Good afternoon, everyone, and thank you for joining us today. My name is John Hester. I am a healthcare analyst here at Bell Potter. I am based in Sydney. For my sins, I cover the healthcare sector, including a whole bunch of Aussie biotech companies, including the likes of Arovella and Anteris and Imugene, all companies involved in cell therapy of one form or another. This is an area of science that is evolving very rapidly as cell therapy is now a dominant form of new treatment in oncology. This afternoon, I am joined by Chairman David Williams. Welcome, David. Assisting him is Nicole van der Weerden, who is the Acting Chief Executive of the company. Hello. I just want to start with just one or two other comments, is that it is not just for blood-borne cancers that the likes of these cell therapies are being developed. Sure. There are obviously those applications for the likes of lymphoma and so on, but there are numerous applications in areas of autoimmune disease, such as lupus and Crohn's, that are also very attractive. As a result of that investment, not only by Arovella, but by many of the large, top-tier pharma groups, there have been some enormous prices paid for some of these assets at very early stage development. I suppose that is what I think the key message is this afternoon, is that these assets have got a huge amount of value despite having relatively modest amounts of data from the clinic. David, that is my two cents worth. I am going to hand it over to you to say a few words and introduce Nicole. Thanks, John, and thanks you and Bell Potter for hosting this for us. I do not think, as you led into it, that anybody needs convincing about how cell therapy is revolutionizing cancer treatment. There is a very crowded space, even in the listed space in Australia, so how to differentiate those. Before I go there, I recently watched Sam Neill from Jurassic Park fame die, and he had had a few years of chemo, and he really had no time left to live. Went into a cell therapy program, six months, nearly killed him again, but he was cancer-free by the end of it. Unfortunately, he recently just died, but it was an immune system thing rather than a cancer thing. That taught me a lot of lessons. Apart from the fact that I knew him, it taught me a lot of lessons which are relevant to the discussion today. One was, I think, speed of treatment, and the other one is cost of treatment. We think when you start to look at this whole tapestry of cell therapy companies in Melbourne and Sydney and Australia, forget about the rest of the world, what is it that we think we're different? We think we're very different because we think we've got the most advanced donor-derived cells in the market, which both have a speed effect and a cost effect, quite apart from the science, which Nic will go into in a moment. But there used to be an ad for those people on this call, John, you're obviously old enough, but in the '80s, when you used to go and get your petrol, you used to check your oil, and there was a Castrol GTX ad I remember became very famous, where a gangster was talking to a nervous mechanic who was putting the wrong oil in his car. This ad came out. The mechanic's name was Sol, but the ad was, "Oils ain't oils, Sol." The guy was very nervous, thought he was going to get killed. I could say the same thing here. Cells ain't cells, mate. We have got an iNKT cell which is very different from other cell properties, and not just in cost and speed, but in science as well. We've got some great preclinical data that we've seen in gastric and pancreatic. The most exciting thing, and Nic's going to cover this, is that we've got FDA approval for an IND, and we're about to dose, hopefully in the next couple of weeks, our first patient, which I think, Nic, will be in The Alfred. We've got a fantastic scientific team, a couple of guys that actually looked after Sam Neill, believe it or not. But we're heading into the clinic, we're heading into first dosing. I think the other thing that I want to come out of this is that we are not developing a product. We are developing a platform. As you quite rightly said, John, there's a number of applications in this area. We're going into clinic in bloods, but we're also working towards solid tumors and immuno as well. Nic will cover off some of this. But I really want to get across today the message that we're different, how we differentiate ourselves, that we're close to first dosing. The final thing I want to get across is that we've got a platform technology, a la those people. I see a few people on the line that are from PolyNovo, a la PolyNovo. Anyway, I'd like to introduce Nic, who is the acting CEO. She's got my complete support, and I'm training her, training her as we go. No, she's training me. I've started from nowhere, and now I'm sort of halfway up the learning curve. Nicole, welcome. Thanks, David, and thanks John and Bell Potter for hosting us today. We will teach you about iNKT cells, David, that's for sure. I'm going to share my screen here. Hopefully everybody can now see my presentation. Yes, we can. Thank you, Nicole. Okay, great. I will be making forward-looking- Just while you're talking, Nicole, I should have said that this presentation on the screen is not the presentation that's been put up to the ASX. That's a longer presentation. It covers everything that's in this presentation, but this is a cut-down version for the purposes of fitting the time that we've got today. Correct. This is a shortened version to really cover the highlights. I will probably refer to a few things today where there is a little bit more data and information in the full deck on the ASX, for those that are interested. I will be making forward-looking statements. This is our disclaimer. I think oncology has really moved and cancer treatments have really moved over the last several decades from these kind of highly toxic, non-specific radiation chemotherapy to much more targeted approaches. Immunotherapies with better specificity, lower toxicities, better safety, and better efficacy. I think one of the most revolutionary of those, and the newest of those modalities, are these cell therapies, which John and David were just talking about. Cell therapy really has revolutionized blood cancer treatment. The first product was approved in 2017. We now have seven approved products for blood cancers, and you can see there that the top three selling products all did well over AUD 1 billion of sales in 2025. CAR T cells have really delivered great efficacy to blood cancer patients, and we are now starting to use cure and cancer in the same sentence for blood cancers, which was unheard of a decade ago. On the bottom right-hand corner of the slide there, you will see two photos. The first one is Emily Whitehead. She was the first pediatric cancer patient that was treated with CAR T, and that photo is of her celebrating 10 years cancer-free. I think she is now up to about 12 years cancer-free. She really has become the poster child for CAR T therapies from early clinical trials. Of course, Sam Neill, David mentioned that he himself was cured of a blood cancer and remained cancer-free until recently when obviously he passed away, but it was not related to the cancer coming back. He was really an advocate recently in the media and things for trying to improve patient access for these really revolutionary treatments. Obviously that has driven strong sales. The efficacy of these products has driven strong sales in the sector. But even with all that good news, there is still 40%-60% of patients that actually relapse after these products. There is still a large unmet need. A little bit about- Nicole, just a question from me. Yeah. If you can jump in on that slide. Perfect. 40%-60% of patients relapse after treatment with YESCARTA and others. These are like $500,000 therapies, right? Correct. What is the profile of the patients who are most likely to relapse? Yeah, look, I think there are several reasons for relapse. One of them is often, I think, patients whose T cells. I actually might go to the next slide to answer that question while I talk through a little bit about what CAR T is and what the challenges are. CAR T therapies are, you take a patient's own T cells, right? You take their blood, take their T cells out of that, so one of their immune cells. Then you genetically modify that to give it a chimeric antigen receptor. That is where the CAR term comes from, and that really turns those T cells into GPS-guided cells that will go and hunt down, find, and kill the cancer cells. That manufacturing batch is patient specific, and that creates not only a really high logistical burden to have to make one batch per patient, but it is also highly costly, and that then leads to this $ 500,000 a dose for these therapies is usually the price. In addition to that logistical challenge, these patients have gone through lots of therapies, prior lines of therapy that can really damage their immune system. Often their T cells are actually not that fit that you are starting with, right? Because they have been damaged. That is one potential cause of failure and relapse, is that the T cells just are not that effective because they are exhausted and damaged. CAR T, the cells can last a very long time in the body because they are the patient's own cells, but they do not last forever. Or sometimes they do not last forever. If those cells have gone and then there is a trace of the cancer to come back, obviously then a patient will relapse. I think they are still learning a lot about CAR T therapies, and efficacy, and what drives that relapse. But it is often caused by the T cells themselves not really being effective enough. Okay. The other downside of a patient-specific manufacturing process is time, right? It takes three or four weeks for these patients to have their blood collected. The product for Australian patients often gets sent back to the U.S., modified, and then has to be shipped back. That three or four weeks could be a really long time for a patient with aggressive disease. Patients do sometimes die while waiting for these cells to be manufactured. Only limited centers can actually collect, manufacture, and reintroduce this therapy. There is only a handful of centers in Australia and nothing in regional Australia. I think patients always have to travel to city centers, often for more than a month, with a carer, to be able to access these treatments. Patient access is a real barrier for these individualized medicines. What is Arovella's solution? We are developing an off-the-shelf CAR T product, right? We take blood from healthy donors, and I will talk a little bit about how we do that and our unique cell type. But we are able to then manufacture our product, create multiple doses from a single manufacturing batch, and then have that product ready, available, sitting in the freezer so that it is ready to dose patients within a week, right? That reduces cost and increases access, and we use a really unique cell type to do that. It is a CAR-iNKT product rather than a CAR T product. Why do we think we are special at Arovella and why invest in Arovella? As David mentioned, we really see what we are developing as a platform designed to support multiple future therapies, and we see ourselves as structurally differentiated because of the unique immune cell that we are using, which is an iNKT cell, and I will talk a little bit more about that in a minute. We have got near-term clinical validation, so we are about to dose the first patient in our phase I clinical trial in the coming weeks. That is supported by a U.S. FDA-accepted IND, and we are expecting preliminary data from that trial in early 2027. It is a scalable platform. As I mentioned, it is off-the-shelf manufacturing. We start with healthy donor material, and we can produce multiple doses per batch, so that really reduces the cost to generate the treatment. The platform supports pipeline expansion across blood cancers, solid tumors, and autoimmune disease, which again, I will talk a little bit more about later in the talk. We are not doing one product, we are really building a platform that can support multiple future therapies. This is where we get into the science a little bit, and I will try and explain why we are so excited about iNKT cells and why we think they are a really powerful immune cell for use in CAR-iNKT or cell therapies. One thing that is important is they are allogeneic without the need to gene edit. Normal T cells cannot be given from one patient to another. Those T cells will recognize the patient as foreign, and they will start attacking their normal tissues, and that is because of the T cell receptor that they have, and I will try and get my pointer going. They have this T cell receptor that will recognize the patient as foreign. iNKT cells are called invariant natural killer T cells, and they have an invariant T cell receptor. My TCR and my iNKT cells is the same as your TCR and your iNKT cells. They can be given from a healthy donor to a patient without the need to edit out that T cell, and they will not cause graft-versus-host disease. They are allogeneic from the start without the need for gene editing, which is a real benefit. They then have multiple ways to actually attack and kill the cancer cells. I mentioned this chimeric antigen receptor. That is the sort of GPS-guided targeting piece that we put into the cell so that they can go and target the cancer cells. Sorry. The CAR that we add in allows them to specifically find a cancer antigen, and we can use different CARs to target different cancers, and that is where it is a real platform that we can expand across different products. This is what is normally added for a CAR T cell, but what is unique about our iNKT cells is our iTCR can also recognize, it is called lipid-bound CD1d. That is not important about what it is, but it is often found upregulated on cancer cells, so the TCR is sort of another naturally targeting thing for cancer cells, and this NKG2D, which recognizes NKG2D ligands, which are, again, normally upregulated on cancer cells. iNKT cells are known to have a protective role in cancer in normal people. We not only have the CAR targeting mechanism, but we also have these additional two natural targeting mechanisms that can help improve efficacy. We know that iNKT cells infiltrate tissues and tumors better than T cells do. We think, again, particularly in a solid tumor setting, that can really help drive access to the cancer cells and improve efficacy. Lastly, they can modulate the tumor microenvironment, which you hear a lot about sort of being a barrier to cell therapies and CAR T in solid tumors, whereas iNKT cells are actually able to block and kill some of the pro-tumor cells in the tumor microenvironment. Then they release molecules that actually attract other immune cell types, such as T cells and NK cells, so that they can actually come in and help attack the cancer. They're a really powerful immune cell, well-placed for an allogeneic cell therapy product. Arovella's core IP is really around a manufacturing process that can take these powerful but rare immune cell type from healthy donor blood and then manufacture up to very large scale. We have spent the last several years developing a semi-automated process that's suitable for large scale and late phase clinical development that's supported by a U.S. FDA-accepted IND. It's also a patented process. We take healthy donor blood. We're then able to isolate the iNKT cells out of that blood, and this is where we engineer them to add the CAR or the GPS guidance system. We use a lentiviral vector for that, which is just a special reagent, a viral vector that adds the DNA in. This is where we can change out this lentivirus to change the CAR that we're adding into the cells and create different products that target different tumor types. Once we have these CAR iNKT cells, we can then expand them up. We grow them up for a few weeks. While they're a rare immune cell and we start with low numbers, they proliferate, grow, and expand very well. We can end up with billions of cells in one manufacturing batch that then we vial and freeze and have that ready to dose patients, and obviously generate multiple doses per batch. We think we've got one of the most advanced donor-derived CAR iNKT development programs, and obviously on the back of that FDA-accepted IND. Although it's sort of a single platform that we have, we really view three different ways to create value from that platform. The first being blood cancers, and that's our CD19 targeting ALA-101 product. CD19 is a validated target for blood cancers. Several of the approved products target CD19. This product for us will really prove the safety of our iNKT cells, our dosing, and also our persistence of our cells. It really creates a regulatory and CMC precedent. We will use the same manufacturing process for future products, which means the regulatory pathway is very well defined. Our phase I trial here will generate B cell depletion data, and I'll talk a little in a minute about why that's important. The second area is really around solid tumors, and this is where we really think the biology of iNKT cells is really well suited to treating solid tumors, because they can infiltrate into tissues better and modify that tumor microenvironment. They have those additional natural targeting mechanisms that can help prevent the antigen escape that you sometimes see in solid tumors where it is difficult to target all of the tumor cells in a solid tumor, and we have naturally got multiple targeting mechanisms. Our lead product there is a Claudin 18.2 targeting product, ALA-105, for gastric and pancreatic cancers. This product really will test our iNKT solid tumor biology. It will leverage our armoring technology, which I am not going to talk a lot about today. For those that have not seen it, we do have an explainer video on how that armoring technology works. That is some specific technology that we have in-licensed that really enhances the efficacy of our iNKT cells, particularly for solid tumors. The data from that product will support expansion to future solid tumor targets. The third area of value creation we see is really around autoimmune disease. This is actually using the same product as we use for blood cancer, so our ALA-101 product, same target. B cells that cause a lot of blood cancers also cause really severe autoimmune diseases. Those abnormal B cells can cause severe autoimmune disease when those B cells start targeting your own tissue instead of recognizing foreign tissue. There is nice data emerging from clinical trials now about CAR T products being really effective in removing those abnormal B cells and acting like an immune reset, so that then patients, their symptoms improve, they are able to come off various treatments. We will see from our phase I data for our blood cancer study that our product is able to deplete those B cells, and that supports then an expansion for ALA-101 into autoimmune disease. We will be able to learn a lot from those coming before us with CAR T products in the autoimmune space about where they are likely to be the most effective. ALA-101, I just mentioned that it is CD19 targeting for blood cancers. Our phase I study is expected to commence next month, and that is a validated target for blood cancers with the potential to expand. This is really the things I have mentioned earlier about how it addresses the key challenges for CAR T. From a safety perspective, we have a low risk of graft-versus-host disease, and the natural properties of iNKT cells also mean that they are likely to have decreased toxicity relative to CAR T. Some of the side effects you see in CAR T, if you have heard mentioned CRS or ICANS, we think there is a potential for those to be lower with our iNKT platform because of some of the properties of iNKT cells. Scalability and cost, allogeneic off-the-shelf. We think both of these, the safety and the scalability, really lead into the potential for improved patient access, right? Even potentially administering these products in an outpatient setting, in regional hospitals and things. That is really a goal for us, is how do we get these treatments to more patients. Then, back to your question at the start, John, around the healthier starting material and avoiding that dysfunction that is often seen for cancer patients that have been through a lot of really harsh treatments. Our phase I study will be in adults with relapsed and refractory lymphomas and leukemias, or CD19 positive lymphomas and leukemias. Patients will undergo screening to confirm they are eligible and their disease status. They will then undergo lymphodepletion, which is a conditioning therapy to prepare their immune system and things to receive the CAR-iNKT product. They will then receive a single infusion of ALA-101, and then they will be followed up on study for obviously safety, response, biology for two years, and then later transition to a long-term follow-up study. It is a dose escalation study, so we will be testing increasing doses of ALA-101, because this is a first-in-human study. We will be actually able to expand and backfill into dose levels that are shown to be safe and efficacious, and that will enable us to get dose response data that really helps us select a dose for a future phase II study. So we are looking for the recommended phase II dose from this study. It is planned to enroll up to 46 patients. What are we looking for in the study? We are really looking for obviously safety. It is a first-in-human study. Are our cells safe? Do they expand and persist when we dose them in patients? Do they control the cancer, and can they deplete B cells? This B cell depletion data obviously supports the expansion down the track to autoimmunity. While this is our phase I blood cancer study, it really does teach us a lot about our cells and our platform that is applicable across solid tumors and autoimmune disease. Hey, Nicole, I might just jump in there. Yeah. And give you a- Please. give you a rest for a second. This trial, can you be a little bit more specific about the indication? Exactly what sort of patients are you going after here? Yeah. For CD19 positive blood cancers, it's a pretty basket trial in terms of we will take all comers that meet that. So that's non-Hodgkin's lymphoma, different subtypes of non-Hodgkin's lymphoma. A large proportion of them will be this DLBCL, diffuse large B-cell lymphoma. It's just the most common. But we're actually really excited to see some of these other subtypes, such as marginal zone and mantle cell lymphoma. A, some of the current CAR T products aren't approved for those indications, and they're known to have CD1d, which is the natural target for iNKT cells. And then leukemia patients as well. We will take CAR T failed patients. Some of these patients will have had a CAR T in the past and relapsed, but that's by no means a requirement. Any patient that wasn't eligible for CAR T but meets our eligibility criteria would still be able to join our study. Okay. So it's pre and post failures on- Yes. on autologous CAR T. Okay. That'll be an interesting one. CAR T is currently second-line therapy in the U.S.? In the U.S. for some subtypes, yes. Yeah. Okay. Yeah. Okay. It's really that border. I think they're still third line here. Yeah. I think that's about right, yeah. Yeah. What's the idea behind the lymphodepletion step? Lymphodepletion is used even with autologous CAR T, and they refer to as kind of making space for these other immune cells to expand. I think it is really about kind of depleting the immune system to make space really for the cells that you add in to be the dominant ones and for them to sort of get a chance to expand and be able to target the tumor cells. It is even more important in an allogeneic setting because while our cells will not recognize the patient as foreign, the patient will recognize our cells as foreign, and eventually those cells will be eliminated. Being able to give our cells time to be able to go and attack the cancer and do what they need to is, I guess it is more effective by doing that lymphodepletion first, removing the patient's immune system. Just last question on this slide. Duration of response is always an important one for investigators and for regulators alike. What is your hope for duration of response? I hope for a good duration of response beyond six and 12 months, and I think- Yeah. Some of the data in our longer deck shows that our product is really very potent. We do think that it will come in and do a really good job of clearing those tumor cells out quickly. What I will say in terms of duration, because this is an issue for any allo product because their cells won't last long term, is a lot of these patients will have failed CAR T therapy. They don't have a lot of other options. Will we see patients that are 10-year cancer free? Probably not at the same numbers as autologous CAR T. But, can we give a really meaningful clinical response to patients that have failed CAR T? Yeah, I think we can. Obviously as we expand our platform, with allo products, there is the potential to look at redosing. You only get one CAR T in your life because it costs $500,000 a dose. Cost is much lower for an allo product. We are exploring whether it is possible to give multiple doses of our product. I think one, two years additional progression-free survival or treatment without relapse is very valuable for these patients who don't really have any other options. Okay, let's move on. Okay. That's it on the blood cancers and ALA-101. Touching on quickly, ALA-105. This is our first solid tumor product targeting Claudin 18.2. It's also a validated target, so there's an approved monoclonal antibody for Claudin. Actually, the first solid tumor CAR T product was recently approved in China targeting Claudin. It's applicable across a broad range of cancers. Initially, we're targeting gastric and pancreatic cancer, and we really think for solid tumors is where these iNKT, our iNKT cells have the potential to outperform T cells because they naturally infiltrate better. They kill pro-tumor cells, and they can target additional targets on the tumor cells. Again, safety, low risk of GVHD. That's the same argument as with the ALA-101, and the scalability and cost and access for these patients. We've recently shown data that we are actually developing a novel Claudin CAR. We've released data, and it's again in the longer deck, showing that that CAR is performing very well in iNKT cells, particularly with our armoring technology. We're really excited to be advancing this product towards the clinic. Lastly, really just touching on our highlights over the past six months for 2026. We finished up 30 June with AUD 14.4 million in the bank, and that's expected to fund our preliminary ALA-101 clinical safety and efficacy data, and then also advancing ALA-105 towards the clinic. We hit some really important milestones over the last six months. We had our U.S. IND accepted for ALA-101, and that really does set the precedent for all future INDs for our platform. We got ethics approval to commence our study, and we've engaged our clinical trial sites, The Alfred Hospital in Melbourne with Dr. Sam Fiorenza as our lead PI. That site startup is all going underway at the moment, and we expect to start dosing patients next month. We manufactured our first clinical batch that is undergoing release testing at the moment. Then, yeah, we are also generating some really compelling preclinical data for our first armored solid tumor product, ALA-105. That is the end of my presentation. Happy to answer- Okay. any additional questions. Thank you. For anyone who would like to ask a question, please use the Q&A button at the top of your screen there. We have got room for just a couple of questions. I will vet those as they come through. Nicole, just from me, look, this is a very competitive space you are in. Not only have we got the autologous product, you have also got the bispecific drugs that are being developed by Roche and others. How do you expect the ALA-101 will differentiate itself from some of those? Yeah. ALA-101, the CD19, obviously CD19 is a very crowded space, but I do still see there is a high unmet need there and a lot of value for a product like ours because we see patients lining up for our clinical trial, right? Yeah. That currently don't have other options. I think there's I still think there's an unmet need there, despite the competitive nature, and I think a product that delivers safety and efficacy will still find a space in this market. Obviously, it expands into the autoimmune setting with that same product. Again, the CAR T products have performed much better than the antibodies and bispecifics to date. I think that just sort of really targeted killing by the immune cells is important. In terms of value for Arovella, I think it's not just ALA-101, it's our solid tumor products and things where the CAR T data has not been as good, and we really think the iNKT biology really drives better efficacy in that setting. Okay. Just a couple of questions coming through from the floor. How do you plan to recruit this trial in the U.S.? Can you be any more specific on what other subtypes are a priority for you, and potentially leading to an accelerated approval? We will start the study here in Australia. Obviously, we've got the IND, we can expand into the U.S. But we've got really good engagement with our Australian sites. They seem to have a good list of patients ready to go for our study. We will look at when the right time is to expand into the U.S., and engage in that setting. We're also looking at jurisdictions like New Zealand that don't have publicly funded CAR T. We've got potential there to recruit patients maybe that haven't had CAR T therapy before. What was the second part of that question? Sorry. Just- John. Can you be any more specific? Oh, the subtypes. You talked about diffuse large B-cell, and there is also mantle cell lymphoma and others as well. That is right. Have you got any idea of which is the sort of greatest unmet need there that perhaps you could target? Yeah. That will be data-driven, right? Our goal is to enroll all sorts of patients into the study and see which ones respond best. I mentioned marginal zone and mantle cell lymphoma- Yeah. have that CD1d aspect, so iNKT cells may naturally target that. Yeah. But yeah, right now we'll kind of learn from the data in the phase I, which are the best subtypes to target. Are you worried about cytokine release syndrome as well? That's obviously one of the major downstream effects from a safety perspective. What's the profile that emerged in your preclinical work there? Yeah. Our iNKT cells are really interesting, and this gets a bit scientific, but they have sort of an immunomodulatory, so they're not quite as inflammatory, and they don't release the same types of cytokines that T cells do that lead to that cytokine release syndrome. We think naturally they will have a lower level of cytokine release. There is a previous CAR-iNKT cell study, an academic center study, where they used CAR-iNKT cells, and they didn't see high-grade cytokine release. We think, and we'll test this in our study obviously, that we'll actually see an improved safety profile relative to the CAR T therapies. Okay. Well, it sounds like a really exciting next six months or so. You're just about to dose first patient imminently? Yes. That sounds great, Nicole. Thank you very much for that. David, just to help us wrap things up here. Obviously, you've got a lot of data to emerge over the next six months or so. What are your thoughts after hearing the presentation there today? Well, none after hearing it. I read it many times before we gave it, so nothing special there. I'm increasingly excited about the data we've already got, and we're going to be hanging on the data coming out of the dosing of patients. I think it's probably worth saying something here, Nicole, about the speed with which we're dosing, because we'll dose one patient, then we'll wait to see the effects, then we'll dose another patient. Please don't send me emails after one week saying, "How many patients we got?" Or, "How are they traveling?" Just put it in the back door till December and then start pestering me. But I'm pretty excited about it. I'm also excited about the platform aspects of this because you know my attitude, John, in the PolyNovos of the world and other things I've had, is that if you really believe in it and the data looks like it's going to come, then crash or crash through them. In other words, don't wait and do it sequentially. If we start to see some good results out of the bloods, then we'll progress very quickly, I think, onto solid tumors and immuno. I think that may take a bit more money, but I think if we're starting to see good results, the share price is going to look after itself anyway. Yep. David, have you had any engagement from the big end of town at this point? No. Well, we're getting a lot of engagement by smaller companies in the space because people are running out of money, and I think we're in the whole sector, by the way, I think we're going to see a lot of mergers between now and even the end of December. We've got a half-reasonable market cap, so we're attractive in that sense. We've got a differentiated cell product, and we're attractive in that sense. What I want to do is do what we've done now. Let's dumb it down. Let's get the patients coming through, and then we'll talk to the big end of town ourselves, because there's certainly plenty of interest in it coming out of North America. I'm not necessarily putting up a for sale sign, but if the big boys, you've seen the transactions that are getting done on very little data and very little patience. The more help we can get in terms of geographical coverage and scientific help, the better. Yep. We'll put really If I don't have many skills myself, but one of the skills I do have is being able to push these things hard. Okay. Nicole, just concluding comments from you, and I'll just ask you to perhaps highlight the news events over the next six months or so, starting with first patient enrolled and when should we expect some clinical data? Yeah. Obviously, we're anticipating first patient in September. We're kind of imminently going through site startup and things for that, and we need release of our clinical manufacturing material. This is a first in human study. We do need to stagger dosing for safety, right? We'll be dosing one patient at a time. We are starting at a- lower dose level, and that will increase up. As David said, right, probably first very early in next year, we should have data that we are able to start releasing. But in the meantime, we have also got advancements on our ALA-105 solid tumor program, and getting that towards clinic. So we are expecting in vivo animal data from that product in the coming months. Then advancing that in towards an IND and then, also looking at potentially new combination, things and sort of platform expanding activities that we will be undertaking over the next six months as well. Okay. All right. And David, just a quick comment on the register. What are you thinking? Well, we are like a lot of small biotechs, even though we have got a half-reasonable market cap, you are left essentially with moms and dads. There is no big end of town or even medium-sized institutions on the register. But that will fix itself. The share price will fix that, and the results will fix that. So it is just a matter of time. Look, I think we have got ourselves reasonably focused now on what we are going to be doing for the next six months. So, turn our attention to how we can accelerate that to the extent we can. In accelerating it, part of that will be talking to all and sundry about where we can cross over and what help we might need in North America or elsewhere for that matter. I am not wedded to North America. Mm. Okay. All right. Well, look, that has been a great run through. Thank you, David, in particular. Thank you, Nicole, for your explanation of the science there. That is indeed very, very exciting. Plenty of news over the next six to nine months. Yep. We look forward with great anticipation to having some very nice efficacy data with long duration of response and hopefully the side effect profile is as lean as it can be. If you put those three things together, then you have got a winner on your hands here. Yeah. No. Thank you, and I will look forward to reading that in your next update. Good on you, David. Thanks very much. Thank you both for your time. Thanks for the opportunity. Thanks. Appreciate it. Thank you very much for joining me. Thanks for hosting it. Thank you. You are welcome. Thanks everyone for listening. Bye.