Okay, I think we're just allowing a little bit of time for people to log in. I think we're ready to start. Welcome everybody to our webinar today to present a progress update. Hopefully, at the end of the presentation, you'll agree we've seen an enormous amount of very good progress at Actinogen in the last few months, with a lot more good stuff in the pipeline. As you know, a number of our senior leaders will be joining me for the presentation, and will do, in fact, most of the talking, including in the Q&A session. It's all about our lead compound, Xanamem®, which we're using to control brain levels of cortisol, which is a well-known toxic hormone in neurodegenerative disease. We also saw in our positive phase IIa some effects in depression as well. With that, I'll just go to the disclaimer. We will be making forward-looking statements. The agenda. Thank you, Michael. Sorry, back to the agenda. I'll start with a few slides of overview and introduction. Dr. Dana Hilt, Chief Medical Officer, will cover clinical and regulatory. Dr. Fujun Li, Manufacturing. Mr. Andy Udell has two real hats at the moment. He's our Chief Commercial Officer concerning commercial readiness, which is very, very important and making great progress there, but also heading our business development and partnering work based in the U.S. We will cover financials and Michael Roberts, the Investor Hub facility, briefly. I'll come back and conclude. The Q&A will be all done at the end. Please keep an eye on your questions. You can submit them during the presentation, but the answers will be grouped together and answered roughly in sequence at the end. We have in total a 45-minute presentation and Q&A session planned. The presentation itself shouldn't be much more than 25 minutes at the most, leaving plenty of time for Q&A. To ask a question, just type your question in the Q&A window and hit Enter on your keyboard to submit the message. It's as simple as that. We'll remind you of the method for asking questions at the end of the presentation. Next slide. What we're going to cover is a broad range of the progress that we've been making on many fronts as we mature into the late stages of our Xanamem® clinical program and clear the pathway to Alzheimer's approval. In particular, we'll focus on the important pivotal phase II-B/III study that is ongoing in Alzheimer's disease, very much on track with the screening closing this week, and our recent FDA meeting, which was extremely positive, agreeing on a fairly streamlined development program to reach a full and comprehensive approval with only one additional pivotal study. This was a very good agreement for us. It It had many other aspects to it, including agreement on manufacturing terms and other ancillary studies. In addition, for the Xanamem® clinical program, as well as the current trial going extremely well, we are constantly monitoring safety, and our excellent safety profile has been maintained. We're now on track for our interim analysis of safety and efficacy of futility in late January, as we've said before, and now on track for top-line final results in the middle of Q4 of next year. Previously, we'd said any time in Q4, thinking it may be late Q4. That's now been narrowed down to the middle of the quarter based on full enrollment by the end of the year. In addition, we haven't talked about this a lot, our open label extension phase for the trial opens in the first quarter of next year. This is very, very important and has been part of the reason that we've been able to get rapid enrollment in the Xanamem® trial itself. That enables anybody, past and present Xanamem® participants, to then proceed on to an open label active treatment phase for up to 25 months. This is very important to patients, carers, and physicians, and will provide really useful data from long-term safety and observation of efficacy variables as well. In addition, we're planning phase III with the FDA minutes in hand and commencing discussions or in full discussions with potential partners regionally and globally. More detail on all of this in the coming presentation. Next slide, please. None of this could be done without the right people. As you'll see from the presentations of the assembled here, a very experienced team, but also a very experienced board-level team as well. I'm not going to pick out everybody individually, but you can see down the bottom there a lot of collective experience at multiple different companies here in Australia and particularly in the U.S. We really are doing things to a very high, I would argue, U.S. biotech or Biopharma standard. I think that is going to bear fruit in the next few months as we go into further discussions with commercial partners and get to the end of the study at the end of next year. Next slide. Before I hand it over to the rest of the team, I'd love to show you our newest mechanism of action video. We have a unique mechanism of action, and Andy quite rightly discussed with thought leaders around the world that we really needed to explain this better in the context of how our drug works and is differentiated from other proposed anti-amyloid therapies for Alzheimer’s disease and potentially depression. For those who haven't seen it, we'd like to play it again. It's quite short, two minutes. Alzheimer’s disease is defined by the pathology of amyloid plaques and tau tangles. However, targeting these proteins has had mixed therapeutic success. Research suggests chronic excess cortisol, the stress hormone, plays an important pathological role upstream of neurodegeneration. Elevated brain cortisol levels are strongly linked to Alzheimer’s disease and major depressive disorder, disrupting brain cell metabolism and damaging neurons through excessive synapse pruning and impairing neurogenesis. Over 50% of brain cortisol is generated locally by the enzyme 11β-HSD1, which converts inactive cortisone into active cortisol. 11β-HSD1 is highly expressed in brain regions critical for memory and mood, and its levels increase with Alzheimer’s and depression. Xanamem® (emestedastat) readily crosses the blood-brain barrier and is the first and only potent oral inhibitor of Brain 11β-HSD1. By selectively reducing cortisol in key brain regions, Xanamem® is designed to slow Alzheimer’s and treat depression while maintaining adrenal production and normal plasma cortisol levels, avoiding adrenal insufficiency. Additionally, its action in the liver and adipose tissue may provide anti-inflammatory and metabolic benefits. In summary, phase II clinical trials have shown Xanamem® to be safe and well-tolerated, with promising disease-modifying activity in Alzheimer’s disease and improvement in depressive symptoms. Great. Hopefully you agree with me that that's a really excellent introduction to Xanamem®, how it works, and why it's different than other drugs. Certainly, in a number of presentations where I've used it previously, it's been very well received universally by various stakeholders interested in our program. Next slide. I think this is where I hand over to Dr. Hilt to take us through our recent clinical and regulatory progress. Thank you, Steve. It's a pleasure to talk to you all today. I want to emphasize something that Steve mentioned and that the video showed, that one way to think about what Xanamem®, emestedastat, is doing, it's reducing the stress response in brain. Cortisol is deleterious to brain function. Importantly, cortisol in the brain is made by a different enzyme than is made in the adrenal cortex. Emestedastat allows us to selectively decrease cortisol while systemic cortisol levels stay normal. Thinking about this reduction in the stress response in the brain, what emestedastat does, it can produce both rapid changes in signal transduction, cell function, neurotransmitter levels that occur over hours or days, but also has slower long-term modulatory effects that may take days or even weeks, leading the brain to reset to a lower stress level. Overall, there's a vast literature, frankly, about the deleterious effects of cortisol in the brain. This is really the first agent that really has shown to decrease the cortisol levels in the brain. Next slide, please. This is some of the evidence for that. What we see here, and we've published these data now, is that on the left side is a probe to 11β-HSD1. You can see the bright staining or the illumination of the 11β-HSD1 with a probe. If you give that same probe in the presence of 5, 10, or 20 mg of Xanamem®, what you see is a great diminution of the intensity of the signal. This means that doses of 5 mg and 10 mg get into the brain and inhibit the production of cortisol by binding to the enzyme. This is called in the Trade Target Engagement. This is a very important point for CNS drugs because we can't take a piece of the brain out and measure this. We have to do it indirectly by these imaging methods. This drug is really the first in its class to show this kind of, you know, rock-solid evidence of target engagement at the doses that we're using. Next, please. If one looks at the drugs that have been approved, the anti-amyloid antibody drugs that have been approved in Alzheimer's disease, what I'm showing here is the natural history of progression over time. I'm showing on the x-axis a decrease in the CDR sum of boxes over time as the patient progresses in the dotted orange line. Both lecanemab and donanemab have a pretty modest effect, and that's shown schematically in the solid orange line. The area between those two curves is really the benefit of the drug, the antibody. The area above the solid orange line in blue is the unmet medical need. There is, yes, an effect with the monoclonal antibodies, but they're obviously not going to be the cure or the standalone therapy for Alzheimer's disease. The field now generally accepts this. At most of the Alzheimer's disease meetings, there's talk now about combination therapy or trying to address different mechanisms other than just amyloid or tau. Of course, Xanamem® is addressing a different mechanism. Next, please. This is an example of what we think the drug can do. This was the initial pilot study in patients with Alzheimer's disease. Initially, the entire study was clinically diagnosed, and we looked at the subset of patients who we know have Alzheimer's disease in this study by having positive biomarker pTau 181 elevation. What we see here in the light purple line is over a three-month trial, the progression in the CDR sum of boxes of worsening going down in patients with this biomarker-positive Alzheimer's disease. In the solid purple line is the effect of Xanamem®. There's a very substantial effect that even can be seen in three months of treatment. This Cohen's D, which is a measure of this magnitude, is 0.4, which is clearly a clinically significant benefit. These strong data were the basis on which we designed the present ongoing phase II-B/III study that Dr. Gourlay mentioned. Next slide. This is a diagram of that study. This is 10 mg vs placebo. The treatment, it's one-to-one randomization. The treatment period is nine months, 36 weeks. What we're doing is enrolling patients that have a clinical diagnosis of Alzheimer's disease plus elevated pTau biomarker positive in their plasma. The primary endpoint is the CDR sum of boxes. This is a universally accepted metric of overall disease severity and clinical significance in patients with Alzheimer's disease. All the regulatory authorities in the world recognize this as a registration endpoint. Key secondary endpoints in this study are measures of cognition, as well as measures of activity of daily living. How well can the patient conduct their normal activity of self-care, feeding, out shopping, buying groceries? These are very important measures as well of clinical benefit. The study was initially started in Australia. We've expanded, we have now expanded into U.S. sites, and that's greatly enhanced the enrollment, the denominator in the United States, larger, bigger population. The trial was originally designed for approximately 220, and we've seen a robust increase in screening and enrollment over the last few months. We think the final projection of the size of the trial will be more in the neighborhood of 240 patients enrolled. We'll be doing a futility analysis, interim analysis, in late January of 2026. This is for safety and efficacy. A futility analysis is basically asking the question, we're not going to unblind the data, and we're not going to stop the trial if the drug is having effect. We want to know, is the drug going in the right direction? This is basically an analysis to say that, yes, we're on the right track. We also, as Dr. Gourlay mentioned, are planning to initiate an open label extension to start enrolling patients in Q1 of 2026 after the interim analysis in late January of 2026. We're very happy with the uptick in enrollment and enthusiasm for participating in the trial, and things are going very well in that regard. Next slide. Also, Steve mentioned the fact that we've done an initial phase II-A study in approximately 160 patients with treatment-resistant depression. These are patients that have a significant history of major depressive disorder. Most of them, 80% of them, are on an antidepressant. They've had 4-5 episodes of severe depression before. This is a tough group of patients to have an impact in. We saw that in patients on SSRIs, which are the standard treatment for depression, that the drug seemed to have a beneficial effect. This is another piece of evidence supporting the conclusion that the drug is active and biologically effective in now two different conditions, Alzheimer’s disease and depression. Importantly, you know, depression is a risk factor for Alzheimer’s disease. Depression frequently occurs in patients with Alzheimer’s disease. This may be also part of the beneficial effect that we might see in patients with Alzheimer’s disease with emestedastat. Next slide. As far as the regulatory perspective, we have an Innovation Passport for innovative drug, which was awarded in the U.K., in 2024. Dr. Gourlay mentioned we had a very positive interaction with the U.S. Food and Drug Administration. Importantly, they said that only the 10 mg vs placebo, only the 10 mg dose vs placebo, one more additional pivotal trial would be necessary, and the open-label safety studies to get the necessary long-term safety with the drug. The ICH guideline for that is 1,500 individuals. We also had very clear guidance from them on a core group of non-clinical and clinical pharmacology studies, such as QT studies or drug-drug interaction studies. We plan a similar EMA meeting in 2026, now that we have the U.S. FDA guidance in hand over the last month or so. This has really, I think, clarified completely what we need to do to get the drug to the finish line and get it to patients. Next slide. I will turn the discussion over to Dr. Fujun Li, who's the Head of Manufacturing, and she'll update you on manufacturing and quality. Fujun. Thank you, Dana. It is my pleasure to provide an update on the Xanamem® manufacturing. This year, we have successfully manufactured a large batch of the Xanamem® drug substance. The manufacture was conducted at IC Chem in China. IC Chem is highly regarded in the pharmaceutical industry for its high-quality standards and has strong expertise in the manufacturing process that is used for Xanamem® drug substance production. We currently have two process patent applications in progress for drug substance. To support the open label extension study, this batch of the drug substance is being used to scale up the manufacturing of tablets at Cortland in the U.S. There were no tariff issues on the import of the drug substance from China for clinical trial material manufacturing. We also have a formulation patent application in progress currently. We recently reached agreement with the FDA on the designation of the regulatory starting materials for the drug substance synthesis. This is a critical step to define the synthetic role for our manufacturing process. Also, recently, we completed a clinical pharmacology study, which confirmed the 10 mg tablets provided similar exposure to the Prevus capsule formulation, and the tablets are suitable for the once-daily dosing. That is also good for us. In addition, Actinogen carefully provides quality oversight of the CDMOs for all the manufacturing activities. That's all the manufacturing update. I'll hand over to Andy. Thanks, Fujun. As you've heard from Steve, you heard from Dana presenting the science and the unique mechanism of action, as well as our clinical results, Xanamem® is something truly different in the Alzheimer's treatment landscape. I am going to review with you the market opportunity, the voice of the physician, and momentum we are already creating around Xanamem®. As you can see here, Alzheimer's, and I'm sure you're very well aware, is already one of the largest and fastest growing healthcare challenges we face in the U.S. alone. It's over 7 million patients today and is supposed to double, nearly double by the year 2060. By 2050, halfway through the century, mid-century, it's supposed to be about a trillion dollars. Despite this enormous need, there's still no safe, effective oral therapies that truly slow the disease. That's why our approach targeting cortisol control represents such a compelling scientific and clinical opportunity. We know that cortisol levels are elevated early in Alzheimer's, and that lowering cortisol through inhibition of the 11β-HSD1 has shown full neuroprotection in preclinical models and promising results in phase II-A patients, as Dana reviewed. In short, it's a large and growing market, and we have a strong scientific rationale to meet a huge unmet need. Next slide. When we look at the voice of the physician, we want to see what the treating prescriber is saying. We've spoken to a lot of KOLs, but we also want to talk to the treating prescribers. We did some primary market research with Spherics Global Insights with over 100 physicians that average covering or managing, I should say, over 220 Alzheimer's disease patients each. No surprise, their current market perception is 91% of them agree there's a high unmet need for disease-modifying therapies in Alzheimer's disease. Also, somewhat interesting, 86%, a lot of them are pretty optimistic, and they feel the approach to treating Alzheimer's disease is going to change over the next five years. This quote on the slide, I think, is important because I think this is, I've been hearing Dana say this for a while now, and Alzheimer's disease is a chronic disease that's going to be treated most likely with several different mechanisms of action, several different components and products. There's no silver bullet, as they say, in development right now, which is certainly encouraging for us that it will be treated with multiple modalities since Xanamem® is so unique. If you go to the next slide. We wanted to expose these physicians to a target product profile, generally conservative product profile of Xanamem®. These are the same, you know, over 100 physicians. You could see here they reacted very positively to Xanamem®, very, very high on the fact that its oral safety profile and its MOA being unique and the efficacy. Interestingly, also on the right side, you could see here that when they were asked of their current patient loads, what do you think are appropriate patients out of the 200 and whatever patients you're currently managing? They feel over 52% of them would be appropriate for a product with Xanamem®'s profile immediately, right away. That's encouraging. That's what we would say is our addressable market. Obviously, it's a massive number. If you're talking about over 7 million patients in the U.S. alone, half of them would be a pretty good-sized market. Also interesting that they feel over 80% of them said that they would prescribe Xanamem®, a product with that profile, within the first six months on the market. You'd be surprised. I've done a lot of these research projects, and you see physicians are generally pretty honest, and they'll sit back, especially with something that's a new chemical entity. They'll sit back, and they'll want to see how a product develops and how it does from a safety perspective when it hits the market. They pretty much felt comfortable with the product profile here and certainly based against the need and what they currently have available. It was very encouraging. To bring it together, we're at a critical point of development, and we need to build a strong insight of market insights, and we need to build this enthusiasm. What are we doing? If you go to the next slide. The first thing you see is we are driving the awareness. As Steve showed you the MOA video, that's an important component. We feel in our market research and speaking with physicians, we've learned that there is a gap. They need to understand this mechanism of action and why it would have the clinical results that it has and we anticipate it's having. We created that. We're also looking at scientific publications, review articles on cortisol and its impact on Alzheimer's disease. We've been engaging with KOLs. We have awareness. We have advisory boards, and we're creating awareness wherever we can with our attendance at meetings and taking educational initiatives. Next slide. After laying the groundwork with our market insights and commercial—whoops, go back—commercial preparations, I'm going to shift to business development where we see we've been seeing meaningful momentum. We remain real active, present, and continue to build relationships both global and regionally with partners of global size and regional size. We've been at attendance in both Alzheimer's-specific or neurology-based meetings such as APDP, AAIC, and others. SACS Neuroscience Conference will be at JPMorgan. We're also attending business meetings like BIO. Dana and I attended, Dr. Hilt and I attended in June in Boston, where there was really—we met with a lot of new companies, new regional-based companies with a lot of interest that we really hadn't met with before. Dr. Gourlay and I are going to BIO Europe in November next week, actually. We have a ton of meetings aligned, a full slate of activity with thought leaders as well as companies, both regional and, you know, global companies. This has really resulted in all this activity is a lot more activity and diligence. We have had a lot of people and companies actively in our data room, and we're really excited about this progress that we've made. It's also, I think, worth noting that this interest is happening in the context of the M&A activity across neuroscience and the industry. Just as you saw yesterday, Novartis announced its AUD 12 billion acquisition of Avidity, which really underscores how much strategic attention and value is returning to the space. Next slide. With that, I think I turn it over to Will. Thank you, Andy. Great to have everyone along. I'm just looking at the attendee list here, and I think the number of attendees is indicative of the interest in the company that we're seeing at the moment. It is wonderful to be here. We released our quarterly last week, which most people would have seen, gives us a pro forma cash position of AUD 12.9 million. The reason I say pro forma is that we've got about AUD 1.9 million pending from an R&D tax rebate. Our activity across the company is both domestic and international. Where we do international activities, we need to confirm with our industry that that is eligible for R&D. That is why we had to wait for that approval. We've received the approval. The income tax return has been resubmitted. There is another AUD 1.9 million coming this quarter to take us to that AUD 12.9 million position. That gives us runway right out to mid-2026 and potentially beyond that. As we are rapidly approaching full enrollment, as we've discussed here today, our cash burn really starts to plateau out. We really have a good handle on exactly what our outgoings are as we move forward from here. Importantly, there are a number of different potential sources of funding as we move into 2026 or the latter part of 2025 and into 2026. We've got four tranches of options out in the market. Two are listed. Quite a few people on the call, I know, will be aware of those. You can buy and sell those. They're trading in the sort of AUD 0.018 to AUD 0.017 at the moment. They have a AUD 0.05 conversion price. The fact they're trading there obviously gives you an indication that people think there's value in this company well above AUD 0.05. We also have two unlisted tranches of options at AUD 0.0375. If they were all to convert, that's about AUD 6 million of funding that would come into the company at that price. We did see last year when we went through that price that we had about AUD 1 million of conversion of those options in about three weeks. Those option holders have the capacity to convert those options and provide additional funding to the company. Earlier this year, we entered into an agreement with Endpoints Capital, who are an experienced biotech R&D loan provider. They only lend reasonable amounts of money, and they only lend to companies where they've done significant due diligence. We were pleased to build that relationship with them, which is a multi-year relationship at our call. We have the ability to borrow from them should we need to for some additional funding. I think it's important to point out here this money that we're spending, you know, this company runs very lean from a sort of G&A perspective and from an overhead perspective. The money goes into the program. For every dollar we spend on R&D, we get nearly 50% of that back from the R&D rebate. As our spending has increased, as this trial has really ramped up this year, obviously what that means is we're building up a bigger accrual in terms of what we're likely to receive back by way of R&D rebate from the tax office in our 2026 return. We can borrow against that at any point during the year as we move forward under that arrangement with Endpoints Capital. The other potential source of capital that we've been talking about is a possible partnership deal. Generally, the structure of those involves some upfront capital, and that's what we would be targeting and what we would expect. That would also clearly provide us with additional funding to take us beyond where we're currently funded to. I think what you've heard here and what we're seeing here today is that there is increased interest in the company as we rapidly approach these significant milestones. That's broad brush. Steve and I and Andy have been on the road over the last couple of weeks, meeting with investors, with analysts, with banks, retail, high net worth, and institutional investors are certainly sitting up and taking notice of this program and where we're at. I think the reason for that is that they've seen, you know, if you think about a mental list of all the things you need to do to get a drug through clinical trial and into development, this company has done nearly all of those. We've been through the whole preclinical process. There's been 10, 12, 15 years of research and development gone into getting the company to this point where we are right now. All of those de-risking elements in terms of, you know, that Dr. Fujun 's described in terms of manufacturing, that Dr. Dana 's described in terms of interaction with regulatory agencies, that Andy's described in terms of interaction with the prescribers, the people at the end of the day that are going to sell this drug. All of those boxes have been ticked or substantially ticked. We're very, very close to the finish line. I think that's why investors and analysts are really just sitting up and taking notice. I think that reflects what we're seeing, you know, what Andy's described on the business development side. That's because we're still trading around AUD 100 million market cap. Obviously, a drug that is successfully approved for Alzheimer's disease has a valuation many, many multiple times above that. That's why I think we're at this really, really crucial point where people are starting to really recognize that potential value inflection point is really not very far away. I think we can move on. Okay, it's over to me. I'm just going to quickly, very quickly, just talk about Investor Hub, which we've launched in the last month or six weeks or so. For those of you who have used Investor Hub before with other companies, it'd be the very familiar format. I may as well just click to show you here. You can read those bullet points. As we go into the hub, you're faced with this if you go to the general intro page, but generally landing on ASX announcement if you're accessing via an announcement. There you can engage directly with the management team. There might be a video there. Here's an example, annual report to shareholders where there was a shareholder question from Sandalwood Capital. We provide answers there. We make most of the Q&A public, especially where there's interest to other investors. One investor asked a question, so we'll make public so everybody else can see them. You can sign up when you first go there. You're asked to sign up with an email address so we can send out price-sensitive ASX announcements. You can identify as a high net worth investor, which is really useful too if we go into capital raisings and things like that. Overall, very, very interactive and gives you an opportunity for interacting directly with the management team here. We try to get back to you as quickly as possible on questions. I'll leave it there and hand back to Steve for the wrap-up. Thanks, Steve. Thanks, Michael. Sorry we went a bit long, but hopefully the presentations from everybody explained the answers to some of the questions that I've already seen. I've got eight questions on the books here. Just to summarize, I hope you agree that we've made a huge amount of progress in recent months, particularly with the FDA meeting being very positive for a very capital-efficient marketing approval for this drug, way less than any European or U.S. company could have done. It is really a wonderful testament to the ability of being able to develop drugs to a very high global standard here in Australia. We'll have a full enrollment of our Xanamem® by the end of the year, probably around the 240. Interim analyses in January, final results, top line in the middle of Q4 next year. Really great stuff. The positive phase II-A in depression validates our dose and the mechanism of action, albeit with a different disease, but that's very encouraging. Manufacturing is going well. Commercial planning is going well, as you saw. Our partnership activities are ramping up as there's such a lot of new interest in our programs. We've got funding out to mid-2026 and beyond. Lots of other good milestones, publications, regulatory events, various other things as well. A very exciting time for the company. Final results are not much more than a year away, which is a really big deal. If, as we believe, as the pilot data from the phase IIa biomarker study showed, we have a much stronger efficacy and much better safety than any of the other antibodies, for example, for amyloid for Alzheimer's, that would be essentially the holy grail for Alzheimer's disease and obviously a very valuable asset, making the company a very valuable proposition for investors as well. We're going to start the Q&A, and I'll try and group the questions together. We will go to about the top of the hour because we're starting Q&A a little bit late. For those who need to go at 11β-HSD 1:45 A.M., I'll try and do the most important ones first. Remember, just type in the Q&A icon and hit Enter to submit your message. With that, I will start, Will, with the first one, but you've sort of covered it. Isaac asked, when do you need to raise money again? In other words, when is more cash required to finish the trials, etc.? Yeah, as I was just describing, we're funded out to mid-2026, as we've explained, but there's a number of different sources of potential capital coming into the company. Some of those sources are non-dilutive, in particular, obviously an upfront from a partnership arrangement. Similarly, the ability to borrow against our 2026 R&D rebate. Of course, there's the options conversion funding that I talked about as well. There's a number of different pathways for us to fund ourselves all the way beyond the end of the trial next year. We're obviously exploring all of those options. Some of them will be market-based and some of them are in our control. We're working on that. Thanks, Will. There's a little bit of, there's a few questions about the futility analysis. Dana, I might just get you to explain that a little bit. Mark, for example, asked how long will the subjects in the futility analysis have been treated for. Maybe you could clarify. Right. The futility analysis, a futility analysis is basically an analysis to show that it isn't futile to continue and finish the study. If the treated patients are doing as well or better than the placebo patients, the trial has a possibility of success. This is going to be looked at by an independent data safety monitoring board, which has a neurologist, a safety physician, and a statistician. We're not being unblinded internally. As I mentioned, the trial will not be stopped for success. We'll continue it to the end. It's going to be based on when 100 patients get to six months of treatment. The primary endpoint in the trial is nine months, as we mentioned. If we have 100 patients to six months, we'll have data on many more patients for some shorter period of time. The futility analysis will be on a fairly substantial group of patients. I don't know, Steve, if you wanted to. Thanks, Andy. Just to clarify, Mark, there will be a decent-sized group of patients who have finished the full 36 weeks. They will be in the analysis. Essentially, it's a cut of all of the available data at a certain point in time so that the independent committee will have information on people who've been treated for 12 weeks, 24 weeks, and 36 weeks. It'll be roughly half the data in the trial. I think hopefully that answers the question. This same group of experts are also keeping an eye on the safety of the trial, and that's an ongoing activity. Yeah. Shane had some questions, Dana, about the pTau screening. I think you sort of answered the why is pTau screening closing early, because I think we've just seen such a rush of volunteers for the trial. We have to close it with a certain cap. His question was, are we expecting the pTau distribution in this trial to be the same as the pTau distribution in our previous analysis of the phase II-A? The previous phase II-A study used a slightly different pTau assay, so the numbers are not exactly identical. We're looking for patients that have clear elevations of pTau. To the first approximation, I think it's going to be roughly similar to what we previously showed in the previous pilot study. Yeah. Okay. Thank you. There's a couple of questions about competition. Maybe I'll answer one question quite quickly from Mark. The top line results from our current pivotal study, which is the first of the pivotal studies in mid-Q4 next year, a year from now, does not include the data from an additional phase III study that we have agreed with the US Food and Drug Administration. That study will commence in early 2027 and take two to two and a half years to complete. Just to be clear, however, having a very large positive Alzheimer's study for a safe and effective oral therapy in Alzheimer's is truly a phenomenally valuing event. We do expect there to be a huge amount of interest incoming from large and medium pharma alike and the world of investors as well with a positive result this time next year. Question from Isaac about companies as biggest competitors, where, I guess this is for you, Andrew, where do you see Xanamem® sitting in the competitive landscape in terms of safety and efficacy? I guess what's approved now and what's in the pipeline? Sure. The quick answer is there's nothing that really works the same way we do. As I said earlier, this disease, nothing in development seems to be a cure. This is likely a disease with a large unmet need that's going to need multiple different mechanisms. There's nothing like Xanamem®'s. Having said that, there's a lot of anti-amyloid therapies that you've seen. They're working on delivery, but they have had challenges with efficacy and certainly safety. You have a lot of anti-Tau therapies that have not made it through the clinic. GLP-1s, there's a large study that's going to come out shortly next month. We see that that may have a positive impact in certainly validating some of our mechanism, components of our mechanism different. The jury's still out on how that's going to do, and we shall see. As far as safety and efficacy, I think as the research showed, safety came out very favorable. Efficacy, even in a conservative case that we projected in the TPP, it was very interesting to them. The fact that the product's oral and combined with that efficacy, even if it matches in the worst-case scenario, but we think it's going to far exceed anything that's available, it's being oral. With that safety profile, it's going to do very, very well. It was very favorably received. In a sort of a related commercial question, David asked, what other forms of dementia beyond Alzheimer’s disease might be suitable for Xanamem®, and would further studies be required? I guess potentially a broader question about other indications, I guess. Andrew? For me? Yeah. I think we're looking at. Or Dana? I thought that would be a Dana question. No, that's fine. I mean, I think because this mechanism is, it's not amyloid or Tau dependent, this drug has shown positive procognitive effect in older normal volunteers that had beneficial effects in patients with depression. One could imagine that one could apply this drug to a variety of neurodegenerative diseases. Cognitive decline is common in all of those diseases: Parkinson's disease, Huntington's disease, Lewy body dementia. One simply has to go to the neurodegenerative disease section of the neurology textbook and leaf through it. Almost all of those diseases, in theory anyway, could be responsive to this type of intervention. I think, you know, we're a small company. We're focused on Alzheimer's disease. We did do the study in depression and showed activity there. One could think broadly about a drug like this. I'm sure if there's a partnership with a larger company, they will think broadly about it because it could help a variety, a number of different patient populations. Thanks, Dana. Yeah, good answer. Andy, this is one for you about the data room. Shane asked, "Are pharma companies in the data room just kicking the tires, or is there real potential for a partnership to be finalized in the short term?" It's always hard to say until a deal is signed. Do they want to see the positive interim? Do they want to wait for the final results? Basically a general question, as much as you feel is appropriate to answer. I think they vary. I think that, you know, I've been in these situations, as Steve, I know you have as well. They have different paces that they work. Companies, some of the bigger companies sometimes work slower, and it's developing a relationship. It might not even be a new inflection point. Sometimes it is. We've had companies that have come back in when we got the FDA minutes. These are the kind of things that you're just never sure what's going on on the other side. I will say, I think the interim analysis for regional partners, I think that they realize that potentially, you know, if they wait too long, they might be priced out if something like this is as successful as we anticipate for the full trial. That could put them out of the market. There's no one answer for any company, but we remain encouraged by the activity. Yeah. Thanks, Andy. We're just going to try and keep the different questions from different people mixed up a bit. Dana, could you sort of elaborate a little bit for Ange on what the open label part of the trial entails starting in next quarter? He asked, actually, is this expanded in clinical trials? What are you hoping to see, etc.? The open label will be basically crossing the patients who are on placebo onto active and then continuing them for the foreseeable future for one, two years, a long period of time. Because the drug has really been safe and well tolerated, the density of visits, the complexity of the visits is reduced. This is to streamline the open label, make it frankly less expensive to conduct, but also less of a burden for the patients and the centers. We will be measuring the key efficacy variables like the CDR sum of boxes and the ADL and select cognition testing over that, usually about every three months during the conduct of that open label extension. It is very important not only to show durability and maintenance and perhaps even a continued progression of a beneficial effect, but also to obtain the safety data necessary that the regulatory authorities want for long-term safety. We need at least 100 patients followed for a year and a total of 1,500 patients exposed to the drug. There are multiple reasons to do the open label. Long-term safety, maintenance of effect, these are the key factors. It will be less intensive for the patient, easier for them to participate over the long term. I would add, because it's an open label study, we can actually report on the progress of patients and their data whenever we choose to look. We may be able to report on what would seem to be slower progress than expected on active drug from time to time. We don't have to wait for the very end of the study like you do with a big, large randomized study like the Xanamem® pivotal study we're currently running. Because the question involved when do we hear news about how the study is going, that sort of thing can happen more than once a year. I'm conscious of our time, so just trying to mix the questions up. If the new patents you're working on are successful, how long are you hoping to have market exclusivity for? The new patents, several of them, the newest ones obviously would be the 20-year patent life stretching to the early to mid-2040s. That would provide a long amount of patent protection. The composition of matter patents with extensions till 2036 in virtually all markets. Europe is a bit longer. There is some data exclusivity protection, particularly long in Europe, but also is being developed and implemented soon in China. Overall, we have good core IP, and we are supplementing with what was called a picket fence of multiple new patents that hopefully would extend the patent life and protect against generic competition. In our conversations with various stakeholders, the strength of our intellectual property portfolio has generally been agreed with and a real asset for us. Mark asked, what will be the treatment period, Dana, in the next pivotal study? The present study, as we've already outlined, is going to end up being 240 patients for nine months. If that study is a positive result, then one could imagine that that's sort of the lower boundary. What we're really envisioning right now is a year-long study, probably a treatment period of a year. If we do two treatment groups, it will be larger than the present study to make sure that we get another positive study, but also to get the necessary safety database that we need to file the NDA and marketing authorization. It'll be in the hundreds per group, two groups, and for a year. Obviously, we have an open label extension, and we'll maintain that. Patients from that next study can also look forward to an open label extension of their treatment as well. Yeah. Thanks, Dana. Will, Ashley asked, and apologizes if she missed the answer or he missed the answer, what amount of funds could the listed options raise if exercised? You mentioned the unlisted, which is about AUD 6 million, but I'm not sure that you mentioned the listed. No, I didn't. If the listed options were converted, it's more like another AUD 20 million+. I think it's about AUD 22 million in total. Obviously, holders of those have the opportunity to trade them on the market if they want to realize value in the near term, or if they're looking for more liquidity, they can convert them and receive the shares. There's a substantial amount of funding that's potentially available through exercise of all of the different tranches of options. Yeah. Thanks, Will. Dana, there was one question early on about sort of mechanisms of action and this sort of concept you put on the reducing the brain stress slide. Are we measuring those sort of brain stress things that you mentioned, such as gene changes in gene transcription, etc., in the brain? Is that part of the study we're doing now, the clinical study? Not measuring gene transcription per se, but we do have a battery of biomarkers that are going to be analyzed. We're collecting them. We don't have the analysis done now, but we'll be doing those. Those will include different pTau species, which are indicators of neurodegeneration, NFL1, neurofilament 1, which is also another sign of neurodegeneration, and a variety of other biomarkers that are indicative of neurodegeneration. We'll be measuring those to determine whether those are also showing some signs of benefit. The most important one, of course, is the clinical measures, which are the CDR sum of boxes and the ADL, activities of daily living scales. Yeah. Thanks, Dana. Probably a good question to finish on from Dev. What is the potential for doctors to prescribe Xanamem® as a prophylactic when a patient is identified to have a significant risk of developing Alzheimer's? I get this question a lot. If a patient, for example, is an APOE4 homozygote, they have a very high chance of eventually, as they age, of developing Alzheimer’s disease. When you look at the antibodies, you have to have PET scans. You have to have serial MRIs. You have bleeding, cerebral edema, side effects. I don’t think that the antibodies are going to have a lot of traction as far as prophylactic in the general population unless you have a familial form of Alzheimer’s disease, which is a very small fraction. Xanamem® and emestedastat seem to be safe, well tolerated. It’s easy to take. It’s once a day. There’s no monitoring by MRI. I think the question’s a good one. As a clinician, as a neurologist, which I practice the neurology and took care of patients with Alzheimer’s disease, this would be the sort of thing that one could consider giving early in the course of the disease or patients that have high risk factors. That’s an open. I don’t have a definitive answer, but certainly the profile of this medicine fits one that could be given prophylactically safely. Thanks, Dana. I think we're out of time, and I apologize to those people who, there were a couple more questions, but I think we covered most of the topics. This slide deck is in the ASX release from this morning. Please take a look at that if you have any additional questions or missed something. Thank you to our presenters and the management team for doing such a wonderful job over this last year or two to really de-risk this program. We have an interim analysis in January. Final results are a bit over a year from now. Things are looking very promising in our discussions with partners and with other stakeholders. There's a lot of people taking notice of the company, as Will said. We have a good cash runway through to the middle of next year. I thank you all for your attention, your interest in the company. We very much value your support. Hopefully, Investor Hub is now a much easier way for you to interact with us. We look forward to seeing you in person if you can make it to the annual general meeting in November. Otherwise, we're often in the other capital cities if you're not based in Sydney, and look forward to meeting some or all of you then. Thank you very much. Thanks, everyone. Thank you.