Alligator Bioscience AB (publ) (ATORX) Earnings Call Transcript

So hello, and welcome to Alligator Biosciences 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 e-mailed to IR at 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 life cycle management opportunities and how we will utilize a so-called investigator-initiated trials to expand the clinical application of mitazalimab. And after having discussed mitazalimab, we will talk about HLX22, an innovative HER2 antibody that Alligator has a stake in the future royalty stream. And as Greta just alluded to, we will end with a Q&A session. And if I could have the next slide, 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; and 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, and Yago will lead you into some of the clinical data on mitazalimab. So 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. And here, our lead asset, mitazalimab, have 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. And 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 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. And finally, as I said, HER2 monoclonal antibody, HLX22 represent 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 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. And as we already said, a lot of life cycle management opportunities, we believe, are based on flows 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 is around 85,000 patients diagnosed with the metastatic pancreatic cancer in the U.S. and the major European countries. And the survival -- the 5-year survival rate for these patients is well below 5%. Definitely unmet medical need there. And for these patients, for most of these patients, chemotherapy is the only option. And there, you can expect a median overall survival of around 8 to 11 months. These chemotherapies are associated with severe and often treatment-limiting side effects. And 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 we'll 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 for FOLFIRINOX triples the 24-month survival rate of these frail patients. And that is really without adding significant side effects on to the chemotherapy. And these two things in combination really puts with mitazalimab at the cusp of being a potential game change in this indication. And 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 2-part trial consisting of the Phase Ib and the Phase II part. In the first part, 2 doses were assayed at 450 micrograms per kilogram and 900 micrograms per kilogram for safety. Once the higher dose was deemed safe, we moved on to Part 2, where we completed several milestones included -- including a futility analysis and 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 and 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. And that's what we called Part 3, where we actually recruited additional patients at this lower dose. If you could give me the next slide, Greta. So 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 not 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 agonist or first generation. And so basically, we are seeing a safe and manageable combination treatment of mitazalimab with the chemotherapy backbone for FOLFIRINOX. Can you give me the next slide, please, Greta? And 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 in each of the patients. And 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 has been a considerable number of responders. This means patients that have had responses below 30% and a reduction in their tumor. And these responses, they're also -- they're very deep. And 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 100% reduction in nontarget lesions. And one of them had a reduction -- 100% reduction in nontarget and target -- in target and nontarget lesions. So we are seeing that mitazalimab in combination with modified FOLFIRINOX is giving us very deep responses. And 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 this fire 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 so aggressive as FOLFIRINOX. But 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 2 years. The important thing, again, not only of these five patients that remain on treatment is not only that they are still on treatment as of the last cutoff but two of these patients have been on monotherapy for one and more than 2 years each after having stopped any chemotherapy backbone. So we can see that the responses are not only deep but they are durable as well. And with that, you can give me the next slide, please. Greta? So when I'm talking about durable, we can translate that into a duration of response and 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 a patient has to be stopped treatment. And historical controls have shown us that for FOLFIRINOX this is around 6 months, 5.9 in the FOLFIRINOX trial. But in the OPTIMIZE-1 trial, we've seen these numbers skyrocket, even doubling that those expected from the historical control to 12.6 months. And 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 are seeing that the median overall survival, the definitive endpoint is superior to that and observed in historical controls with 14.9 months when compared to the 11.1 months. And finally, in the different readouts that we've been carrying out and with mature data, we can see that the patients not only have a nominally median overall survival. But this -- the 18 months and 24 months overall survival rates are clearly superior to that historical controls. You can see that at 18 months, we can compare our 37% overall survival rate versus 19% in FOLFIRINOX. And in addition to that, even more surprisingly, is a 2-year survival rate, which is 29% in the OPTIMIZE-1 trial versus the reported 8%. So 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 the patients -- 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. And if you can give me the next slide, please? Okay. And in addition to the nominal comparisons that I was showing in the previous slide, we've also done -- analyzed buying direct 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 FOLFIRINOX or the recently approved in NALIRIFOX. And you can see from this data that we presented at ASCO earlier this year at ASCO GI, [ mitaza ] the OPTIMIZE-1 trial comes out ahead of this pool of data with a clear benefit in overall survival. If you can give me the next one, please, Greta. And finally, I don't want to end this report without sharing some of the dose comparison data, dose characterization. As I mentioned in the first slide, we compared -- we were asked by FDA to further characterize the lower dose in order to comply with their Project Optimus guidelines. And you can see here from the data that the -- even with a very short follow-up, the 900-microgram per kilogram dose is superior in all the endpoints that we tested to the 450 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. So finally, you can give me the next one, Greta. And in this -- just this is a summary, just you can see that we delivered a primary endpoint -- a positive primary endpoint earlier in January 2024. We have done 18 and 24 month follows. And 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%, and 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 and which we'll be using median overall survival as its primary endpoint. And with that, I think I can move on to our CSO, Peter Ellmark, which will be talking about some of the biomarker that is coupled with the clinical data that I just showed.

Thank you, Yago. Sorry if I can have the next -- thank you. So we have performed an extensive biomarker study to analyze how mitazalimab treatment affects immune cells and the tumor microenvironment. And 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. This data, we're 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. And what you see here, what we could 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, reduction of fibrosis, and this sensitize the tumor to chemotherapy and results in more immune cells infiltrated tumor. Further, we -- 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. But we're going to have a bit of a look at the data and mitazalimab does not only activate immune cells in the periphery, but this immune cell activation is actually associated with clinical and predicts clinical outcomes. And 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. So this is why we know that this is mitazalimab induced activity only. It's before any chemotherapy is given. So if the patient responds by having more proliferating T-cells in the blood, they almost double their overall survival. So 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 new cells in the periphery, but we can also see that mitazalimab triggers activation of immune cells in the tumor, and what we show here is data from -- obtained from patients that response to treatment. And what we have done is that we have looked at -- looked at gene signature or gene pathways that are activated after treatment. And what you can see is that mitazalimab induced activation of T-cells and myeloid cells, which confirms with the solid modest of action and shows that we have achieved what we set out to achieve. And 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 you in the next slide that we have identified a new baseline fibrosis-related gene signature that identified mitazalimab responders. In this study, we have looked at biopsies of the tumors in patients before treatment. So these are baseline patient biopsies. We then looked at the immune signatures to these patients, and we identified pathways that were related to overall survival. And the one we found here on the top is extracellular matrix organization pathway. This is something related to fibrosis and stroma and patients that have high expression of these genes, they are doing much better, as you can see in the middle graph in terms of overall survival. This was really exciting finally because this is directly linked to the mode of action of mitazalimab. As you can recall, so mitazalimab acts by activating macrophages that degrade stroma. And this data really means that if you have more of basically the target of mitazalimab, you will do better. And this data not only provides a potential biomarker, but it also further supports the contribution of mitazalimab to the clinical activity that we see OPTIMIZE-1. So I can summarize the biomarkers by clearly stating that mitazalimab induced immune activation is associated with improved survival. We have identified a new baseline signature. And taken together, these biomarker data shows how mitazalimab contribute to the clinical activity and efficacy in OPTIMIZE-1 and informs on potential patient selection strategies for future studies. So 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. Now one thing is to have clinical Phase II data and being able to explain your mechanism of action to move forward to Phase III is, of course, also important that you have material of the right quality and in the right quantities available. And this is not something that we have talked a lot about. But over the last years, the dedicated Alligator team have worked to develop novel Phase III and commercial GMP manufacturing process. I can proudly say that we have done so together with Thermo Fisher, now at commercial 2,000-liter scale, cost-effective. And as industry standard something that really supports the continued development of mitazalimab. We've also manufactured both the drug substance, but more importantly, the drug product and now has a full supply to support the future Phase III study in first-line metastatic pancreatic cancer. And together with all this, the team have had a proactive regulatory dialogue both with the U.S. authorities and also the European authorities that have derisked also the manufacturing path to approval. So not something that is often discussed but a cornerstone in companies and Alligator's ability to move mitazalimab forward. If we take the next slide, we can see that we've 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've already discussed, the drug has orphan drug designation in the U.S. and also in Europe. And during the first half of 2025, we have finalized our regulatory interactions of pre-Phase III regulatory interactions both with FDA and EMA. And the conclusion on this, as we believe we have communicated several times, is that the agencies have endorsed 900 micrograms as the Phase III dose, that Phase III started design is acceptable for both agencies for regulatory submissions in both agencies. The nonclinical program is adequate and completed. And as I just discussed, the manufacturing and release strategy has been endorsed with both agencies. So 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. Now what does the Phase III program look like? What is the trial outline? And to talk a little bit about that and also discuss our indication expansion efforts. Tom, please join me and...

Sure. Thank you. So first, the Phase III study. This is a very straightforward Phase III design. So 1:1 randomization between an experimental arm, which is mitazalimab that the FDA agreed dose of 900 mgs per kilogram plus standard mFOLFIRINOX chemotherapy compared to mFOLFIRINOX alone as the control arm. Treatment is until progression. The primary endpoint, as a standard for many Phase III oncology studies is overall survival. The study would undergo an interim analysis. This would be -- this would function both as a potential futility and also is a potentially early stop in the event of very strongly positive data or the study would progress to the final analysis. As we've, I think, indicated already, this study design has been endorsed by both FDA and EMA following on 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 in the future, potentially for mitazalimab. Next slide, please. So 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 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 offer -- possess different tumor anatomy and immunology, but we do see opportunity for particularly treatment of hot tumors with 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, though, is taking from this -- 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 future Phase IIIs 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 and 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. And 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 mita's footprint is quite beneficial to Alligator. We support the drug supply, and we support some safety operations on the back end. But 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 irreversible electro operation. This is ongoing in the U.S. at the moment. And as I think some of you have already picked up, we also have an interesting pilot study about a Phase II study looking at mitazalimab in the treatment of oral potentially malignant disorder. So these are a range of different disorders, particularly in the oral mucosa that are prone to malignant transformation essentially becoming oral cancer. And 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 a similar role. So 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. And then 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, and this would provide us with the 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. So just in terms of mitazalimab summary, what we have shared today is that mitazalimab efficacy data show significant long-term survival benefit in first-line metastatic pancreatic cancer patients and 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 confirmed the mechanism of action of mitazalimab and link it directly with the immune activation in the tumor, in the periphery and with clinical outcomes. And definitely, 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. And we have a clear path to approval in first-line metastatic pancreatic cancer. And as I said before, Phase III preparations are so complete as we can take them without actually starting the Phase III study. And then 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 indication -- indications and also in new settings. And we really believe that this is building tremendous -- will be building tremendous value to the program, to Alligator and a future partner for mitazalimab. And if I could have the next slide, talking about partnership and business development, we have -- over the preceding 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 focused are located in London. There was a number of active confidential dialogues with Global Pharma ongoing as we speak. And as we speak, they are also active due diligence processes underway. Alligator is continuing the outreach process together with Moelis and we will both engage both existing contacts as data materialize. And of course, we are also contacting and exploring new potential context. And just to make it absolutely clear Alligator is both open to global partnerships, but also regional deals U.S., Europe, Southeast Asia. But we will, of course, keep you updated as we have been doing it a whole with the information about the partnering effort. And 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 is 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 cancer. So what is called gastroesophageal junction cancer, GEJ and gastric cancer. And here Phase III -- global Phase III study was initiated in Q4 last year. And recently, Henlius also took HLX22 into breast cancer, initiating a Phase II study in the second quarter of 2025. And the molecule was recently granted Orphan Drug Designation in gastric cancer by FDA. And just very briefly, who is Henlius? Are they -- 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 6 marketed products, 6 active marketing applications and a total of 19 clinical candidates currently in more than 30 ongoing clinical studies. So definitely a competent development partner for this molecule. So if we move to the next slide and talk a little bit about how do we see the potential upside of HLX 22. First of all, I think it's important to mention that the Alligator is not privy to any confidential information, everything is handed or handled at arm's length. So we can only rely and relate, 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 to 12 months. And of course, therefore, the main project value is attributed to royalties following HLX launch. And it's, of course, always difficult to assess the future value of a molecule like HLX22, not only because we don't know the underlying development projects 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 in valuation model have taken a more cautious approach even though we see basically HLX have the blockbuster potential in at least 2 indications. And 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 in -- on an annual basis. And just to stress, as I said before, we will communicate major regulatory and commercial milestones based on public information from Henlius. And we might, from time to time reevaluate our valuation and have that as part of our quarterly communication. So with that, let's look at the summary and outlook before we go to the Q&A. So I think we have made the case that the Phase II study and the data warrants registrational development, the first-line PDAC and that we've established the regulatory pay it forward to commercialization for the drug should have Phase III started to 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 client. 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 PDAC in these IIT trials where Alligator primarily provides mitazalimab to the investigators. And as I said, the partnering efforts are ongoing with continued focus and diligence. If we look at the other pipeline, especially 4066, we believe, represent a future strategic development opportunities beyond mites. And we, of course, continue to focus on monetizing these pipeline assets, together with some of the underlying technology, both on antibody libraries, our Neo-X-Prime technology and our proprietary bispecific format, Ruby, not to forget. And then, of course, we believe that the royalties from HLX will represent a significant potential future financial upside for Alligator. And 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. And we will, as per policy, press release when the first patient has been dosed in these trials. So if I can have the final slide here, just to remind you that in connection with the rights issue that we did early in the year. There is a series of warrants outstanding with the exercise price being announced Thursday next week, August 28, and the exercise period starts September 1 and runs to September 15, with September 11 being the last day of trading of the TO 13. Importantly, should you decide to subscribe if you hold warrants, which we hope that you would make that positive decision, please come forward with your bank or platform as these -- as the last trading days or exercise date may vary from bank to bank. And with that, I will initially thank you for listening to us. And now we will open the floor for Q&A, and we have around 15, 16 minutes for this. And if there are extensive questions, we will probably run over for those of you who are interested. [Operator Instructions] I will moderate the session. Today, I'm lucky to have both Tom, Yago and Peter to help me answer your questions. And I think Tom, why don't we hit it off with you.

And we have a question here around the IIT in oral pre malignancies. Have you -- have we valued the indication? And 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. It's -- we're at early stage with this. But what we can say is that studies suggest that the global prevalence of the OPMD oral potentially malignant disorder that we're considering is in the region of 4% to 5% globally. So there's certainly a significant potential patient pool there. However, we 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. And just to clarify, regulatory documents have been filed and we are waiting to enroll the first patient. Good. Let's go to a series of questions from Richard, from Redeye. And Yago, the first one is to you, and Tom chip in 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?

Yes, that's a fantastic question to answer. I mean patients that are -- remain for a longer time on treatment are regardless of the second-line therapy that they receive are going to be end up surviving more. And this duration, longer time on treatment means that the longer time these patients will be benefiting and can benefit even after progression on designing that. So basically, if you stay longer on treatment, you are most certainly going to be surviving for longer.

That's a good question. You can say that durability of responses sort of equals tumor control in the individual patients, you could say that. Then we have -- let's stay on the Phase III program here. And there is a question for you, Peter, are you ready to ask how important macrophage activation, stronger breakdown and T-cell activation in the tumor how important these parameters are for the data that we've seen?

Sure. Happy to. So both mitazalimab acts both by activating macrophages that in turn then degrade stroma and by activating dendritic cells, which leads to more T-cell recognized in tumors. I believe that both these mechanisms are important, and they are likely linked. I would say that when we -- considering the very strong duration of response and overall survival data, in particular, the very high OS18 and OS24 data that Yago presented. There are clear signs that these are clear signs that T-cells play a very important role for the long-term control of the disease. So for the long-term control, I would imagine that the T-cell activation in mitazalimab is very important. But as I said at the beginning, they are both linked, both mechanisms are important.