Good afternoon, ladies and gentlemen, and welcome to Scancell Holdings plc investor presentation to report strong phase II data on iSCIB1+ in advanced melanoma. At this time, all participants are in listen-only mode. Later, we will conduct a question and answer session through the phone lines and instructions will follow at that time. I would like to remind all participants that this call is being recorded. I will now hand over to Mary-Ann Chang, Investor Relations, to open the presentation. Please go ahead. Thank you. Good afternoon, everyone, and thank you for joining Scancell's webcast on the SCOPE study result update. My name is Mary-Ann Chang, Investor Relations for Scancell. Presenting today are Phil L'Huillier, our CEO, who will provide opening remarks. Professor Lindy Durrant, our founder and CSO, who'll provide important context on our DNA active immunotherapy, and Nermeen Varawalla, our CMO, who will walk you through the results in detail. Following the presentation, our CFO, Sath Nirmalananthan, will join the Q&A session, and you may submit written questions during the webcast. You can also access the slides directly on the webcast page. Next slide, please. Before we begin, I'd like to draw everyone's attention to this statement. Today's discussion will include forward-looking statements which are based on current expectations and assumptions. Actual results may differ, so we encourage you to review our filings for more details. With that, I'll now turn the call to our CEO, Phil L'Huillier, to get us started. Phil? Thank you, Mary Ann. Welcome, everybody. Good afternoon to everybody in the U.K. and Europe, and good morning to those that are joining from the U.S. We're very excited today to share with you this significant update of clinical data, potentially practice-changing clinical data from the SCOPE study. As Mary Ann said, I will open the presentation, and I'll be joined by my colleagues, Lindy Durrant, Founder and CSO of the company, and Nermeen Varawalla, CMO. They will talk you through the design of the program but also the data from the program. Can I have the next slide, please. Scancell is now two entities, two companies, Scancell Clinical and GlyMab Therapeutics. Today, we're focused on the lead product, the lead program in advanced melanoma in phase II, and we're going to share with you some really impressive efficacy data, strong durability, and very good safety. Next slide, thank you. Let me jump straight in and share with you some high-level perspectives on the data and put it into context. The middle of the slide perhaps shows this best in the orange box. Impressive efficacy data, robust safety with excellent tolerability, and durable responses that we're seeing prolonged progression-free survival. On the right, you can see a progression-free survival curve, and on the left, we've summarized the efficacy data. Let me just talk you through that. Cohort one, the SCIB1 product. On the back of standard of care, nivolumab and ipilimumab, we see an overall response rate of 68.4% and a disease control rate of 89%, nearly 90%. Cohort three, which is the iSCIB1+ product. On the back of the standard of care, we see an overall response rate of 68.9% and a DCR of 86.2%. Thirdly, in the orange box on the bottom, we've pulled together the two datasets from cohort one and cohort three, and we've done this because this is the population that we will go forward to develop further in, so we can pull together this larger dataset. Here summarize the overall response rate, 68.6, and the disease control rate, 88%. Most importantly, also for the types of patients that we are working with, is the durability of the responses. On the right-hand side, you can see an early progression-free survival curve, where we've plotted the two cohorts, cohort one and cohort three, the top line. We've plotted that against standard of care from a clinical study, CheckMate 067. You can see these curves start off together and then diverge over time. Now, although early, we are seeing a significant divergence of these curves, indicating that our patients are having greater durable responses than the historic control, the standard of care, which really bodes well for the patients. This product is safe, efficacious, but also the responses are lasting well in the patients. Next slide, thank you. Let me put this into context. First and foremost, we've been able to say today that we're selecting the iSCIB1+ product for further development and are accelerating the next phase of development. We said we would select the product in the middle of the year, and we're coming back and doing that today. We've selected iSCIB1+ on the basis of the potency and the safety, but more importantly, the efficacy is seen in a wider population, some 80% of the population, versus SCIB1, which is closer to 35%-40%. Lindy and Nermeen will talk you through the basis of those calculations. Additionally, iSCIB1+ has a much longer patent life through to 2039, so that's important for further development. Also from this study, we've been able to identify a potential selection marker for patients that will respond, and this marker could be used in the registrational study. I think this is a really significant finding and has enormous potential to improve the likelihood of success of the registrational study, but it also moves us much closer to new medicine. How do I put this into context? What's the commercial size of the opportunity? Well, if one reflects back to the time when nivolumab was added to ipilimumab, the benefit of doing that is very similar to the benefit we're seeing of adding iSCIB1+ onto these two checkpoints, the standard of care today. The combination of ipi and nivo has captured 65%-70% of the US market in metastatic melanoma. That sizes the commercial opportunity we've got here. The context for patients is on the right-hand side here. Here is Shaw, the lead for the skin cancer service at UCLH and also the SCOPE principal investigator has commented that these findings highlight the potential for a significant clinical benefit for patients with advanced melanoma. In advanced melanoma, there's still an unmet need. Now, I'd like to turn and ask Lindy Durrant to go back in time and tell us the basis of the design of these two products, SCIB1 and iSCIB1+, and the hypothesis that you proposed for how these products would work in pre-clinical, but also in clinical studies. Then from there, Nermeen Varawalla will do a deeper dive into the clinical data. Lindy. Thank you, Phil, and good afternoon, everyone. Could I have the next slide, please? Just to remind those that have been with us for a long time or and anybody who's new, what SCIB1 is a DNA vector and what it encodes is an antibody. What we have done is we have replaced the CDRs of the antibody, which normally bind the antigen, with T-cell epitopes. Okay? We preserve the Fc function of the antibody because that's how we target the high-affinity receptor CD64, which is on activated dendritic cell. You need to target these cells if you're going to get strong, potent, good T-cell responses. Okay? With the initial vector, the SCIB1, we encoded epitopes predominantly from HLA-A2. A2 is the HLA type that presents the CD8 epitope. As Phil's already said, we knew that was only about 35% of patients, but we wanted to check that the vaccine worked and it was working well before we went ahead and put in more epitopes. SCIB1 has two epitopes, two CD8 epitopes, one from GP100 and one from TRP2. Those are both enzymes involved in the production of melanin or the colored pigment in skin. Of course, melanoma is predominantly a skin cancer from those skin melanin-producing cells, so virtually all melanoma has dark skin and expresses our antigen. The success of SCIB1 in our initial studies made us go back and think, "Right, we probably need to target more than just 35% of patients." We did two things. We put in more epitopes, and I'll show you in detail how we did that, again, from the same two antigens, but again binding to more HLA types. We also put in the modifications in the Fc, which we call AvidiMab, which enhanced that binding to CD64. To make sure we got those best T-cell responses and good targeting of dendritic cells. Next slide, please. There you go. We have the differences here. The initial epitopes, there were three in iSCIB1, and then we added three more. That meant we have more TRP2 epitopes. That gave us the best chance of targeting both antigens, not just one. Equally, some of these epitopes now were predicted to stimulate responses or the epitopes would bind to A2, A3, A31, B35, A33, and B44. Okay? That's quite a broad range of HLA types, so we were hoping to cover as many people as possible by using this broad range of HLA types. One of the things that we're saying here and in our patients is when we look at this, we are actually targeting 80% of melanoma patients with these HLA types, and they are the responding patients. In essence, if you have the right HLA type, the vaccine can work, and you do a great deal better, as Nermeen will go on to show you. Next slide, please. This is just showing you some of the new data that we haven't presented before from cohort three. There are forty-nine patients that have been immunized in cohort three, but so far, we only have T-cell responses in thirty-one patients. This is an ongoing study, and we're continuing to collect blood. Okay? If you look there and you look to see the number of people who made a positive response in whether they had a complete or a partial response, that's 79%. Most of those patients had stable disease, at least half of them still also made a good response. The progressive disease patients basically made very poor T-cell responses, and that correlates beautifully again with the HLA type. If you had the right HLA types, you are more likely to be a complete or partial responder or SD. Okay? Again, on the right-hand side, we just show you a fraction of those responses. You can see basically the lines go up because once we immunize, we get better T-cell responses. We get better T-cell responses to all the epitopes we encoded. There are occasionally patients who already make a response to those epitopes, which is as expected, that's why they were picked. Again, we have boosted those responses. The bottom line is T-cell responses correlates with better clinical outcome and is predicted by the vaccines that we put the HLA type. Next slide, please. We then went on to say over half of the patients in cohort one and even more in cohort three responded to both TRP-2 and GP100. That's important because it is possible that you could lose one of those epitopes and basically still continue to be a melanoma. It's much more difficult to lose both of them in what we call immune editing. This makes sure that the responses are durable, and that's what we're seeing over time. We're also showing you that between 58% and 68% of patients in the two cohorts responded with a very strong response to at least one or more of those epitopes. Again, when you see that combined data set, you begin to see those really strong responses coming through. As I say, bear in mind, cohort three is still ongoing. In cohort one, we now have a number of patients who've been on study for two years and having that very strong memory T cell responses. One of the other things that we have found is when we looked at the data, most patients make a CD4 response, but the best responses for this vaccine are CD8 responses. It's the CD8 responses that are presented on that MHC class I, and they were the alleles that I talked to you about that predict the response, and that is our biomarker. You can see in cohort three there, if you had a CD8 response, 83% of them made a good clinical response. Again, the vaccine is working as we predict really well in these extremely advanced melanoma patients, and that's why we're so excited. Next slide, please. Now, one of the questions we've been asked are these T cells really what we call polyfunctional? Do they do multiple things? The answer is yes. They produce cytokines like gamma interferon and TNF. Perhaps even more importantly, these markers in the middle, granzyme, perforin, and granulysin are markers of killer cells. It's the killer T cells, the killer CD8s that are getting rid of these tumors, removing them, and causing tumor regression. Indeed, that's exactly what our data. This is from specific TCRs that we've cloned, we've validated, and we've looked at single-cell analysis on multiple patients. This data is really exciting. If I now hand over to you, Nermeen, so you can run us through in more detail the clinical data. Thank you, Lynley. Good afternoon, everyone. I'm pleased to share with you, and I hope the next slide will allow me to do so, the data from this, our SCOPE clinical program. Let me remind you that the SCOPE clinical program is evaluating Scancell's off-the-shelf immunotherapy or DNA plasmid vaccine as a first line in patients with advanced melanoma when combined with standard of care checkpoint inhibitors. This is a phase II open label, parallel multi-cohort study that's being conducted at sixteen clinical trial sites across the United Kingdom, enrolling over 140 patients. The objective of the program is to select the product and the target population for the follow on randomized phase III trial. I now walk you through the four cohorts that are included in the program. Cohort one that has immunized 43 patients, trials SCIB1, which as you've just heard, and I remind you, is our first generation vaccine along with standard of care double checkpoint ipi/nivo in patients with only the HLA-A*02:01 haplotype. Cohort two does the same. However, here the standard of care is single checkpoint pembrolizumab. Cohort three is when we introduced the next generation vaccine, iSCIB1+, which is being trialed along with standard of care ipi/nivo. As you've just heard, iSCIB1+ is effective against a larger HLA haplotype pool, and hence the patient population that's been immunized includes patients with multiple haplotypes. It's no longer a restricted haplotype population. Cohort four that's ongoing and has immunized 30 patients to date. Again, trials iSCIB1+ in the manner that I've described with two modifications. One is that cohort four introduces what we call accelerated dosing, where the priming doses are delivered in an accelerated quicker succession manner. The vaccine, iSCIB1+, is administered intradermally. The purpose of our investigations is we seek to improve the reported outcomes with standard of care. I remind you that for double checkpoints ipi/nivo, the ORR that's been reported by CheckMate 067, the landmark study was 50%, while that reported in real world settings is lower than that, and the number I suggest for our consideration is 48%. While the ORR reported for pembrolizumab alone in the KEYNOTE study is 41%. Based on our evaluation of the population and our understanding of the HLA types in which our vaccines are effective, we now have a clearly defined target population. This target population excludes patients with acral melanoma and active brain metastases, patients unable to reach the week 13 first imaging point, and patients with HLA MHC class I that includes one of A2, A3, A31, A33, B35, and B44. This group, it's very important, this group represents 80% of the global patient population. Now, what I'd like to do is share with you the preliminary readouts from each of these cohorts in this target population. May I have the next slide, which will talk us through cohort one. Remind you, SCIB1, first generation standard of care, double checkpoint. The next slide will show us the ef... Will show us very compelling efficacy and durability. You see the waterfall plot, which is the RECIST 1.1 best overall response that's plotted on the left-hand side of your screen. Here you will see that the overall response rate is 26 out of 38, which makes it 68.4%, while the disease control rate that includes patients who have not progressed and have stable disease is 89.5%, 34 out of 38. On the right-hand side of your screen, you will see the spider plot for these 38 patients, and you will note that those patients who achieve a response once they have achieved a response, this is a durable response. The curves go down, and then they remain down. Moving on to the next slide, I will show you the progression-free survival curve for this population. As you can see there, the PFS at 22 months is a very impressive 64.6%. Moving on to the next cohort two. Here we are trialing first generation iSCIB1 along with standard of care, single checkpoint pembrolizumab. Next slide, please. Where you will see the waterfall plot in this target population of nine. You can see the overall response rate is 77.8% with a disease control rate of exactly that same number. You can see the durable responses on the spider plot that's displayed alongside. Given that the standard of care has changed in the U.K., recruiting patients into this cohort was not possible anymore. Hence, the cohort has been stopped with only nine patients in the target cohort, in the target population in this cohort. Now let's move on to cohort three. May I have the next slide, please? Cohort three, I will share data with you with our next generation vaccine, iSCIB1+. iSCIB1+, as you've heard, works and is effective in a much larger group of HLA types, HLA haplotypes in our patients. Moving on to the next slide, you will see that the best overall response, the waterfall plot in this cohort of 29 patients is 68.9%. The disease control rate is 86.2%. Again, you see a durable response on the spider plot that's been plotted for each of these 29 patients that I display alongside. The next slide shows you the progression-free survival for this cohort, and that is an impressive 80.8%, almost 81% at 11 months. Although this data will mature, at this stage what is very clear is that the response is durable. This is a very important and exciting finding, much more so because it is this, it is this endpoint that the regulators will accept for market authorization and registration of the product. Moving on. Now, I'll show you the data from cohort one and cohort three. The first thing I want to remind you that here the standard of care in this cohort is the same. All these patients receive ipi/nivo. The only difference is one group of patients have received the first generation vaccine, the second group of patients have received our second generation vaccine, iSCIB1+. The data that I'm going to show you, all the patients in this cohort meet the definition of our target population, which I've already explained to you. Remember, it is this target population that we seek to take forward into our registration study. If I may have the next slide, please. Here you will see a very impressive waterfall plot that plots the best overall response, RECIST 1.1, for 67 of these patients that sit in cohort one and cohort three, all with the same standard of care, first-line advanced melanoma who have received one or two of our vaccines and fit our definition of a target population. Here you see an overall response rate of 68.6%, 88% disease control rate, with 12 patients who've experienced a complete response. Now if we move to the next slide, you will see a really impressive progression-free survival curve. The progression-free survival of this cohort at 22 months is 69%. This has been plotted alongside the progression-free survival curve for patients who've received standard of care ipi/nivo, as shared with the CheckMate 067 study. There's a remarkable 20% difference, 20% uplift on PFS with the against standard of care. For those of you who follow the field of oncology, this is a truly remarkable finding. In patients with advanced metastatic melanoma, to demonstrate a progression-free survival benefit of over 20% is truly exciting. It is this that excites us, and it's this that motivates us to move at speed to progress the development of this product further. If I now move on to get the next slide. I would now like to share with you another very important aspect of our vaccines, which is their high degree of safety, robust safety, and they're extremely well-tolerated. You're all aware of the toxicity associated with checkpoint inhibitors. Hence, it's really important that these patients are not burdened with additional toxicity. The line that I would like to share to draw your attention to in this table that summarizes treatment emergent adverse events reported for all patients in all of our ongoing cohorts. If you look at the events that are classified by our investigators, by their treating physicians as being an adverse event greater than grade three, that is, this is a severe debilitating adverse event. You see the numbers that are deemed to be related to checkpoint inhibitor is 113, while those believed to be related to the vaccine is only 30. This is very, very reassuring for us as we consider using our vaccine not only in the advanced setting but also in the earlier setting, in the neoadjuvant-adjuvant setting. If I now may move on to what I believe is my last final summary slide. I would like to summarize by saying we've now shared with you a very compelling, exciting readout of our phase II open label parallel multi-cohort study. In particular, I want to draw your attention to the cohorts treated with iSCIB1+ and double checkpoint standard of care. You see the response rates there with those who've received SCIB1, iSCIB1+, and combined in this target population. We have an ORR of 68.6%, a DCR of 88%. Enough evidence to demonstrate that the response is durable with a prolonged progression-free survival. We very, very squarely ticked the safety and tolerability box. On the back of this, we are very excited to plan our follow-on phase III study, the selected product being iSCIB1+. We have a clearly defined target population, along with a very clear precise biomarker to select the HLA patients that we know fit the criteria of the target population in which group they can be expected and be confident that they will enjoy the efficacy that the vaccine gives. We agreed on the control arm, which is standard of care, double checkpoint ipi/nivo, and we will adopt what we are calling accelerated dosing, accelerated priming. With that, I will hand over to Phil. Thank you, Nermeen. Could I have the next slide, please? The next slide. I want to summarize the development plans we have and also the commercial opportunity. Before going there, let me use this slide just to pull all of the data that Nermeen has presented together and put it into context alongside the existing standard of care. You can see here, the final bullet on this slide really summarizes the point I want to make. The clinical benefit of iSCIB1+ with standard of care over standard of care equates to a 20% improvement in all parameters, the response rate, the DCR, as well as the PFS, the progression-free survival. Some of these measures continue to grow. We're very excited about what will come. This, as Nermeen said to you, is on top of the fact that this combination is very well-tolerated and safety is excellent. We're in a very, very strong position to move forward. On the next slide, I bring us back to the clinical pipeline and the advances we're planning for the pipeline for iSCIB1+. In the middle of this slide, you can see the SCOPE study and the four cohorts of the SCOPE study that Nermeen laid out. Just to remind you that the fourth cohort, the intradermal cohort with the accelerated immunization, is ongoing, and we will come back to you towards the end of the year with data from that cohort. On the bottom of the slide, I've highlighted where our plans are going. We are determined to accelerate the planning to move to the next phase of development, a registrational study, an adaptive two by three study in the metastatic melanoma population that we're working in now. We're planning to really accelerate the move into that study. On top of that, given we see activity across multiple checkpoints, and given that we believe this product will work even better in earlier stage disease, we're also exploring the possibility of going into the earlier settings of the neoadjuvant/adjuvant population. Early days in the planning there, but it's another possibility for the product. A lot already happening in the pipeline, but more exciting stuff to come. Before we move off this slide, I also put it here for an important point. At the top, you can see the monotherapy study with SKI001. I mentioned this study where we saw really impressive long-term responses in a resectable population, so at the earliest stage of disease, which bodes well for the possibility of the neoadjuvant study. I wanted to highlight this for two reasons. One, I know very well that pharma are particularly interested to see for combination studies like we have here for combination products, activity in monotherapy. Just a reminder that we have seen very, very good activity from our SCIB product. Secondly, also there's a number of people out there in the industry that believe activity of a combination in phase III correlates pretty well to monotherapy activity on top of the combination activity. We're in a very strong place with pharma, but also based on our data and today in the monotherapy data to move forward into later development. Next slide, please. Let me finish off by talking to you about the market opportunity and then our milestones. We've mentioned a couple of times already on the left the unmet need. It's a significant unmet need in metastatic melanoma. It's in fact the fifth largest cancer. A significant number of deaths unfortunately. Checkpoint therapies have made a significant difference to these patients, but still only about half, and in the real world setting, we think it's even less than half, get any long-term benefit from checkpoint therapies. There is a significant unmet need. In the middle of the slide, you can see where Scancell is positioned in the frontline setting and in the unresectable population, the stage 3-B and stage four. That's where we're working at the moment. We are exploring the possibility of moving to earlier stages, the resectable population. On the next slide, please. You can see we've summarized the global market opportunities here. There are sizable market opportunities, first and foremost in the unresectable melanoma, now for iSCIB1+ patient population in our target market and a potential market size summarized there. If we explore the possibility of moving to neoadjuvant, adjuvant and even larger patient population, again in our target HLA market. As I've said to you before, there is the possibility in the future, given the safety that we're seeing with this product, of the possibility of going into high risk populations in a more preventative possibility. Significant market opportunities. Let me just finish with the last slide to highlight to you what's coming up. We've told you during this year that we would share data from the SCOPE study, and we've done that early in the year. We said in the middle of the year we would share this data set with you, and we've done that. We've been delivering on our milestones and our timelines. Over the next quarter, the latter part of the year, I'm really excited to be able to see how the PFS progresses from these cohorts, but also early overall survival data. We'll also see, as we've mentioned, of course, early data from cohort four. We're not going to wait for that data to move on, but that data will be interesting to explore. Then, as both Nermeen and I have mentioned, we're kicking on with planning for the next phase, the randomized studies, and are already underway with the preparation of regulatory filings for both the FDA and other jurisdictions. Then finally, just let me say two further things. One, we have a good cash position, cash through to the second half of 2026, and we are very proactive in our business development perspectives to explore the possibility of partnering, licensing, co-development for the programs, as well as further investment for us to take the program forward. Let me finish there and we'll open up for questions. Thank you, everyone. As a reminder, participants can also submit questions by clicking the question button on the webcast page. Please submit these and the company will get back to you in due course. If you would like to ask a question on the phone line, please signal by pressing star and then one on your telephone keypad. We will pause for a moment to assemble the questions. Our first question comes from the line of Julie Simmonds with Panmure Liberum. Your line is now open. Thank you. Excellent. Thank you, guys. Couple of questions. Firstly on the PFS, which is obviously really impressive so far. I was just wondering how long you are gonna be continuing to follow these patients for, to start with? Because clearly it's still extending at the moment. Yes. Hi, Julie. Thanks for the question. As for the protocol, our patients are on study for two years. Many of our patients are still very much on study and we will therefore report the PFS at the end of 24 months. Also we will in due course be in a position to report some of the overall survival data. You are right in that our data is at varying stages of maturity and we expect it to mature even further. What is very encouraging and indeed exciting for us is the evidence we're getting of durability in that once our patients achieve a response, they maintain a response. We look forward to confirming that with longer PFS follow-up data. Excellent. Thank you. I must admit that is a particularly impressive graph you have on that there. Secondly, just on the selection of patients, it's clear you've got what looks like quite an interesting biomarker for potential use in the registration trial. I was just wondering how routinely it's currently tested for or if this is a novel biomarker, and you'll need to do some development around that too. Again, great question. What our biomarker does is examines the HLA, the HLA haplotype of our patients. To be clear, we're looking for type one MHC HLA alleles. This can be done by serological tests, which is what we do in the United Kingdom, and it can be done by molecular tests in the United States. Happily, this is a very accepted standard test, and there are a number of laboratories all over the world that do it. It's good news for us that it's, and for our patients, that it's a test that's readily available. We, in the course of our study, managed to get a turnaround often within 48 hours. It's a very robust method for which we can use to very effectively and accurately select our patient population. Lovely. Thanks very much. The next question comes from the line of Mike Gednal of Investec. Your line is now open. That's right. Just for a second question. So you mentioned the possibility of looking at earlier stage disease. Following on from Julie's question a moment ago, could the use of the HLA biomarker stratify patients in both metastatic and earlier stage disease settings, or is it at least more limited at the earlier stage? Mike, I think I understood the question in terms of we, do we use it, is there, is the HLA typing a requirement for both resectable and unresectable? The answer is for both groups. The basis, as you've heard Lindy explain, for the HLA type, is that those are the epitopes that the vaccine will work on. Patients who do not have the appropriate HLA type are not in a position for our iSCIB1 vaccine to work. We will use this, the HLA, typing that I've described, which covers 80% of the population for both the resectable and unresectable patients. Great. Thank you. Just looking at the next stages of the development campaign, thinking about the manufacturing, delivery, stable delivery, stability and price of one plus, what are the sort of things that you need to bear in mind at this stage? That's a very good question, Mike. We have a very strong team in Scancell on the development and the CMC side, and the team has already optimized manufacturing and is in the process of scale up. You'll also remember that this product is an off-the-shelf product. Some of the challenges that others have with the personalized approach, it doesn't apply to our therapy. It's a straightforward, so to speak, manufacturing process. It's been optimized and is currently being scaled and delivery of that to the patient and immunization of the patient has been worked out through this study. I think we're very, very well placed in relation to the CMC questions. Okay. Many thanks for that. Great day for the day. Congratulations. Thank you. Your next question comes from the line of Edward Sham of Singer Capital Markets. Your line is now open. Hi there all. Congratulations on an excellent set of data. I think my first question is just around the kind of phase data, and that really should be putting you on the map of large pharma and biotech. I just want to kind of understand how much weight does that have in kind of future and current partnering discussions? That's a very good question. I think it's significant data in any context, but it is also important data in the context of potential partnering discussions with pharma. We are very proactive around exploring the possibilities with pharma, really around all avenues of licensing as well as co-development with pharma, of the program. Yeah. That's definitely helpful. My second question is just probably around the kind of inclusion of the AvidiMab in iSCIB1+. Did that lead to any measurable improvement in immune response or clinical efficacy? I know there was a statement that said the data appears to be equipotent to SCIB1 on a patient basis. I'm just wondering if there was any visible benefit, and was that in line with your internal expectations? Lindy, would you like to take that question? Yeah, definitely. I think we've had two benefits really. One is, as I say, we are getting better responses to both TRP-2 and GP100, which is a significantly better thing for the patient and I think that's reflected in the better durability. Now, we have to be a little bit careful because the PFS for cohort three is not as long as cohort one. At the moment, if anything, the AvidiMab is helping in that durability of the response. I think it's a bigger population for sure, which is really interesting, and that's really what we went for. I think the AvidiMab has probably just made that response as, a little bit better and a little bit stronger. At the moment, we don't have compelling data for that. No, great. Thanks. Then just maybe one last one on cash runway. You guys mentioned that a potential accelerated kind of plan for the typical registration trial and engaging with FDA by the end of the year. Does that impact your cash runway? Which I think our current guidance forecast kind of goes through to second half 2026. We've considered that, Ed. As you say, I think we're in a very strong cash position. I think we've got a further 15 months, if I can add more detail to our runway, as well as upside opportunities on that too. I think there's a very healthy cash runway, and we've certainly incorporated the early spend on these regulatory activities and allowing us to accelerate through to the next stages of development. It doesn't materially impact the guidance I'm giving you on our cash runway. It still remains very positive into H2 2026. Great. Thank you very much. There are no further questions on the conference line. We will now address the written questions submitted via the webcast page. I will now hand over to Mary-Ann Chang, Investor Relations, to read them out. Thank you. Our first question is for Nermeen. Do you believe cohort four will improve on these results, and how does it compare on initial readouts? Thank you for that question. Let me be clear. Cohort four, although we've immunized 30 patients, and it's, we've been enrolling these patients at a great and very rapid rate. The first of those patients have not yet reached their week 13 scan. As yet, I'm not in a position, we're not in a position to give—to have any sense on the efficacy of cohort four. It's too early for us to comment on that. That's the first thing you should know. As you heard Phil say, we will be in a position to comment on the readout of cohort four in the fourth quarter of this year. The two other things to say is that, given... We await the outcome of accelerated immunization. We await the outcome of intradermal administration of the vaccine. One thing remains clear from our data that the PFS advantage that we've shown over standard of care of over 20% is very compelling and compels us to move the product forward to the next phase of clinical development. If the delta were to improve in cohort four from the present 22% to, let's say, 35%, sure, we would reconsider that. Given it's advanced disease, the chances of that happening, even in our wonderfully designed cohort four, is not that high. The answer is that we've taken some lessons. Of course, we will wait for the final readout. Very, very importantly, we owe it to our patients to complete the cohort, if we will. I would be very, very amazingly and happily surprised if that cohort could beat, in a significant way, the results that we've demonstrated so far. If it does, yes, we would be thrilled to include that in the IND submission as we progress with our conversations with the FDA. Thank you. That's clear. Another question for you, Nermeen. Can you explain why you've combined data between the two cohorts only to report the 69% ORR and why you think that's relevant? I think I was very clear in the presentation, but I'm very, very happy to go through it again because it's really important. We have defined what is the target population for all patients. The target population are, we're excluding acral melanoma and active brain mets. We're excluding patients that don't reach the first endpoint, i.e., the week 13 imaging scan. We are only including patients that match the HLA class I MHC HLA haplotype that our vaccine works in which, and as far as that is concerned, that's 80% of the population. We have to be really clear on what the target population is. Having defined that, then if you look at cohort one and cohort three, the only difference between the two is cohort one has our first generation vaccine and cohort three has the second generation vaccine. Therefore, in an effort to give us comfort with a larger denominator base, I feel, and we feel very comfortable in combining cohort one and cohort three, understanding that the difference between them is only with respect to the first and second generation vaccine. Therefore, we combined them and had that denominator of 67%. On that, we achieved a very impressive ORR rate of 69%. May I remind you, the real world evidence suggests that ORR with standard of care ipi/nivo is 48%. This, if you use that, it represents a 21% delta. That sits in very nicely with the PFS delta. On the basis of all of this, we have a great deal of confidence. That combining cohort one and cohort three in our target population, using the parameters I've defined, is exactly the combination we need to take forward to a larger randomized controlled phase III setting. Great. Very good. Thank you. Moving to Lindy, this has already been somewhat answered, but you may have something to add. You mentioned a biomarker enabling optimized recruitment for the phase II, phase III trial. To what extent do you expect this to improve iSCIB1+'s performance for that trial? Again, just to clarify, because I know it's very complicated. The epitopes that we have put in iSCIB1+ can only be presented by certain HLA types. Okay? What I find amazing is the epitopes we put in and the HLA types we predicted are indeed where we are seeing the T-cell responses and the clinical responses. Therefore, our biomarker is saying, for the vaccine to be effective, you have to have the HLA types that we are talking about. Let's say 80% of the population, so that's fantastic. That's a good number. We've doubled our market, which is massive and really exciting. It re-emphasizes the science. What we predicted is true. We've immunized all patients just to make sure, but it's actually come back very strongly to say, "Yes, you were right. Your prediction was right, your hypothesis was right. These are the patients that are benefiting, and these are the patients you must select for your phase II, phase III randomized study. Great. Thank you. Nermeen, back to you. Given the high response rate and unmet medical need in advanced melanoma, do you think Scancell could be eligible for accelerated approval or breakthrough therapy designation from the FDA or similar regulatory bodies like the MHRA in the U.K.? In a word, the answer is yes. On the back of this very compelling data, and mind you, as somebody who works very closely with our physicians, is in continuous contact with our patient support groups, there's a huge need for the therapy we have. We have the opportunity to transform the care of these patients and allow large numbers of patients to live cancer-free. Just think what an important thing that is, and we are on the brink of that. In my word, the answer is yes. We are working very hard to swiftly have scientific advice conversations with multiple regulators, the FDA, EMA, MHRA, with an effort to get this designation and swiftly move to make these therapies available for our patients, both in the advanced as well as in the resectable settings. Great, thank you. Sass, one for you. There are a number of questions on financing. After grouping them together, how are you thinking about funding for the next stage of development? Thank you. As I said, I think we're in a pretty healthy cash runway position. To reiterate, we've got circa 15 months of cash as well as upside opportunities on that cash runway too. As Phil has highlighted, we are in proactive conversations on the business development side, and now we've got data on cohort one, cohort two, and cohort three. I expect those conversations to deepen, and in some cases we will be revisiting existing conversations to tell everyone how compelling this data is. Partnering and co-development are clear opportunities for us, and we have the cash runway to explore those and to really drive and assess what's best for the future development of the iSCIB1+. It is clear that if we consider and we decide that future financing is what we need to push us forward, that's something we will consider. We have time, and we have the data to explore what's right with shareholder value in mind. Very good. We have answered all the questions. I'd like to hand back now to Phil, for closing remarks, please. Thank you, Mary-Ann Chang. I think today you've seen an amazing set of data, and you've also seen the excitement from the team, but also our determination to move this program forward to patients and for a return to investors. I'm a believer that what makes a good drug is strong foundational science, a good understanding on how it works, and then the testing of it in the right patient population. That's what Scancell has done and will continue to do. Let me just finish by acknowledging that all of this work started with Lindy and her scientific team in the laboratory. Kudos to Lindy. Thank you, everyone.