Now I will hand the conference over to the speakers, CEO Erik Manting and CFO Lotta Ferm. Please go ahead. Good afternoon, everybody. Good morning for those of you from the U.S. joining, and welcome to the Q3 Financial and Business Update from Mendus. It's a public company. We have to show our disclaimer. It's also available on our website. The Q3 of 2025 has mainly been focusing on the progress in myeloid blood cancers. It means we have followed up our ADVANCE II Phase IIa trial and have indicated a positive outcome now at 48 months median follow-up. Also, those data give us a lot of confidence about the potential of the product in the broader AML setting. We have started, and that trial is ongoing, and recruiting the AMLM22 Cadence trial together with the Australasian Leukemia Lymphoma Group; in short, Cadence trial. This is a Phase IIb combination trial with a drug approved for AML patients that have been treated with high-intensity chemotherapy called oral azacitidine. That trial is gaining momentum, and we have set a goal to enroll 20 patients by the first quarter of 2026, after which we will also prepare an initial readout. Another important step is that the AML first-line treatment landscape is evolving, and we have to adapt to that. Next to high-intensity chemotherapy, there is now a very successful regime of two drugs called venetoclax and azacitidine, used as a means to get chemo-ineligible AML patients into complete remission. That is a growing patient population, which is also in a very high need of post-remission immunotherapy. We want to be able to be part of that transformation of the AML landscape. We are now preparing, with Andrew Wei, the same professor who is also heading the AMLM22 Cadence trial, a trial called DEVA, which is a Phase I trial to, for the first time, study vididencel in combination with azacitidine and venetoclax. Also importantly, and as a very attractive market segment in myeloid blood cancers, we have decided to position vididencel in chronic myeloid leukemia. We will share a few details about the background of that new indication in the upcoming slides. Also importantly, we have already prepared in detail the trials to enter into this field, with a Phase I and a Phase IIa trial scheduled to start in 2026. To compensate for the additional trial costs that we anticipate in 2026, we have decided to reduce our staff, including also some of the management team members, to compensate for those additional trial costs in 2026. Mid this year, we announced that the U.S. Patent and Trademark Office, the USPTO, granted us a patent covering the use of vididencel in ovarian cancer. That is a part of an ongoing trial, the ELLISON trial in Phase I. This also validates the use of the product in ovarian cancer, and it gives us a nice optionality to see how the ELLISON trial plays out and is, of course, in a good way protecting our product specifically for use in that indication. We have a platform that we have been developing. A lot of research, preclinical research, has been going on in our labs. We have made the preclinical research subject to partnering. We actually also announced in the third quarter that we have closed an initial partnership with an international biopharmaceutical company in a research collaboration with our lab. Going to the financial information, Lotta, can I hand it over to you? Yes, please. Hi, everyone. Yeah, there is not much to say about the financial, as usual. We have an operating result of SEK 20.4 million. The cash flow, the negative cash flow, is SEK 21.4 million, so it is more or less in line with the result. It depends, and it is because we now have went into a more late-stage Phase with NorthX Biologics, so we do not have costs every month because the cost for the batches will come when they will be delivered to us. The cash position end of Q3 is SEK 37.6 million, and we expect that to have finished to have a cash runway into the beginning of 2026. Thanks, Lotta. As a high-level summary of why we are in AML, AML is a very aggressive blood-borne tumor, with basically immunotherapy being the only chance of cure. The only approved immunotherapy currently in AML is bone marrow transplant, or hematopoietic stem cell transplant, also in short, HSCT. This is a very high-risk procedure, which is inaccessible to most AML patients. Without transplant, AML patients face imminent relapse due to residual disease, and actually, the five-year survival of AML has been dramatically low, well below 30%. Why are we relevant? We offer a safe immunotherapy to reduce relapse by providing immune control over the residual disease. We have shown that this leads to durable clinical remissions, but also, very importantly, our product is safe, so we preserve health and quality of life for the patients treated. This is the 48-month data that I alluded to. What you see is a nice plateau. It means that after the initial patients that failed to respond to the therapy have suffered from relapse, you see a relatively large population responding with long-term survival. That is the plateau, the flattening of the curve that you see when you go to the right-hand side. Also, you can see that a number of patients have already passed five-year survival. This is a very striking result. As you know from our previous presentations, we have also looked in a lot of detail into the immune system of the patients, and we could show that actually all the patients that had a reasonable immune system at the start of treatment were able to build up immune responses against leukemic antigens after treatment with vididencel. Also, all of them became long-term survivors. The majority of patients are still alive at 48-month median follow-up. That is a great outcome. That gives us the confidence that we can push vididencel in the broader setting in AML. This is an overview of the AML treatment landscape. Again, HSCT is still the only curative approach, but for the many patients not able to undergo HSCT, there are actually two solutions, which is one, oral AZA, but oral AZA or oral azacitidine is not very effective. It does give some progression-free survival benefit, but when you look at long-term overall survival, it has very limited effect, and it is still below 30%. That patient population is the patient population we are currently treating in the Cadence trial. On the bottom, you see the patient population, which is currently classified as chemo-unfit. These patients do not get the classical high-intensity chemotherapy but a combination of azacitidine and venetoclax. There is no transplant option. The need for immunotherapy to make sure that these patients do not relapse is actually even larger than in the chemo-eligible patient population. This is the reason, plus the fact that the treatment is so effective that it is being used more and more as a first-line treatment, even for patients that are classically classified as chemo-fit, which means that is a very fast-growing patient population in need of post-remission immunotherapy. This is why we want to expand the positioning of vididencel with the DEVA trial, which is a Phase I trial addressing azacitidine-venetoclax-treated patients. Overall, the time to market has not changed significantly to our earlier plans, which were to execute on a more narrowly defined trial with oral azacitidine in only MRD-positive patients. Now, there's two reasons why we have adjusted the strategy. First of all, the developments in the AML landscape and the growing opportunity for post-remission immunotherapy. We want to make sure that we adjust to that evolving landscape and are optimally positioned for vididencel in terms of reaching the market and also the overall market potential. We have to adapt the execution of a clinical trial to what's happening in the field. Also, the use of MRD has changed. Where MRD was not part of our Phase I trial because it was not commonly used in clinical practice, in our Phase II trial, the ADVANCE II trial, we just looked at, we could use it to stratify patients into an MRD-positive, being a high-risk patient population. Nowadays, MRD is used a lot more continuously to monitor disease, and there's also a variation in MRD levels depending on how the disease is also monitored. There are different techniques to do it. In a nutshell, MRD is a very important parameter and part of AML treatment, but the use of it has become a lot more diverse and a lot more continuous rather than just a black-and-white classification of MRD-positive and MRD-negative patients. All in all, we want to first move to beyond MRD-positive patients. That is what's currently going on in the Cadence trial because we treat both MRD-positive and MRD-negative patients. As said, the azacitidine-venetoclax patient population, very fast-growing patient population in need of post-remission immunotherapy, in principle, also not eligible for transplant, so an even higher unmet medical need. We really want to make sure that we capture the broader AML opportunity and also that our plans to go to market with this product have the best chances of reaching the market and also having the recruitment to support the Phase III trial in the best possible way. The overall timelines to get to market, we estimate, are not so different from the original planned time to market. We just optimize the chances of getting there. Of course, we've had an end-of-Phase II meeting with the FDA. We are also preparing for large-scale GMP production. We have a manufacturing alliance with a company called NorthX Biologics. We have entered into the production Phase of that alliance, so we are currently evaluating the batches that we have manufactured. Of course, as soon as we can state that we have successfully been able to manufacture and release those batches, we will also notify the market. The alliance is on track and a very important part of supporting the late-stage development of vididencel in AML. I will spend a little bit more time on the CML field. The reason is it's a new field that we aim to enter. Acute myeloid leukemia and chronic myeloid leukemia do share antigens. That is well documented. We have done some preclinical work ourselves that we presented last year at the ESH conference, showing that vididencel actually stimulates immune cells to build up immunity against CML, which is, of course, a starting point for an active immunotherapy that we try to accomplish immune control over the residual disease. Why is it so relevant in CML? CML is a disease that is driven by a specific oncogene called BCR-ABL. Because this oncogene is so specific, it can also be effectively controlled with inhibitors, ABL1, tyrosine kinase inhibitors, or TKIs. It means that the disease is, in principle, under control and that treatment focus has shifted from short-term disease control to quality of life and cost reduction. The quality of life is heavily affected by lifelong TKI usage. Patients really want to try and stop their TKIs, and that is called a treatment-free remission, which has become a key therapy goal in CML. However, if you need to put pressure on the disease with TKIs and you take off the TKIs, you stop with the TKIs; it, in a lot of patients, quite quickly, within the first 6-12 months, leads to rising levels of disease. In that situation, patients have to be put back on the original or a new generation of TKIs, and the limited success of TFR is basically still an unresolved question. Going back to immune control, CML, before the invention of TKIs, was treated with hematopoietic stem cell transplants, so with bone marrow transplants. Because it's such a dangerous procedure, it's hardly used anymore. The other immune drug that has been tried in CML is interferon alpha, but also that is a very difficult-to-use drug with toxicity, with a difficult therapeutic window. People are really looking for new immune therapies to improve TFR success, to make sure that the immune system is able to control residual disease and you don't need to take your TKIs for the rest of your life. That is a big unmet medical need. Also, when you look into the patient numbers on the right-hand side, you will appreciate that CML is a much larger field than AML, and the main reason is that CML patients stay alive. It is a growing patient population. The estimated numbers now are roughly 150,000 patients in Europe and 150,000 in the U.S., adding up to roughly 300,000 patients in Europe and the U.S. alone. Almost all these patients have one single goal, which is to live a healthy life without being convicted to lifelong drug usage. What we will try to accomplish in 2026 is, first of all, safety and early signs of efficacy based on the molecular levels of disease that we can monitor, but then also quite quickly step up and start a PPhase IIa trial after the initial Phase I safety readout. We will focus in that Phase IIa trial on patients who have previously failed TFR attempts. The reason to do that is that the failure rate in the first year at the first TFR attempt, and this is patients that have had very stable, very low levels of disease so that they can finally stop their TKIs, is 50%. If it then fails and patients try after a couple of years of, again, stable disease suppression, a second TFR attempt, that failure rate is even higher, roughly 75%. This is a good patient population to start and try and pick up the signal that an immunotherapy like vididencel allows patients to have a better outcome of their TFR attempt. The start of both of these trials is planned for 2026. Moving to the summary in the outlook. The positive ADVANCE II Phase IIa data that we have presented with 48-month median follow-up data showing really that these patients have a chance of durable clinical remissions without having to pay a price of toxicity, so with a very safe treatment, really boosts our confidence to position vididencel more broadly in the AML landscape. This we are currently doing in the randomized control Cadence trial with oral azacitidine, but we will also expand to the chemo-unfit patient population in the DEVA trial in combination with azacitidine and venetoclax. The clinical data we expect from both trials in 2026, plus the anticipated first-line treatment landscape in AML, will guide our optimal go-to-market strategy in AML. The indication expansion to CML with a clear rationale based on a very large and growing patient population with unmet medical need will open up large additional market potential for vididencel in myeloid blood cancers, and we have already drawn out in detail the clinical trial strategy to open up that indication. I should also mention in ovarian cancer, we have published positive data in the middle of this year at ESCO, and we will continue to follow up these patients. We expect the next readout of the ovarian cancer trial before the year end. As near-term clinical milestones, we have the continued long-term follow-up of the ADVANCE II trial, including an update before the year end. We have the long-term follow-up data from the ELLISON trial in ovarian cancer, and then in the expansion of the positioning of vididencel to the myeloid blood cancer space, we have a number of key readouts already in 2026, being the Cadence trial readout based on the first 20 patients in the trial, the DEVA trial readout based on initial safety and efficacy data, and the initial safety and feasibility data in CML, which, of course, is the first big step into the remainder of the Phase I trial, but also the start of the Phase IIa trial. With that, I would like to hand it over to the Q&A session and welcome to answer any questions. If you wish to ask a question, please dial pound key five on your telephone keypad to enter the queue. If you wish to withdraw your question, please dial pound key six on your telephone keypad. The next question comes from Christian Binder from Redeye. Please go ahead. Hi, and thanks so much for taking my question. I was wondering about potential late-stage development in AML. Previously, you've remarked that you could get to market with a relatively small Phase III trial. Is that still the case, or would it potentially need to be expanded given the broader positioning? Hi, Christian. Thanks for your question. Yeah, I think the short answer to your question is we will expect a somewhat larger patient population if we, let's say, broaden the addressable patient population post-chemo, so to include also the MRD-negative patients, which tend to have a somewhat longer period before potential relapse. The recruitment and, in the end, also the probability of success in running that trial will also significantly improve because you, first of all, have a much broader patient population, but also you overcome the complexity of first having to assess according to standardized methods that the patient is considered to be MRD-positive. We anticipate a trial to be bigger. Initially, we said 150-200 patients. We now think that the registration trial in that setting will require around 250 patients, but the lack of complexity and a much broader patient population to be included will certainly facilitate the recruitment of that trial. All right, perfect. That was all from my side. Thank you so much. Thanks, Christian. The next question comes from Aaron Aatkar from Edison Group. Please go ahead. Hi there, Erik. Lotta, nice to see the presentation. Thanks for taking my questions. The first one I've got is, could you provide some more detail on the trial design size and endpoints that might be used for this Phase I b -DEVA trial? Yes, absolutely. It's going to be a typical Phase I trial, Aaron, and we anticipate to enroll 24 patients in 12 months' time. This is a much more prevalent patient population, and yeah, we think, therefore, that we can run a relatively quick trial with the initial safety and feasibility signal already established in 2026, but the trial, of course, extending into 2027. Okay, if I'm understanding correctly, then, there'll be 24 patients in 12 months, but then the initial readout would be in sort of mid-2026. Will that interim sort of readout be, well, an interim readout, not corresponding to the full results? Is that right? Exactly. Like in the Phase I for CML, in the first eight patients, you want to establish safety and feasibility. Safety, of course, is clearly monitored on a day-to-day basis in all of our trials, but feasibility will also be to see if we can pick up some initial molecular responses on the disease level. Okay, thank you. My next question, looking at the CML stuff in a bit more detail. Assuming successful with the Phase I trial, for the planned Phase IIa trial, am I right in thinking that that will be vididencel evaluated as a monotherapy? Are there any more sort of details you can provide on the design and whether it will be self-sponsored? Yeah, so apart from whether the trial's being accompanied or investigated, sponsored, because that question is always a matter of, on the one hand, the financials involved, but also the need for a certain, let's say, coordination in the execution. I think the centers we work with in Australia, and as you know, the center running or coordinating the Cadence trial is run by Andrew Wei. That's an investigator-sponsored trial. Same thing for the DEVA trial, which will also be led by Professor Wei. These are very experienced clinical centers who also have all of the infrastructure to monitor these trials. There you don't have to step in as a company. The same is true for the DEVA trial, sorry, the P hase IIa trial, which will be supervised by Professor Timothy Hughes, who's also a very renowned KOL. These groups know what to do. In principle, we don't have to step in as a company, and those will be investigator-sponsored trials. The Phase I in CML, because it is a new indication, we want to have a little bit more control of. We will work, so it will be a corporate-sponsored trial, but we will work with the group in Bergen University led by Professor Björn Gersten, who also was so kind to give an interview for the Q3 report. He is very experienced with the product because he's also been part of our AML trial. Everything is in close coordination with the investigators, but with some nuances on whether it's a corporate or an investigator-sponsored trial. Okay, thank you. Sorry, just in case I missed it, the Phase II design, is that sort of to be determined still in terms of size and endpoints or? Y eah, sorry. Yeah, I forgot to answer that part of the question. Sorry, Aaron. The idea is, no worries. I'll describe it in a little bit more detail. There's basically two main issues with TFR in CML. First of all, you're formally only eligible for a TFR attempt as a patient if you've had very deep and consistent responses on TKIs. A lot of patients don't reach that point, so that's called suboptimal responders. That is a patient population that we will enrich for in the Phase I to see whether we can already make or see a difference in the patients that have difficulties reaching those very deep molecular responses on TKIs only. The Phase I will be a combination trial. In the Phase IIa trial, we will focus on patients that have achieved those deep molecular responses, but where the expectation is that as soon as they stop with their TKI, their probability of rising disease levels is very high. That is a different trial. That is where you start the treatment of vididencel while the patients are still on TKI, and then you do the stop of the treatment, and you see whether you have an improved outcome of that TFR attempt because then the immune system has to basically control the disease and hopefully prevent rising disease levels as soon as you stop the TKI. Does that answer your question? Yes, that's super helpful. Thanks very much. No more from me. Thanks, Erik. As a reminder, if you wish to ask a question, please dial pound key five on your telephone keypad. There are no more questions at this time, so I hand the conference back to the speakers for any closing comments. Thank you, everybody, for joining. Have a lovely day, and speak to you soon. Yep, thank you.