Hello and welcome to Alligator Bioscience's R&D Event, 19th of August 2025. My name is Greta Höög, the IR and Communications Manager at Alligator. Shortly, our CEO, Søren Bregenholt, will introduce you to our colleagues who will take you through an R&D update, after which they will be happy to answer any questions you may have. These questions can either be posted in the Q&A function of the webinar, or they can be emailed to ir@alligatorbioscience.com. As you know, Alligator is a publicly listed company, and I'd like to note that today's presentation may include forward-looking statements. Please refer to the disclaimer on this slide, which applies to the full presentation. With that, over to you, Søren. Thank you, Greta, and once again welcome to this Alligator R&D update here on August 19, 2025. If we can have the next slide. What we'll do today is that we will cover some of the background of mitazalimab, our lead candidate, our phase III ready candidate. We will share some of the clinical data, some new data that you have not seen before, and we'll talk about lifecycle management opportunities and how we will utilize so-called investigator-initiated trials to expand the clinical application of mitazalimab. After having discussed mitazalimab, we will talk about HLX22, an innovative HER2 antibody that Alligator has a stake in the future royalty stream. As Greta just alluded to, we will end with a Q&A session. If I could have the next slide, Greta, I want to introduce my colleagues here with me today. I have our Chief Medical Officer, Tom Moore, with an extensive background from Global Pharma and drug development in these companies. We have Peter Ellmark, our Chief Scientific Officer and inventor of mitazalimab. Finally, we have our Medical Science Director, Yago Pico de Coaña, and Yago has been instrumental in driving the phase II study with mitazalimab in first-line metastatic pancreatic cancer. Yago will lead you into some of the clinical data on mitazalimab. If we can have the next slide, just to remind ourselves that Alligator is a phase III ready biotech company. We are developing best-in-class immunotherapies, first and foremost in metastatic pancreatic cancer. Here, our lead asset, mitazalimab, has demonstrated solid clinical efficacy and long-term survival benefit in this indication with high unmet medical need. Based on this, we have created a clear path to approval in the indication with both the U.S. FDA and European authorities. As we'll discuss later today, there is a number of development opportunities beyond pancreatic cancer that we will start exploring in the coming period. In addition, we have developed a drug called ATOR-4066, which is a bispecific follow-up molecule to mitazalimab that we hope to be able to develop more targeted in the years to come. Finally, as I said, the HER2 monoclonal antibody HLX22 represents a potential future financial upside to Alligator. If I could have the next slide, Greta, this is a representation of the pipeline, as you see it, with several late-stage programs that represent significant opportunities for continued value creation in Alligator Bioscience. The next slide will focus on mitazalimab. We will spend the next 25 minutes on this drug. mitazalimab is a CD40 monoclonal antibody designed for an optimal therapeutic window, having the best balance between efficacy and safety. So far, we have generated positive phase II data in pancreatic cancer. As we already said, a lot of lifecycle management opportunities we believe are based or flow directly from these positive data, whether that is in combination with chemotherapies, with vaccines, or with checkpoint inhibitors. If I could have the next slide, just as an introduction to metastatic pancreatic cancer, it's an indication with a significant unmet medical need. It's expected to be the second largest cause of cancer death in the U.S. in the coming decade. Currently, there are around 85,000 patients diagnosed with metastatic pancreatic cancer in the U.S. and the major European countries. The five-year survival rate for these patients is well below 5%. Definitely an unmet medical need there. For most of these patients, chemotherapy is the only option. You can expect a median overall survival of around 8- 11 months. These chemotherapies are associated with severe and often treatment-limiting side effects. Basically, we have not seen any significant improvement in clinical outcomes over the past 15 years. We believe that mitazalimab and the data that we have shown so far and will share with you today really have an opportunity to change clinical practice in the disease. What we see is that the drug, in combination with chemotherapy FOLFIRINOX, triples the 24-month survival rate of these frail patients, and that is really without adding significant side effects onto the chemotherapy. These two things in combination really put mitazalimab at the cusp of being a potential game changer in this indication. With these words, I will leave the stage to my esteemed colleague Yago to tell you and bring you through some of the key results from the phase II study. Thanks, Søren. If you can give me the next slide, please. Okay, so you can see here is an overview of the whole OPTIMIZE- 1 trial, which was initially a two-part trial consisting of a phase I-b and a phase II part. In the first part, two doses were assayed at 450 μg/kg and 900 μg/kg for safety. Once the higher dose was deemed safe, we moved on to part two, where we completed several milestones, including a fertility analysis and a primary analysis. After our primary analysis, which was successful, we have also delivered different readouts, which you will see the data from the last one, the 24-month follow-up that was released in February 2025. Additionally, during the trial, FDA asked us to further characterize the lower dose before establishing a consolidated phase III dose. That's what we called part three, where we actually recruited additional patients at this lower dose. You could give me the next slide, Greta. The safety-wise, the main message that OPTIMIZE- 1 has yielded is that there's a good safety profile, which is consistent with modified FOLFIRINOX, meaning that there are no signs of added toxicities. On top of that, one of the concerns from first-generation CD40 antibodies was the appearance of cytokine release syndrome. We haven't seen any of those events or either liver toxicity. As I said, these were associated with CD40 agonists or first generation. Basically, we are seeing a safe and manageable combination treatment of mitazalimab with the chemotherapy backbone FOLFIRINOX. Can you give me the next slide, please, Greta? Now, actually, these two panels, you can see here on your left, is the waterfall plot, which shows the best reduction in time for each of the tumors and each of the patients. On your right is a follow-up in time of these tumor reductions. If we want to focus on the left panel, you can see that there's been a considerable number of responders. This means patients that have had responses below 30% in reduction in their tumors. These responses, they're also very deep. By deep, we mean that a very big number of patients went below 40% reduction. The five arrows you can see in these plots are symbolizing patients that remained on treatment. Of these patients, all the three best responders, you can see them to your right, had a 100% reduction in non-target lesions. One of them had a 100% reduction in non-target and target and non-target lesions. We are seeing that mitazalimab, in combination with modified FOLFIRINOX, is giving us very deep responses. There's a strong reduction in the tumor volume in these patients. This reduction is not punctual. As you can see on your right panel in the spire plot, these reductions are consistent over time. Chemotherapy is expected to give fast and quick reductions in tumor volume in the initial start of the treatment, especially a chemotherapy backbone as aggressive as FOLFIRINOX. What is remarkable here is that these deep responses not only stay, they're only deep, but they stay down in time. We're keeping these patients on treatment for a long time. A lot of patients, a large number of patients have been on treatment for more than a year, more than 18 months, and as you can see here, even more than two years. The important thing, again, not only of these five patients that remain on treatment, it's not only that they're still on treatment, as I was last cut off, but two of these patients have been on monotherapy for one and more than two years each after having stopped any chemotherapy backbone. We can see that the responses are not only deep, but they're durable as well. With that, you can give me the next slide, please, Greta. When I'm talking about durable, we can translate that into duration of response. Duration of response is measured from the point that a patient has a radiological response, meaning a reduction in 30% of their tumor lesions, until the patient has to be stopped treatment. Historical controls have shown that for FOLFIRINOX, this is around six months, 5.9 in the FOLFIRINOX trial. In the OPTIMIZE-1 trial, we've seen these numbers skyrocket, even doubling those expected from the historical control to 12.6 months. This is actually quite remarkable, meaning that these patients, the patients that respond, benefit from the therapy, from the treatment for more than a year on median. In addition to that, we're seeing that the median overall survival, the definitive endpoint, is superior to that observed in historical controls with 14.9 months when compared to the 11.1 months. Finally, in the different readouts that we've been carrying out and with mature data, we can see that the patients not only have anomaly median overall survival, but the 18-month and 24-month overall survival rates are clearly superior to that of historical controls. You can see that at 18 months, we can compare our 37% overall survival rate versus 19% in FOLFIRINOX. In addition to that, even more surprisingly, is a two-year survival rate, which is 29% in the OPTIMIZE-1 trial versus the reported 8%. In summary, we can say that the responses are not only deep, they're durable. This means that patients stay on treatment longer because the treatment is safe, and also that this leads and translates into a better overall survival. With that, I want to add that we will be delivering a final readout in Q3 this year, where the trial completion data will be released. If you can give me the next slide, please. In addition to the nominal comparisons that I was showing in the previous slide, we've also analyzed by indirect treatment comparisons the data from OPTIMIZE-1, the OPTIMIZE-1 trial, and compared it to a pool of historical phase II and III data where the trials where the chemotherapy regimen was a FOLFIRINOX or the recently approved NALIRIFOX. You can see from this data that we presented at ASCO earlier this year at ASCO GI. The OPTIMIZE-1 trial comes out ahead of this pool of data with a clear benefit in overall survival. You can give me the next one, please, Greta. Finally, I didn't want to end this report without sharing some of the dose comparison data, dose characterization. As I mentioned in the first slide, we were asked by FDA to further characterize the lower dose in order to comply with their Project Optimus guidelines. You can see here from the data that even with a very short follow-up, the 900 μg/kg dose is superior in all the endpoints that we tested to the 450 μg/kg dose. This means not only that we can use, and this dose has been endorsed by FDA for our phase III, but it also means that in our opinion, this exposure response correlation is hinting that mitazalimab is responsible for the good numbers in duration of response and overall survival that we're seeing. You can give me the next one, Greta. This is a summary just that you can see that we delivered a primary endpoint, a positive primary endpoint earlier in January 2024. We have done 18 and 24-month follow-ups. In all these data, as the data matures, we are confirming that the duration of response is more than doubling that in historical controls. We have extended median overall survival by more than 30%. We have fantastic overall survival rates at 18 and 24 months. This, combined with the fact that we've done indirect treatment comparisons, shows us that in a potential phase III, we are ready to go ahead and move forward with this phase III study, which will be using median overall survival as its primary endpoint. With that, I think I can move on to our CSO, Peter Ellmark, who will be talking about some of the biomarker analyses that are coupled with the clinical data that I just showed. Thank you, Yago. Thank you. We have performed an extensive biomarker study to analyze how mitazalimab treatment affects immune cells and the tumor microenvironment. What we can show is that mitazalimab-induced activation is associated with improved survival and clearly supports mitazalimab's contribution to the clinical efficacy that we see in OPTIMIZE-1. We are really excited about this data. It will be published shortly, so keep an eye out for the publication. I'm going to present some highlights here today. What you see here, what we can show is summarized in the figure here that mitazalimab activates immune cells in the periphery. These can then traffic to the tumor. Mitazalimab treatment results in degradation of stroma and reduction of fibrosis, and this sensitizes the tumor to chemotherapy and results in more immune cells infiltrating the tumor. Further, mitazalimab treatment results in activation of immune cells in the tumor microenvironment, and this in turn then leads to tumor shrinkage and durable survival benefits. We are going to have a bit of a look at the data. mitazalimab does not only activate immune cells in the periphery, but this immune cell activation is actually associated with clinical and predicts clinical outcomes. What we show here in this slide, and what you can see to the left, is activation of T cells in the blood following the first dose of mitazalimab. This is why we know that this is mitazalimab-induced activity only. It's before any chemotherapy is given. If the patient responds by having more proliferating T cells in the blood, they almost double their overall survival. Mitazalimab-induced immune activation before chemotherapy is associated with longer OS. This confirms the mode of action of mitazalimab and supports the role of mitazalimab in the clinical activity data that Yago was showing you. We are not only activating immune cells in the periphery, but we can also see that mitazalimab triggers activation of immune cells in the tumor. What we show here is data obtained from patients that respond to treatment. What we have done is that we have looked at gene signature or gene pathways that are activated after treatment. What you can see is that mitazalimab induces activation of T cells and myeloid cells, which confirms mitazalimab's mode of action and shows that we have achieved what we set out to achieve. These effects are, as I said, it's responding patients, so these effects are associated with shrinkage of the tumor. In addition to this, we can show in the next slide that we have identified a new baseline fibrosis-related gene signature that identifies mitazalimab responders. In this study, we have looked at the biopsies of the tumors in patients before treatment. These are baseline patient biopsies. We then looked at the immune signatures in these patients, and we identified pathways that were related to normal survival. The one we found here on the top is the extracellular matrix organization pathway. This is something related to fibrosis and stroma. Patients that have a high expression of these genes are doing much better, as you can see in the middle graph, in terms of overall survival. This was a really exciting finding because this is directly linked to the mode of action of mitazalimab. As you can recall, mitazalimab acts by activating macrophages that degrade stroma. This data really means that if you have more of basically the target of mitazalimab, you will do better. This data not only provides a potential biomarker, but it also further supports the contribution of mitazalimab to the clinical activity that we see in OPTIMIZE-1. I can summarize the biomarkers by clearly stating that mitazalimab-induced immune activation is associated with improved survival. We have identified a new baseline gene signature. Taken together, this biomarker data shows how mitazalimab contributes to the clinical activity and efficacy in OPTIMIZE-1 and informs on potential patient selection strategies for future studies. With that, I would like to hand it over back to Søren. Thank you, Peter, and also thank you, Yago, for taking us through the phase II data, the excellent survival benefits that we see in patients, and Peter, for very clearly linking the mechanism of action of mitazalimab not only with the pharmacological response in the patient, but also linking it directly to the superior clinical outcomes that we see in these patients. One thing is to have clinical phase II data and being able to explain your mechanism of action to move forward to phase III. It's, of course, also important that you have material of the right quality and in the right quantities available. This is not something that we have talked a lot about, but over the last years, the dedicated Alligator team has worked to develop a novel phase III and commercial GMP manufacturing process. I can proudly say that we have done so together with Thermo Fisher, now at a commercial 2,000 L scale, cost-effective, and as industry standard, something that really supports the continued development of mitazalimab. we have also manufactured both the drug substance, but more importantly, the drug product, and now have a full supply to support the future phase III study in first-line metastatic pancreatic cancer. Together with all this, the team has had a proactive regulatory dialogue, both with the U.S. authorities and also the European authorities that have de-risked also the manufacturing path to approval. Not something that is often discussed, but a cornerstone in a company's and Alligator's ability to move mitazalimab forward. If we take the next slide, we can see that we have also been working diligently on the regulatory side of things. We now have a safety database with more than 200 patients being treated with mitazalimab in total. As we have already discussed, the drug has orphan drug designation in the U.S. and also in Europe. During the first half of 2025, we have finalized our regulatory interactions, our pre-phase III regulatory interactions, both with FDA and EMA. The conclusion on this, as we believe we have communicated several times, is that the agencies have endorsed 900 µg as the phase III dose, that the phase III start design is acceptable for both agencies, for regulatory submissions in both agencies, the non-clinical program is adequate and completed, and as I just discussed, the manufacturing and the release strategy has been endorsed with both agencies. In terms of phase III readiness, we have pushed mitazalimab or advanced mitazalimab as far as we can without really pushing the big green button to officially start a phase III study. What does the phase III program look like? What is the trial outline? To talk a little bit about that and also discuss our indication expansion efforts, Tom, please join me and... Sure. Thank you. First, the phase III study. This is a very straightforward phase III design. It's a one-to-one randomization between an experimental arm, which is mitazalimab at the FDA-agreed dose at 900 µg/kg, plus standard and FOLFIRINOX chemotherapy compared to FOLFIRINOX alone as the control arm. Treatment is until progression. The primary endpoint, as is standard for many phase III oncology studies, is overall survival. The study would undergo an interim analysis. This would function both as a potential futility and also as a potentially early stop in the event of very strongly positive data, or the study would progress to the final analysis. As we've indicated already, this study design has been endorsed by both FDA and EMA following discussions. Next slide, please. What we'd like to do now is to broaden the discussion beyond the existing data, beyond the potential phase III study towards what else might be in the future potentially for mitazalimab. Next slide, please. If we think very broadly, we see many opportunities for the future of mitazalimab. First of all, if we just focus on pancreatic cancer, we see opportunities for within the metastatic first-line setting, we can see opportunities for broadening the chemotherapy backbone, potentially broadening the patient pool available to us. Otherwise, we could move to locally advanced pancreatic or resectable pancreatic cancers. If we move beyond pancreatic cancer, there are opportunities in other GI cancers which potentially share similar tumor anatomy and/or immunology and also share a similar standard of care chemotherapy backbone. These would include biliary tract, colorectal, and gastric cancer. Lastly, moving even further afield, we see opportunities for treatment of cancers far away from the GI tract, which may possess different tumor anatomy and immunology, but we do see opportunity for particularly treatment of hot tumors currently treated with PD-1, PD-L1, or chemotherapy backbones. These might include renal cell cancer, melanoma, triple-negative breast cancer, or urothelial cancer. Next slide, please. What we've been putting quite a lot of work into recently is moving from this vision and focusing in on the next steps for the clinical footprint of mitazalimab. What we're looking to do is explore additional indications beyond pancreatic cancer, expand our database of clinical and translational data, and in particular, we're looking for opportunities that help us to generate decision-making data. For example, this might be initiation of phase III trials, or it might be pilot studies that support more meaningful human studies. Based on the positive data we've seen from the OPTIMIZE-1 trial, we're pleased to have received significant interest from a wide range of leading cancer centers at academic institutions around the world. We've received over 20 proposals for investigator trials with mitazalimab across a wide range of tumor types. There's a focus on GI cancers, but others have been included as well. There's been strong interest in combining mitazalimab with a range of different tumor treating modalities, chemotherapy, immuno-oncology, radiation, and vaccines. Next slide, please. It's important to note that the approach we're taking, utilizing investigator-initiated trials to broaden mitazalimab's footprint, is quite beneficial to Alligator. We support the drug supply, and we support some safety operations on the back end. In general, the trials are funded by grants or by institutions. We have two trials which are approved and either active or close to active. First of all, we have a trial in pancreatic cancer where mitazalimab is being used alongside an experimental surgical treatment for pancreatic cancer and an irreversible electro-operation. This is ongoing in the U.S. at the moment. As I think some of you have already picked up, we also have an interesting pilot study about to start a phase II study looking at mitazalimab in the treatment of oral potentially malignant disorder. These are a range of different disorders, particularly in the oral mucosa, that are prone to malignant transformation, essentially becoming oral cancer. We're exploring the benefit that mitazalimab can bring in these cases by delaying or preventing that malignant transformation. Beyond that, we've recently been working on three additional trials. More information will be released on these in due course. Firstly, we have a trial of mitazalimab plus chemotherapy in a GI cancer that's quite similar to pancreatic, and the chemotherapy is similar also. This is a randomized trial and will provide us with direct decision-making data. We have a trial of mitazalimab with a more experimental immuno-oncology agent. This is in pancreatic cancer and is a multi-arm trial in the U.S. Lastly, we have a pilot study, quite an early stage, in a very different form of cancer, which again is a combination of mitazalimab with an IO agent. This would provide us with decision-making data to support moving into more formal human trials in the event of a positive outcome. I'll hand back to you. Thanks, Søren. Next slide, please, as well. Thank you for that update, Tom. In terms of mitazalimab summary, what we have shared today is that mitazalimab efficacy data shows significant long-term survival benefit in first-line metastatic pancreatic cancer patients. The safety data that Yago discussed supports continued and long-term dosing in these patients in combination with chemotherapy. Importantly, Peter showed us that biomarker data from these patients confirm the mechanism of action of mitazalimab and links it directly with immune activation in the tumor, in the periphery, and with clinical outcomes. Some of these biomarker data might inform potential patient selection strategies in future trials. The commercial manufacturing process has been developed, and phase III GMP material has been successfully manufactured. We have established a clear path to approval in first-line metastatic pancreatic cancer. As I said before, phase III preparations are so complete as we can take them without actually starting the phase III study. Lastly, as shared by Tom, and quite importantly, we have embarked on an extensive clinical phase I and II program in collaboration with leading oncologists globally in a program through exploratory trials, but also in randomized phase II settings to establish and expand mitazalimab's use in new indications and also in new settings. We really believe that this is building tremendous, will be building tremendous value to the program, to Alligator, and a future partner for mitazalimab. If I could have the next slide, talking about the partnership and business development, we have over the seeding period here discussed with a number of different global partners, either through our direct outreach or through our investment bank, Moelis, a global life-focused investment bank located in London. There is a number of active confidential dialogues with Global Pharma ongoing as we speak. As we speak, there are also active due diligence processes underway. Alligator is continuing the outreach process together with Moelis. We will both engage both existing contacts as data materialize. Of course, we are also contacting and exploring new potential contacts. Just to make it absolutely clear, Alligator is both open to global partnerships, but also regional deals, U.S., Europe, Southeast Asia. We will, of course, keep you updated as we have been doing here at home with information about the partnering effort. With these words, we will move on and spend a little time on HLX22, a program, if I can have the next slide. HER2 antibody, HER2 is a molecule expressed on a number of tumors, including breast cancer and various gastric cancers. HLX22 is an innovative monoclonal antibody, and it's currently being developed by a Chinese company called Henlius under a license from AbClon, a Korean company, and following a discovery collaboration with Alligator that allows us a stake in the future revenues from this molecule. HLX22 is currently being developed in a number of clinical trials, first and foremost for the treatment of gastric cancers, what is called gastric esophageal junction cancer, GEJ, and gastric cancer. Here, a global phase III study was initiated Q4 last year. Recently, Henlius also took HLX22 into breast cancer, initiating a phase II study in the second quarter of 2025. The molecule was recently granted orphan drug designation in gastric cancer by FDA. Very briefly, who is Henlius? Do they have the capacity to develop drugs, develop and manufacture drugs, and commercialize drugs globally? Absolutely. Henlius is a big company with a significant market cap, currently six marketed products, six active marketing applications, and a total of 19 clinical candidates currently in more than 30 ongoing clinical studies. Definitely a competent development partner for this molecule. If we move to the next slide and talk a little bit about how we see the potential upside of HLX22. First of all, I think it's important to mention that Alligator is not privy to any confidential information. Everything is handled at arm's length. We can only rely and relay what is already publicly communicated by Henlius. We've also taken a stance and say it's only Henlius news and Henlius information that we will communicate and comment on. We expect to receive the next development milestone from the molecule. That's a phase II milestone within the coming 6- 12 months. Therefore, the main project value is attributed to royalties following HLX launch. It's always difficult to assess the future value of a molecule like HLX22, not only because we don't know the underlying development priorities from Henlius, but also because it's just in the beginning of its phase III development. Words have been out of a market capital or a full market value or peak sales of $10 billion. I think Alligator in our outside invaluation model has taken a more cautious approach, even though we see basically HLX has the blockbuster potential in at least two indications. We believe that the future revenues from the peak sales would amount to somewhere between SEK 150 million and SEK 400 million to Alligator on a fully developed molecule on an annual basis. Just to stress, as I said before, we will communicate major regulatory and commercial milestones based on public information from Henlius. We might, from time to time, reevaluate our valuation and have that as part of our quarterly communication. Let's look at the summary and outlook before we go to the Q&A. I think we have made the case that the phase II study and the data warrants registration and development in first-line PDAC, and that we've established the regulatory path forward to commercialization for the drug should a phase III study be positive. We are ready to launch a phase III study, but as we've communicated previously, we need a partner to be able to initiate such a trial. While we are working on that, we continue to build value both for patients, for stakeholders, and shareholders in mitazalimab by exploring additional indications beyond the PDAC in these IIT trials where Alligator primarily provides mitazalimab to the investigators. As I said, the partnering efforts are ongoing with continued focus and diligence. If we look at the other pipeline, especially in ATOR-4066, we believe it represents a future strategic development opportunity beyond mitazalimab. We, of course, continue to focus on monetizing these pipeline assets together with some of the underlying technology, both our antibody libraries, our Neo-X-Prime technology, and our proprietary bispecific format, RUBY, not to forget. We believe that the royalties from HLX will represent a significant potential future financial upside for Alligator. If we just stay on this slide, as was evident from Tom's slide, we see that these investigator-initiated trials will commence during the second half of this year and the first quarters of 2026. We will, as per policy, press release when the first patient has been dosed in these trials. If I can have the final slide here, just to remind you that in connection with the rights issue that we did earlier in the year, there is a series of warrants outstanding with the exercise price being announced Thursday next week, August 28th. The exercise period starts September 1st and runs to September 15th, with September 11th being the last day of trading of the TO 13s. Importantly, should you decide to subscribe, if you hold warrants, which we hope that you would make that positive decision, please confer with your bank or platform as the last trading days or exercise date may vary from bank to bank. With that, I will initially thank you for listening to us. Now we will open the floor for Q&A. We have around 15, 16 minutes for this. If there are extensive questions, we will probably run over for those of you who are interested. We will do it as we normally do in our quarterly calls. You have the opportunity to write questions in the chat. I will moderate the session. Today, I'm lucky to have both Tom, Yago, and Peter to help me answer your questions. I think, Tom, why don't we hit it off with you? We have a question here around the IIT in oral premalignancies. Have we valued the indication? If not, how many patients potentially would be treated with a drug like mitazalimab? Thanks, Søren. We don't have the direct answer to that question. We're at an early stage with this. What we can say is that studies suggest the global prevalence of the OPMD, the oral potentially malignant disorder that we're considering, is in the region of 4%- 5% globally. There's certainly a significant potential patient pool out there. However, we've also got to be cautious saying that the progress of moving from hopefully positive pilot data through to figuring out how to integrate mitazalimab in a meaningful way within treatment of this disorder is work that we have yet to do. Thank you, Tom. Just to clarify, regulatory documents have been filed, and we are awaiting to enroll the first patient. Good. Let's go to a series of questions from Richard from Redeye. Yago, the first one is to you and Tom, keep in if you feel like it. How is the duration of response related to overall survival and maybe equally important to the survival rates at 18 and 24 months? Yeah, that's a fantastic question to answer. I mean, patients that remain for a longer time on treatment, regardless of the second-line therapy that they receive, are going to end up surviving more. This duration, longer time on treatment, means that the longer time these patients will be benefiting and can benefit even after progression on mitazalimab. Basically, if you stay longer on treatment, you are most certainly going to be surviving for longer. Yeah. That's a good question. You can say that durability of response sort of equals tumor control in the individual patient. You could say that. Let's stay on the phase III program here. There is a question for you, Peter. Are you ready to ask how important the macrophage activation, stromal breakdown, and T cell activation in the tumor, how important these parameters are for the data that we've seen? Sure. Happy to. mitazalimab acts both by activating macrophages that in turn then degrade stroma, and by activating dendritic cells, which leads to more T cell recognizing tumors. I believe that both these mechanisms are important, and they are likely linked. When we are considering the very strong duration of response and overall survival data, in particular the very high OS 18 and OS 24 data that Yago presented, there are clear signs that T cells play a very important role for the long-term control of the disease. For the long-term control, I would imagine that the T cell activation induced by mitazalimab is very important. As I said in the beginning, they are both linked. Both mechanisms are important. Thank you, Peter. There is one for me here, also from Richard: have you produced drug materials for the entire phase III program? That's a good question. The answer is very short. It's yes. The team has developed a very good process with high yield and high quality. In terms of drug manufacturing, a single batch was enough to secure the entire phase III program, and then some in addition to that. That box has been ticked. Also from Richard, and this goes to you, Tom, how many patients will be recruited for the interim analysis in the phase III study? That's a tricky one. Thanks. There is no straight answer to this because the timing of the interim analysis would be driven by the number of events that were needed to be seen rather than being capped or related directly to a recruitment target. It sounds counterintuitive, but honestly, it's likely that the study would be mostly or even fully recruited by the time of the interim analysis, although that prediction is a little bit uncertain just based on dynamics like the number of sites and the ultimate recruitment rate that we'd see. We'd probably be close to fully recruited, if not fully recruited, by the time that event-driven analysis happened. Great. Thank you for that. A question comes from Luisa at Kempen. Maybe I can go on that, and then Yago or Tom, you can help me. The question is really, would you consider revisiting the phase III trial if and when, let's say when, a partner comes in, and how early could this interim analysis in the potential phase III take place? It's clear that a partner that takes full ownership or partial ownership of mitazalimab would have a strong say in how we would run the phase III study. The design that we have discussed today is very traditional. It's what we have endorsed by the FDA. It's a good starting point for any modifications. The second part of the question here, how early could this interim analysis potentially take place? Tom, do you have a qualified answer for that? I can. As I say, it's event-driven. It's after about 60% of the events in the study. It would be reasonably earlier, but I don't have a precise timeline that I can offer today. Good. We have a question from Luisa, and that goes to you, Yago, regarding the 10 patients currently on long-term follow-up. These were the data from July that we showed in one of the slides. What is the reason for discontinuation of treatment with mita or mita treatment? Yeah, that's quite straightforward, Søren. It's just disease progression. These patients have been a long time on treatment, and eventually, in pancreatic cancer, they just progress. Absolutely. Thank you. We stay in mitazalimab here. I think you've already shared this, but a question from Philip here at Red Eye, Tom. Could you share some insights on the possibility of using an interim readout in a phase III trial with mitazalimab to support an earlier regulatory filing? Yeah. I mean, it's absolutely part of the current study design. As I said, any interim that takes place can lead to a stop of the study for futility. If it meets superiority, it could also lead to the study essentially reading out early and being filed earlier. Yeah, that's absolutely something that's in the design. Great. A question here, also from Philip. Do you see breakthrough therapy designation as a suitable path for mitazalimab in metastatic pancreatic cancer and/or other indications? Yes, we are definitely considering whether to apply for that based on the 24-month data and some of the biomarker profile data that we discussed today. I think it's important to state here that breakthrough designation is, of course, a nice thing to have. It gives you direct dialogue with the FDA, but as such, does not speed up the regulatory process significantly. That's definitely in our considerations. Anything to add there, Tom? No, I don't think so. Thanks. A couple of other questions. One from Luisa here about HLX22. How much will the next development milestone amount to? That we are not privy to share. That's in an agreement between AbClon and Henlius. Unfortunately, we will, of course, share it once we have the money at hand. We have a question here from Johan Ransdam. As you reason for the monetary value of HLX, why can't you do the same on mitazalimab? I assume the question here goes to, can we monetize the future value of mitazalimab and use that to develop the drug, use that model? That is definitely something that we are discussing with so-called royalty financiers or trial financiers as part of our business development efforts. No doubt about it. That is a potential path. I think experience shows that the money you get from these transactions is pretty expensive when you look at how much of your future stream you have to give up to be able to finance a phase III study. We also have a question from Johan. Are there negotiations or only discovery processes ongoing? I think this goes to the business development effort. I would say that there are everything from non-confidential discussions going on, which we can call early discovery, and all the way to discussing potential structures for how a mitazalimab license could look like. We have a couple of questions also on HLX22 from Carl Magnus Van Veen. The first question here, have you considered selling the share of the HLX22 license to fund a phase III study yourself? I think that's a good question. I also think that the reality is that the risk-adjusted net present value of that future royalty stream, if we sold that today with the phase III study just starting, I don't think that that amount of money would allow us to fund the phase III study. It's definitely something that we are considering. What is in the best interest of the company and its shareholders holding on to the long-term opportunity, mid to long-term opportunity, or cash in now? That's definitely something that we are considering on an ongoing basis. Magnus also had a question here. How will you protect the value of HLX22 for shareholders if you do not secure a deal for mitazalimab? First of all, it sounds like there is a direct link here between the survival of Alligator and getting a deal for mitazalimab. That's not how management and board see it. We believe that we continue to build value based on the data and the initiatives that we have shown today. We will definitely continue with strict cost control to secure the runway, as I hope we have relayed to you today. We are closing down the phase II, the OPTIMIZE-1 phase II study, and the majority of the CMC, the vast majority of the CMC investment is behind us. We will maintain Alligator's operation, continue to build value at a lower burn rate, which I also believe we communicated at the quarterly meeting. We are approaching 5:00 P.M. I think there is a question here from an anonymous attendee. Please provide some column design of OPTIMIZE-1. Specifically, why was the duration of response chosen as the primary endpoint for the phase I-b study while meeting overall survival is selected for the upcoming phase III trial? Just to be clear, the primary endpoint of the OPTIMIZE-1 study was the objective response rate. We cleared that primary endpoint already at the top line readout. I think it was January 2024. Is that correct, Yago? January 2024, we did the primary endpoint, which is overall response, as you mentioned. Meeting overall survival is simply a request by the regulatory authorities, as Tom alluded to earlier today during our call. That is why that is a request for the phase III study. We don't have any more questions from the audience. I would like to thank all of you for listening in, sticking along a little bit later than the projected time. A great thank you to Tom, Yago, and Peter for not only providing input to the slides, but also for providing input on data, biomarker data, and clinical design and future plans, and for answering questions from the audience. If you have additional questions, please feel free to address them to the team here at the investor relations mail at ir@alligatorbioscience.com. Thanks a lot. Goodbye.