Good afternoon, and welcome to the Poolbeg Pharma PRC investor presentation. Throughout this recorded presentation, investors will be in listen-only mode. Questions are encouraged and can be submitted at any time via the Q&A tab situated on the right-hand corner of your screen. Simply type in your questions and press send. The company may not be in a position to answer every question it receives during the meeting itself. However, the company can review all questions submitted today and publish responses where it is appropriate to do so. Before we begin, I'd like to submit the following poll, and I'll now like to hand you over to Jeremy Skillington, CEO. Good afternoon, sir. Good afternoon, Lily, and thank you for that introduction. Good afternoon to everybody, and thank you for joining us today at lunchtime. Hopefully, you have your sandwich or bowl of soup in front of you, as we want to give you some very exciting, very important updates from Poolbeg just over the last short while. My name is Jeremy Skillington, the CEO of Poolbeg Pharma, and delighted to be joined today by Professor Brendan Buckley, who sits on our Scientific Advisory Board and as an NED as well, and Dr. Liam Tremble, our principal scientist. Today, I do want to go through and give you a sense of where Poolbeg are. I know we are familiar to many of you, but for those maybe not so familiar, we are a very highly experienced team with a proven track record, lots of years in the biotech and pharma industries. We've got a very exciting pipeline of high-value programs targeting critical unmet needs, and we're going to go through in great detail today POLB001, our lead program, which just recently got announced to get orphan drug designation from the U.S. FDA. Very exciting time for that. I think importantly for investors, we've got multiple near-term value inflection points, and these are clinical value inflection points, and we'll talk about those as we go through. As I said, right now we're focused on execution of these clinical trials and ultimately leading to partnering. We can touch upon this maybe in the Q&A, but lots of good discussions with pharma partners who are very excited to see us execute on the POLB001 CRS clinical trial, which we'll speak to, and again, leading to partnering thereafter. We did announce last week a fundraise, GBP 4.865 million of conditionally raised, obviously pursuant to a general meeting at the end of June, but this added to our cash balance of GBP 6.2 million that we had at the end of March, gives us a really nice cash runway into 2027 as we have to execute on these clinical trials and then importantly achieve these milestones and partnering. This is the Poolbeg pipeline as we stand today, the lead program POLB001. It's a p38 MAPK inhibitor. This is a master regulator of the immune system, of the immune or inflammatory response, and we are pursuing this drug in cancer immunotherapy-induced cytokine release syndrome. This is a really significant or serious issue for patients who are already undergoing cancer therapy, but their immune system goes awry, gets overexcited, you could say, and causes significant issues to these patients. We've got a small molecule, orally available drug to prophylactically prevent CRS, which we're putting into clinic later this year. As I mentioned, very exciting news that came through to us late on Friday that the FDA has granted us orphan drug designation, and thankfully, Professor Buckley will go through the details of that later on. I mentioned the clinical milestones are very important, so we're on track, the first patient to be dosed in the second half of this year, H2 2025, in this phase 2A trial. Yes, that will be in multiple myeloma patients, and that was specifically a request from Pharma Company. They want to see the safety and efficacy of this drug in patients. This is a very rapid trial, so we'll have interim analysis, interim readouts from a subset of these patients in the first half of next year. Again, looking to see the cytokine release syndrome, how POLB001 impacts or prevents CRS in the first half of next year, and then the full top-line data the second half of next year. Again, we have a nice momentum of milestones, but I think importantly, we're going to get really good data quite quickly, essentially quite quickly. The second program we won't touch upon today, but we've got an oral encapsulated GLP-1 program. I think the world is getting very excited and acknowledging the importance of these GLP-1 receptor agonists, those on the market, the majority of which are given by injection, and we've got an oral encapsulated version of that. Again, planning to take this into the clinic for a proof of concept, a proof of technology clinical trial, again later this year with top-line data again, very rapid in the first half of next year. Two AI programs come from kind of our legacy collaborations with CytoResin and OneThree around identifying new and novel drug targets to influenza and novel drugs to RSV, respiratory syncytial virus. That is the pipeline as it stands right now, but as I said, the majority of the focus today will be on POLB001 because, as I say, on the back of this orphan drug designation given by the FDA on Friday. I will walk you through CRS, cytokine release syndrome, the dramatic impact it has on patients, but I think importantly as well, the benefit that we could bring to the marketplace and ultimately contribute to a market that we have estimated to be over $10 billion. Cytokine release syndrome, CRS, is a severe, potentially life-threatening side effect of cancer immunotherapies. Now, cancer immunotherapies do a terrific job of reorienting your immune system to go after a tumor. Not an easy thing to do because that's your cell tissue, your cell tumor, but they do a really good job, particularly in the hematological cancers, of increasing surviving of these, for example, multiple myeloma patients. You do have the side effects. Upwards of 70% of the patients receiving either a bispecific antibody or a CAR T -cell therapy develop cytokine release syndrome, CRS. This is a significant issue for the patients themselves, obviously. They're not feeling well. They're on cancer treatment anyway, but they're not feeling well, and these CRS can escalate where these patients are essentially, they're on respirators to begin with, ventilators, and their low blood pressure, but ultimately this can go down to multi-organ failure. It is a significant issue that needs to be stopped. As I say, with a small molecule, POLB001, we feel we can potentially prevent this from happening in the first place. There are no approved therapies for the prevention of CRS. Right now, it's kind of managed in a reactive manner where these patients are given tocilizumab. This is an interleukin-6 antibody that's already on the market for rheumatoid arthritis. They give it as a rescue to try and manage that CRS symptoms that they receive. I said, nothing is out there yet to prevent CRS, particularly grade 2, and we, as I said, planning a clinical trial later this year to demonstrate that proof of concept. We've done some independent analysis last year. We talked to a lot of key opinion leaders, we talked to clinicians, we talked to payers, and we estimate that we could potentially enter into a $10 billion market opportunity. I'll touch upon this in greater detail later on, but I think right now we're at a really interesting time as the growth essentially of these bispecific and T-cell engagers and CAR Ts. As I say, if we can manage CRS as a support therapeutic, then I think we'll have a very exciting market ahead of us. I do want to comment on Poolbeg as we were. Many of you know we started off looking at infectious diseases. We spun out of hVIVO in 2021, and I think we really kind of opened up a very exciting opportunity in the oncology space. We were pursuing POLB001 for severe influenza. Many of you will remember we got terrific data using an LPS challenge study. Liam will present some data on that later on. I think what grabbed our attention a few years ago was this urgent need to prevent CRS in this oncology, in this immuno-oncology setting. We kind of dived into that deeper, and it became very clear to us that this would supersede by an enormous factor the market for influenza. We pivoted in that direction. We were rapid in 2023 filing patent applications in this immuno-oncology space, and at the time we had data coming through from our LPS challenge study that we presented at the American Society of Hematology Conference in the U.S., and that got the attention of the hematologists, recognizing that here could be something of benefit to their patients who receive these bispecifics and CAR Ts, but unfortunately also develop CRS. Again, we did our analysis in 2024, $10 billion market opportunities, talked to a lot of key opinion leaders. We generated additional preclinical data in a mouse model of CRS. We presented that at the ASH conference, American Society of Hematology, again back in December. That was very well received. We are building a nice momentum and getting a very good network. Where we are today, as I mentioned, we are phase 2 ready, planning to go to the clinic later this year, first patient dose in the second half of this year. As I say, strong indications that colleagues at Big Pharma, who we from a business development standpoint have talked to, updating them regularly on our activities, they have strong indications they will provide us with the bispecific antibody for that clinical trial free of charge. They see the benefits that this could improve the outcomes from there, the safety outcomes from their drug, so they are willing to give us this antibody free of charge. So then we can take that forward into our study in combination with POLB001, and as I say, study that CRS aspects of these multiple myeloma patients. I think excitingly then for the company, we announced just yesterday after receiving news late on Friday that the FDA has granted us orphan drug designation for the prevention of T-cell engaging bispecific antibody-induced CRS. That was a really nice way to end the week last week, and as I say, we're building on the momentum that we've generated over the last three, six, 12 months. On that, I do want to pass across to Professor Brendan Buckley now. Brendan will talk you through the aspects of the FDA orphan drug designation. Brendan, over to you. Thank you, Jeremy. I'm a Non-Executive Director of Poolbeg and also direct the Scientific Advisory team. My background in orphan drugs is that I was a member of the Committee for Orphan Medicinal Products at the European Medicines Agency and also was a faculty member for a good number of years on an advanced course on clinical trials in rare diseases that the FDA used to run for their internal staff. I'm a former Professor of Medicine Pharmacology and also former Chief Medical Officer of ICON. Next slide, Jeremy. What's the significance of orphan designation? The first thing to say is it's not a license from the FDA to put the drug on the market yet, but it essentially gives us a lot of incentives and help to develop what they regard now as a drug with plausible promise. In 1983, during the Reagan presidency, an Orphan Drug Act was passed to facilitate development of drugs for rare diseases. These are defined as diseases affecting fewer than 200,000 persons in the U.S. at any given time, and they provide for financial and other incentives to develop the drugs to treat, diagnose, or prevent these diseases and conditions. The act tells us what we have to do to designate these drugs, and effectively we have to prove the incidence that we're fewer than 200,000 a year in the U.S., but they also make us show that it is plausible that these drugs will work, that they have a good prospect of turning out to be effective in the disease and the condition. In a sense, a regulator granting orphan drug designation is an external review of the plausibility of what we're doing, and it confirms that we're on the right track in our supposition that this will work. Again, to reiterate, granting orphan designation is not a license to market the drug. That comes later at the end of trials. Next one, Jeremy, please. Thanks, Brendan. You froze there a little bit, Brendan. Can you do your last couple of sentences there, please? Sorry. We have to provide data to the FDA, which demonstrates to them that we have a plausible basis for expecting the drug to work in this indication. The fact that we've got orphan designation tells us that the FDA are happy that we're proceeding in the right direction and we're not following a dream. We're following something which is highly plausible that may work. Brilliant. Thanks, Brendan. The orphan designation, of course, is not a license. I'll reiterate that again. Why are we so happy? Why was it a great Friday? The benefits of this designation, the kind of highlight ones, come both during development of the drug and when the drug is on the market. Importantly, we sit into a nice relationship with the American regulator in that, for example, by designation of orphan, we do not have to pay regulatory fees, and that is a considerable benefit. It is of the order of more than $200 million U.S. dollars. Anybody who normally applies for a drug to get an NDA to go into clinical trials or to proceed towards a market authorization application has got to pay very hefty fees. Basically, the drug developers pay the drug regulators, and we have a favorable regulatory engagement with the FDA, and this includes free advice from them on how appropriate or otherwise the protocols that we're going to use in the clinical trials are to getting us to the endpoints that we're looking for. Finally, for qualified clinical trials, there are tax credits down the line in the U.S.. This is very helpful during development and again extends our runway considerably. Once the drug gets on the market, if we are successful in that, we have Uncle Sam protecting our intellectual property to an extent for seven years, so nobody else can compete with us in this area if they have a drug which works similarly to us. The orphan designation protects us from Metoos. Somebody can come along with a drug that is subtly different in molecular structure but works the same way to POLB001 and get it on the market. We're protected by the regulator from that. Also, it's recognized that during drug development, you lose patent life, and the orphan designation allows the clock to be rewound to start later so that your loss of patent life begins much later than if we didn't have orphan designation, and this can add several years to the patent along the line. The effect of the Orphan Drug Act in the United States was really to start the whole biotech industry. Companies like Genentech and so forth, they all started off with the Orphan Drug Act, which enabled them to develop drugs for rare diseases that otherwise were considered not worthwhile commercially. You can see why we are really incentivized by this and very energized by it now. Thanks, Jeremy. We'll move next to Dr. Liam Tremble, and Liam is our Principal Scientist who's in charge of this program. Liam has a very strong background in immunology, and I would have to say he's probably one of the best drug development scientists I've ever worked with over the years. Thank you, Brendan. High praise. Hopefully, I can live up to some of that, but thank you all for your time today. I'm just going to speak through some of the existing preclinical and clinical data that we have so far and some of our clinical plans as we move forward. On the slide in front of you, I'm just going to take a little bit of time that the result is straightforward in that we were able to show that in a mouse model, in a humanized mouse model, that POLB001 was effective in reducing CRS. The detail on the slide, I'll just go through and explain it a little bit in a little bit more detail. Essentially, cytokine release syndrome is quite challenging technically to study in animals. This is largely because they need to be humanized, so to induce a human immune system. In the top bar, this is what we're looking at, that we use a special strain of mice that have genes knocked out, including major histocompatibility complex, so they do not have any rat or mouse immune cells. What happens is we give them human immune cells, and we pre-select these for high reactivity. We give them about five days before we induce cytokine release syndrome to allow those cells to go into the tissues to mature and to really make the mouse humanized in terms of we're studying the human immune system rather than the mouse immune system. Similar to what our plans are in the clinic, we prophylactically dose with POLB001. What we did in this case was we induced CRS with a CD28 super antibody. CD28 binds on T- cells and essentially to get a very vigorous and violent activation of T- cells that stimulate your cytokines and then drive symptoms. That is the important part that we really wanted to study and that we were not just interested in the prevention of cytokines, but we really wanted to test if POL could reduce cytokines and have a clinical improvement. This model is quite specialized. The Jackson Labs in the U.S. does it for us, and they have a special strain of mice where one of the challenges with a humanized mouse model is you always get a residual level of immunogenicity against the human immune system. This is called background graft-versus-host disease where the mouse immune system, residual immune system, still recognizes the human immune system. We can basically minimize that because the symptoms overlap with cytokine release syndrome, and that allows us to see cytokine release syndrome physically manifest in these animals over what we would see in background graft-versus-host disease. In the graph on the left-hand slide, as you're looking at it, the difference between the navy and the red lines, this is essentially without POLB 001. We had a CRS score of 2, which is no CRS really. It's background graft-versus-host disease. What we can see is when we introduce CD28 into the red, we see actually the clinical score increase where they have symptoms of cytokine release syndrome. You can see we introduced three different doses of POLB001, and actually what we saw was that it brought the CRS right down to the background graft-versus-host disease, indicating that we completely reduced or diminished the cytokine release syndrome. In this model, we also used an anti-TNF antibody. In the clinic, as Jeremy introduced, there is an antibody, Tocilizumab, which has anti-IL-6 receptor use. In this case, the difference was purely a technical limitation of the model in that an anti-TNF antibody is better than an anti-IL-6. This was really the gold standard that we wanted to use in this model. As you can see, it was also effective. When we looked at the biomarker responses, we looked at a number of biomarkers, but for simplicity, I have only shown IL-6 and TNF alpha here. What we can see is that the red line where we induce CRS, as we expect, we get an increase in various cytokines that increase with the clinical manifestations. As we introduce POLB 001, what we see is these cytokines really go down greatly, almost in the terms of IL-6 to background levels of graft-versus-host disease of the navy line. Interestingly, in terms of the anti-TNF antibody, POLB also outperformed this antibody for almost all markers or for all markers with the exception of TNF, and that's because an anti-TNF antibody will quench TNF, so even the assay is going to be a little bit biased. We were really impressed and promised and enthused by these results. This is some new data that we haven't shared before and we'll share a little bit more later this year, but essentially as part of the orphan application, one of the things we did really want to do was to say, well, look, we've looked at cytokine release syndrome in an animal model using this CD28 stimulus, but we really wanted to use specifically a bispecific antibody as we intend to do in the clinic. What we used here is a CD19, CD3 bispecific antibody, essentially equivalent to Blincyto, an acute lymphoblastic leukemia drug that's currently in the clinic. The important part here is that it stimulates T- cells by CD3, so it gives equivalent indications as to the other multiple myeloma drugs, which are BCMA, CD3 bispecific antibodies. What I'm showing you here is similar to the last slide with IL-6. This was a slightly shorter model just for technical limitations, but here we can see that in this model as well, POLB greatly reduced IL-6 levels, giving us an indication that we will hopefully see clinical benefit as we move forward towards our planned clinical trial. On this next slide, this is one that some of you may have seen before, so I'm just going to give a brief summary of our previous LPS challenge trial that we conducted. This is a phase 1B clinical trial where we use lipopolysaccharide, a component of the bacterial cell wall, to induce an acute inflammatory stimulus. Similar to how we intend to dose in our upcoming trial, we administered POLB 001 prophylactically for four days before we gave an intradermal and then an intravenous dose. I'm going to focus on the intravenous dose because that's more representative of a systemic inflammatory response, which is what we're kind of comparing to as we move forward with cytokine release syndrome. As we can see here, again, I'm focusing on IL-6 because we know this is a clinically important cytokine in cytokine release syndrome. What we can see is actually the two upper doses that we used in that trial of 70 mg and 150 mg twice daily were both highly beneficial to the patients or to the healthy volunteers in this indication. One of the strongest parts of the LPS challenge study in its relevance as we move forward with cytokine release syndrome is LPS doesn't just induce cytokines, but these cytokines are coupled to clinical responses. In our case, we were able to see a heart rate elevation and also an increase in heart rate driven by the LPS. As we introduced POLB001, what we saw was that these elevations were actually decreased. Again, give us an indication that hopefully we'll be able to drive meaningful clinical benefit as we move towards the prevention of cytokine release syndrome. I mentioned the trial we're hoping to do later this year or to start later this year. This is a trial in multiple myeloma patients receiving a bispecific antibody. The bispecific antibody induces cytokine release syndrome, and what we're planning is prophylactic dosing to cover the entire step-up dose region, which generally occurs over the time course of about five to seven days. This is the highest risk period of cytokine release syndrome and currently requires patients normally to be given the bispecific in a hospital setting. What we're interested in is obviously looking at the biomarkers as POLB 001 is introduced, but then also looking at the incidence of CRS, specifically grade 2 or higher CRS, which tends to be more clinically severe, clinically challenging. If we can reduce that or eliminate that completely, then obviously the drug will have high value as we move forward. One of the other things that we're interested in is to see if we would still need the same level of Tocilizumab usage for, as Jeremy said, rescue use of cytokine release syndrome. The trial is designed as a simple, rapid trial that will allow us to get proof of concept data as we move forward. Twice daily oral dosing, single arm, open label, using an approved bispecific. We have really been focused on making sure that we design a trial that will allow us to get rapid clinical data. For this trial, we have had strong indications from Big Pharma that they are willing to provide the bispecific antibody free of charge. That is, again, a big boost in terms of making sure that this trial moves quickly and that it recruits quickly. We are hoping to start in H2 2025, and we are hoping to have top-line data at the second half of next year. We have had leading myeloma clinicians enthusiastically participate on this trial, and that is something that I know I am personally excited to be able to share later in the year. We will definitely give you more updates as we are able to share more information. We do have extensive engagement with myeloma experts and key opinion leaders in the field, such as Martin Kaiser and Gareth Morgan. They have all highly enthusiastically endorsed the program, which is really exciting for us at Poolbeg. As we move forward, I'll hand you back to Jeremy for the moment to go through some of the market opportunities. Brilliant. Thank you for that, Liam. It's, as I say, comprehensive, very exciting time for the company to get into the clinic and test this in multiple myeloma patients. But it's worth pointing out, as I say, in my kind of last few slides here, I don't want to leave time for Q&As, obviously. But in my last few slides, I do want to talk about the market. I mean, we come at this from a scientific standpoint, a clinical standpoint, patient benefit standpoint, but it is important for us to understand the marketplace and what the market size should be. I just want to kind of take you through the logic of that and the work that we did last year to kind of estimate what impact POLB001 could have on the marketplace. As mentioned earlier on, I mean, this is a significant market opportunity. The uptake of bispecifics and CAR Ts in the immuno-oncology space is quite significant. On the right-hand side graph here, you can see it's estimated that these drugs alone will generate revenue of upwards of $120 billion by 2030. Sorry. Again, as we see, I've lost the presentation there. Thanks, Lily. Sorry. Just moving on. As we see this, as these drugs are kind of driving increase in sales, we also hope to have POLB 001 in parallel with these drugs as a supportive care to prevent CRS as they're getting into patients. Right now, I mentioned there's nothing on the market for prevention of CRS. As I say, the market and the clinicians and the payers are looking for effective CRS management across both bispecifics and CAR Ts. We did a deeper analysis on this where we looked at just two tumor types in the hematological space. We looked at multiple myeloma and diffuse large B-cell lymphoma who patients currently receive the bispecific antibodies and CAR Ts. We are estimating that about 500,000 patients by 2030 will be diagnosed with multiple myeloma and diffuse large B-cell lymphoma. That is in the U.S. and the EU5 only. Again, that is kind of a subset of cancers, you could say, but a subset of the world, and we decided to focus in on there. As I say, the potential to kind of treat these patients is really what is driving us from a motivation standpoint. The key here is that these patients receive their bispecific and CAR Ts in a dedicated cancer clinic. We talked about Tocilizumab earlier on as an antibody. If they receive that, that's given as an IV infusion. You have to be in the clinic for that. One of the key advantages of POLB 001, not just from, we hope, an efficacy standpoint, but it's a pill. It's a small molecule that can be orally delivered. The patients can take this at home. That really takes a lot of pressure off the healthcare system and the patients themselves. When we dug into it deeper, and I think this graph kind of summarized it well, you've got 500,000 people coming into the system, coming into these dedicated cancer clinics, lining up to receive their bispecifics and CAR Ts. There is a bottleneck because if you come into the cancer clinic, the fear of CRS is that you have to stay there for a week or 10 days or two weeks just in case CRS develops before they are able to send you home. Our belief is that if you can prevent CRS in the first place, but also have POLB001 as an orally available, or patients can take it home, you are going to open up this bottleneck. You are going to get more patients through the system. We can charge, obviously, for POLB001, but I think importantly, and we have discussed this with pharma partners, that they see that there is the potential that they will increase their revenue of their own bispecific and CAR Ts because we are opening this bottleneck. Liam referred to Martin Kaiser, and he has a nice quote there. If there was a therapy that was orally delivered, a whole lot of the infrastructure requirements falls away. That is the number of beds required for these patients, the clinicians, the nurses, etc. Very exciting time for the company, as I say, very keen now to move forward and get this clinical trial up and running. My last slide here before we go to questions is just a reminder. I mean, we feel at 001, we are addressing a critical unmet need here, and it could be attractive to pharma companies who are seeking to gain competitive advantage in the space. A lot of them are going after the same tumors. There are a lot of them going after the same targets, even on the same tumors. If you can have a drug that kind of eliminates CRS, I think they'll see that there's going to be significant benefit in the marketplace for their particular drugs. As I say, we talked about expanding the market for them, getting them through the system, more patients go through, and that will obviously generate greater revenues for these bispecifics and CAR Ts. Importantly, improving patients' lives and taking pressure off the healthcare system. As Liam's mentioned and I mentioned, I mean, great discussions with pharma companies. They want to see this data coming from these multiple myeloma patients. They've agreed to give us free of charge. They've kind of indicated that they give us free of charge the bispecific antibody required for this study. That's going through the various kind of discussions right now with regard to paperwork required for that. As I say, that's great validation from them that this is a clinical trial they want to see started and obviously see the data come out the other end. We see with this data, with this 2A data in hand, I think that's going to be of great interest to multiple pharma companies when it comes to whether they can apply to their bispecifics or CAR Ts. It'd be great. We hope a lot of interest in pharma companies with this positive data in hand. As I say, having the orphan drug designation in hand strengthens our hand there as well because, as Brendan mentioned, seven years of exclusivity on the market in the U.S. with this orphan drug designation once it's launched. Again, that gives us an inside track, let's say, in building up and generating rapid revenues from POLB001. That's where I will finish up. Again, appreciate your time this Wednesday lunchtime. What we'll do, we'll switch on now for Q&A. I'm just going to grab a little bit of water before I do that. Jeremy, Brendan, Liam, thank you very much for your presentation this afternoon. Ladies and gentlemen, please do continue to submit your questions just by using the Q&A tab situated on the top right-hand corner of your screen. Just while the company takes a few moments to review those questions submitted today, I'd like to remind you that recording of this presentation, along with a copy of the slides and the published Q&A, can be accessed by your investor dashboard. As you can see, we've received a number of questions throughout today's presentation. If I could hand back to you to read the questions and give responses where appropriate to do so, I'll pick up from you at the end. Happy to do so, Lily. And thank you. Water on board. Again, thanks to everyone submitting questions. I see they're kind of coming through here. I'll kind of read them down again. We've got about 10 minutes or so, so apologies if we don't reach all of the questions, but we'll do our best. What I'll do, I'll read the questions. Since, let's say, I'm chairing the meeting, I'm going to point a finger at Brendan or Liam or even myself to answer the questions, but we'll get through as many as we can here. I'll start. James C, thank you. Will there be an early indication of success on POLB001 trial before 2026? Just to go through the various milestones we talked about there. In H2 this year is kind of starting of the trial, getting the first patient on board. Liam talked about the clinical trial design. Again, we're looking at that immune response. Just to be clear, we're not looking at, let's say, kind of overall survival or progression-free survival at the various oncology endpoints. We will have a very rapid kind of immune response data set. Now, we did talk about having it is an open-label trial, so we can see the data as it comes through. We will have interim readouts of the patient data, let's say the first six patients or eight or ten, first small number of patients. That would be in H1 of 2026. That will be in the first half of 2026. As these kind of patients enroll, we'll have the data coming through with the full kind of top-line data set by the end of the year. I would not say before 2026, but I would say in the first half of 2026 is where we will see some of this, as I say, patient data coming through for, as I say, the prevention of CRS. Again, appreciate the question. Second question coming through here. Keith M, thank you. When will we hear which pharmas will provide the bispecifics for POLB 001 trial and confirmation that this would be free of charge? Really good question. I mean, pharmas are kind of interesting. As I say, we have had multiple discussions with all of the bispecific pharmas, the CAR T pharmas. I like to kind of comment that they do not know that CRS is an issue unless, just say, they do not kind of shout it from the rooftops. Sometimes they will give us the drug, and maybe they will not want us to publish which pharma company is doing this for us. We will, as I say, hopefully that will kind of give us a springboard or accelerate discussions ultimately with a partnership. That partner will then be named. I think what's interesting in the way we've kind of set this up from a clinical trial standpoint and even from a Poolbeg company standpoint is that we still want to be somewhat agnostic. We don't want to have ourselves kind of in the throes or in the arms of kind of one pharma to do this trial. We want to get data with one bispecific, obviously, but we believe this will apply to other bispecifics and other CAR Ts. We feel that we want to keep all of the pharma companies hungry so that we'll get the best deal possible for Poolbeg when we have this data in hand. I say sometimes pharmas do not want to be named for various reasons, but if they allow us, of course, we will name them. Very, very good discussions with these pharmas. We have a meeting set up in a few weeks at the European Hematology Association Conference that is going on in Milan. Again, sitting down with pharma talking about this clinical trial and endpoints, etc. Really good engagement there. Question from Peter, or sorry, from Keith. When will we hear? Sorry, that was the one I just already asked. Apologies. Next one. Did any large pharma participate in the recent fundraise? No. Short answer is no, they did not. As I say, when it comes to kind of contribution to the trial, obviously, we are getting the bispecific antibody if you want to count that. The recent fundraise was really kind of from the Irish kind of high net worth networks, some funds, some institutions in London, and some, as I say, some generalist investors as well, but no pharma in particular. David T, Jeremy mentioned a huge potential market for POLB001, but the orphan drug designation affects fewer than 200,000 patients. How does this square up? I mean, I can start, but Brendan, I see there you're kind of lounging back. Do you want to take this one or? Yeah. There appears to be a kind of an inherent contradiction in this commercially. Indeed, the original act was set up to recognize the headwinds that drugs would have to make money with rare diseases. On the other hand, the history since 1983 is that this has been a very successful effort. Companies like Genentech are founded on the Orphan Drug Act originally. Part of it is pricing. The argument in reimbursement of drugs like this recognizes the cost of development. That is an important part of the negotiation with payers on both sides of the Atlantic. The nice thing about POLB 001 is that if it works, it will be very cost-effective. If I'm a hematological oncologist and I want to book a patient for a bispecific antibody treatment, I've really got to book an intensive care unit as well. If I save intensive care unit days by using POLB 001, it will be enormously valuable. One of the big barriers to drugs these days, like all of these antibodies that are coming out, is that they're very expensive. Getting past reimbursement, even at a significantly elevated cost for our drug, will not be a problem. Working off the experience of lots of other drugs in this area, people are a high proportion of all drugs now going through regulators and subsequently making money for their investors are drugs for rare diseases or for rare subsets of common diseases like breast cancer and stuff like that, where there are 15 different kinds of. That's a good point. All medicine is becoming, all diseases are becoming rare diseases now as we recognize the molecular subtypes and stuff and as we personalize medicine. The costing and reimbursement model is adjusting and has adjusted to recognize that. We do not have any difficulty in being very confident in the potential market if this experiment works. Yeah. I think one point I had to wrap around in my mind is like, yes, it's 200,000 patients, and that's right today. As you say, we know the market is growing. These number of patients are growing. The people who receive these bispecifics are growing. That's irrelevant if it goes beyond 200. We expect that it will. As of today, we're in good shape. Having that improvement, I think, is fantastic, which leads nicely, a nice segue into the next question. What would you say is that, sorry, does orphan drug designation significantly increase the potential value of POLB001 to potential partner? Have you already shared news with them? Which, again, is kind of a good question. I mentioned earlier on about that seven years of market exclusivity in the U.S. essentially, that's blocking everybody else out. Nobody else can have a p38 MAPK inhibitor in this prevention of CRS. It gives us that nice little market exclusivity, which, again, is very interesting to pharmas. We know that the pharma space is very competitive, without question. All the innovators are looking to get their drugs as quickly as possible onto the market. First mover is critical. There is some really good data out there about if you're the first drug on the market for a particular indication, you seem to have kind of got it cornered. New innovators come through, but it's really hard to kind of usurp the first across the post, as it were. As I say, it would be similar for POLB001, as I say, just having that CRS prevention. Of course, yes, we've shared that information with our pharma partners. You saw the splash yesterday and obviously getting the word out there because it is an important time for the company. It's an important, as I say, kind of affirmation, I guess, from the FDA that we're kind of this is something that's of interest. And as Brendan said earlier on, kind of convinced us we're on the right track. This is a significant unmet need that we feel that POLB 001 can meet. Okay, moving on. When would you say is the next real value inflection point will be in the POLB journey that investors can look forward to? I mentioned the three in particular. The start of the clinical trial, the second half of this year, of course, we'll update the market for all of the activities that are going on, interim data in the first half of next year. As I say, we'll update the markets on that as well with the first, say, subset of patients. Then following that will be the full data set towards the end of next year, the top-line data. As I say, there'll be multiple inflection points. As things happen for the other clinical trial, I say that'll be updating the market. I think those of us who know Poolbeg, we're kind of we like to share information. We like that engagement with our investors. As I say, we're working hard to kind of reach these important milestones. Obviously, we'll update the markets as soon as they occur. Again, appreciate the question and interest. A question here from Stuart. As a long-term shareholder, the recommendation of the failed Huckabee deal surprised many. All right, we'll go back to Huckabee. Following the recent funding completion, the company trajectory appeared much brighter without Huckabee. Very good. Would you please comment on this matter and whether the long-term plan is to pursue a U.S. primary listing? We've got about three minutes left, and this could take a full this may take all of it. I do want to give a few snapshots here. When we were kind of merging with Huckabee, and this was kind of we stated to the market last year that Poolbeg, we were interested in getting onto NASDAQ. We thought the U.S. market is terrific. We thought it would be good for our shareholders, get kind of more exposure, more traction. Huckabee had a very interesting pipeline that we thought was overlapping well with us insofar as they had some virology programs that they partnered with Gilead in an oncology program that we did some diligence on. I was very impressed. It was about to go into the clinic. We did walk down the road quite a bit with them. As many of you know, it was, I think, essentially all agreed, but their board at the very last minute decided they would not pursue. As I say, we do not kind of question their decisions. I mean, they are obviously taking things forward themselves. One of the key feedbacks was when we were talking to potential investors in the U.S. was that they really liked the POLB 001 story. They saw how the T-cell engagers and the CAR Ts were kind of growing in that direction. A lot of companies are building new CAR Ts and bispecifics. CRS is always an issue. They saw this as a very nice drug and very nice to develop. I think if we learn anything from the Huckabee, it is like this is the POLB 001 is what investors really liked. That really, when the Huckabee deal did not go forward, we said we will turn and we will switch our focus now to POLB 001, the GLP-1 program. That is where we are right now. We are kind of blinkered visions now. We have delighted with the fundraise. It is a very tough financing, biotech financing environment. Very happy with the fundraiser we got. That allows us now to be extremely focused and get these programs moving. It was kind of maybe a double-edged sword, but listen, we'll take the feedback we got about POLB 001 from these U.S. investors and move it forward, as I say, at pace to get this clinical trial up and running and obviously excited to see the data at the end. Again, appreciate the question, but it could be a very kind of convoluted or complicated answer. What we'll do in the one minute or 30 seconds we have left, last question, why aren't pharma paying for the full trial? That's a good question, but I would say that's kind of a Poolbeg decision because delighted that they're going to give us, as I say, indicated they'll give us bispecific antibody to run the trial. We want to keep ourselves, let's say, independent. We want multiple suitors for POLB 001 when the data comes out next year. We do not want to be locked into one pharma company right now because if they fund the trial, they will have expectations of options or have expectations of first-rider refusals. That really kind of paints us into a corner that we do not want to be in. I think from that standpoint, it is the right decision that with our fundraise, Poolbeg will fund it, getting the antibody for free. Then, as I say, having that data in hand, that really kind of improves or increases the Poolbeg leverage for an impressive deal with that data in hand. We will leave it at that. I say that is our 45 minutes up. Again, great appreciation for everybody who joined this lunchtime. Did not get a chance to get to all the questions, obviously, but we always endeavor to try and have follow-up. If there's anything pertinent, we're happy to engage as a follow-up. Again, thank you all for your time, and we look forward to updating you and the markets over various Poolbeg activities in the not too distant future. Thanks to Brendan and Liam for subbing in as well. Appreciate it. Jeremy, Brendan, Liam, thank you for updating investors today. Can I please ask investors not to close this session as you'll now be automatically redirected to provide your feedback in order that the management team can better understand your views and expectations? This will only take a few moments to complete, and I'm sure will be greatly valued by the company. On behalf of the management team of Poolbeg Pharma, we'd like to thank you for attending today's presentation, and good afternoon to you all.