Welcome to today's webinar presentation, discussing the positive outcome of our independent Data Monitoring Committee for the XanaMIA pivotal trial. We're very excited to report the positive outcome from that, and we'll just explain in some detail what that all means, and how to interpret it, and how we are increasingly confident of a positive outcome when we reveal top-line final results for the trial in November, in patients with mild to moderate Alzheimer's disease. Just to step back a bit: as you all know, oral Xanamem is a really good-looking once-a-day low-dose oral pill, with great pharmaceutical properties, great manufacturing properties, and of course we have a lot of clinical data showing activity in Alzheimer's disease and in depression, and this molecule may well have other important roles to play in treating the diseases, including anxiety diseases. And so today we will also cover the fundraising which was announced today: an AUD 12 million placement and an approximate AUD 5 million share purchase plan that many of you are eligible to participate in, up to AUD 30,000 per holding, not per investor. With that I'll just move to the next slide, which is our usual disclaimer. I'm not going to go through this all. We will be making forward-looking statements. This can be read on our website and in the presentation released on the ASX today. Next slide. I'll briefly summarize what we're going to talk about, and I'm not going to dwell on every word on this slide. But fundamentally, as you know, very important program developing Xanamem for Alzheimer's disease, potentially depression as well as other diseases. Independent DMC, what we call it a DMC for short, made us a positive recommendation which is very pleasing, and we've cleared essentially the pre-specified safety and efficacy, futility hurdles, and we really have maintained a very promising safety profile with this molecule, having treated more than 500 people, many of them now for 36 weeks, which is a major tick for safety, and the efficacy/futility hurdle is another tick for efficacy. So, our company outlook now is that we get focused very much with our resources on the Alzheimer's program, and with this additional fundraising we have the ability to get past final results in November and at that point plan to engage with major global strategic partners with whom we all have a, well, I have a very, and the other parts members of the team also already have a very good relationship. They're watching us closely. In the meantime, if we do get a smaller, perhaps regional deal that makes sense favorably, for the company in terms of financial and pragmatic terms, we will consider doing that, but only if the terms are favorable during the year. As a result of the placement we have firm commitments for AUD 12 million via a non-underwritten placement, and we are expecting to raise approximately AUD 5 million additional in a share purchase plan, which will open today—well, which we are notifying today and will open shortly. We've directed participation of just AUD 666,667 as well, including AUD 500,000 of additional personal cash which I am committing, which brings my total commitment of personal money to the company of about AUD 2.5 million. I don't do this flippantly; I took this job because I was so impressed at how Xanamem five years ago was a somewhat de-risked Alzheimer's disease molecule. I believe that with greater certainty today. And, you know, my probability of success for the outcome of the trial in November—I've been saying for several years 70%-80%—I'm even more sure of that outcome. Well, not guaranteed. That's a very good probability of success for a major clinical trial, and I hope and expect we prove that correct when we undo the results in November. And with that, to the next slide. And just at the very beginning I want to say how important it is to have experienced people with track records running this kind of a program. We have that with our board of management and the management team, a strong track record with hundreds of drug development years and many successful exits between us all. I'm very pleased to say the team is excited, totally engaged, and doing a great job. With that I will hand over to a very important team member, Dr. Dana Hilt, who is joining us from the U.S., to run us through the interim analysis story and some background on the molecule, and its clinical data. Thank you, Steve. So in many trials, like this, an interim analysis is done, and the interim analysis is something to help determine whether or not there's a safety issue, number one, and number two, to really globally say it, is that the trial headed in the right direction. You know, is the trial going to be essentially non-futile? And the recommendation of this external committee. They had the unblinded data. No one within the company had any access to any unblinded data. They recommended after review of this comprehensive review of this data that the trial continue exactly the way it's being run with no adjustments or amendments. Now this external DMC, as Steve has stated, we call it, was chaired actually by Dr. Hans Moebius. He is a neurologist, an expert in the field. He's the one that actually developed and got Namenda approved for the treatment of Alzheimer's disease. So he chaired a committee that looked at all the data. They looked at not just the data of 100 patients at six- months, but the totality of the data. This includes 52 patients that actually completed the entire study, many patients that had more than six- months' worth of data. It's approximately 37% of the total data. The first step was looking at the safety, and we have, to date, a very safe and well-tolerated drug. There were no serious adverse events that are actually attributed to the drug or associated with the drug. So that passed very well. Secondly most importantly is the futility analysis. So when one does an analysis like this, one has pre-established thresholds basically to lead one to the conclusion or not whether the drug has a chance of success in this trial and whether there's any chance that the drug would be doing worse than placebo. And so the positive results, as stated here in this box, confirmed that the trial cleared these pre-specified hurdles and definitions. The unblinded safety review also, the drug passed that very well. These, both of these things, both of these analyses we think materially de-risk the program and advance us forward to the top-line results in November, as Steve has indicated. Next, please. Now I don't need to tell you this, but unfortunately the Alzheimer's disease market is large and growing. In the U.S. there are almost 8 million. This is going to, as aging populations both in the U.S. and around the world progress, this is going to become increasingly a major problem. And while the monoclonal antibodies to amyloid have produced a benefit to patients, this benefit is fairly modest. I'll get into that in a minute. And even the dyed-in-the-wool amyloidologists who really believe in treating amyloid for Alzheimer's disease now admit, and embrace the notion that combination therapy, additional mechanisms need to be developed that can be either used in combination with the monoclonal antibodies or even before or after. And so this Alzheimer's disease is a chronic disease. Almost all chronic diseases require multiple therapeutic mechanisms. The size of the market here is very large. Next, please. I think Michael will show you a two-minute animation loop that really explains some of the features of this drug and the rationale behind how the drug is working in patients. While that's being queued up, just to recap while Michael is getting it going: the key here is this is a selective inhibitor that blocks cortisol production in the brain without affecting systemic cortisol. I see Michael has it up, so I will stop talking. 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 11-beta-HSD1, which converts inactive cortisone into active cortisol. 11-beta-HSD1 is highly expressed in brain regions critical for memory and mood, and its levels increase with Alzheimer's and depression. Xanamem/emustadostat readily crosses the blood-brain barrier and is the first and only potent oral inhibitor of brain 11-beta-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. Okay. So I think that film loop is a very nice definition of some of the properties of Xanamem and how it exerts its activity. Michael will put back up the presentation. I'll just continue with a few more slides. The key points to remember from this loop is that it selectively inhibits the production of cortisol leaving systemic cortisol normal. Next slide, please. So I think increasingly Xanamem has a clear path to hopefully a positive phase IIb phase III study and approval. We've had a Type C meeting with the FDA. We've reached agreement on all the key points on the remaining activities to be done to push this across the finish line. We will be having an EMA meeting, in this next—in this year, in 2026, to make sure that the European regulatory agency is in agreement as to the program to, again, to push this towards a submission of a dossier for approval. One additional pivotal study of 10 mg versus placebo is what the FDA said we would have to do. This is important. We won't have to do a dose ranging study versus placebo. So this will focus us down on the to-be-marketed dose of the drug 10 mg. We had received clear guidance on the CMC manufacturing, the clinical pharmacology ancillary studies that are going to be necessary for an NDA. The pivotal trial, the phase IIb/III trial, which is ongoing now and to which the DMC did the interim analysis, is, of course, as you know, fully enrolled in the U.S. and Australia. It has an excellent safety profile. We've had two DMC reviews. The first one was a safety review. The one that was just executed is a safety and efficacy futility review. We've passed those, I think, with flying colors. And we're on track timeline-wise for our top-line results in November of this year. What we're planning on doing, while not spending a lot of money on it but investing effort, is to get the phase III outline that the FDA agreed with us would be the next trial and the final trial, to start planning that, identifying sites, talking to CROs, getting that in shape to be pushed forward very rapidly once we have the top-line data from the phase IIb/III ongoing study so that we don't lose precious time. Next, please. So if we look at the treatment landscape, and this is not completely comprehensive, but I think here is a summary of the drugs that have been approved and the drugs that are in a later stage of development. The older drugs that are on the market are really for symptomatic boosting acetylcholine or modification of glutamate. They're symptomatic therapies. They have modest effects. They do have some side effects. Some patients don't tolerate them very well. Now, two-three actually, monoclonal antibodies to amyloid have been approved over the last five years. One is no longer marketed, Aduhelm. Two, lecanemab and donanemab, are marketed. These have modest effects, and I'm going to illuminate that a little bit with some graphical presentation of the data. Now, there's a second generation anti-amyloid antibodies coming along that are using the transferrin receptor shuttle, to try to enhance the penetration of the antibodies into the brain. These may be safer, and they may lead to a more rapid clearance of amyloid, but the two that are on the market now that produce very modest effects quantitatively remove amyloid. So you can't get better than that. If you remove the amyloid, yet you have very modest clinical benefit with patients, that's telling us something. That's telling us that removing all the amyloid is not going to stop the disease from progressing and is going to very likely have a very modest effect. So emustadostat—excuse me—Xanamem, is the only drug really that is focused on cortisol. And as we've already mentioned, it's in a phase IIb/III trial. It's 247 patients. We'll be reading that out in November. There are a few other drugs that are in later stage development. Blarcamesine is an interesting drug. They had a mixed result in their phase IIb/III trial. They submitted that to the EMA, and that was not approved, rejected by the EMA, so they have more work to do. The anti-tau therapy approaches have really, unfortunately, multiple trials have been executed, and none of them have been positive. So, you know—and there have been (not listed here on this slide) there have been a number of compounds and entities that have gone into larger phase II trials that haven't been successful over the last two or three years. Next, please. So what gives us confidence? Well, we have a very strong rationale, scientific rationale, in Alzheimer's disease, and I don't have the time to go into it in detail. There are slide sets on the company's website that explain in detail some of the rationale here. This target (no one has to date, except for this drug) has really been able to show substantial target engagement. We have positive target engagement in a human PET scan study. This is the only drug in this class that's been able to do that. We did an initial Alzheimer's disease study, which has been published, and we looked at the subset of patients that have high p-Tau. Now, that's important because the high p-Tau patients, A, definitely have Alzheimer's disease, and B, are more likely to progress. In that subset of patients with high p-Tau, the drug had a very nice, robust treatment effect. We also showed clinical activity of the drug in patients with pretty significant depression. These are patients that had, by and large, treatment-resistant depression. I'll just show you one slide on that data. That then is the ground or the basis then to design and execute the trial we're now doing, the XanaMIA trial, in 247 patients with clinical diagnosis and p-Tau elevation confirmation of Alzheimer's disease. Next, please. So this is a little bit of that scientific rationale that leads one to hypothesize that blocking brain production of cortisol would be good for Alzheimer's disease. So higher cortisol levels lead to a greater risk. Patients with APOE4, which, as you know, is the biggest genetic risk factor for Alzheimer's disease and leads to a more aggressive form of Alzheimer's disease. Lo and behold, they have higher CSF cortisol levels. High cortisol predicts probable Alzheimer's disease after age 75, and higher CSF cortisol levels in 80 patients are associated with a more rapid malignant course for the disease. So there's a substantial amount of data out there suggesting that, you know, cortisol level may be detrimental and a risk factor for leading to Alzheimer's disease and accelerating its course. Next, please. This is the data I was mentioning about PET scan. And so in neurologic psychiatric drug development, one of the first questions one has to ask oneself is: do I have target engagement? Does the drug get into the brain, bind to the target? If it doesn't, it won't have a chance of working. So this is the only drug in the class of 11-beta-HSD1 inhibitors that has this type of data, and this has been published. The left panel is slices through the brain like this, transverse slices, and a probe to 11-beta-HSD1. As you can see, the probe, the lighter areas stand out as binding to neuronal-rich areas in the brain, neuron-rich areas in the brain neocortex. Now, if one gives the same dose of that probe in the presence of five, 10, or 20 mg of Xanamem, you can see a dramatic reduction. What that means is that Xanamem is getting into the brain and binding to the target and inhibiting the binding of the probe. So this is de facto evidence that doses—pretty low doses of five and 10 mg, 20 mg—get into the brain and substantially inhibit the binding of a probe to this enzyme. So that really is gold standard data then that we have target engagement, in the brain. Next, please. Now, this is the pilot data from the XanaDU study that I mentioned. So this is in the 34 patients who had elevated p-Tau181, which is a marker—a diagnostic marker, if you will—of Alzheimer's disease. Now, on this graph, the placebo is the light line, and Xanamem is the darker purple line. The y-axis is the CDR Sum of Boxes. This is a clinical dementia rating scale. This is a global scale that is universally used to rate the severity and the progression of patients with Alzheimer's disease. Down is worse. The patients are getting worse. On the x-axis is time through three months. So you can see in the light line that the placebo patients have a substantial decrease over three months. You can see in the solid line that patients treated with Xanamem have much less of a decline. So this is a Cohen's d. That's a fraction of a standard deviation. It's about 0.4. The mean change is 0.6, which is a very substantial change, particularly over such a short period of observation of three months. So this data is very positive and very suggestive then that the drug will have a beneficial effect in patients. And this is some of the data that we used coupled with the PET scan data to design and then now execute the larger phase IIb phase III trial that we're conducting. Next, please. Now, this is another piece of data that suggests the drug is getting into the brain, having a beneficial effect. These are patients that I mentioned that have MDD, major depressive disorder, and these are, these are basically treatment-resistant patients. 80% of these patients are on background antidepressant therapy. They've had four major depressive episodes previously, and they have substantial residual depression, even though 80% of them are on a background antidepressant. What you can see here over time is that, the patients here, the patients that are treated but is worse, but you can see that there's a and a separation here by weeks six to 10 in Xanamem having a very nice, therapeutic effect, significant, and a Cohen's d of 0.64, which is a very robust measure of the magnitude of a treatment effect. Next, please. So all of these data then fit into the design of the phase IIb/III trial, which is now being conducted, the interim analysis, which I told you about. This is 10 mg of Xanamem. That would be the targeted to be marketed dose of the drug versus placebo. It's 36 weeks of observation. The key inclusion criteria in this trial is a clinical diagnosis of Alzheimer's, as well as a blood p-Tau181 biomarker elevation, p-Tau181, we're using. The primary endpoint is the universal endpoint that everyone accepts as a robust measure of disease severity in Alzheimer's disease - the CDR Sum of Boxes. It integrates both cognitive and functional measures at nine months. The key secondary endpoints include a measure of activities of daily living - functional measures of everyday life activities - self-care, hygiene, you know, cooking, and so forth and so on - activities - as well as a cognitive test battery. This trial is being conducted in Australian and U.S. sites. It's fully enrolled, as I mentioned. We've had two interim analyses. The last one last week was a futility analysis that I mentioned, and I've already mentioned - and Steve has mentioned - that we'll be reading the results out in November of this year. Next, please. So we plan to initiate an open-label study of 10 mg, and this will be starting the end of Q1, Q2 of this year. And this will basically be offered to all patients, whether they've been treated or on placebo, active or placebo, in the XanaMIA phase IIb/III trial. And so patients can continue on this for a period of time. There won't be any placebo group here, and the data from this will provide longer-term safety analysis, tolerability analysis, and we'll also be looking at some efficacy endpoints, and we will keep the treatment during the initial phase blinded during this extension. So we'll see if we produce a benefit, does this benefit persist? And if that's the case, you know, then one can start to talk about the potential of a disease-modifying effect of the drug. And so this will be very interesting, and of course, it's very encouraging for the patients who want to get access to this drug for longer term. Next, please. So I think I'll be handing over to Steve and make one more comment here. I've already mentioned that the antibodies that are approved, they do have a modest effect, but the patients, for example, have to go to an infusion center once or twice a month. They have to have a half a dozen MRI scans. They have the risk of having ARIA, brain edema, and hemorrhage. And so these antibodies don't—they come with a risk associated with, and they have some benefit. So clearly, the experts and the patients and everyone are looking for additional therapies. And we think that Xanamem, being an oral once-a-day medication—no risk of ARIA, no risk of brain edema, no risk of brain hemorrhage like the antibodies—this is an easy-to-use, convenient, safe drug with an advantageous profile. We think patients and clinicians will gravitate, gravitate to. We are focusing on showing that it can produce both cognition and functioning benefit for these patients and slow down the rate of progression. Because it's not focused just on amyloid, this drug could potentially be used in a variety of different neurodegenerative diseases. In some ways, this may well be a pipeline in the pill, if you will, that it could be used and adapted to a variety of neurodegenerative and neuropsychiatric conditions. Next, please. This, I've already mentioned in part that, schematically here, I've already mentioned the CDR Sum of Boxes gets worse over time. The dotted line here is the placebo. So you can see over—this is an 18-month window we're looking at here—that over a year and a half, patients decline. Both donanemab and lecanemab have a pretty modest treatment effect that's characterized by that solid orange line. So the area between the dotted line and the solid line is really the clinical benefit over time. However, if you look, the largest segment on this graph is the area above the solid orange line up to the flat blue line. This is the unmet medical need that's not treated with anti-amyloid therapy. So, that is why the attention in the field is now moving beyond amyloid and beyond tau to other mechanisms. And we think emustadostat Xanamem is an excellent example of a mechanism that can really help patients and is focusing not just on amyloid and tau. It may be that amyloid and tau are the manifestations of the disease, not the cause of the disease. And so, that's why we think emustadostat may be helpful to patients. Next, please. And this is another typical, another example, if you will, or another depiction of this. Remember that mentioned that even at three months there was a substantial difference. If we look at the benefits that both lecanemab and donanemab produce at three months, the results that we saw with Xanamem and emustadostat was larger. A beneficial effect was larger than either lecanemab or donanemab was at three months. So we're hopeful then that improved profile, if you will, more robust treatment effect will hold out in this study, and we can really help these patients more effectively. Next, please. I've already mentioned this, in part. The drug is oral once a day. It's well tolerated. It's safe. There have been no serious adverse events in the entire program associated with Xanamem. We're looking at cognition and activities of daily living as well as the CDR Sum of Boxes, which is an integration of function and cognition. So there's robust measures in place to measure clinical benefit for patients, and that's what we're intending to do. Next, please. And I think I'll turn it back maybe for Steve to make some final comments. Yeah, thanks, Dana. And that was great to go through that in detail. And especially explain to people the open label. So just to be clear to some people who've been confused, you can't swap out of the active trial into the open label. You have to complete your period of Xanamem or active therapy in the main trial, do a four-week follow-up visit, and then you are eligible. You're also eligible even if you stopped six or nine months ago and had a big gap, after finishing the final trial. Though we are still making that eligible to patients. So commercial planning. We've done some primary, original market research with U.S. neurologists, all of whom embraced the product profile of the drug. And 60% of them indicated, or 80%, sorry, indicated that they would prescribe Xanamem in the first six months of a launch, which is a phenomenal potential launch. And it just shows that there is no safe and effective, you know, disease-slowing, oral therapy, available or credibly in the pipeline except for Xanamem, now in its first pivotal trial. So that's very exciting. So currently we're planning potentially, if the deal firms are right, for one or more regional partnership deals. Many of those parties are active in our data room. But the final results, in November, we trust will be excellent and excite multiple global partnership bids. Potentially, because the Europeans have already accepted one application for Alzheimer's disease with a single pivotal trial, it may even - and this is a bit of a long shot - excite regulators to consider allowing us to get expedited approval and do a second phase III in parallel as opposed to marketing commitment. But that's a long shot, but there's no guarantee. But we will be talking to the Europeans about that in the second quarter. Next slide. And so in summary, we've got a very experienced team with proven track records of getting things done as well as getting successful exits for their various companies. We're on track with the trial. Positive market research shows that we're not dreaming. We've got a really big rapid potential launch on our hands. We've got a streamlined agreement with the FDA on a path to Xanamem approval, which we hope to replicate in our discussions with the EMA. Great intellectual property, growing, and I would say a lot of excitement around what we're doing both in the major and the mid and smaller tier companies interested in Alzheimer's disease. And now, as Will will explain, we're funded beyond the top-line results in November, which is an important milestone for the company. And with that, I think we will pass over to Will. Sorry, just near-term milestones. I'm not going to go through all of these, but we do have the peer-reviewed journal publication of a depression phase II. We're starting the open label. A number of scientific conferences and a discussion with the EMA. You know, if we do do a regional deal, obviously that will get—that will be published at the time, but we can't comment on any details until a deal is done. So we'll move over to Will. Thanks, Steve. Obviously the other really important bit of news for today on top of the great news about the interim analysis that was announced late last week is that we have now fully funded the company beyond the final results in November this year. So we're announcing a AUD 12 million placement at AUD 0.42 per share. And importantly, all shareholders will have an opportunity to participate on those same terms through a follow-on SPP that will be launched in the coming weeks. So the offer is not underwritten. We're confident that the follow-on SPP will be well taken up. We've allowed for up to AUD 5 million and possibly over AUD 5 million depending on demand. The offer price represents a modest discount to recent pricing, but a significant premium to our last round, and there are no attaching options. So we think it's a very strong, strong funding round and was well supported by both existing and new shareholders. I think we can move to the next one. As Steve mentioned, the directors, as a pool, have contributed AUD 667,000 to the placement, including AUD 500,000 from Steve himself, bringing his contribution to close to AUD 2.5 million so far. And I think that's a strong endorsement of the program. I don't think I need to go through the details of the SPP again here. There's further information both in the presentation and also in the accompanying ASX release, so people need to keep an eye out for that. I see there's a—you know, there's a good turnout of people on this call, so let everyone know. You can participate up to AUD 30,000 per holding. There'll be some time during February. I think the offer will be open for approximately three weeks for people to participate, get their money together, and get their applications in. Next one, Michael. So importantly, what's the money for? Well, it's really two things. Obviously, it's to give us the strength to get beyond the November results. So you can see there are intended uses of funds, primarily going into finishing off the Xanamem trial, but also getting this open-label extension program open. We have some other R&D and manufacturing activities to undertake. The great news from the FDA meeting we had last year, which we announced to the market, is that there aren't too many other studies that need to be done, and so there's not too much expenditure associated with those, and some of those can be done later in the program. So that's really great news. We can really focus the funding on the clinical trial itself. And then obviously, supporting working capital and cost of the offer. People would have seen in our quarterly, if they had a look, that was released on Friday that we closed 31 December with AUD 6.5 million in the bank. Subsequent to that, we announced that we raised AUD 4.3 million in non-dilutive funding by borrowing against our accrued R&D rebate to 31 December. So, as the program ramps up, as we got to full enrollment, obviously our spending profile increased. Most of the money goes into R&D, which is, you know, shareholder value accretive. But importantly, we then get the opportunity to recover, you know, close to half of that through the R&D tax incentive. But naturally, that creates a bit of a working capital cycle because you don't get that until you file your tax return towards the end of the year. And so those loan proceeds allow us to extend our runway, and allow us to fund our way through to that R&D rebate later in the year. When you combine that with the funds that we've raised today and the SPP coming up, then we've got pro forma cash balance as at 31 December of close to AUD 30 million. Next, Michael. Look, I won't go through this in detail other than to say that the money for the placement is now in the bank and we are going to issue those shares this week. So that's done. And as I said, the SPP dates—I don't think they're on the slide here, Michael—but that the offer opens. So the record date, if you were a shareholder on the 30th of January, then you'll be entitled to participate in the SPP. The offer will open on the 10th of February and be open until the 24th of February, and then the shares will be issued on the 2nd of March and traded from the 3rd of March. So by that time, we'll have the full funding in the bank. We will be funded to beyond the November results. So we anticipate that with that funding, milestone behind us and the great news of the successful clearing of the interim analysis hurdle, that there should be significant opportunity for the valuation of the company to increase as we get closer to that really important milestone to reflect, you know, the real potential of the company as we close out this Xanamem program. Have we got any other slides, Michael? That's it. Thanks. And thanks, Will. It was a great explanation. And just also to point out that many of you may be holding non-listed options for AUD 0.375. Some of these expire in September of this year, i.e., well before the final results. I hold a fair few of those. So if you do want to purchase those shares, they need to be exercised and purchased before September. We potentially have around AUD 5 million of revenue coming in from that, and we may well get revenue from an upfront payment in a you know, regional deal if, as I said, those the terms, including the milestones and the partnering logistics, are favorable to the company. So we do have other sources of funding, but it's also a little reminder for those people to consider when they want to exercise those, options and when a capital gains event may occur. Obviously, if we have very exciting results in November, we'll go into a phase of negotiation, hopefully with multiple parties. That'll probably take some months, but, a lot of those parties may well have done pre-diligence, so it could happen fairly quickly. So anyway, just to point that out. So for Q&A, just as a reminder, and I think we've had some questions already, down at the bottom right-hand side of your screen, you see a question box there. You just click the question box, type a question in, and hit the arrow return button, and your questions will come up. So we've had some initial questions. Well, first one for us to you, Will, from Matt, who was the broker who did this book build? Yeah, so we were supported by Canaccord. They were the lead broker, and also the co-manager was CBA CommSec. We have, you know, a significant number of our 5,500 shareholders are on the CommSec platform, so those guys worked together, did a great job. You know, we ended up, with oversubscriptions and we had to make some adjustments to scale people back to get to that AUD 12 million number. So we're anticipating some strong demand in the aftermarket, and we appreciate the support of those guys. Yep. So So we had a question, a few questions from Dev. The first one was, you know, congratulations and can you please shed some light on the results from the open-label extension trial could be published during the course of the year? So just briefly, I'll answer that one, and Dana, you can jump in if you want. Open-label trial, of course, means that you're monitoring the data constantly and you can report the data at any stage for any number of participants, but we do need a substantial number to be able to, you know, compare at least 30- 50 patients who have had an ideally at least six months treatment from starting to the next data point. And we'd be comparing those patients' pre-Xanamem results from the current pivotal trial with other historical data. So it's a little uncertain how much value we can produce in a clinical presentation before November, but we may well have a rush for the front door when the trial opens in March, and so we'll have to wait and see. But subsequent to that, we'll have a lot of interesting data, as Dana said, about the transition between either placebo or active onto everybody being on active, and then every six months or so we'll have a new data report which we can compare to our own Xanamem data and to other sources of historical data for both the CDR Sum of Boxes and also some other endpoints as well. So that's that's the basic story of the open label and how it will be reported. What is the approval of this current trial? About well, I'll just it's a question it's an FDA question from Dev, so I'll just try and unpick it, actually. So the FDA approval of the design of our next pivotal trial is important because basically we're just doing a larger version of the current Xanamem trial. Secondly, we specifically said, do you agree this is a pivotal trial, one of the two, to get it approved? And they said yes. And so and then we also asked, do you do you get the plans for the interim analysis and that they won't spoil the statistics of this trial? And they agreed with that as well. So overall, both the current trial, blessed as a pivotal trial, and the next bigger trial, also blessed. So, and then a quick question from Dev on depression. Depression is parked for the moment. We have strong indications of activity in a very difficult-to-treat population, as Dana explained. And depression is common in Alzheimer's, and so having perhaps an additional depression trial at maybe in older individuals would potentially be very helpful and important for marketing Xanamem. Sorry, but in the situation we think we're in where there wouldn't be any direct competition, it may be better to focus our resources on Alzheimer's disease. But certainly with a bigger partner, depression could be part of the story. Matt asked how many patients are currently using the competing antibody drugs. So it's kind of an anti-question, but it's a remarkably low number. You can Google and find the sales numbers. And that's the reasons for that are obvious. A lot of our doctors that we interviewed in the U.S. for our drug said, you know, they don't recommend it to most of their patients. Even if the patients have it recommended, when they look at the risks, they don't choose to take it up on in many occasions. It's not well reimbursed, and some countries have really refused to put it on, as Australia has not put it on, the PBS. So yeah, it's not being successful, and that's because the drugs are not that good. So Andrew asked why did you raise AUD 17 million at those prices when you're, Steve, I can jump in on this one. Yeah, yeah, yeah, okay, that's fine. I think there's a little bit of confusion, so maybe I can just clarify the pro forma cash position. So that pro forma cash position essentially outlines where we would have been at 31/12/2025, not 2026. The question, I think, assumed that that was our cash balance at the end of 2026, not 2025. So what you do is you say, okay, well, the reported cash is AUD 6.5 million at 31 December. If we add to that the cash that's coming in in January, what, you know, what's essentially our opening position on 1 January 2025? And that's what the AUD 29.7 million is rather than the end of the calendar year. So that puts us in a great position. There's also a question about directors' participation. The directors have participated in every capital raising round and have been extremely supportive. And obviously, Steve in particular has committed another AUD 500,000 to this round. So just to reiterate that there's strong support from the board on the program and a strong belief in the success at the end of the year. Yep. Thanks, Will. Mark asked about where the bar is set for the efficacy futility hurdle in our recent Data Monitoring Committee review. I'll comment a little bit on the statistics because I'm a bit of a statistician among other things. There are a couple of different ways to do efficacy futility. One is to do something what's called a conditional probability model, but normally you have a probability of 80% or 90% for a positive trial when you define the number of patients you need for a statistically significant result of p less than 0.05. Typically, those conditional probabilities, because you're only looking at a subset of the data, are set at 30% or 40%, which means that actually placebo could be winning, but there's still a bit of a chance the trial would be positive at the end. So we chose not to use that method, but instead we chose an algorithm which largely says Xanamem has to be winning, basically based on the gestalt of the primary endpoint and the other secondary endpoints. And we also rely on the wisdom of the committee and the highly experienced chair, Hans, to say, hey, maybe it looked complete, you know, equal at the beginning, but there's separation as the drug is being treated for longer, which is something you might expect. So we don't know what those data show because if we break the code and look at the data ourselves, we have to sacrifice the stats and the pivotal nature of the trial. But that's fundamentally an algorithmic model that we used. So then, Will, do you want to have a look at? Yeah, look, I just—there's another follow-on question in relation to the raising and the pricing, so I'm happy to take that. People will understand that biotechs at this stage of their life have quite a volatile pathway, particularly from a share price perspective. And it's, you know, it depends on a multitude of things, including people's perception as to when you're raising money, people's perception around the actual trial and the science itself, market factors, liquidity, interest rates, and so on. All of those things go into the mix to set your price at the time when you do your capital raising. That timing was determined by the interim analysis rather than, you know, able to be selected, opportunistically by us. So the stock has traded up into the AUD 0.10, has traded down into the ones and twos. We're very comfortable that raising money at this sort of overall valuation at this sort of price without giving any additional options and getting strong support for that is the right thing to do for the company. Now that the funding's in hand, it takes away that perception of an upcoming fundraising which lots of people trading in the stock are concerned about. So now that we've done that, we're anticipating continued share price appreciation into, you know, into these results later in the year. So, you know, that's that's why we made the decision to raise the money at the price we did. Yep. Thanks, Will. And then Andrew just asked about putting up the pro forma. Again, just as a reminder, the pro forma is essentially AUD 30 million at end of December 2025, and that combined with some income, some monies from option exercises and potentially a deal—well, we don't need the deal, but some option exercises, et cetera.—more than sees us through the November final result. And as Will mentioned, but we're not being specific about; we know how big the tax check will be from the R&D incentive. It is a big number. Our biggest in the past was AUD 9 million something. Given our increased spending over the last year on R&D, which is eligible, we expect that number to be higher than that. So you know that our pro forma includes that very certain income later in the year from the R&D tax credit. Yeah, I think just to add that now that the program is fully enrolled and all the sites are ticking over and, you know, we know exactly how many people we've got in the program. People will remember we were planning to enroll 220. There was such demand for the program towards the tail end of last year that we closed it, but, you know, 27 more snuck through. So we ended up with 247. So now that we've, you know, we've settled on that, that gives us a much narrower range of uncertainty around our budgeting for the year. We've got a great track record of being able to, you know, hit our budgets, and so we anticipate we don't anticipate any surprises between now and the end of the trial from a, you know, from a budgeting perspective. Yep. Thanks, Will. All right. I think we're pretty much out of the questions at that stage. If I just call for any last-minute questions, but otherwise I think we're at 55 minutes, which is pretty long for a webinar of this sort. So just to summarise, very pleasing outcome from both the positive DMC review for the trial and from support from new and existing investors in our placement and coming in the SPP. I will just add in this placement we had a number of existing smaller Australian institutional investors support and participate, largely super pro rata, and some quality new Australian institutionals joining the register. So we do feel this funding, which is, you know, a pretty modest amount compared to our market cap, so there's relatively little dilution to existing shareholders, is substantially adding to the quality of our register. So with that, I think we'll say thank you, and we look forward, we're happy to answer questions from you individually, and, you know, really looking forward to your participation in the SPP from your various holdings if you haven't already participated in the placement. And thank you for your support. We are excited to bring this trial to a positive top-line conclusion in November, which is just a few months away. Thanks, everybody. Thank you. Thanks, everybody.