Good morning, and welcome to the Avacta Group plc interim results investor presentation. Throughout this recorded presentation, investors will be in listen-only mode. Questions are encouraged and can be submitted at any time by the Q&A tab situated in the right-hand corner of your screen. Just 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 will review all questions submitted today and publish responses where it's appropriate to do so. Before we begin, I'd like to submit the following poll. I'd now like to hand you over to Alastair Smith, CEO. Good morning to you, sir. Morning. Thanks very much. Morning, everyone, and thank you for sparing the time to listen to the interim results presentation. Let's crack straight on. It's quite a lengthy deck. So, I'm aware that most of you will be very familiar with the company, so, you know, just very brief introductory slides. The group comprises two divisions, therapeutics and diagnostics, with, you know, a combined objective of improving patients' lives, leveraging the two proprietary platforms, Affimer and pre|CISION, that we own. I won't read through all of the investment highlights, but let me just sort of focus on, you know, the key points. Certainly, throughout the reporting period and post period as well, the outstanding progress with AVA6000 in the clinic is clearly attracting a huge amount of attention, and we'll talk through that. I'll—everyone is up to date, but I'll go through the most recent announcements again in this deck. Following behind that, our second pre|CISION prodrug, which is 3996. We'll talk a little bit about that. Still on target to get into humans, so the second pre|CISION drug into human later next year. On the diagnostics side, I'll give you a quick update on the progress building a significant pan-European diagnostics business. We'll talk through the vision and the mission for that division. Focus right now is on growing the acquired businesses. So the two businesses we'll talk about briefly. The focus now is not on additional M&A to add to that at this point in time, but really focused on benefiting from the synergies across the division. I think it's worth saying, and Tony will speak through the financials in a moment, but it's worth saying that with that balanced business model and a really, you know, clear understanding of where capital allocation has to be made within the group at the moment for, you know, greatest growth and shareholder value, we are, you know, well-funded, and we have plenty of optionality around non-dilutive commercial sources of funding, as well as, of course, dilutive funding. But we're well-funded through to late next year to achieve the milestones that we're, you know, all focused on. I'll hand over to Tony to talk through the numbers, please. Thanks, Alastair. Good morning, everybody. Just to run through the financials for the half year. In the income statement, we reported revenue of just shy of GBP 12 million, which was the biggest revenue number Avacta's reported in a six-month period. And as you can see from the slide, significantly ahead of the position in 2022. The revenue in the first half of the year obviously has the benefits of Launch Diagnostics for the full period, and the acquisition of Coris, which came on board at the start of June. Scrolling down the P&L, the most important number, I guess, on the face of the P&L, is the adjusted EBITDA line, which is essentially our, you know, cash usage from a P&L point of view. So we're just shy of GBP 8 million cash EBITDA loss in the period, compared to GBP 15 million December 2022. The items below that on the P&L are all essentially non-cash items, with the exception of the tax, which is R&D tax credits, which we will receive back over the course of the coming years. The retained loss, obviously GBP 11.5 million. And if we just move on to the next slide, we can see how we've broken that down by the divisions. And the important point here on it is the diagnostics division, which, you know, we are aiming to be a profitable EBITDA business in the near term. You can see the loss in the six months was just over GBP 400 thousand, compared to GBP 2.5 million the previous six-month period. So that is progressing well. We will obviously have the full benefit of six months of Coris and Launch in the second half of the year. So we're hoping to see that become positive in the not-too-distant future. The biggest spend, obviously, is the research costs in therapeutics. There you can see the GBP 5.3 million as we continue to progress the clinical trials. Moving on to the cash flow. We started the year with GBP 42 million. The GBP 8 million outflow ties back to the adjusted EBITDA that we mentioned earlier. The investing activities of GBP 7 million relates to the acquisition of Coris, whereas obviously in the period to December 2022, we had the acquisition of Launch, the disposal of the animal health business, and some CapEx costs there. So the cash at the end of June was GBP 26 million. At the end of August, it's about GBP 24.5 million. And we've received a tax refund of GBP 2.3 million to do with 2022 tax. So that cash runway gives us good runway through right into the back end of 2024. From a balance sheet perspective, obviously, the key assets are the goodwill and the leases around buildings and facilities. Given the increase in the Coris acquisition, the cash position there of GBP 26 million, and then the convertible bond. There's been a subsequent amortization and conversion since the end of June, so the amount outstanding on the bond is now down to GBP 43 million, which we anticipate will all be settled in equity. I'll pass back to Alastair. Thank you. Great. Thanks, Tony. Okay, so let's go through the business update. Obviously, looking back at the reporting period, but also post-period end. So focusing on therapeutics, predominantly. And just to run through a few introductory slides for those of you who aren't familiar with the company. So I mentioned that we have two proprietary platforms. We're focusing initially on the pre|CISION platform, but I will talk through, give a little bit more detail on the Affimer platform, later on in the deck. So the challenge that we are addressing with the pre|CISION platform is one of the fact that chemotherapy, when it's delivered to a patient IV, the whole patient's body gets exposed to that therapy, and these are quite potent toxins, so the whole body receives a systemic exposure to these toxins. And that limits the tolerability for patients, where I think we're all aware from personal experience of people who've had chemotherapy treatment, and it can be very unpleasant. That limits the tolerability, and through that, limits the way in which the drugs are dosed, so the dosing regimen, and that has an effect on efficacy, of course. It's that safety aspect and tolerability for patients that's the real issue with chemotherapies. Many of them are very effective drugs, but they're not tolerated by patients. So the solution to that, a solution to that, is to target the active chemotherapy into the tumor tissue. And the way we are doing that with the pre|CISION platform is to selectively activate the chemotherapy in the tumor. As you'll see on the subsequent slides, when a drug is modified with pre|CISION, it is inert as it goes around the body and then activated in the tumor, so we get a significant reduction in the systemic exposure, and that improves the safety and tolerability, and thereby, the efficacy. So pre|CISION is made to work effectively by an enzyme called F-A-P, FAP. And so it's worth just talking through very, very briefly some details around FAP and the pre|CISION platform. So pre|CISION, as you'll see in a moment, is a bit of chemistry, ultimately. It's a bit of chemistry, which is recognized by this enzyme, FAP, and it is removed from the chemotherapy by this enzyme. So that's the mechanism by which pre|CISION drugs are activated. And you'll see in the middle panel on the slide that shows you the amount of FAP in a range of different tumors. You can see going from the bottom upwards, sarcoma, salivary gland, CUP, if you didn't know, is cancer of unknown primary, esophageal, and so on. So these cancers have very high levels of FAP, and FAP is not present in most healthy tissues. So this is an enzyme which is very much, you know, very much specific and particular to tumor tissues. So when the pre|CISION modification is made to the chemotherapy and it then can't enter the cells as it's going around the body, that renders it inert and relatively harmless, and we'll see that when we talk through the clinical safety data that we're observing for the first of these drugs, AVA6000. When it gets into the tumor, as I said, the modification's removed, and it's only removed by FAP. So really, to emphasize that third bullet on the left, that's where the IP and the real value lies in the IP. The fact that pre|CISION is absolutely specific to FAP. There is no other human enzyme that will release the drug, and therefore, you get a very tumor-specific release. That's the key to the real value of the technology. So just a little bit, just to delve into that a little bit more, 'cause I want to make a specific point. You know, it's very easy to get focused on AVA6000 and forget the fact that this is a platform, okay? So the fact that AVA6000 is generating such good clinical data, which we'll talk through, it serves to validate the mechanism of pre|CISION in human. Therefore, the platform, you know, the mechanism of the platform is being validated by 6000. So we're not just developing an individual asset, we have a platform. And very briefly, to talk through the nature of that platform, give you a little bit more detail than I may have done in the past. So there's four components to a pre|CISION drug. It's easiest to think about on the right-hand side to begin with. The active agent, the drug. In 6000's case, it's doxorubicin. In the case of 3996, which is the example I've used here on the slide, it's a proteasome inhibitor. So that's the drug, that's the cytotoxin. There are then three other components. You can insert a spacer after the drug before you get to the FAP substrate. We don't do that for 6000 or 3996, but it can be done, and it affects the rate at which the drug is released. So that, then, that's an important control lever, if you like, in the structure of a pre|CISION drug. The FAP substrate, I guess what we ultimately call pre|CISION is the bit that is selective for FAP, and you can see that in red below. As I said, it's a small chemical. It's actually a peptide that's very specific to FAP. And then there is an additional tail, if you like, on the molecule that, again, can be used to modulate the way in which the drug is released and the way in which the drug is cleared, and so on. So there are four components to the structure of a pre|CISION drug. And to try and illustrate that in a simple way, I've indicated the drug as a pill, so that's the drug on the right. And then the pre|CISION substrate is the bit that keeps that locked up as it's in circulation, and FAP is the key that releases it, and of course, FAP is predominantly in the tumor. So just to use that, you know, that way of looking at things with AVA6000. How do we get rid of that? On somebody else's computer. There we go. The doxorubicin then on the left is connected to pre|CISION, and that's AVA6000, okay? Locked up and inert as it's administered to the patient IV, that goes around in the circulation until it goes through the tumor tissue in the circulation, where it encounters FAP, which, again, just to add a little bit more detail, as people understand the technology more and more, that FAP is predominantly on what are called cancer-associated fibroblasts. So this is really. You may have heard the word stroma. This is really the bulk of the tumor, you know, the dense stroma that surrounds and makes up most of the tumor mass. And that is what is very rich in FAP. And when, of course, the AVA6000 encounters the FAP, which is the key, it unlocks the drug and releases doxorubicin. So hopefully, that mechanism is, A, very clear, but B, it's very clear that it is a platform technology. So the value here is not just in a single asset, it's in a whole range. A whole range of established chemotherapies and other more potent toxins that have never been used as chemotherapies because they're too potent. And we can now begin to think about using those as systemic treatments. Well, we're moving along. There we go. Thank you. Okay, so AVA6000 is, as you all know, in a phase IA safety study. The primary outcomes of a safety study are obviously safety and tolerability. We will touch on and talk about the efficacy signals that we're now seeing, which has been—I mean, that's a huge landmark step for us to be seeing efficacy in this group of patients, as well as getting the remarkable safety data that we've been getting, is a huge step forward, and we'll talk about that briefly in a moment. But the phase IA dose-escalation study is a safety study. The primary objectives are to understand the safety and the tolerability, and to identify, if there is one, a maximum tolerated dose, or define the dose to move on to the phase II study. So, as the name suggests, it's a dose escalation through increasing levels of treatment with AVA6000. To cut a long story short, we are now into the seventh cohort, which is dosing patients at 385 mg/m², which, to give you a benchmark there, is equivalent to about 3.5 times the normal dose of doxorubicin that a patient would receive. So significantly higher levels of equivalent levels of doxorubicin being given to patients. To then just talk through, many of you will have seen this slide before, but clearly, I've updated it for the most recent completion of cohorts 5 and 6, and I've underlined the changes that I've made here. So we've now had 35 patients through the study with a broad range of solid tumors, actually. You know, many with soft tissue sarcoma, but many with a range of other cancers as well. We are currently dosing patients in the seventh cohort, as I said, and a couple of weeks ago, we announced that cohort seven would be the final cohort. We'll discuss the reasons for that on the next slide. So thinking about the safety data, we continue to see, you know, what I've described as remarkable safety data. All the clinicians involved in the study would, you know, would use the same word. It's, you know, it's better than we really imagined it could be. We are seeing an almost complete absence of the serious toxicities, the grade 3 above toxicities that we see all the time and would expect to see with doxorubicin. There are some. The most serious ones, neutropenia, thrombocytopenia, anemia, that affect the dosing of doxorubicin and limit it to 3-weekly dosing. We'll talk about that on the next slide. We're seeing an almost complete absence of that, whereas neutropenia is a 50% incidence with doxorubicin, I believe. So despite delivering, you know, multiples of the normal dose of doxorubicin, we're also seeing none of the typical drug-related cardiotoxicity that affects the long-term number of cycles a patient can receive because of cumulative damage to the heart. So, in a nutshell, the safety and tolerability for the patients is very good indeed. We have done a number of biopsies from patients where we gain consent. That's up to nine patients now. We've reported previously, and I don't have the detailed table in this slide because it's quite a long presentation, so... But we've reported previously that we're seeing very high levels of doxorubicin in the tumor tissue, and that continues with the new biopsies that we've taken out of Cohort Five. So the, you know, that trend is continuing with the new biopsies that we've got. And then the new news, I guess, that we announced a couple of weeks ago, and really, really important progress for us, is that we have seen-... Very clear signs of clinical activity for the drug, which you would expect, of course, but if you're releasing dox in the tumor, then some of these tumors will respond. You would hope, even though these are late-stage patients. But we now, we now have those clinical signs of activity. In particular, one patient that's shown a very significant reduction in tumor volume, that's a patient with soft tissue sarcoma. But other patients which have stable disease or who have stable disease, that may be sarcoma patients or indeed, patients with, with other cancers. So, all in all, phase IA dose escalation is going extremely well, and we're now into the final cohort, which will complete before year-end. So then thinking forward about the clinical development strategy, some of this is not, not new. Focus on soft tissue sarcoma for the reasons I think you're all aware of. But what is new is that now that we have got these very clear signs of efficacy, we don't believe it's necessary to go through quite an extensive and expensive phase IB expansion to convince ourselves of the efficacy signal before we go into the phase II. So what we plan to do now is to run alongside the last cohort in the phase IA three-weekly dosing, a fortnightly dosing group. Now that there's a reason for that, obviously. I mean, it's well known in the development of cytotoxins that more frequent dosing often gives better outcomes for patients. So rather than keep putting more drug into patients with a three-weekly dosing regimen, which is only the regimen because of doxorubicin's historical toxicities, it is very likely to give better outcomes for patients if we can move to fortnightly dosing, and we should be able to with the safety profile that we've got. So we've designed a relatively short two-weekly dosing study that will take us through to the middle of next year, when we'll be able to define the dosing regimen for the phase II, and initiate that study, which would have previously begun in 2025, but is now brought forward, we hope, into 2024. So that phase II study will be in soft tissue sarcoma. We'll release more information on, you know, which subtypes and, you know, more detail on that phase II study when we, when we can. But it'll be a study in soft tissue sarcoma, and it will be designed to be a registrational study in the U.S. So as I say, we'll give more detail on that, you know, as we, as we can, when we can. But right now, we should be at least looking forward to a registrational study that begins in 2024, and which should finish, we would expect, because these things are variable, by the end of 2026 or into early 2027. Okay, so let me move on. You know, on the back of that very, very positive clinical progress for AVA6000 and those thoughts about, you know, the potential of a platform, the potential to take, you know, existing chemotherapies or new potent chemotherapies, and improve the safety and efficacy, you know, the thoughts about, you know, what comes next in the pipeline, you know, there's huge, huge opportunities. So 3996 is the second in the pipeline. We've talked a little about this before. The warhead you see on the right, circled in blue, which we rather nattily name AVA2727D, that's a proteasome inhibitor. And the proteasome inhibitor affects the way in which cells clear up a degraded protein. So it's effectively, if you want to call it, the garbage disposal of cells. If you block that up, then that leads to cell death. So proteasome inhibitors are approved or on the market, but their toxicities, their systemic toxicities, have really limited their use to liquid tumors, to multiple myeloma effectively. So our approach, of course, is not to think about going head to head in multiple myeloma. Now, we have an opportunity to take proteasome inhibitors into solid tumor indications because we should not suffer from the same systemic toxicities, but we should be able to release that proteasome inhibitor in the solid tumor. So really interesting, exciting opportunity. I'm not gonna talk more about the rest of the pipeline now, but of course, we have other pre|CISION molecules in the pipeline. I hope we can get to a point where we can talk about that, you know, relatively soon. But 3996 is the next one. This is a little bit dense on data, but I think those of you who would like to see the data will enjoy seeing this. You know, 3996 is looking very good in preclinical. We're aiming to file an IND next year, and we're still on track for that. And this is mouse data that shows the efficacy of 3996 in a melanoma, a skin cancer model, but also shows the improvement in safety compared to VELCADE, which is the leading proteasome inhibitor on the market. So, very quickly, these graphs that you see here are the increase in the tumor size in a mouse. So it's a human tumor that's implanted in a mouse, and the tumor grows very quickly if you do nothing, which is the black line. If you treat the animals with VELCADE or bortezomib, as it's known, or with 3996, you get quite a significant reduction in that tumor growth. So there's clearly an effect, an efficacious effect on reducing tumor growth. But if you look at the animal's body weight, when they're treated with bortezomib, the animals lose significant body weight, and that's a surrogate for the systemic toxicities, whereas, of course, with 3996, because it's released in the tumor, the animals are not suffering in the same way. In fact, the animals on bortezomib had to be given a five-day break and then put back onto the treatment. So this is a mouse model of course, it's not, it's not human data, but it's very, very encouraging. And when you're comparing this final graph, this is again, tumor volume. And the green line is the standard of care for melanoma, so you can see that 3996 is performing as well as the standard of care, trametinib, in this melanoma PDX model. So in summary, the takeaway for 3996 is really promising preclinical data. We're now into the IND-enabling studies around tox and so forth, which should bring us to an IND filing, next year, and a second pre|CISION drug in the clinic before the end of next year. Just moving then on to the Affimer platform. Now, this has, I guess, played second fiddle to the pre|CISION platform for a little while, purely because of focusing resources on pre|CISION for understandable reasons. The Affimer platform, for those of you who are not familiar, is a biologic platform. In simple terms, it's a replacement for antibodies. So it's a simple, small protein that you can use to generate binders to drug targets in the same way that you can use antibodies to do that. But there are a number of technical and commercial benefits. I mean, it's a small protein, it's very stable. You know, small and stable usually means that you get good pharmacokinetics, good tissue penetration into solid tumors. It's a very flexible molecule in the sense, as you'll see on the next slide, that we can build other structures by combining one or two or three or four Affimers to create multi-specifics that really allow you to start thinking about some interesting drug modalities. So that flexibility and that stability and then feeds through into the fact that we can make these things. You know, a lot of technologies like this suffer from manufacturing issues once you get into the more exotic structures. But the Affimer platform behaves really well, even in those multi-specific structures, we can still manufacture these things. That's what high expression levels means. You can manufacture these things quite straightforwardly. From a commercial perspective, this platform is proprietary to Avacta, of course, so there is... It's completely unencumbered in terms of IP, whereas, of course, the antibody space is relatively complex from an IP perspective. So the other interesting angle around the Affimer platform is it's not an antibody, clearly, and it's not related to an antibody in any way, so there is freedom to operate, where there is a heavily based, antibody-based, IP. I mean, the key things really are, how can you differentiate the therapies that you develop? And there's a number of elements to the Affimer benefits. One is we have shown numerous times over the past few years that we can get binders to targets that are traditionally difficult for antibodies. So one example is something called GPCRs, which are a very interesting and important drug class, but very difficult to generate antibodies to bind against, and we can generate Affimers that bind this important drug class. So, so one of the differentiators for Affimers is that we do seem to be able to generate binders to what are quite tricky drug classes for antibodies. The second is that we can make Affimers that are very, very specific to the target, so exquisitely selected for the target that we're aiming for, which is clearly important in drug development as well as diagnostics, of course. And then that final point around flexibility and being able to build multi-specific formats. That's not straightforward with many of these types of technologies or with antibodies, whereas it has proven, serendipitously, if I'm honest, to be very straightforward with the Affimer platform. So that's the platform. You know, we have three programs, internal programs, and two partner programs that I'll talk through briefly. As I say, the Affimer programs have, to some extent, played second fiddle, for obvious reasons, to the pre|CISION. Now, that's where we've put our capital over the last couple of years to get the clinical proof of concept with the pre|CISION platform done. But let me talk you through the, you know, the programs that we've been keeping going and now properly resourcing. And in fact, we'll be presenting some data on the first of those in a couple of weeks. So the, I guess the lead Affimer program is a bispecific PD-L1 antagonist with a cytokine called IL-15. So clearly, there are good biological and clinical reasons for wanting to combine PD-L1 with a, you know, with a cytokine and IL-15. There are others you could choose. IL-15 is our lead and preferred option. So that's the data, the preclinical data that we have, which is looking quite interesting. That data will be presented very shortly in a couple of weeks. And we'll then get that post onto our website, and I'll produce a, you know, a teaching video to try and talk you through that. That preclinical data, as I say, is looking very interesting. The second multispecific program that we are moving forwards is a PD-L1 LAG-3 bispecific. So those are both immune checkpoint targets, as I'm sure many of you are aware. So those use, as you see in the picture at the bottom, those use Affimers to bind the the drug targets and the central part is actually a part of an antibody to provide size, to give the right amount of time in the bloodstream before the drug is cleared. In contrast, the PD-L1 IL-15 drug uses our own half-life extension technology, the Affimer-XT. So in fact, it's a, you know, it's a tri-specific binding PD-L1 IL-15, and a human serum albumin. So all of those programs are now in later stage research, and we'll be publishing the data, say, later this year and through into early next year. The third program, which is a really interesting with, you know, many of you... I'll have talked to many of you about the TMAC program in the past. That remains. We've now actually built out our chemistry team a little further to be able to keep pushing that forward. That is a combination of the two technologies, so the Affimer and the pre|CISION chemistry, to create a novel drug conjugate, where the payload, the toxin, whatever that is, is released in the tumor microenvironment. But just to put things into context, you know, there are a lot of a lot of unknowns in a TMAC molecule. You know, there's a new toxin in there. There's pre|CISION, which, of course, now is much more validated in the clinic, but there's the Affimer, which has not yet been into human. We'll talk about that with the partners in a moment. So there's a greater degree of risk in terms of developing a TMAC molecule. So those are the reasons why we have focused resource from an Affimer perspective on the better understood bispecific programs on the left-hand side of the screen. But that does not mean that TMAC is not still in our sights. It's just a lower priority for us. So going on to those partner programs, and I'll again, I think you know what these are, but I'll briefly introduce them for those who don't. We have a partnership with Daewoong Pharmaceutical, and that's actually a joint venture. So we are a co-owner in a joint venture in South Korea called AffyXell, which is actually a cell therapy company. So Daewoong's IP that's in AffyXell is around stem cell therapies. And what we have shown is that we can put the genetic code of an Affimer into a stem cell to get the stem cell to make its own immunotherapy. So when the stem cell is in situ, it will generate its own immunotherapy to support its function. Really novel, you know, a real next-generation step in terms of stem cell therapy. Clearly early stage, but we've been making really good progress with the first of those, which uses an anti-CD40 ligand Affimer in GVHD. So that program, if you just look over on the right, that is still slated for an IND filing next year. So we believe, and we certainly hope that AffyXell will get an Affimer into human later next year, if we can work with them to support that IND filing in 2024. The second program, we've got a target that we've generated Affimers against. Those have now gone into AffyXell, and the way our relationship from an equity perspective works with AffyXell is we don't put cash in at their funding rounds, so they raise capital with regional VCs, Samsung Ventures, others. And of course, we get diluted at that point, because we don't put cash into that JV. But when we put the Affimer to a target in, and we transfer the IP, so the patent ownership into AffyXell, then we regain an equity share. And we've just gone through one of those processes. We are going through a formal process in South Korea as to exactly the increase, what the increase in our ownership will be, but it is going to rise from about 19% to about 25%. So AffyXell are making really good progress with the first and the second program. And they have the ability to choose other targets as well. Now, LG Chem is more straightforward from a, you know, from a technology perspective. It is a partnership, a research partnership with LG Chem for multiple targets. The first of which is a PD-L1 inhibitor, so this is a straightforward immune checkpoint inhibitor. I guess, novel in the sense that it's an Affimer, but also novel that the half-life extension is provided by our own Affimer-XT, which binds to serum albumin in the blood, and thereby extends the amount of time the drug spends in the bloodstream before it's cleared. So we believe that LG Chem are taking that program forward. The work is done entirely internally within LG Chem. We don't have any involvement in that. So we would expect and hope to see an IND filing from them sometime next year. They also have rights to other targets, which, of course, we're working with them on what those other targets might be. So I think the takeaway from the partner program, certainly with AffyXell, is we've got sight of an IND filing and that would be the first time that we've had the Affimer platform in human. Okay, then, just to summarize, and I won't, I won't read through the pipeline. Just to summarize, that is now the pipeline as it stands of our pre|CISION and Affimer wholly owned and partnered programs. Okay. Just five minutes on the diagnostics division to provide you with an update. I know we've got plenty of questions, and I want to get around to those. So the vision that we have for diagnostics is to build a significant European IVD business. I'll explain what I mean by full spectrum in a moment. Focused on professional healthcare and also broadening access to diagnostics. The mission really is to make sure we deliver high quality diagnostics to a broad range of people for both treatments, you know, for both diagnostics in that sense, but also to monitor health and fitness for individuals. Okay, so full spectrum, you can look at that in two ways. I mean, we are focused on the professional healthcare market, so not consumer testing, buying tests online and testing yourself at home, focused on professional use. There's two settings for that, really. The centralized hospital laboratory testing, and the decentralized testing, which is more GP clinics and pharmacies and other settings. Now, there's a big push in the U.K. for community diagnostic centers, so there's more effort in the U.K. and, of course, in Europe and the U.S., going into decentralized testing to take that pressure off centralized path labs. And then the modalities of testing run from pathology laboratory, which is big equipment and very high throughput in hospitals through rapid point-of-care testing, which primarily means lateral flow tests. And those are used in hospitals as well as in the more decentralized setting. And then there is an opportunity to get individuals to sample, but not do the test themselves, to then send the sample away for the test to be done in a professional setting, and for the results to be communicated with some clinical support. So that's our universe, if you like, of the way we see a full spectrum IVD business. If you think about the value chain, and this goes to our M&A strategy, and we'll see how Launch and Coris fit into the strategy on the next slide. This talks to our strategy. We see the value in the diagnostics value chain at the start and at the end, frankly. So the sales channels, the customer relationships, the market intelligence that tells you which tests to develop, that's very high value. And the IP, the new novel product development, the competitive product development, that is also of high value. Manufacturing is a little bit more commoditized. As you know, Coris have a manufacturing capability, so it tends to come with. But if you need more volume, then you outsource. It's a very commoditized market in terms of manufacturing IVDs. So then just thinking how the acquisitions we've made fit that strategy, and thinking about that full-spectrum IVD market, Launch is the largest distributor of- or the largest independent distributor, now part of Avacta, of course, but the largest distributor of IVDs in the U.K,, has a growing business in France and some business in Belgium and Ireland, and we'll talk about expanding that in a moment. It's a very well-respected, well-established, profitable business, selling into centralized professional healthcare, so mainly hospitals in the U.K. and Europe. So the NHS obviously is a huge customer for Launch, but private hospitals in the U.K. as well, and in France and other places in Europe. Coris, so the strategy, just to step back, is simple, right? If we can build those routes to market and own those routes to market, and then expand our own product portfolio through development and acquisition, and put those down our sales channels, then we get decent margin sales. The margins on IVDs sold through third-party distributors are pretty tight, so what's attractive about this is owning the routes to market as well as owning the products, or some of the products. Coris is a lateral flow test, a rapid test developer. They have a range of tests, primarily focused on infectious diseases. And an area of their portfolio that I think is, or we all think is particularly interesting, is in antimicrobial resistance, so that's perhaps, you know, what you know it as antibiotic resistance. So those are a range of tests that allow you to determine which resistance pathway. So if you have an infection that is resistant to antibiotics, you know, what is it? Which antibiotic should you choose? And that's a growing market, and again, one that we can grow with Coris going forward. So that's how those two acquisitions fit in, and I'll talk about the synergy with the Avacta in a moment, in a moment. Of course, that's related to the Affimer platform and Coris' products primarily. So it's critical that we grow these businesses. We've talked through these slides before, so I won't dwell on them, then we can get onto the questions. But the key area in which we think we can grow Launch significantly in the coming sort of three years or so is by expanding their business into Germany, and we're actively pursuing that. I hope I'll be able to give you an update on that soon. So Germany is the biggest IVD market in Europe. Launch have a fantastic reputation in the U.K. and France, and they're well-known in Europe, so expanding that business model into Germany makes absolute sense. And that, as I say, I hope I'll be able to give you an update in the not-too-distant future. And then with Coris clearly expanding their product portfolio, using the Affimer platform to improve or create new tests for the Coris portfolio, that's a really important synergy that we're working very hard on realizing. But also actually, with Coris growing and improving their distribution now, we're obviously using Launch within the markets where Launch operates, but also just improving the quality and the management of the distribution network globally, to grow Coris sales through that route. Okay, and the final slide, just to make the point that I've just, just made, which is that the Affimer platform, you know, we've talked a, a lot about the, the therapeutic opportunities, but it, it also is a, an ideal reagent platform for generating immunodiagnostics, which the lateral flow test, of course, is. So it gives us a, a real opportunity to create competitive advantage with better performance, ultimately, and also new targets that are difficult for antibodies to difficult for antibodies to, to reach. So that, that is work that's ongoing now. As I said, right at the start, I think, you know, the real focus now is on realizing those synergies, so we've paused any further acquisitions, and we're working on those mechanisms for growth, organic growth in those businesses, expansion of Launch into Germany, and getting Affimer reagents into Coris products. Okay, so I won't re-read through the whole summary, but I think the key points are really the outstanding performance of AVA6000 in the clinic, and I'm saying these things multiple times, but that really has validated the mechanism of pre|CISION in human. pre|CISION works, so we now need to think about what the pipeline really looks like beyond 6000 and 3996, and I hope in, you know, in due course, we'll be able to talk to you about other opportunities. We certainly, at the AGM, we talked about the commercial opportunities now that we have. The clinical data that we have, we're getting increased commercial attention, of course, because everyone's been waiting to see whether, you know, whether we get those clinical signs of efficacy. And that allows us to think about partnering, not our assets necessarily, because we want to take those forwards, but allows us to think about partnering the platform, potentially with toxins owned by other companies and so on. We talked through that in detail at the AGM earlier this year. And just a final note on the capital allocation. As I said, no further M&A activity. We have great optionality that I've spoken about in terms of commercial opportunities with pre|CISION for non-dilutive funding, and that's a very high priority for us, you know, as well as potential for dilutive funding. But as Tony mentioned, our current cash runway is to the back end of 2024, to be able to deliver on 6000 and 3996, as we all would hope to. So I'll pause there. And perhaps we can start to take some questions. Perfect. Alastair, Tony, thank you very much for your presentation. Ladies and gentlemen, please do continue to submit your questions just by using the Q&A tab, which is situated on the top right-hand corner of your screen. We have received a number of questions from investors today, and I want to start up the Q&A session with this question here, which reads as follows: What funding options for further phase of the pre|CISION platform, both AVA6000 and other prodrugs are back to considering? Will these be in the best interest of shareholders and create minimal dilution? Yes, it's obviously a good question. I think I've probably dealt with that in the last sentence at the end of the presentation, but, you know, we are fortunate to have plenty of optionality regarding, you know, the way we fund the business, non-dilutively as well as dilutively. The clinical progress that we've made, is, you know, is giving us, you know, an uptick in commercial interest, as I mentioned recently. So, you know, that gives us one option for non-dilutive funding, which is the real focus of the question, of course. And, you know, we've also hinted at the potential to spin out the diagnostics business at some point. And again, that, that's another way to produce non-dilutive funding for the group. So, you know, we have plenty of optionality, and, you know, that's always at the front of our, as a board of directors, always at the front of our minds, so, so don't worry about that. Perfect. Thank you very much, Turning to next question: Will the short fortnightly dosing study, that is to run in parallel with C7 of phase IA, also be a dose escalation study, or will you pick a single dose level based on the phase IA data up to C6 or C7? Yes. Yeah, so it will be a dose escalation study, but it'll be quite a short one, because without going into lots of detail, from the three weekly study, we know where we can start, as it were, so we don't have to go back to the beginning. So we'll be starting in the middle of the dose range, and we would expect two, three dose escalations, you know, maybe four at the most. But we know where we can start in the middle, and the idea is to run that very quickly and have it finished, you know, by the middle of next year. Perfect. Turning to the next question: Will phase II treat early-stage STS patients or only very late-stage patients? Yes. So phase II is an efficacy study, so it's designed to be a registrational study, and then so it will be a first-line treatment for soft tissue sarcoma patients. So very different from a phase I study, where many of those patients are in late-stage disease, and of course, many of them, not soft tissue sarcomas. So the answer to the question is, it will be first-line treatment, so early stage is the question, to put it, first-line treatment of soft tissue sarcoma. And it'll be particular subtypes of soft tissue sarcoma as well, and we'll give more information about that when we can. Perfect. That's great. Why did investigators elect a 385 mg final dose if no MTD is likely to be found and not 400 mg? What factors led to this decision? Okay, well, that's very straightforward. During the study, the FDA put a limit of a 25% increase in the dosing between the cohorts, so it's a simple calculation of 25% increase over the previous cohort. So it's, it was an FDA requirement that later in the study, we stuck to a 25% increase. Perfect. Thank you very much. Can you explain how effective AVA6000 is at attacking the stroma in more detail? Yeah. So we touched on this a little bit in the presentation, but you know, the stroma, as I mentioned, is non-cancerous cells, non-immune cells, and it's you know, the tissue that's associated with the tumor. So it's the bulk of the tumor, really. And generally, the stroma's a very dense mesh of fibroblasts, as I think I mentioned during the presentation, and it's actually that structure, that dense structure that prevents some therapeutics or larger therapeutics, like antibodies, from penetrating. So that you know, the question about attacking the stroma is a really important one because breaking down the stroma allows other therapies to penetrate the tumor more effectively. You know, that's another thing we didn't talk about during the presentation, but it is, it is important to think about opportunities for use of doxorubicin or AVA6000 to work in combination with immunotherapies. And to answer the question, the majority of the stroma is made up of cancer-associated fibroblasts, or CAFs. Those are the bulk of the tissue, and they're the cells which have FAP on them, you'll remember. So those are the ones that are directly targeted by AVA6000. So we know that doxorubicin has an effect on the stroma, to break it down. We've got data where we have, so, in vitro data, where we've what's called co-cultured, so we've grown CAF cells with tumor cells, and we can show that the sensitivity of the tumor cells to AVA6000 is greatly enhanced when we have the presence of CAFs. So all the data that we have and the knowledge about doxorubicin points towards the fact that AVA6000 is likely to have, as doxorubicin does, you know, an effect on breaking down the stroma, which means it can be used in combination with immunotherapies as well. Perfect. Thank you very much. I know you might have just touched on this. I know you'd mentioned CAFs, but could you also explain how effective AVA6000 is at attacking MAFs as well? Yeah. So that's, I mean, it's quite a specialist question, isn't it? But, for most people, MAFs are metastasis-associated fibroblasts. So these are the... So CAFs are the fibroblasts in the tumor, the primary tumor, and MAFs are similar, well, the equivalent, if you like, in the metastases. And we know that MAFs also have a high level of FAP, which is really interesting because, you know, from a treatment perspective, you don't need to know, with a pre|CISION drug, you don't need to know where the metastases are because they're rich in FAP. So the drug will find them through the circulation, and it'll release the chemotherapy in the metastases. So, our biopsy samples from the clinical trial are almost all, they may all be, but certainly almost all from metastases, from metastatic sites. So, you know, so we, you know, we know that we can detect significant levels of doxorubicin at those sites, so that suggests that 6000 is going to be as effective on the metastatic sites, the MAFs, as it is on the CAFs. Perfect. Thank you very much. Next question here: What is happening with FAPI-PET? Okay, so it may be worth explaining to some people on the call what FAPI-PET is as well. So the I in FAPI refers to a small molecule that binds to FAP and stops it working. It's an inhibitor, hence the letter I. So the first bit of that thing, FAPI-PET, is basically a small molecule that binds to FAP and PET imaging, everyone's heard of PET imaging. So that inhibitor, that small molecule, carries a radionuclide with it, so allows us to do PET imaging in the normal way that you're aware of. So FAPI-PET gives us a way of doing whole body imaging and seeing where the FAP is within the body, if that makes sense, 'cause the radionuclide binds through this small molecule to FAP. So for us, it's a really useful research tool. So one that we can use during drug development. It's potentially a companion diagnostic, although I would just sort of make the comment that it's a very expensive imaging system, so it's not widely available, and I think that might be challenging in terms of companion diagnostic. But just to answer the question, what's happening with it? We are getting close to getting FAPI-PET working in Memorial Sloan Kettering Cancer Center. So that's the center running the AVA6000 study in New York. So that should happen in the next few months. So that will be very important for research, as I've said, but also for the phase II study next year. So the real challenge... I mean, we've been talking about FAPI-PET for a while. I think the questioner is basically saying, "You know, why haven't we got it working yet?" So to answer that, the challenge lies in manufacturing, because the radioactive label has to be manufactured right next to the site where it's gonna be used, because it's got a short half-life. So basically, it's not very easy to implement in a hospital, and you need specialist facilities, and that's not worked in the U.K. in the way that we'd hoped. But as I say, we plan to have that in place in Sloan Kettering in the next few months. Perfect. Thank you very much. I think we've probably got time for maybe two more questions. So let's go for this one here: "Will Avacta consider adding additional indications in P two? Not initially. So the phase II study that I've outlined, I mean, I realize I've given very little detail, but the phase II study that I've outlined is gonna be focused on one or two subtypes of soft tissue sarcoma, and that is a regulatory strategy that's designed to get registrational approval. So that can be done in the U.S. It's more difficult to take that approach in Europe. So it's a strategy to make sure that we get to the end of phase II and get approval for AVA6000 in those selected indications. Now, clearly, that can then be expanded into other sarcoma subtypes and other indications that we've spoken about in the past. I know we had a meeting before this, where we talked about breast cancer, and that's an obvious one. So, we will, and those opportunities may be, you know, may be partnered, because studies in breast cancer, as I'm sure you're aware, are very large studies, and may be something that we would partner rather than do ourselves. Perfect. Maybe the final question: "Going forward, will the FDA be the lead regulator? Well, I mean, we obviously keep all our options open. I think everyone's aware that there's delays in the U.K. with the MHRA. So I think it's very likely that the FDA is gonna be the lead regulator for, you know, for a period. Let's hope those delays are shorter than the U.K., but we keep all our options open. Perfect. Alastair, Tony, thank you very much for that. We've just hit the hour, and I think you've addressed those questions you can from investors. Of course, the company will review all the questions submitted today, and we'll publish those responses on the Investor Meet Company platform. Just before we direct investors to provide you with their feedback, which we know is particularly important to the company, Alastair, could I just ask you for a few closing comments? Yeah, sure. Thank you for your time. Now, it's a real pleasure to be talking about such an exciting period in the, you know, in the therapeutic division's development and the group as a whole. It's been a super, you know, 12 months, and the last few months as we've seen those efficacy signals is genuinely transformational for the company in many ways. So it's a very exciting time to be in the company, hopefully an exciting time to be an investor. We have so much to do. But yeah, it's an exciting picture moving forward. So thank you for your time, and looking forward to next opportunity to speak to you. Perfect. Alastair, Tony, thank you once again for updating investors today. Could 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, but I'm sure it will be greatly valued by the company. On behalf of the management team of the Avacta Group plc, we'd like to thank you for attending today's presentation, and good afternoon to you all.