Good afternoon and welcome to the Avacta Group Plc Investor Presentation. Throughout the quarter presentation, investors will be in listen-only mode. Questions are encouraged and they can be submitted at any time by the Q&A tab situated in the right corner of your screen. Just simply type in your questions and press send. Due to the attendance on today's call, the company may not be in a position to answer every question it received in the meeting itself. However, the company can review the questions submitted today and publish responses where it is appropriate to do so. Before we begin, I'd like to submit the following poll. I'd like to hand you over to CEO Christina Coughlin. Good afternoon. Good afternoon and thank you for being here. We are thrilled to bring our new chapter at Avacta for everyone. Joining me today is a number of members of our team. Let me have each of them introduce themselves, and then we'll get started with the presentation. Dave. Hi, my name is Dave Liebowitz and I'm the Chief Medical Officer here at Avacta. I have about over 30 years of clinical development experience with 25 of those years being in industry. Happy to be presenting here today. Great. Francis? Hi, I'm Francis Wilson. I'm the VP of Chemistry at Avacta. I started my career in big pharma for 10 years, and then I spent the last 20+ years in biotech. And Tom? Hi, I'm Tom Clough, Senior Medicinal Chemist at Avacta. I joined after a postdoc in medicinal chemistry at the Institute of Cancer Research and a PhD at Imperial College. Great. Ruairidh? Hi everyone, I'm Ruairidh Edwards. I'm a Translational Scientist at Avacta. I've worked at Avacta for three years in the Translational Science role, and prior to that, I worked in the University of Miami as a postdoc and did my PhD at the University of Glasgow. Great, thank you so much. Okay, we're going to dive right in. As part of the presentation, myself and team members will be making forward-looking statements. The pre|CISION platform at Avacta is a FAP-activated drug delivery platform. Let's look at how this works. We attach a FAP-cleavable peptide to a given cancer drug. What this does is it inactivates the cancer drug so that essentially normal tissues and even the tumor don't get exposed to that highly toxic active drug. We call this a mask-in-release technology. The masked toxic payload now with the peptide attached cannot enter cells, and it is silent in the bloodstream but it is active in the tumor because there is a tumor enzyme FAP that specifically cleaves the peptide and releases the active drug right in the tumor where it is supposed to be active. The mask-in-release technology then essentially allows us to concentrate the active drug, the released drug, right in the tumor and enhances that concentration and it limits the blood exposure. What we've seen this translate to in a couple of specific diseases is prolonged treatment beyond what would normally be used for conventional therapy because we are controlling those toxicities, but that is also translating to enhanced survival. This is with our FAP-doxorubicin program. Dave will give you a couple of insights there. Let me turn it over to Dave to talk through the mechanism of action of these and Ruairidh to give you some insights into the translational pieces. Thanks, Chris. Yes, on this slide we have depicted the pre|CISION platform's mechanism of action and it works through a bystander effect. I'll walk you through the diagram to give you a better idea of how this works. If you look at the left side here, you can see the peptide drug conjugate and Chris already spoke to you about the properties of this. It's inactive in this conformation. It binds to FAP on the surface of cancer-associated fibroblasts and it binds to the active site. It's then cleaved, the peptide releases the drug in the microenvironment and once the peptide is released from the drug, it's free to move inside the cells and kill them through the drug's mechanism of action. What we're excited to speak to you about today is a dual-payload version of our pre|CISION platform. This mechanism of action is very similar with a couple of slight differences. In this, one FAP cleavage can release two separate payloads. You can see, similar to what we showed earlier, it has a FAP peptide and a linker. This linker has two attachment points so we could put two payloads on the linker and it's self-immolient. Once it's cleaved, the linker can release both drugs. They're in the same proximity in the tumor microenvironment to the cancer cells. Once they're released, they can be taken up by the cancer cells and through the complementary mechanisms of action of the drugs, the cancer cells die. I'll now turn it over to Ruairidh to present the next couple of slides. Thanks, Steve. Dave's given an axial overview of the mechanism of action of pre|CISION, but what we've then done from the translational perspective is to look at what actually happens inside the tumor. This particular slide focuses on the spatial organization of FAP expression in the tumor. On the left here, you can see these two images which are of a tumor from a salivary ductal carcinoma patient. Essentially, what we're looking at here is in green, we can see these rivers of FAP in the green there surrounding the aqua tumor cells. In red, we can see the blood vessels. What is really exciting about the pre|CISION platform is that it harnesses the proximity to the tumor cells. The FAP-positive cancer-associated fibroblasts surround the tumor cell nests. Not only that, we also have blood vessels in close proximity to the FAP-positive fibroblasts. Therefore, you get drug delivery through the vessels, cleavage of pre|CISION by the FAP-positive cancer-associated fibroblasts, and then bystander cell killing of the tumor cells once the payload has been released. If we look at the next slide, this slide here is an excellent overview not only of just the spatial localization of FAP, but then if we look much further into the cancers that express FAP, we teamed up with our collaborators, Tempus AI, and harnessed the AI technology they possess using their Lens database to basically identify the FAP landscape of cancer. We essentially evaluated all the solid tumors, over 160,000 samples. When we separated out based on tumor type, we found that 90% of all solid tumors expressed FAP. The opportunity in terms of indications, in terms of treatments using precision medicines, is very high. I'll pass over to Dave, who can talk a bit about AVA6000. Thank you, Ruairidh. Yeah, I'm going to speak to you a little bit with some high-level results that we've seen in our phase I study with AVA6000 or FAP-enabled doxorubicin, which is a FAP-enabled version of doxorubicin. As we're aware, if we start on the left side of this slide, cardiac toxicity is essentially the dose-limiting toxicity for doxorubicin. It's been reported to occur anywhere from 6%- 20% depending on the study. In the doxorubicin label, it's around 20%. What we've seen in our study with a fair number of subjects enrolled is that we've seen no cardiac toxicity to date and certainly nothing severe. This compares very favorably to what is observed with doxorubicin. Additionally, there are other side effects of doxorubicin, including GI and bone marrow toxicity. We've also seen very limited severe neutropenia. One of the most exciting things we've observed, and this really validates the mechanism of action that was described earlier, is that there's a high concentration of doxorubicin in the tumor compared to the plasma. What we've noticed is that if you look at the doxorubicin concentrations, there's a 100 to 1 tumor-to-plasma ratio. It's very highly concentrated in the tumor compared to what the systemic circulation sees. In addition, Chris already alluded to this, but we've seen encouraging clinical activity, anti-tumor responses in patients with salivary gland cancer and sarcoma. Here are some comparisons of our pre|CISIO peptide drug conjugate platform versus antibody-drug conjugates or ADCs. First of all, in terms of payload release, ADCs have some non-specificity to the protease-cleavable linkers that are employed. You see organ toxicity such as pneumonitis and hepatitis. In contrast, if you look at the pre|CISION platform, the release is very specific by FAP. As we've shown on the previous slide, you have a 100:1 concentration of the drug, in this case doxorubicin, in the tumor compared to the plasma. This would really limit the amount of systemic toxicity that's observed. I've already shown you that the cardiac toxicity is better than what's seen with conventional doxorubicin. We've had no pneumonitis or hepatitis that we've observed during this study. If you look at the drug-to-antibody ratios during manufacturing, either with single or dual-payload platforms, there's heterogeneity in the ratio. You have an inhomogeneous product. If you look at the pre|CISION platform, the peptide-to-drug ratio is stable and is well controlled in the manufacturing process. Depending on whether we're looking at single or dual-payloads, we have a one-to-one or one-to-two ratio peptide-to-drug. Bystander effect and tumor penetration, if we look at that, the bystander effect with ADCs is complex. You have to have the antibody penetrate the tumor, and it's a relatively large molecule. Intracellular release and drug extrusion is how the bystander effect would work. You have to have antigen-positive cells which take up the ADC. If you look at the peptide drug conjugates, they're small molecule-like, and they penetrate the tumor quite well. As we've shown on one of the previous slides, it's a pretty simple extracellular mechanism of release. You can thereby, with the bystander effect, kill both FAP-positive and FAP-negative cells. In terms of the market opportunity, each ADC, their market is narrow because of single antigen expression levels on different tumor types. FAP, as Ruairidh already showed you, is expressed in 90% of all solid tumors that we've looked at. The bystander effect is active and can be released. We've demonstrated in the AVA6000 program that even low-level expression of FAP, one plus by immune histochemistry, is able to have activity. I will pass this on now to Francis, who will take it on from here. Thank you, Dave. What I'm going to take you through now is essentially how we've taken the pre|CISION technology forward from our previous single payload molecules into now the dual-payload work. Why a dual payload? It allows us to, because we're hitting the tumor with two potentially distinct mechanisms, we can circumvent the resistance mechanism that you would see with one. Potentially, we can also maximize the therapeutic effect because we can use two complementary mechanisms. We've looked now, and we'll show you some data as we go forwards, looking at both combining two distinct mechanisms. With MME and exatecan, and also where we have complementary and then synergistic mechanisms where we combine an exatecan with a DNA damage response element. What we've basically done is to build on the work that we've done with AVA6103 that releases exatecan. What we did there was to evolve our technology to allow us, if I take you through this slide, what we see on the left-hand side is the capping group and the pre|CISION peptide. The pre|CISION peptide is what gives us our unique exquisite selectivity for FAP. The capping group sits in the active site of the enzyme and can be modified to extend plasma exposure and the PK of the molecule. Where we've built now is with the linker piece where we have the ability to put multiple payloads. We're showing here two distinct payloads. We also still retain, and this is the key piece that we built on from the AVA6103 program, we've retained the ability to interact with FAP and to modulate the PK of the speed at which these payloads are released. What we show here is essentially, this is using mass spec to detect both of the payloads. You can see clearly from a single FAP cleavage, we get equal amounts of the two payloads. The linker is self-immolative just as before with AVA6103, but now it's releasing two distinct warheads. I'm now going to pass you over to Tom and he's going to show you some of the data that we've generated with this exciting new development. Thank you, Francis. That previous slide showed FAP-dependent release of two payloads from a single molecule, both Exatecan and MME. This slide shows biological evidence of release of both of those payloads. On the left-hand side, this is biomarker data which shows release of Exatecan specifically from two FAP-Exatecan-MME compounds. We've called them Compound A and Compound B, and these differ in the nature of the self-immolative linker in them. In the biomarker data at the top, this is showing levels of topoisomerase 1, which is inhibited by Exatecan. For both Compound A and Compound B alone, without FAP, this enzyme is still present. In the presence of FAP, both of these compounds see loss of topo1, which is indicative of Exatecan release from both of them. We also see DNA damage coming from this release. Upregulation of phospho-tech-1 and gamma H2AX is present in both A and B when you add FAP. Both compounds are releasing Exatecan and we're seeing a biological effect from that. On the right-hand side, we're looking at MME-specific activity. The biomarker data is levels of phosphohistone-3. During M-phase arrest, which comes about when MME stops tubulin polymerization, we see that is upregulated from both Compound A and Compound B in the presence of FAP, but not in the compounds alone. In the plots below, this looks at the percentage of tubulin depolymerization from both compounds. The light blue line is the compounds in the presence of FAP, and you can see that we get depolymerization equivalent to MME alone when both compounds are in the presence of FAP. This shows we are releasing both payloads in a FAP-dependent manner and we can measure the biological effects of that in multiple different ways. This slide looks at some cytotoxicity profiles of these two compounds. Compound A and Compound B have been designed to be cleaved by FAP at different rates. Compound A is cleaved more rapidly and Compound B more slowly, and you can see that from the cytotoxicity profile. I want to draw your attention to the lighter blue lines on both of these plots. You can see that Compound A in the presence of FAP exhibits activity comparable to Exatecan, which is the pink line, and Compound B shows less activity in the presence of FAP. This is indicative of the slower rate of cleavage of Compound B, so it's less FAP sensitive. That came about through design of the compound and changes to the self-immolative linker and shows that we can modify rate of release from the chemical structure of our peptide-drug conjugates. What's potentially more exciting is the incorporation of DDR or I inhibitor, DDR inhibitor. This allows us to potentially overcome a key resistance mechanism to topo1 therapy. Topo1 inhibition, which is caused by exatecan, induces single-strand DNA breaks during replication. This can be compensated for in cells by activation of the DNA damage repair pathway. If that pathway is activated successfully, then the cancer cell can survive topo1 inhibition. One way to potentially see a synergistic effect is through inhibition of this pathway that would stop any repair mechanism in cancer cells affected by topo1 inhibition and overcome this key resistance mechanism to topo1 therapy. What we've done is used the pre|CISION dual-payload technology to target this topo1 resistance pathway by introducing inhibitors to two enzymes involved in DNA damage repair: PARP and ATR. We've made two different compounds, one incorporating a PARP inhibitor and another incorporating an ATR inhibitor. You can see from the plot on the right-hand side that we are releasing exatecan from both of these compounds as well as the DDRI compound, so either the PARP inhibitor or ATR inhibitor, and that this occurs only in the presence of FAP. Similar to the exatecan MME compounds, we are releasing a DNA damage response pathway inhibitor in a FAP-dependent manner. Again, this is more biomarker data. On the left-hand side, we're looking for key biomarkers that come about from activity of ATR inhibitors. Phospho-CHK1, you can see that exatecan administration doesn't affect the levels of phospho-CHK1, but we are seeing that with our compound in the presence of FAP. We're also seeing upregulation of gamma H2AX, which is indicative of DNA damage only in the presence of FAP, as well as increased levels of cleaved PARP, which shows we're inducing apoptosis. In addition, with the PARP inhibitor compound on the right-hand side, we're also seeing upregulation of cleaved PARP, again showing that we're inducing apoptosis. We're also seeing downregulation of PAR, so this is synthesized by PARP. You can see that in the presence of FAP, our dual-payload compound is reducing the levels of that. We're seeing DNA damage response pathway inhibition in both of these compounds. What's potentially really exciting is the potential for synergy with these compounds. We have some preliminary cytotoxicity data, which suggests we are seeing synergy. If you look at the cytotoxicity plots on the right-hand side, the turquoise curve is our compounds plus FAP, and the peach curve is exatecan alone. What we're seeing is an increase in tumor cell kill from the dual-payload exatecan DDRI compounds, as much as five times greater tumor cell kill from these compounds in the presence of FAP above that achieved by exatecan, which could potentially be due to a synergistic mechanism, preventing that DNA damage repair from occurring after exatecan has had its effect. We have also looked at this effect in a co-culture model. This is a system where we incubate tumor cells with fibroblasts, which produce FAP, and measure the rate of tumor spheroid death. You can see from the plots at the bottom of the slide, we are getting similar activity to exatecan when we have our compound in the presence of tumor cells and fibroblasts. We're not seeing any tumor cell death in the absence of these fibroblasts because FAP is necessary to release those payloads and kill the tumor cells. When we add a FAP inhibitor in, we see a reduction in activity, which tells us that this tumor cell death is due to the activity of FAP. FAP is responsible for payload release, and without that, we wouldn't see any tumor cell death. I'll pass back over to Chris now. Thanks, Tom. Appreciate it. Thanks to all of our scientists who jumped in and our physicians who jumped in to take you through these new developments. This slots nicely into our IP portfolio, which starts with our foundational IP, which covers AVA6000, fibro doxorubicin. Our sustained release program IP that we've spoken about previously, this one covers our AVA6103 program now moving towards the clinic quickly. Finally, our dual-payload technology IP. This is just fresh off of its submission. Really exciting leapfrog move for the company, essentially taking the next step in this field of drug conjugate technology. Creating now a combination product in a single vial. In conclusion from our presentation today, these FAP-selective pre|CISION dual-payload technology, it allows us to deliver two drugs simultaneously right at the same point, targeting the same cells from a single stable peptide drug conjugate. It's a single FAP cleavage event that releases those two drugs. We do have tunable kinetics. These two pieces of IP, as Francis and Tom spoke about, these work well together. We now can tune the release exactly as we've done with the single payload AVA6103. Different linkers create different tunable kinetics, as Tom took you through. Now it's an optimization, and each program will go through its own optimization steps as we move through. The dual-payload release has been validated through a number of pathway biomarkers. We do show in the data that each individual drug is having its biologic effects. The dual payloads are released by FAP on the cancer-associated fibroblasts, and that concentrates the dual payloads will both be released in that same location. The dual-payload technology allows that selective delivery. It can now, as we discussed, we can now overcome resistance mechanisms. Critically important, as you know, single therapies, we know that cancer cells will often develop resistance mechanisms. The tumor-specific delivery really has the potential now to change the therapeutic window of both of these therapies and significantly reduce the systemic toxicities that we would see either with a pre|CISION molecule combined with the inhibitory. This allows us now to specifically deliver these right to the tumor. That's the whole idea behind pre|CISION. I'd like to thank our scientists, our physicians for joining us here today. I'm happy to conclude the presentation, and we're happy to take questions at this point. That's great. Thank you very much for your presentation. We have received a number of questions, both pre-submitted and throughout today's live presentation. Obviously, we won't be able to get through all the questions today, but I have spoken to Christina, and she said they will, we are about to, we'll publish responses next week. We will start with the first question here, which reads as follows: How does the pre|CISION PDC technology differ from an ADC? Are there advantages that you see at all? Thanks, Alexander. Yes. Dave went through this new slide that we have in the deck. We do get asked this question a lot. Let me talk about what we see as sort of the four key advantages of the peptide drug conjugate or pre|CISION over an ADC. The first one, which really speaks to both safety and efficacy, is the payload release mechanism. Our release mechanism leverages FAP, which is a specific enzyme. It's a single enzyme that is located, expressed, over-expressed in 90% of solid tumors. That specific release mechanism then allows the payload to be concentrated in the tumor versus any other normal tissue release, which we have not seen. We were actually asked by health authorities to take a look at those toxicities that are associated with the non-specific release that one can see with the cleavable linkers used in many ADCs. Those are lung toxicity or pneumonitis, liver toxicity, hepatitis. We haven't seen a single incidence of either of those. We believe it's because of this highly specific release mechanism. The second advantage, as Dave mentioned, was in manufacturing. We think about this concept of the drug-to-antibody ratio, the DAR. We think about the drug-to-peptide ratio with ours. One of the challenges that we have in trying to create a homogeneous product with an ADC is how homogeneous can one make that linkage in terms of how many molecules of drug are attached to the antibody. They call it the DAR. It's anywhere usually from, it can be as low as two. It can go up to, you know, we've seen eight or just above that. This is because of the non-site-specific conjugation. It appears that in some of the early versions of the dual-payload ADCs, the control of that becomes even more challenging because you have heterogeneity at both the DAR level, but also at the, you know, trying to control how much of each drug is attached. It's very different with the peptide drug conjugates because if you take a look at our approach with the linker, we almost create like these chemical pods, I think of it as, you know, and we know that drug X or payload one gets attached at the first pod. The second chemical pod is where the next drug gets attached. We often get asked, you know, can you put a third one on? That was a question that came up a lot at the meeting. Right now, we can do payload one and payload two. What that allows us to have is then a one-to-one-to-one ratio. We know that there's one peptide drug, payload one will be here and payload two will be here. It's a very homogeneous product, which will be an advantage versus a biologic conjugation, which for those antibodies, it's both stochastic, but it's somewhat unpredictable. The third advantage is both the bystander effect and the tumor penetration. Bystander effect, our bystander effect is incredibly simple. The payload is released extracellularly, and it can move into an antigen negative or antigen positive. The antigen here is FAP. It moves right into antigen negative or FAP negative tumor cells. It's critically important. This is part of our salivary cancer data in that we know that the FAP is not expressed on the tumor cells. It can then move into those FAP negative tumor cells. Importantly, we also know that we get great tumor penetration because the Cmax of the released payload, we've seen this in the animal models, it's seen within minutes. As opposed to an antibody, which is going to have a slower uptake because the tumor penetration of that large biologic, it's a little bit more challenging. We get these high Cmax's right in the tumor right away. We've shown that pretty extensively with some of the recent tumor-to-plasma ratio data that have come out with the exatecan molecule. The final advantage, as Dave described, is the addressable market opportunity. We think this is a pretty big one. 90% of solid tumors will express FAP. There's a number of diseases, gastric cancer, triple negative breast cancer, most of the subsets of breast cancer, whatnot, where we see over 95% and the expression is quite strong in those diseases. That's in contrast to an ADC approach where the utility of that drug is really limited by the expression of the antigen. If we think about an example of HER2, which is a great drug, a HER2-directed ADC, that drug is useful in breast cancer. It's also useful in a small subset of gastric cancer because it's directed by HER2 expression. The broad expression of FAP really speaks to a very large addressable market. It's one of the reasons that for our second program, we wanted to take a mechanism like a topo1 that's very broadly applicable. Great question, new slide in the deck and one that I really like. That's great. Thank you very much, Chris. Turning on to the next question we have here, when can we expect a dual-payload PDC to come to the clinic? Great question. We always get that when there's new information out there. We do anticipate for this one selecting the clinical candidate in the second half of next year. I know today was a bit technical, but I hope that you can all see the tremendous work that the team has put into this development. This one has been quite a bit of work just understanding first chemically how to make the pods, how to attach the drugs, making sure that the self-immolative linker that Francis and Tom spoke about, that it falls apart in both drugs. That's why the biomarker data are so important. Both drugs have to release and we have to get the biologic effects of both of them. The selection of the candidate late next year will be based on another round of optimization as well as the animal models, the full pharmacology, both efficacy animal models, but also it's really important for us to look at the tumor-to-plasma and really tuning, fine-tuning the delivery of each of them. From candidate selection, if we think about it, you know, then we've got, we've defined that specific drug and program that we intend to take forward. It generally there takes about a year to enter the clinic. In that year, we do the GMP manufacturing for the drug to go into patients. The non-clinical toxicology study, so these are not the animal models with tumors, these are the animal models where we push the doses as high as we can go and whatnot and understand the tox. In parallel with those in that last year, we also start the clinical trial preparation. All of these work streams then meet up pretty much where we are right now with the Exatecan program, which is to start the clinical trial. Much of the success and how we're going to be able to move the dual-payload through is going to depend on our initial observations in the clinic with the Exatecan molecule. Francis mentioned a few times that, and Tom, that a lot of what we're doing with the dual-payload is based on a lot of the learnings in the lab with the Exatecan molecule. We expect to learn a lot about this molecule, the Exatecan molecule, as we move it into the clinic. That's going to inform a lot about our newer molecules, you know, the dual-payload. The learnings in the clinic coming up in the first half of 2026 and whatnot will inform, you know, exactly how quickly we're going to move the dual-payload through. Perfect. That's great. Just following on from that, what advantages and disadvantages does dual-payload AVA6207 have over two pre|CISION drugs, exatecan and the other drug, administered together consecutively or with appropriate spacing? Another investor's also asked us in a shorter form, why not just combine our AVA6103 with the ATR inhibitor? A question that we've had a number of times. To be honest with you, we've debated this internally at Avacta Group Plc as well. If we think about the clinical development, let's fast forward and assume that we've hit the clinic now. There are two really critical advantages to a dual-payload molecule. I'm going to put them out simply and then we'll go through it a little bit. One, the release of these two drugs, especially as we're targeting resistance mechanisms, occurs in the same timeframe and in the same location. Essentially, timing and location are critical. It's important that we release both in the same location. We believe that this is going to make this much more effective than dosing two medicines at the same time and relying on those two medicines to find the tumor at the same time, kill the tumor, induce those double-strand or single-strand breaks that we talked about, but also to inhibit the resistance mechanism. If we use the pre|CISION dual-payload, we deliver them both at the same location at the same time. We don't have to risk or think about Brownian motion and how drugs move through, how they're taken up by tumors and whatnot. As we think about the clinical development, I'm going to talk a little bit here about regulatory. The second advantage is cash and timing. A single drug, like a dual-payload, is much faster to develop and get on the market. It's much cheaper. It's nearly half the cost if you think about it. It's easier to get it on the market from a regulatory perspective than to try and get a drug approved in combination, especially because many of the, I don't want to say sexy, but many of the agents that we're looking to combine with aren't actually on the market. Exatecan isn't on the market. ATR, there is a PARP inhibitor on the market, but none of the ATR inhibitors have made it to the market. The drugs that we're looking at and getting what we call a novel novel combination on the market is really hard from a regulatory perspective. Combination drug development to get a new medicine is very time-consuming. You have to do a phase I of each. Then you have to do a phase I of the combination. It takes more trials. It essentially doubles the cost of manufacturing because you now have to manufacture two drugs instead of one. Again, two individual phase I trials, the combination phase I trial. In contrast to that, if we think about it, having the two drugs released, one medicine, those two key advantages, location, location, and timing, but also half the cost, half the time to get it to market. Although we have put a lot of effort into essentially inventing this new technology, just like the sustained release mechanism, the last piece of IP that we put out there, these new linkers with essentially two chemical pods where we can attach the drugs, it's now almost a plug-and-play mechanism. It was worth the effort and the time to develop that linker because now we can develop multiple combination products from here. It's not just the few medicines or the few payloads that we've talked about today. We almost, you know, the world is our oyster. We almost have a number of different approaches that we can take there. Developing a combination product, a single product, is much easier than doing that drug A, drug B combination therapy in the clinic. Perfect. Thank you very much. Another question we have here. Can the dual-payload use a sustained release technology? How does this work with two payloads? Yeah, it's a great question. We've had this one, and actually we had this one at the poster from a few different people. The answer is yes, the dual-payload technology actually came from some of the linkers that we've developed as part of the exatecan sustained release program. We adapted these linkers from that work to have those two binding ports, two places where it's easy to conjugate a drug onto the linker. That conjugated linker dual payload is then conjugated to the peptide. All of it is small molecule manufacturing, which is important. There's no biologic component here. Just to brag on our chemistry team again, what they have invented is really remarkable. Now it's a tunable release mechanism with two different drugs. If we want, we've talked about the pharmacokinetics. We can get a nice high Cmax because of that tumor penetration. It really allows us to tune the release of both of the payloads. It's really exciting times coming up in the next few months as we optimize this. Perfect. That's great. The next question we have here, can you explain why manufacturing is an advantage for the PDC? Yeah, another one, and this was a pretty frequent topic that we saw at the poster on Saturday, which is explain to me why manufacturing is an advantage for you. In order to address this, let me talk a little bit about how we manufacture antibodies because that was a drug class that came after small molecules. When I say small molecules, I mean chemical drugs. Many of the pills that we take out there, acetaminophen and whatnot, those are small molecules. Those are chemicals which have a much faster and cheaper manufacturing process. A biologic drug, of which an antibody is the main drug class in there, these are very large protein-type drugs. We don't have chemical manufacturing abilities here. What we need is we need cells to make them. We either use bacterial cells or human or animal cells to actually manufacture them. We have to change DNA because they're based on recombinant DNA to proteins. The antibody drug conjugates have three different manufacturing processes. First, you have to manufacture the biologic, and that's an expensive cell-based process. Then we have to make the payload. The third part of that is the conjugation of the payload and the biologic. The advantage that we have is that our peptide is not, it's not a biologic. It's considered a small molecule, and we can go through just a simple chemical manufacturing process. Excuse me. It's then conjugated to the payload, and it's simple and it's fast, and the drug is ready for startup much sooner. The complex process needed for biologics isn't needed here. We have a faster and less expensive manufacturing process. It becomes really important as we move towards the clinic because the manufacturing of a drug for clinical trials, believe it or not, that's one of the most expensive parts of clinical development just because an investigative drug has so many checks and balances that we have to do. It becomes almost the most expensive part. The manufacturing, it's not sexy, it's not interesting, but it really is one of the key advantages that we have of a peptide drug conjugate over an ADC format. Thank you very much, Christina. Turning to the next question we have here, how does this dual-payload development factor into the commercial strategy? I’m guessing that this one really is relating to deals and partnerships as opposed to, you know, the commercialization of a drug. We can't comment on the ongoing conversations. However, what I can tell you is that this development continues to be of interest to potential partners that we do have ongoing conversations with. We do continue in multiple conversations. It is important also, though, to realize that this IP is really only a few weeks old at this point. It's an exciting, it's a really exciting development for Avacta. It really is, I call it almost a leapfrog step because we've taken Avacta, you know, single payload peptide drug conjugate and really taken a very large step forward. There's a number of preclinical, a couple of clinical dual-payload ADCs really, really looking to target resistance at the same time as putting a potent payload forward. We're super excited to move this one forward. It has been a topic of conversation, but only for a couple of weeks since the IP was filed. That's great. The next question is almost a forward-looking question. When can we expect news of a partnership or a license deal for any of the drugs in our pipeline? We do continue in multiple conversations. I can't comment on timing. We've had a number of, I would say, longstanding conversations. There are potential partners out there that are waiting for a little bit of additional data. This was some of the data that folks were waiting for. What I can tell you also is that there is interest in our technology despite only one drug in phase I B. I've mentioned before, you know, when you think about platform companies like ours, platforms become a platform when one has done it twice. Doing it twice really means not inventing a second one, but really getting another one into the clinic. An important point for our company is really as we move forward with our exatecan program and showing the world, you know, that we're able to do this twice. We are, you know, within just a few steps, really, of putting the exatecan program forward. We were very pleased that we were able to raise that small amount of money. It's not inconsequential in that, you know, it really allows us to move our exatecan program forward. As we mentioned in the RNS, to retain 100% ownership of that, which is an important factor as we continue the conversations with potential partners. We have actually continued on multiple conversations regarding AVA6000, and we're very much looking forward to, you know, pulling those conversations forward. Thank you very much. The next question we have on the panel, why do we continue to add new work in the pipeline when the company should focus on getting AVA6000 on the market? This really feeds back, I would say, Alexander, into the previous question. At the heart of this, you know, we're a platform company. A platform is only a platform with multiple entries. Otherwise, it's a single drug. When one only does it, we have to do it more than once. It's an important point. We have constructed multiple molecules. Very early on in my tenure as the Head of R&D, we did disclose that we had constructed multiple molecules, up to 10 at that time. However, we have only put one thus far into the clinic. Moving into the clinic is extremely expensive. GMP manufacturing and putting a clinical trial together, you move from budgets of hundreds of thousands into multiple millions as you move forward into the clinic. We think very hard. We think for a number of reasons, our Exatecan program, we're extremely excited about it. That's how it got its nickname, The Beast. The IND stage is really the hardest in the development of a molecule. I've seen things all the way through, but figuring out really how to translate key scientific findings into it being a drug for patients and how to develop it in the clinic is part of what I've always loved to do, but it's really the hardest part. For a platform company, too, like Avacta, it's critically important that we develop a pipeline and continue to move our programs forward. At the same time, focus on what the company is best at doing. For us, the Exatecan molecule is really the next big event for us. It's on track to begin its phase I in the first quarter. We will follow on with the dual-payload. We're going to learn a lot, as I mentioned previously, we're going to learn a lot in the Exatecan program that will feed right back into the dual-payload. You have this almost continuous learning. The next chapter coming up is very exciting for us. We're really super excited to move The Beast into the clinic. It's also in this question to think about how drugs are approved and thus, and how can we, you know, then sell them for profit on a global scale. In most clinical development settings, the company would perform the phase I, and that is where we select the dose and regimen. We may potentially also see proof of concept, especially in oncology where we go right into patients in a specific patient population. We would then conduct a phase II trial. The phase II trials are usually used to define what are the endpoints that we're ultimately going to use, and then what are the statistics around those endpoints for the approval strategy. Many of our investors, you've seen us conducting our phase Ib or our expansion cohorts, mainly because in salivary and salivary gland cancer, you know, that's a small enough disease setting, and we kind of know from the phase I population what we're going to be looking for. After that phase II trial, the company would then conduct the pivotal or the definitive phase III trial to show that the drug is safe and it's more effective than standard therapy. There are expedited programs, and those exist with the various health authorities, and they often are seen with rare cancers. It's one of the reasons that we like starting with salivary gland cancer, rare cancers really with a high unmet need. We are trying to tap into those with the health authorities. I think that the point that I often make here is that drug development is a marathon. It's not a sprint. Just because we say that we see proof of concept in phase I, that doesn't mean that this is a drug that can be approved. We go through the regulatory steps. We're hopeful to not have to go through a long process, but it does take several years for these pivotal trials. The company does continue to plan for those next steps for FAP-activated doxorubicin and look for a partner at the same time, you know, back to the last few questions that we answered. We do also continue to progress the FAP-exatecan program forward. It has several big advantages over the FAP-activated doxorubicin program. With that, we're also going to continue to progress the dual-payload PDC technology. It's a small company, you know, there's only just over 20 of us in the company. We've had investors comment to us that that's a lot of work. It is a lot of work. We have some consultants on the outside as well. It's really important that we keep the whole platform moving forward and that with each different drug that we put forward, that we make sort of, I like to call them leapfrogs and really move the whole technology forward, a whole new set of IP. That's what keeps the technology and the company really moving forward at a rapid pace. That's great. Thank you very much. Another question we have here, I think you have touched on it, but how is the progress on the AVA6103 program? Are we still on track to start the trial soon? We are very much so on track. The IND filing is coming together. The clinical trial is deep in its planning and prep work. Sites are being selected, and we look forward to treating the first patient in this study in, we're guiding to the first quarter of 2026. Perfect. That's great. The next question we have here, which ATR and PARP inhibitors have been used in these studies? Can we expect these to be the next program in the Avacta pipeline? I've got asked that also at the poster a number of times. In fact, there was one scientist who was really trying to get that out of us. We have not disclosed either the PARP nor the ATR inhibitors that were used in these studies. It's important, I'm going to link back to Francis's comment that anything, well, almost anything can be used. If it's used in an ADC, we can implement it in a PDC. As we work through candidate selection, we will be identifying sort of which of these we're going to be wanting to move forward. No big decisions have been made, and we continue to work on these. Thank you very much. We are approaching the hour, so maybe just time for a few financial questions just to wrap up with. Clearly, the management and the board of Avacta are publicly very bullish on the stock and its value for money at current prices. Yet inside ownership remains in the very low single digits, and we never see open market purchases by the board and management. If you can comment on that, that'd be great. Yes, the board and the management team are in fact very invested in the Avacta story. I did invest in the placing that took place in early 2024. I was a board member and had just become the Head of R&D. I know that former board members have actually participated as well. The big difference that we have right now is that we are planning for a potential dual listing. It's not immediate. It will be in the future. Tapping into some larger capital markets is something that we've had good discussions and lots of planning. The difference there is how equity is treated with directors in the two different markets. In the U.S. markets, directors can be compensated with equity instead of cash. Because directors are usually in possession of material non-public information, that precludes buying in the open trading in the open market. Placings can be different in that we often disclose that kind of information at the time. The management team is a little bit different in that we are taking sort of a U.S.-based approach in that the team is compensated with options. They're at different strike prices, and so there are differences between U.S. employees and UK employees. We are looking at a management team that does have a good deal of skin in the game. The management team really does have a key goal to continue to work towards the share price. We believe as a management team, and everyone holds this value very dear, that if we do very right by our patients, we will be doing very right by our shareholders. We are looking for benefits for both patients and shareholders alike. Thanks for the color on that. Maybe the final question for today. With the recent raise, what does the cash runway look like, and what are the financial plans from here? Does the raise assist with the AVA6103 phase I trial? We had disclosed previously that our cash runway prior to the raise was into the first quarter of 2026, and we now have runway into the second half of 2026. We do have several events, several catalysts before that cash out timing. Specifically, let's think about that we have the salivary gland cancer data, the expansion cohort data that we'll report on. It will still be ongoing because of the long PFS that we see. That'll be in late 2025. We will have the initiation of the FAP-exatecan trial. Yes, it will benefit that one. That'll be later in the first quarter of 2026. The breast cancer data then by mid-2026. We do have a number of levers to pull here. Management, myself, Brian, we are actively working with the board in conjunction with what the next steps are and what are the different levers that we have to pull here. It does give us some breathing room as we move forward into a few of these next catalysts. Perfect. Thank you very much for answering those questions from investors. Of course, the company can view all the questions submitted today, and we'll publish the responses out on the Investor Meet Company platform. Just before redirecting investors to provide you with their feedback, which I know is particularly important to the company, Christina, could I just ask you for a few closing comments? Sure. I was peeking as we were talking at the questions that were asked. One of them I actually like, and I'm going to answer it here live. It is, does Christina think that she's going to put a dent in cancer? I guess I've said that previously. I would answer that question in a single word, absolutely. The future is very bright for Avacta. The dual payload is a true leapfrog. We are not just, you know, an alternative to ADC anymore. We have key advantages in our dual-payload technology. We have a number of key points here. We've got a number of catalysts coming up. The next, let's call it several months to a year for Avacta is, we hope, going to be truly transformational. The beast into the clinic, AVA6103, the FAP-exatecan program. Just because this is one of the most potent payloads that we could have selected, it's also one of the most broadly applicable payloads. We have so much to learn in this one, and we are within striking distance with moving that one into the clinic. It's truly one of the most unique medicines I've ever developed in my now 20 years in industry. I go back to that last question, which was the statement of, if we do right and we do great things for patients, we will be doing great things for our shareholders. We are very excited. The future is very bright for Avacta. We have an incredibly dedicated and frankly brilliant group of scientists and physicians. You met a few of them today that I get to work with. We are thrilled. The next chapter is coming up. It is loading, and we're excited that you're along with the ride for us. Perfect. Thank you once again for updating investors today. Could I please ask investors not to close this session as you will now be automatically redirected to provide your feedback in order that the management team can better understand your views and expectations. On behalf of the management team of Avacta Group Plc, we'd like to thank you for attending today's presentation. Good afternoon to you all.