs. I'll talk briefly about that a little bit later. If we have time towards the end, is this better? We will talk about the follow-up program ATOR-4066 and also a molecule called HLX-22 that is currently out-licensed to a Chinese company, Henlius. Metastatic pancreatic cancer, I'm trying here to summarize a horrific disease in just one slide. We have approximately 85,000 cases in the EU and the US on an annual basis. As you can see, the prognosis for these patients is really, really bad. Even in first-line setting with chemotherapy, which is available to most of the patients and the only opportunity for most of the patients, you can expect a median overall survival of between 8 and 11 months. These chemotherapies are associated with severe and dose-limiting toxicities that are really sort of tiring out the patients. We've not seen any improvements in the treatment landscape over the last 15 years. What we can see when we add mitazalimab to these chemotherapies is that will triple your ability or your probability of being alive at two years after diagnosis, not only once, but actually three times. We do not add any significant toxicity on top of chemotherapy, which is important in this indication. We believe that the 22,000 patients that are addressable in first-line setting actually means that mitazalimab have at least a single blockbuster potential. What is the drug? The drug is a monoclonal antibody. It is designed here in Lund. A safe technology bet, no surprises there. My very clever colleagues have optimized the molecule or designed the molecule in a way so it gives optimal safety and optimal efficacy. As I said, that is important when you are developing combination drugs with these chemotherapies that you can manage the safety. What do we actually do in terms of how does the drug do in terms of clinical data? We have conducted a phase II study. We're just winding it down, closing sites. It fulfilled its purpose. As you can see on the right-hand side of the slide, we do not see any of the safety effects that are normally associated with this class of drugs. We do not add any significant safety signals on top of the chemotherapy. That, as I said, is very important. How do we do on the efficacy data? First of all, look on the top. You can see in the median, if you get mitazalimab on top of chemotherapy, we extend your or the median overall survival with approximately four months. If we look at the lower part of the curve here, and I think that's really where the drug shows its true differentiation. Let's see if we can point with this one. We cannot. If you look at the bottom here, you can see that 18 months after diagnosis, your life expectancy or your probability of being alive with chemotherapy alone is around 19%. We double that by adding mitazalimab to your treatment. At two years after diagnosis, you can have approximately 8%-10% probability of being alive. We triple that when we add mitazalimab to your first-line therapy. You can see after two and a half years of diagnosis, no patient being alive has been reported. We still have a fifth of the patients being alive in the study. A significant long-term survival effect for these patients. If we take a little bit closer look at these data on your left, a so-called waterfall plot where we depict the tumor reduction on a per-patient basis. Just one takeaway here is that if you look to the right-hand side of that graph, you can see that we have three patients with complete reductions or complete remissions of their target lesions. This is something you very, very rarely see in this indication. If you look to the right-hand side of this slide, you'll see the spaghetti plot. The same patients just now with a time parameter on the x-axis. What you immediately see is that you have quite a number of patients that are actually still on treatment after two, two and a half years. Several of these patients have actually been completely rolled out of chemotherapy, meaning that they are on mitazalimab alone, which is also fantastic. Not only do we keep the patients alive, but we actually let them lead a much better life than they would do if they were also on chemotherapy. How does the drug work? We hypothesize that that's the idea with this drug, that it stimulates the immune system primarily in the tumor. Here is some data that we recently announced or published in Cell Reports Medicine, where we on the left-hand side looked into the tumor of patients before mitazalimab treatment and after patients that responded to treatment. Those of you who are close enough to read it can see that those gene signatures that actually increase are those that are associated with both myeloid and T cell activation within the tumor, i.e., the proposed mechanisms of the drug. If you look at the right-hand side of the slide, we took this analysis even further and divided the patient 24 hours after their first dose of mitazalimab and said, those who have the highest T cell response in the blood versus those that had the weakest T cell response in the blood, how do they fare in terms of their survival? I think what is obvious, even if you sit in the back here, is that the red curve, which are those with the lowest response, fare like you would expect with chemotherapy alone, where those patients that actually do mount a significant T cell response after mitazalimab have a median overall survival that is double that of the patients with a lower response. A very, very clear mechanistic chain of evidence from the mechanism of the drug to its ability to activate T cells in the tumor and its effect on the long-term survival of these patients. This data has led us to a stage where we've agreed the phase III design with the regulators. We have agreed all the MUCHA, the FAE, the dose, the study design, so on and so forth. We are just now at a stage where we are negotiating with partners on how to get this trial going in the nearest future. How do we expand the clinical footprint of mitazalimab without really spending too much money doing so? Over the years, it has become clear that the data that I shared with you before has really sort of spurred a lot of interest in the scientific community, in the clinical community, not only in pancreatic cancer, but also in other clinical indications in the oncology field. What we have in sort of a deliberate strategy, we have engaged in a number of so-called investigator-initiated trials, i.e., that local hospitals, large clinical networks are going to conduct clinical studies with mitazalimab where Alligator only provides drug that is already sitting in a warehouse. We are paying for pharmacovigilance and some insurance. The real trial cost is paid by various grants. We have announced some of those. I just want you to focus on the middle line there that says biliary tract cancer. This is a randomized phase II study that will be started next year, a study that is based on a grant from the French government system. On the bottom here, we have two other IITs that will start shortly, we hope, at East Coast Ivy League universities in the U.S. with a number of world-renowned clinicians. More about that once we have dosed the first patients in these trials. Very briefly, mitazalimab, strong efficacy data, strong safety data, clinical path, regulatory path to approval. We are really moving the drug forward. Let's jump over this. In interest of time, I have exactly nine seconds to talk to you about HLX-22, which is an old legacy molecule that Alligator has had on its books for a long time. It's currently out-licensed to a Chinese company called Henlius and is both in a couple of phase II and a phase III global study in gastric cancers. Why do I mention this? Alligator is eligible to a part of the financial upside once the drug is on market. We believe that this drug has a commercial potential for Alligator to give royalty revenues in the range of SEK 150 million-SEK 400 million on an annual basis starting in the late 2020s, early 2030s. With those, the full timeline here on the full pipeline. I think we have a young lady here who is eager to ask a couple of questions. With that, Cecilia. I'm allowed to speak. You are allowed to speak, yes. Thank you very much, Søren. You're allowed to applaud as well. You skipped the ATOR-4066 slide there. And as it just happens, I have a question about that. Someone wants to know how it fits into your long-term strategy and how does it complement mitazalimab. Yeah. This is a CD40 bispecific. That is sort of the next-level innovation after mitazalimab. It can do the same, and then it can do much more. It is safer. It is broader immune activating. We believe that it will also be used in a specific manner. It is more like precision medicine. This fits very nicely. I would have loved to push this forward, but we have had to sort of limit our scope and pipeline investments due to the general financial macroeconomics. Once mitazalimab is moved on in development, hopefully with a partner, this is the next clear step for Alligator. It is based on a technology called Neo-X-Prime, which will allow us, and potentially a partner, to do similar molecules addressing different tumor specificities. For now, it's resting, but you have it. We are thinking about it every day. Yeah. Turning back to mitazalimab, could you elaborate a bit on what reactions you've had from potential partners when you're out talking to people? What do they say to you? Yeah. I mean, first of all, I think everybody aligns on the depth of the data on the unmet medical need. It's clear that the indication has been, over the years, very, very difficult to tackle. The patients have very, very poor prognosis and many, unfortunately, what can we say, disease early in the trial. It has been a challenge. No, just to. Development point. No, it's difficult simply because the patients in the studies die. From a medical point of view, it's a really, really high bar we need to go over. I think the phase II data definitely show us that we can. That means that there's a number of companies that is out of it. We're moving ahead with this. We've announced that we'll raise money soon. I'll maybe stay a little bit shy on being too specific here. I can tell you we are moved further than we had last time you asked the question. Yeah. The next time I ask the question, you'll be even further along. Hopefully. Hopefully. Until then, did you? No. I think in terms of timing, and I think there's agreement around that in the networking break. We're just home from SITSI. We're home from BioEurope. The investor sentiment and the pharma sentiment is slowly coming back. We hope and believe that the fact that we have now sort of putting a bow on the phase II study coincides nicely with increased sentiment in pharma and general life science investment. Until next time, Søren. Thank you so much. Thank you.