Good afternoon, everyone. Thank you for joining today. I'm delighted to welcome you to our Capital Markets Update. I'm Namir Hassan. Today I will go through a focused update on Zelluna as we transition into the clinic. What I will cover is what we have achieved so far, what we're aiming to achieve over the coming months, and why we believe we're heading towards a meaningful and significant inflection for the company. I'm thrilled to be joined online by Professor Fiona Thistlethwaite. Professor Fiona Thistlethwaite is a deeply experienced Medical Oncologist working at The Christie. We are privileged to have her lead our first-in-human study. I'll come on to introduce Fiona more fully at the end of the presentation, where she'll give her clinical perspective. We'll open up to questions and answers in the session. Just to remind you, this session will be recorded so that we can make it available on our website. We're entering into an exciting phase where the biology that we have been building over the last several years is to be tested in patients, and importantly, where early clinical data can inform value for patients and value for shareholders. In my presentation, I'll walk through the developments in the field, our platform technology, why we're differentiated, our mechanism of action, our lead program, and the progress that we're making to the clinic, and also go through what we think success looks like in the near term. Before that, I want to start with the big challenge and the major problem that we're aiming to address, in essence, the purpose of the company, our why. Why do we exist? That is because, unfortunately, there are over nine million deaths annually from solid tumors, and over 80% of late-stage patients die from their disease. I'm sure many in this audience will know someone who has been afflicted by a solid cancer. Now, the initial responses that we have seen in the progress that we have made as a field for treatments of solid cancers has been encouraging, but unfortunately have also not been durable or long-lasting. That is fundamentally driven by tumors escaping those treatments. What's needed in the field are therapies that can overcome tumor escape and drive long-lasting responses. That's exactly what we have been building over the last years at Zelluna. We have been building a next-generation cell therapy in order to unlock the treatment of solid tumors. Now, why cell therapies? Well, we know cell therapies have been a clinically validated modality with nine approvals to date. The challenge has been to really unlock solid tumors with that treatment modality. Our platform has been designed specifically to harness the power of cell therapies and target solid tumors. I'll come on to talk about the makeup of the platform. It's also designed to enable the scaling of these therapies in order to provide the treatments as an off-the-shelf, immediate access product. Subsequent to having our clinical trial application approved by the MHRA, we're working towards moving to the clinic, and as we have communicated previously, we're expecting initial data to emerge around mid-2026. The platform technology is really underpinned by a growing IP portfolio, which includes not only protection of individual products, but also protection of the entire therapeutic approach. In essence, we have a differentiated approach built on clinically validated biology that is targeting the largest unmet need in cancer, namely solid tumors. Just to elaborate further on the clinical validation of the therapeutic modality that is cell therapies, I mentioned that we have seen nine approvals to date in the cell therapy space. I show some of those examples in this timeline with the various products that have been approved over the course of the last years. Really there are two key messages from this slide. The first is that small clinical data sets have driven approvals in this therapeutic space. You can see the number of patients highlighted for each product that have driven approvals for those products. For many of those, that's less than 100 patients. What we can also see, as well as the clinical validation, there has been the commercial validation, and you can see some of the sales of a couple of examples on the slide which demonstrate the potential commercial viability of the cell therapy space. What this shows is that cell therapy as a treatment modality has been clinically validated through approvals and also demonstrates commercial viability. Now, the next frontier for cell therapies is to take the potential that we have seen largely in liquid cancers, most of these approvals have been in liquid cancers, to take that potential and to drive that into solid tumors and to do that at scale. That's the next frontier, and indeed, it's the frontier that we've been building towards. Now, another axis to look at when understanding the prospect and the value driven by cell therapies is when we survey transactions that have been of late, over the last 18 months or so, in this frontier of off-the-shelf cell therapies, and I show some of those on this slide. What's demonstrated with these transactions are two key patterns. The first is that these transactions are based on platform technologies that are at the space of trying to deliver cell therapies in an off-the-shelf scalable fashion, as we're trying to do. The second is that these have been triggered by relatively small patient data sets. Just to give an example, you can see here the deal with EsoBiotec and AstraZeneca. It's a deal which was based on the acquisition of EsoBiotec that has been developing an off-the-shelf cell therapy, so-called in vivo CAR T, and that was driven on the basis of treatment of one single patient. Small clinical data sets can drive high value. When we look at how value is created in this field and what kind of data potentially triggers these transactions, what we see is that early signs of efficacy, particularly where the science is translated into the clinic, where the mechanism of action that's predicted from the science is translated in patients, that's where we see value created. Of course, also the demonstration of safety, particularly for novel platforms. These have driven major partnerships and acquisitions, and Zelluna is approaching this very meaningful inflection point. We're on the cusp of the clinic with a platform technology and off-the-shelf cell therapy technology. What we're aiming to do, at least for those early patients, is to understand if the science translates into patients and that the mechanism of action is validated. That initial clinical data, as communicated, is expected to emerge from mid-2026. Just moving on to the biological problem, why is it that we see for patients treated with treatments that have shown promise in the solid tumor space, that some of them can respond where the tumors shrink, but ultimately all relapse and the responses don't last? The reason for that is shown in this illustration. The fundamental driver behind that is shown in this illustration. That is down to the fact that within an individual patient that is harboring tumors, those tumors will have different flavors. And so when you have a targeting agent that's going after a specific flavor of cancer, in this case, it will be demonstrated by the red cancer cells, you may see an initial response where those cancers are eliminated, but parts of the cancer that don't harbor the feature for the treatment will then grow and outgrow. And that's what we have seen clinically in patients. And so what's needed in this space are treatments that can specifically get into tumors, but can recognize multiple features in the cancer in order to eliminate the entire population. And so this is exactly what we believe we have and have been building towards with the TCRNK platform. I'll spend a minute just going through the platform technology. It's a differentiated approach, and we say it's built on clinically validated biology. Now, what do we mean by that? The approach is built on two components. The first component is what's called a T cell receptor. That's shown at the top. It's a homing device, if you like. It's what traffics and enables cells to get to where you intend them to get to. It's a scaffold and a homing device that has been clinically validated as demonstrated by two approvals that are based on this homing device that target solid tumors. Those two are shown in this example, Tecelra and Kimmtrak. These are two approved therapies that are used to treat solid tumors that use this scaffold, the T cell receptor, to drive the targeting to those solid tumors. I was privileged to be leading the early development of one of those approvals in my last organization, Kimmtrak, which is currently being approved for the treatment of uveal melanoma, a type of melanoma that's incredibly aggressive and results in a relatively short lifespan, unfortunately, in patients. This scaffold is a clinically approved targeting mechanism for solid tumors. This is key. This is what differentiates us from any other natural killer cell player in this space. By putting this homing device into natural killer cells, we then allow those cells to target solid tumors. The other component that we have here is the natural killer cell. This is a cell that naturally is considered the most efficient killer cell in the human body. We take that cell and we put into it the homing device, the T cell receptor. The benefits of this natural killer cell, beyond its efficient killing, is that it can be used in a scalable off-the-shelf manner, meaning that healthy donor cells can be generated and expanded and then frozen down as single doses that are then used in patients. Now, this also is a clinically validated biology, as we have seen multiple clinical programs that use natural killer cells that demonstrate safety, their favorable safety profile, which is an important point, and also their efficacy, their ability to kill cancers. That's almost exclusively been in the liquid cancer setting. One example is CD19 CAR-NK, where we've seen efficient killing and high levels of responses in those liquid cancer patients, which demonstrates to us that natural killer cells can kill very well in patients and kill safely. The reason why they have been largely restricted to liquid cancers is the nature of the homing device used in those cases, which is a chimeric antigen receptor, a CAR, and that's the key difference. By putting a T cell receptor that's optimized and shown to target solid tumors, we then enable solid tumor targeting, and we believe unlock solid tumors with this platform. Since no one else is really doing it the way we are with the TCR, we haven't seen the potential of natural killer cells in solid tumors yet. To summarize, what we end up with the TCR-NK platform is a combination of validated tumor targeting and cell killing, as we've seen with the validation of the biology of the individual components, the ability to overcome tumor escape, and I'll come on to talk through that in a moment, and a scalable off-the-shelf approach. We believe, therefore, that we're addressing the key challenges in the cell therapy space. If I then move on to another layer of clinically validated biology that we are building from, that is the nature of the targets we have in our pipeline. We're also going after clinically validated targets. Our lead program targets MAGE-A4. It's a clinically validated target. It's expressed, and it's a feature that's made on cancers across various solid cancer types, lung cancer, ovarian cancer, head and neck cancer, and so on. We believe, and others believe, who are also targeting MAGE-A4, that the treatable patient population is potentially over 50,000 patients. It's an enormous, potentially treatable patient population across a variety of different solid cancer types. The other layer of validation on this target is that others that are targeting MAGE-A4 with different modalities have shown the ability to shrink tumors, reduce tumor size, and these responses have been observed across multiple different cancer indications. Indeed, we have one approved therapy that uses T cells that targets MAGE-A4, again, exemplifying the validity of targeting MAGE-A4. Of course, the limitation of this, as I've described, is that invariably patients relapse, so those that respond, the responses don't last, and also that this type of therapy is limited in its scalability. This is exactly what we're aiming to build on, building on a validated target. We're anchoring, we believe, on a strong footing, but addressing that with a platform technology that can overcome tumor escape and that can be scaled so that it can enable access to the potentially wide population that can be treated. I'd just like to delve a little into the mechanism of action, and this is important because we're going to be looking for features and signs of this in patients. It's exciting to say that because we have a product in the freezer thanks to the brilliant team. Product is in the freezer. Once the product is taken out and infused into patients, what we anticipate, and this is on account of our differentiating element, the homing device, if you remember the T cell receptor. What we anticipate is that the T-cell receptor will guide our product to the cancer and hook on to the feature that the homing device recognizes, in this case, MAGE-A4. Now, we know it does this with other modalities. As I mentioned, this guidance system is a validated biology. It takes cells to their target in this way. We expect this to happen based on what we have seen with other modalities. Once it hooks onto the target, it will then kill those cancers that express the feature for the T-cell receptor. Now, all other current MAGE-A4-targeting treatments will stop there because there is no other function in that therapy to allow killing of other cancers. This is where we have the edge. Natural killer cells are then able to recognize other features in the other flavors of the cancer population, in this case, the blue and the green cancers within that population. The intent would be to have those also eliminated on account of having natural killer cells delivered to that environment. The MAGE-A4 feature, which is the target for the T cell receptor, provides the ability for the natural killer cells to traffic and hook into the tumor environment, and the natural killer cells will then kill the remaining cancers in that environment. We call this a dual mechanism, the initial mechanism to traffic as a consequence of the T cell receptor, and the second bucket of mechanisms where the natural killer cell can recognize different features on the cancers in order for the elimination of the entire population to occur. We will be looking for the translation into the clinic of this science. We've demonstrated that this science holds experimentally. I'll come on to show some of that data. This will be key to the initial understanding of the treatment of patients. I mentioned the off-the-shelf scaling potential of this treatment, and the manufacturing team has worked tirelessly to get us to a point of locking down a manufacturing process, our own proprietary manufacturing process that enables us to generate from a healthy blood donor, material that can be frozen and used at the point of need. At the moment, what we're able to do is from a single batch is generate hundreds of doses that can be frozen and used in patients for their treatment. As we scale, the cost per dose reduces, and that becomes another important feature as we think about the treatment and the reimbursement prospect and the commercial prospect for a platform technology such as this. At this stage, a single batch generates hundreds of doses with lower cost of goods. I mentioned briefly the intellectual property portfolio that underpins the platform technology, and I just wanted to spend a moment on that. That is that beyond individual products, which we will be protecting, as is common practice, what we also have is a granted patent that protects the entire therapeutic field, and that is the approach that we have, which is putting T cell receptors, which is key to targeting solid tumors, into natural killer cells. That approach in its entirety is protected with a granted patent. In thinking about this, what we sometimes communicate is the analogy to, for example, a CAR T patent, which doesn't exist. If there was a CAR T patent that protected the approach of CAR Ts, which as many of you I'm sure will know, has underpinned the approvals of a number of products in this space, as I've shown here, with multi-billion revenue, if a patent had existed that protected the CAR T, then the aggregate value of that, of course, would be immense. We believe the concept patent, as we call it, provides potential high value if we're able to demonstrate the science translating into the clinic. Let me move on to the lead program and provide some further information on the lead program. We are really well on the way in clinical preparations for advancing the lead into the clinic. The scientific team really over the years have done brilliantly to demonstrate the potential of the lead program, and we published a paper on this this year, where we've demonstrated the ability of the lead to outperform the clinical benchmark. You may recall there's one approved MAGE-A4 TCR T therapy. We have used that in the research laboratory to benchmark against, and we've demonstrated outperformance based on a number of characteristics that's been published in the paper. We've demonstrated crucially that the TCR-NK platform can kill diverse tumors. This is the fundamental hypothesis, and we've shown that to be the case, and also various beneficial features that the TCR-NK cells have and potentially can translate into patients. From a regulatory perspective, we have approval from the MHRA to move into clinical studies in the U.K., and we have also, as part of our regulatory pathway, interacted with the FDA and have had favorable feedback, which would support a potential U.S. expansion. From a clinical perspective, we have identified and are targeting solid tumors with a high unmet medical need, where the feature MAGE-A4 is present, where we've seen other MAGE-A4 modalities show tumor responses against those, and where we believe our platform potentially can be optimized for those cancers. Those cancers are lung, ovarian, sarcoma, and head and neck cancers. We're privileged to work initially with a couple of really deeply expert U.K. clinical sites, and I'll come on to say something about those sites, The Christie and The Royal Marsden. We believe we've de-risked our entry into the clinic, and we're aiming for tumors with really high unmet medical need. To talk through and to demonstrate the potential of the platform to kill what are called heterogeneous tumors, these are cancers that may have different features, we demonstrate that with this short video. Just before playing the video, I'd just like to explain that within this picture, you will see green cancers and red cancers. The red cancers contain MAGE-A4. This is the feature for the homing device. If you recall, this will be how the TCR-NK will hook into the tumors, and they will then kill those red cancer cells over the course of this video. If you remember, that's where current therapies will stop. Beyond that, the TCR-NK cells will also kill the green cancers, and that's on account of the ability of natural killer cells to recognize multiple features on cancers. Over the course of this video, what you'll see is both populations be killed, and that tends to happen at a relatively rapid rate, the red cells there dying off and the green cells dying off. These translucent cells are the actual TCR-NK cells that are scouring around, scanning the cells, and then destroying them. We have multiple data sets demonstrating that this platform and the lead can recognize and kill mixed populations. Where are we today? The team have done a brilliant job in executing to get us to where we are today. We're rapidly moving towards the clinic. We're aiming to have our first clinical site activated for early May. We're on track to achieve that, and that's a consequence of a number of key milestones along the way. Initially, manufacturing is being established and clinical-ready, generating a clinical batch of material that we're aiming to use in those first patients, engaging leading U.K. sites, The Christie and The Royal Marsden, selecting a deeply expert CRO to support us in the operational execution of the clinical study. They have deep experience in the cell therapy space and in oncology, submitting our CTA in December and having that approved unconditionally in February, and really being well underway, knee-deep, essentially, in clinical site startup activities that are advancing very well and progressing. As we move towards the clinic, where I mentioned privileged to work with a couple of really world-class clinical sites led by internationally recognized clinical investigators, Professor Fiona Thistlethwaite, who I'll hand the floor to in a moment, from The Christie. The Christie is one of Europe's leading cancer centers with extensive experience in early-phase oncology studies and specialist expertise in cell and immunotherapy trials. We also have Dr. Andrew Furness, again, world-renowned at The Royal Marsden, globally recognized cancer center, pioneer in early-phase clinical development with a strong track record in novel immunotherapies and cell therapies. This is important. When it comes to clinical testing, it's incredibly important to enlist the appropriate clinical sites in order to support high-quality and reliable clinical execution. We're delighted to have them on board. Just to give a flavor of the design of the clinical study, perhaps just to have a picture emerge in your mind, it's a phase I dose escalation study, a classic 3+3 design. What that means is that we will be testing dose levels, and for each dose level, we will recruit three patients. We will start with a dose level that we believe is biologically relevant. In those first patients, we will certainly be looking for signs of mechanism of action as a consequence of the relevance of the initial dose. We will be treating advanced solid tumors. These are heavily pre-treated patients that have failed all other options. They will be screened to ensure that they contain the feature for the T cell receptor that provides that initial hook. That's MAGE-A4 and another feature called HLA-A2. We will need to screen patients to ensure and identify those that have those features. It will be, as I mentioned, for the indications shown, lung, ovarian, sarcoma, and head and neck cancers. The way we'll treat those patients is that we will give them three doses on day one, four, and eight, and we'll continuously monitor them with a safety review committee and also an independent data monitoring committee, which we have now established, again, with world-renowned experts that will independently review the data. As mentioned, we expect initial readout to emerge from mid-2026. The important thing here is that what we will be looking for from those patients, and I have one slide dedicated to that, it's naturally an often-asked question, is we'll be looking for safety, importantly, since this is a novel platform technology, and any signs of the translation of the science in patients, i.e. the mechanism of action. Now, the timing of data emerging will really depend on the pace of patient recruitment and the safety review timelines. In essence, the trial is designed to establish safety and enable early assessment of tumor targeting in patients. Now, I think it's important to spend a moment on safety. Safety is really emerging as a key differentiator in next-generation cell therapies. When we look at the approvals that we have had in the cell therapy space, whilst we have seen tumor responses and we have seen their effect, we've also seen the toxicities that have emerged and the complications as a consequence of those toxicities. With autologous CAR T therapies, which have dominated the approvals to date, and with the newer cutting-edge in vivo platform technologies, which we have seen multiple transactions recently around, we are seeing and we have seen toxicities with those agents, and they're associated with toxicities around neurotoxicity and around multi-organ failure in some cases. Invariably, they have required hospitalization and intensive monitoring. Of course, that limits the broader patient access and scalability of such modalities. What's really emerging as a key differentiator in this field is the demonstration of safety. With NK cell-based therapies, what we know from the innate biology of those cell types is that they have a favorable safety profile. We have decades of clinical development experience with natural killer cells that demonstrate the safety of patients treated with those cells. Key for us initially is to demonstrate safety for our novel technology and our novel product. What that would do, if demonstrated, is support the broader access and improved patient experience. Really, the improved safety profile has the potential to expand access and also allows versatility in the treatment regime. One can treat and retreat and gives various options when it comes to patient treatment. That will be a key important element to understand as we move into patients. Now, what would be exciting for us to see from the first patients treated? Just to remind you, the patients that we'll be treating are heavily pretreated patients. They would have failed past therapies. Unfortunately, they probably would have not very long survival prognosis. These are very ill patients. What we'll be doing is we have a program of assessments in those patients that will look at biopsies, sampling biopsies, what's happening in their tumors, imaging, which will be typical, so imaging their cancers to see what's happening to the cancers, are they expanding or shrinking, and blood sampling to understand what's happening systemically in those patients. Now, initially, we'll be looking for early indicators of success. That will come in different forms. The first and key would be to demonstrate that the first-in-class therapy for this novel platform is safe, that it has a favorable safety profile. That's foundational for this class of therapy, and in the context of my previous slide, where I'd shown that safety can be a challenge and a limitation for other cell therapies. Demonstrating safety for a novel platform technology like ours will be key. Next will be to demonstrate proof of mechanism. We will be carefully looking at those patients to see if TCR-NKs are getting into tumor, and that will be our proof of mechanisms. Do the T cell receptor NKs reach and engage tumors? If they do, then that demonstrates that the scientific hypothesis translates to patients, and then we can continue to build from there. That will be essential and key to the platform technology. Further to that, we'll be looking for signs of that, which will be efficacy signals, tumor imaging, to see the potential shrinkages in tumor. Now, it's important to remember that the maximum effect of this therapy may only occur as we go up the dose in our dose escalation. Initially, what we'll really be looking for is proof of mechanism, and if we establish that, then we'll be able to optimize the maximum therapeutic effect. I'll just say a few words then about our pipeline. Our pipeline is made up of assets that target what we believe are validated targets that cover a whole range of cancer types beyond the cancers that I mentioned for our first-in-human study. Just to reflect back on what we have achieved over 2025, a key year for us, and what we continue to achieve and progress in 2026, which is primarily to advance towards the clinic, as discussed earlier, entering into a zone where early clinical data really begins to inform value. We have seen that with multiple transactions on the back and on the basis of very small human data sets. To sum up, we believe we have a differentiated platform that is optimized to treat solid tumors with a near-term clinical catalyst. I hope I've described in maybe more detail than before on why we believe this is built on validated biology components that are validated, the T cell receptor, a validated homing device with two approvals, and natural killer cells that have been demonstrated to be safe and deliver efficacy, though in liquid cancers, and we bring those two things together. From a inflection perspective, we're heading to the clinic to really understand if the biology translates into patients, and this has been a real significant and meaningful inflection across the field. We're expecting to be able to communicate initial data emerging from mid-2026. It's a platform built on clinically validated biology with near-term data catalyst. This is perhaps the most important slide around the people, and there are a number of others, of course, across the organization that are driving what we're doing. Some of the Management Team are here today. I think it's important to say that across the team, across Management Team, and across the Board, we have collectively deep experience in taking therapies like this to the clinic, including approved therapies, in generating value along the way, both value for patients and value for shareholders. Without further ado, and thanks, Fiona, for waiting patiently. I'd like to properly introduce Fiona, Professor Thistlethwaite. It's really a pleasure to work with her. Fiona is a Medical Oncology Consultant within the Experimental Cancer Medicines Team, Medical Director of The Christie Clinical Research Facility, Clinical Lead for the Advanced Immunotherapy and Cell Therapy, Team Director of iMATCH. iMATCH is the Innovate Manchester Advanced Therapy Centre Hub at The Christie in Manchester. The Christie, it's one of Europe's largest cancer centers, treating over 60,000 patients annually. We're really privileged to have Fiona leading our first-in-human ZI-MA4-1 study. Fiona, I'll put you up on the screen now, and maybe pass on to you and perhaps just begin by asking how you see the nature of the patients that we're aiming to treat, the standard of care, and where you see the TCR-NK platform and our lead fitting in that context. Okay. Thank you very much, and thank you for the introduction and the opportunity to talk today. In terms of these patients, we're treating patients who have metastatic disease, so the cancer has spread. Their disease would generally be considered not curable, certainly historically. We very carefully selected certain tumor types where we feel there's a high unmet need remains. At the moment for lung cancer, ovarian cancer, sarcoma, head and neck cancer, treatment of these patients is still based around chemotherapy, where many patients will respond but for a short period of time. Increasingly, the care pathways for these patients are becoming more complex, so combining with targeted agents. Again, some of those targeted agents, like the PARP inhibitors in ovarian cancer, resistance eventually builds for those patients. For some of the tumor types that we mentioned, the lung cancer and the head and neck cancer and ovarian cancer to a degree, we do use in standard of care immunotherapies, but those are very non-targeted, so the checkpoint inhibitors, where a small proportion of patients may have durable benefit, but the vast majority of patients, a significant majority, don't respond adequately to those and don't get deep, meaningful responses over a long period of time. Taking all of that together, it signifies there's definitely still a high unmet need for these patients, and that's seen through our clinic. I sit primarily within our phase I team, where we get at least 20 or 30 referrals per week from patients across all tumor types who have exhausted all therapies but who remain fit and interested in clinical trials. Yes, they'll have had multiple different lines of treatment. We cream off the very fittest patients, good performance score, few comorbidities, and interested in trials, and those are the patients that we'll be focusing on really for this trial. I don't know if there's other things you want me to kind of highlight here. Anyway. That's great, Fiona. Thanks for that. How do you see the prospect of TCR-NK fitting into that context? I think this is really exciting. We've seen CAR T. It still surprises me to think that CAR T now for hematological cancers have been part of our standard of care treatment for more than five years. We've really struggled to make that inroads into solid tumors in the same way that we have with hematological cancers. There's lots of reasons for that, many of which you've highlighted already. It's that idea that in solid tumors, you need a homing mechanism to get really into the tumor and then to avoid the escape mechanisms of the tumor by having a breadth of response. That's what's exciting, I think, about this CAR-NK approach, where we have available to us both of those signals. Also thinking about, again, what you've highlighted, that we're looking really at validated targets. The MAGE-A4, we've run TCR T-cell therapy trials here with that particular target for T cells, but perhaps haven't, again, made that step change into the types of responses that we want to see across the breadth of the immune response. That's what the NK can bring. That's, I think, what's exciting and what differentiates it from what's gone before. Appreciate that, Fiona. I've tried to express what we believe success looks like from those early patients. I wonder, just from your perspective, what you would be looking for from those early patients. Yeah. I think every patient who comes through our clinic, many patients are looking for cell therapies, actually, and it's rare that we can offer them. Again, that's exciting to be able to offer patients cell therapies. We always talk to patients that these are often first-in-human, very early trials. There are many factors that will need to be optimized. We're looking, as you mentioned, primarily safety. Is it deliverable? Can we select the right patients for the trial through the kind of pre-screening mechanisms to make sure they've got the right HLA subtype, the right MAGE-A4 expression levels? We're confident we can do that. The next step is to say, are the cells getting to the right place? You've highlighted already for readout of the pharmacodynamic, the cells getting into the right place will be really important, and that's where having biopsies pre- and post-treatment, patients will accept that, and we'll select patients where they've got disease that we can easily biopsy before and after treatment. Of course, every patient comes to our clinic hoping that the therapy will control their cancer, and we will be looking for that. I think in the early days of any dose escalation trial, that comes as a potential bonus rather than what we're focusing on primarily, and that's the safety and some indication the cells are getting to the right place and active in the tumor microenvironment. Thanks for that, Fiona. Maybe another one which can come up in terms of recruitment of patients and the pace of recruitment, that's an often asked question. I don't know if you wanted to give a flavor of that, how you see that. I know you see the largest number of patients across Europe, multiple referral centers, and so on. Perhaps just to get your perspective on patient recruitment. Yeah, I think what I can say here is we've got a well-oiled machinery in our specialist team, our advanced immunotherapy and cell therapy team, where we've recruited, as I mentioned, to the MAGE-A4 TCR T-cell therapy trials very well. What we do there is we will have some patients coming in, as I mentioned, 20 or 30 referrals a week across all tumor types, but the ones we've selected here are relatively common, certainly the lung cancer, the head and neck, and the ovarian. Sarcoma is a little bit different. The synovial sarcoma is a much rarer tumor type, but where we see much more commonly the MAGE-A4 expression. We've done both in the past. It's a way of we get volume of patients coming. We'll discuss trials with them, and then if they're interested in the pre-screening, we'll recruit and identify the patients who are potentially suitable for this trial. We keep a waiting list actually of patients where we're trying to match them to the right trial. At any one time, there's around 200 patients on that list. When the trial opens, we'll first of all go to our waiting list to pre-screen for suitable patients. We'll have patients coming to us each week who are referred as potentially suitable phase I trial patients. Finally what we'll do is we'll do an outreach, particularly for the sarcoma. We've built up really good working relationships with sarcoma teams across the country. Many of the sarcoma patients are young and really interested in trials. In sarcoma, there's a particularly high unmet need where there's very limited lines of therapy for patients. We'll outreach to our contacts that we've got already well-established and actually actively request referrals in, particularly for the sarcoma, but we can do that for any of the disease types that we're targeting for this. I think what we'll aim to do is we have to identify through the pre-screening what we call double positive patients, the patients with the right HLA group and whose tumor expresses the MAGE-A4. What we tend to do with this type of trial is keep a kind of steady state of maybe five to 10 patients where we know they're double positive. When the time's right to treat them, because of the 3+3 design, we won't be actively recruiting five patients at once. We'll be recruiting up to three patients in on one go, and we'll need to line up with our clinical wards where we'll actually treat them. We keep a kind of pool of double positive patients, and then we select the patient that we feel is right to move forward on to the actual cellular therapy, at the right time. We're really clear with patients the pre-screening doesn't guarantee them treatment with cells. It just means they might be suitable so that we can pick when the timing's right for the patient and which patient is going to actually potentially benefit the most from the treatment. It's about kind of managing expectations and not screening thousands of patients and ending up with too many that we can't treat everyone. It's about getting that balance right, and we've got good experience here. I have to say that we work really well with the Marsden team, with Andrew Furness. We've collaborated on many different trials and other aspects of research. We're really excited to be able to work with that team, and I'm sure it'll be a really productive way that we find to move forward with patients with recruitment. Brilliant. Thanks, Fiona. Thanks for sharing that dynamic and those insights. Is there anything else, Fiona, that you wanted to share before I open up for questions? No. Not particularly. We're well into our setup for the trial, and we're really looking forward to getting open within the time frames that you've mentioned. As soon as we open, I expect we'll very rapidly be able to start the pre-screening process. It's a bit like they say, like buses, we'll be looking for those double positive patients. Sometimes we get three in one week. Sometimes it takes a week or two for us to start to find those double positive patients, but we're really excited to get going. Brilliant. Thanks for that. In that case, I'd like to open up for any questions. We have a microphone. If I can kindly ask we pass that. Geir Christian Melen has a microphone. There's a question over here. Shall I help? Arne Roset. I have a few questions. Sure. You're talking about a quite heterogeneous material, and you mentioned that these T-Cell Receptors will recognize portion of the cells in the tumor. My question is, approximately what kind of% of these solid tumor cells will be positive for the MAGE-A4? Mm-hmm. Secondly, you have to have the right HLA-A2. Mm-hmm. How many of the rest of the cells do you expect to have this correct HLA concentration? Mm-hmm. Very good questions. When it comes to the first question in terms of the MAGE-A4 feature. Mm-hmm We have a setup that the science team have actually developed together with a partner where we screen patients. Mm-hmm We look for a particular extent of MAGE-A4. That's around 30%. 30? Yeah. Yeah. That's also benchmarked against the approved therapy that have used a similar benchmark. Mm-hmm ... has worked in a different type of setting. When it comes to HLA-A2, we look for the patients being HLA-A2, and that's around 50% of patients generally. And then the tumors may or may not have that HLA-A2 feature, but both are advantages. Where they have the HLA2 and the major four, they'll be targeted with the T cell receptor. If they've lost the HLA, that's another feature of Natural killer cell recognition. So natural killer cell recognize cancers that have lost HLA. Double feature. Correct. This is again where natural killer cells are at an advantage. Whereas with other modalities that target MAGE-A4, they will be silent in the case of HLA loss, they won't be able to act. That's another feature of natural killers. Thank you. Thank you. Any other questions from the audience yet? In the deals you showed, there was a lot of ongoing activity in the in vivo space. Is it, in principle, possible to do this also in the long term as an in vivo therapy, or is there anything that hinders? Yeah, potentially. It would require technology that allows you to, in an in vivo manner, target the cargo, the T cell receptor cargo, into natural killer cells via an in vivo platform technology. Potentially that's possible. I think remembering that, and that's possible and perhaps an innovation down the line, and that could also, we believe, fit within the general protection we have for the TCR-NK space, which covers T cell receptors in natural killer cells. That potentially could be an approach. Now, it's still an emerging technology in vivo CAR T. You may have seen the recent article on the first five patients treated with EsoBiotec, all of which had severe toxicities, and so I think it remains to be seen how that plays out. It's a very emerging technology. What we know from the NK cells that are used ex vivo is that they're very safe, and we're hoping to demonstrate that in our platform technology. In principle, it could be possible. Yes, there's a question. I am Gunnar Kvalheim. I'm previous Head of the Department of Cellular Therapy in Oslo. First of all, congratulation. It looks to be a very interesting study. I have several clinical issues. Are you going to treat the patient three times, every patient, as I can understand? The next would be in the lung cancer, would you select patient that are resistant to checkpoints? Will that also apply to the head and neck cancer? Fiona, do you want to comment on that? Yes. The patients will receive lymphodepleting chemotherapy and then have three doses of cells at intervals of a few days. There is an option to re-lymphodeplete the patients at a later time point and retreat them, but that will be made on a patient-by-patient basis to whether they're suitable and depending on their clinical response. In terms of the patients with lung cancer and head and neck cancer, these will be patients who have not responded to checkpoint inhibitors or who have relapsed following checkpoint inhibitor treatment, by and large, because most of our patients will have received those in earlier lines of treatment. Thanks, Fiona. Thanks for the question. Any other questions before we close? No? In that case, thanks again for joining. I appreciate your time. We'll make this session available on our website, and hopefully, we can bring more news as the weeks develop. Thank you very much, and thanks to Fiona for joining. I appreciate that. We'll stay in touch.