It's a pleasure being here today. So Alligator Bioscience is a clinical stage, phase III ready company. We're situated in Lund, listed on NASDAQ. Our lead asset is a best-in-class CD40 monoclonal antibody that we are developing for first-line metastatic pancreatic cancer. I'll show you some of the data today. I'll talk a little bit about the regulatory status. The drug is phase III ready. And then I'll talk somewhat more about what lies beyond pancreatic cancer for mitazalimab. And then I'll touch towards the end to some of our other pipeline assets. So if we start talking about pancreatic cancer, metastatic pancreatic cancer, it's approximately 85,000 patients that are affected with this annually. The survival rate, as you can see, is pretty bad. It's a horrendous disease. Think about Patrick Swayze, Steve Jobs, even Sven-Göran Eriksson. We all know people that have been affected by this disease, maybe a little bit more personally than those three I mentioned there. For the patients, there's primarily only chemotherapy as an option. And for these patients, so-called median overall survival of less than a year can be expected. And why is that? That is, first of all, because the tumor is very aggressive. These chemotherapies have severe side effects, and they also do not activate the immune system. Hence, the body is not able to build a long-lasting defense against the disease. However, when we combine these chemotherapies, and in this case, a combination called FOLFIRINOX with our drug mitazalimab, we can see that our 24-month survival is more than tripled compared to chemotherapy alone. And we can see that we are able to do this without adding any significant side effects to the patients. If you look at this somewhat niche market, you can see that we can probably treat approximately 25,000 to 25,000 patients in the U.S. and Europe every year, which gives this drug a blockbuster status. Beyond that, there's, of course, also significant interest in the drug outside pancreatic cancer and other solid tumor indications, but more about that later. Just very briefly about the molecule, it's designed in Lund. It's manufactured in the U.S., and it's probably going to be used globally once it's approved. It's a monoclonal antibody, as I said, and it's designed to specifically activate the immune system without giving severe side effects outside of the tumor. I'll show you a couple of slides a little bit later to show that that is exactly what the drug does. We have done a phase II study in treatment naive patients, meaning that these are the patients, one, they're getting diagnosed with metastatic pancreatic cancer. The first drug they actually see is mitazalimab, and then they get treated with chemotherapy and mitazalimab at biweekly cycles, so the patients don't have any more hassle than they would have if they only received chemotherapy. If we look at, that must be your left side of the screen here, this is a so-called waterfall plot where the individual patient's best tumor response is depicted, and you can see that most of the patients are either green or orange, meaning that they have some sort of clinical benefit of mitazalimab. If you look carefully here to the right-hand side of that graph, you can see that there's actually three of these patients that receive or get full remission of the target lesion, meaning that they are more or less tumor-free. If we look at the right-hand side of the graph here, that's exact same patients. Now we add a time horizon to it. I told you before that you, as a patient, could expect around 11 months of survival. You can see that we have quite a number of patients that go beyond 18 months, 24 months, and even 13 months, meaning that these people actually live more or less, not all of them tumor-free lives, but they live with their tumor under control for sustained periods of time. Data that, of course, have caught our interest, enthused us, and also enthused the people that we work with and the pharma partners that we discuss with as well. Then a very fundamental question to all that we are doing here is that we really want to be able to explain our data. We want to put a very strict connection between the mechanism of action, the hypothesis we had, and the clinical outcome. So what you see here, again, on your left side is a diagram showing that in patients that respond to mitazalimab, that if you look at that tumor before treatment and after treatment, we can very clearly show that the genes that are mostly upregulated in these patients are the genes that regulate T cell and other killer cell activation, meaning there's a direct link between mitazalimab and the outcome for these patients. If we take this analysis actually a little bit further and then look into the patients only 24 hours after they have received their first dose of mitazalimab and simply take them in two equally big piles, so to speak, and say the patients that respond the most versus those that respond the least, and then look at their survival, we can see that the patients, if I can, I could not make that happen. If we look at the patients, that doesn't work. In the green there, those are the patients that respond the best, and you can see that they almost survive twice as long as those patients that survive or have the least response to mitazalimab. Very clear evidence that the drug works and that there is a direct correlation between the drug working and the individual patient's survival outcome. So when we look at the drug in comparison to existing chemotherapy, we can see that we extend the lifetime or expectancy on the broad population with approximately four months. But when we look at the patient's probability of being alive after 18 or 24 months, you can see that we more than double and in the later time point actually triple what you can expect with chemotherapy alone. And as early as or as late as yesterday, we announced the last data set from these patients, the so-called 30 months readout, where we showed that at this very extended time point, there were still 20% of the patients alive here. So truly a remarkable set of data. That has also made us ready for the next step. We believe that the data that we show can translate directly into phase III success. The patient population in phase III is going to be the same as in phase III. The endpoints are going to be the same. And we will also have the identical treatment schedule in phase III. So we believe TEAD offers success there. And both the FDA and the European authorities have approved the phase III protocol, and the material that are going to be used in these patients is ready in the warehouse. So what happens next for Mitazalimab? Several times today, we have discussed the financial hardship of the industry. That has also been clear for Alligator. So how to go about that, be able to continue to build in value in your program without repeatedly asking investors for money? So what we have done over the last couple of years is that we have engaged extensively with the key opinion leader or the physicians' community globally. And right now, this means that we are kicking off a program of so-called investigator-initiated trials. So that is phase I and phase II studies where Alligator provides mitazalimab and where the investigators do the trial supported by grants or by government grants. And notably, you can see that we have a couple of studies ongoing. And then next year, sometimes during the second quarter, we expect to start a big phase II, a randomized phase II study with more than 100 patients done in France and sponsored by the French government. This does two things to us. It validates our view that the data from pancreatic cancer is excellent and that they can be transferred to similar solid tumor indications. And it also allows us to continue to build value in the program and get the drug hopefully approved in indications beyond pancreatic cancer. I'll skip this just to let you know we have drugs in preclinical development as well that it builds on what we have done with mitazalimab with a little bit more of additional innovation height. One of them is a bispecific antibody called 4066. We recently published data on this. It looks tremendously good. And then finally, before Cecilia comes up here, I just want to mention that in addition to this, we have a legacy molecule called HLX22, which is a HER2 monoclonal antibody. It's outlicensed to a Chinese company, and it's currently in phase III development in HER2 positive gastric cancers. And we expect this molecule to provide significant financial upsides to Alligator in the early 2030s, so in a handful of years. Thank you. The first question was actually about that, about the HLX22 and how you see its role in what you mentioned there. How important will that be for generating future, alongside mitazalimab, of course, but how important do you see that kind of part of the program? So I mean, of course, any steady income is. I was going to say any money is good money. is, of course, what we strive for. If the drug gets approved in the two gastric cancer indications, we definitely believe that it's going to be a blockbuster and that that will provide somewhere between $15 million and maybe $40 million to Alligator on an annual basis. And I think most biotech companies would sort of be happy for that steady income. So definitely. But it's also, of course, important to remember as an investor that we have no direct involvement. There's no cost. There's no say. And we are only reporting. Their results. Their results. Yeah, absolutely. With the Croco-Bill, which is the new study into biliary tract cancer, how important would you say it is for you to demonstrate that mitazalimab has potential beyond pancreatic cancer? Yeah, but I guess we heard today that antibodies, and especially, for instance, Keytruda is approved in, I think, more than 40 indications. And I think mitazalimab, not that it will be maybe approved in that many indications, but the nature of the molecule and the mechanism of action, the safety profile that we have demonstrated sort of makes it a good add-on in many, many diseases, whether it's in pancreatic and biliary as combination with chemo, or whether it's with a PD-1, for instance, or a PD-L1 in other solid tumors. So that is, of course, an important way for Alligator to expand the clinical and hence the commercial potential of the drug. And in a minute, you're going to ask me whether that is something potential partners would be happy about. And yes, of course. We've done this too often, sir. Of course it is. And you're going to ask me, but I can post that question myself. No, of course they are. I mean, this is, and let's just stay in here, it's basically the French government paying a full phase II study to the value of, if we were going to do it, maybe $40 million. So that is, of course, a tremendous thing that we get for free, more or less. Now let's turn to some of the more medical questions. Someone is asking why the drug is given intratumorally, which is not a word I say every day. So in the phase II study and in the solid indications or the solid tumor indications like biliary tract we just discussed, the drug will be given as an IV infusion. Then we have a few specific indications, like two of them where it's intratumoral. One is an oral premalignancy. So your doctors see that you have sort of a pre-tumor in your oral cavity. And there it's most prudent to give it as an intratumoral rather than a systemic treatment. And the other one that we are running at University of California San Diego is a surgical method where the primary tumor is actually isolated, and then it's sort of zapped with electricity. So a new way of tumor ablation. And there when you have the tumor in front of you, it's, of course, also smarter to inject the drug directly in the tumor. But the main route of administration by far the majority of indications will be infusion. With that, I say thank you so much. Thank you, Cecilia. Yeah, thank you.