Pleasure to open today's webinar to give you an update on our Xanamem program. As you know, we announced today the enrollment of our final patient and the treatment of that patient, the 256th patient in the XanaMIA trial, giving my dyslexia away. And it's a very important milestone for the company, as we will explain. Joining me is Dr. Dana Hilt, CMO, and Andy Udell, our Chief Commercial Officer, both from the US. And as you know, our program is all about bringing what we believe is going to be one of the holy grails or the holy grail in the treatment of Alzheimer's. We've already shown some activity in depression, and we believe this is a unique and groundbreaking program that will transform the treatment landscape for Alzheimer's disease in particular. Next slide.
We will be making forward-looking statements, and this disclaimer can be seen in today's disclosure on the ASX. Next slide. We will be doing online Q&A. Today we're using Investor Hub, our new relationship software and site. So we, as previously, we will take questions by using the chat function. You can find that in the bottom right-hand corner of your screen. Type your question into the box and hit the send icon or enter to submit your question. We will take the Q&A at the end of the presentation, which will take 20-2 5 minutes max. There'll be plenty of time for questions. I will potentially group questions together that are similar. Next. And I would like to start today's presentation just to remind you that drug development is a team sport, and experience and a track record really matters. We have a very strong board of directors.
We have a very strong senior management team shown there, several of whom are with us today. My own more recent experience in the U.S. with Principia Biopharma was taking two small molecules from go/no-go preclinical all the way through phase two and phase three trials to a successful exit to Sanofi for $3.7 billion. So we've all done this before in various different roles, and we bring that depth of experience to this project, which potentially, arguably, will be the most important success any of us have ever had because of the uniqueness and importance of the unmet medical need in Alzheimer's disease. Next slide. As you know, Alzheimer's disease is a huge and unmet market. There are some older drugs that I'll talk about in a minute, and then the newer antibody drugs have very borderline risk-benefit. They only slow disease modestly, as Dana will discuss.
And of course, with the aging population in most countries, the growth of the market and the potential unmet need is enormous. And you see there on the right in the orange bar, just in the U.S. alone, it'll cost more than $1 trillion to treat Alzheimer's in 2050. So this is a very, very large and important opportunity because, of course, patients don't really have any adequate therapies at the moment. Next slide. And so at this point, I'm going to ask Andy to show us our unique mechanism of action animation, which lasts for about 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 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, emestedastat, 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.
Great. Thanks, Andy, and while we're getting the other presentation back, I just have to say, you know, Andy was instrumental in getting a really top-notch animation contractor to do that for us, and I think it really has made a huge difference in a lot of academic and also industry presentations we've been doing so far. Next slide, so where are we today? Importantly, we have a very clear path to an Alzheimer's approval, essentially agreeing with the FDA on streamlined drug development, one additional pivotal study after this XanaMIA pivotal study reads out next November, and we're well down the track in planning the meeting materials for the European Medicines Agency, and that will occur in the second quarter of 2026. Alzheimer's is a relatively straightforward regulatory approach, and the FDA and the EMA are expected to be pretty aligned.
We've got full enrollment as of today in the US and Australia. We've got an excellent safety profile. And this is important because we've previously only treated patients before this study for up to 12 weeks. We've now got quite a few patients who've finished their 36-week treatment, and safety looks exemplary. We've had a first positive data monitoring committee review. The interim analysis of safety and futility will be in late January. And just to clear up one misunderstanding that it seems to be quite common, it uses all available data. The timing of it was triggered when about 100 patients would reach the week 24 visit. However, the committee will look at all of the week 12 data, the week 24 data, and the available week 36 data in making its determination and on track for final results in November.
At the same time, we're initiating the Phase III planning, having discussed it already with the FDA. We'll discuss it with the EMA in parallel with various discussions we're having with potential partners as they look at confidential data in our data room. Next slide. Last slide from me. I just wanted to put up a slide on the treatment landscape for Alzheimer's because it can be very confusing as a lot of different companies are trying different things. A massive amount of money has been spent on these anti-amyloid and anti-tau protein immunotherapies. Essentially, these are intravenous injections or now new subcutaneous injections, which are easier to use at home.
However, they have, as Dana will explain, a very borderline risk-benefit ratio, and there are newer ones that will probably be safer, but very unlikely that any of the amyloid approaches will show greater efficacy than the current ones that strip out all the amyloid within about six months of treatment. There are older drugs shown at the top. Donepezil is a classic one. Boost acetylcholine transmission. They improve symptoms a bit for about six months generally, but they do have a lot of gastrointestinal side effects. These drugs are still used today commonly. About half the patients in our Alzheimer's trials are on these medications, and we know Xanamem appears to work just as well with those drugs as it does without them.
But really, with our Xanamem program, by controlling elevated brain cortisol, a completely unique mechanism with no direct competition, no one else is doing this, we're leading the pack really with a promising, potentially safe and effective oral that can be combined with other drugs quite easily and a very easy drug to use with once daily dosing. So most other approaches look like there are some toxicities or lack of efficacy. And so really, our program does stand out globally as really the leading oral contender for near-term approval by the regulatory authorities. So with that, I'm going to hand over to Dana, who's going to take you through some of the program work, and I'll come back at the end for Q&A.
Okay, thanks, Steve. So first of all, I want to, for the group listening, give you an outline of step by step of what's the background and why do we think that this Phase IIb trial that we're doing now is likely to be effective. First of all, there's a really large literature on the cortisol scientific rationale for Alzheimer's disease. Cortisol is toxic to neurons. It leads to neuronal cell death. I'm going to go over some of that additional background information. But if one does a search of the literature, one comes across, one sees hundreds, even thousands of papers on this subject. The next stage is that you have to show that the drug gets into the brain and engages the target.
Now, this is the only 11-beta-HSD1 targeted drug that actually has human PET data showing that the drug gets into the brain, binds the target, and effectively inhibits the enzyme at very low doses of five and 10 mg a day. And that data has been published. There is a published paper now in a pilot study or initial study in patients with Alzheimer's disease. And this is in patients that have elevated p-Tau, which is really the biomarker now of choice to prove that patients actually have Alzheimer's disease. Now, we're not focusing. Our drug doesn't work directly on amyloid or tau, but looking at this group of patients that have elevated p-Tau assures that, one, that group of patients actually have Alzheimer's disease, and two, they're going to have more rapid progression.
When we did the analysis of this, and this has been published, as I mentioned, we showed a very robust effect slowing the progression of the disease and the CDR Sum of Boxes decline over time in this group of patients. And I'll show you a slide of that data. To also, another independent test of whether the drug has beneficial effects in patients that have elevated cortisol and in which cortisol has been invoked as a mechanism for the disease is in patients with depression. And we did a study, again, that's been reported publicly and is now under review to be published in 165 patients. And these are patients with serious depression, multiple episodes, 80% of them on background antidepressants, yet still have residual substantial depression. These are really treatment-resistant depression patients. And the drug showed antidepressant activity in that group of patients.
All of these data there then informed our design for the ongoing study, which Steve just mentioned. We announced today we've closed enrollment with 246 patients that will be treated for nine months. Next slide, please. So if we summarize some of the very large body of data that is in the literature that indicates that cortisol could be a factor in precipitating neuronal cell death and progression in patients with Alzheimer's disease, individuals that have high cortisol levels have a greater risk of developing Alzheimer's disease. Patients with ApoE4 allele have higher CSF cortisol, and as you know, the ApoE4 allele is one of the biggest genetic risk factors for Alzheimer's disease, and there are many other studies that also predict this. Higher CSF cortisol level in AD patients is associated with a more rapid clinical worsening and cognitive impairment in these patients.
And so there's also a progression as the disease progresses. The CSF cortisol shown in that panel on the right graph goes up. So there's a very large body of data that suggests that cortisol is an excellent target. How does one inhibit that? Next, please. And the way we're inhibiting the production of cortisol in the brain is we have a specific 11-beta-HSD1 enzyme inhibitor. So in the brain, cortisol is made from cortisone by a specific enzyme, 11-beta-HSD1, that is not the enzyme that makes cortisol in your adrenal cortex. So this allows one to selectively by and large decrease cortisol level in the brain while systemic plasma cortisol stays within normal ranges with chronic dosing. Now, this is the PET scan data that's been published. As you see here on the left panel is a probe to 11-beta-HSD1.
You can see areas of the neocortex, the thinking part of the brain, the hippocampus, the frontal cortex light up. And so that shows that that probe binds to 11-beta-HSD1. In the presence of 5, 10, and 20 milligrams of Xanamem at steady state, you see a dramatic decrease in the binding. This means that these low doses of Xanamem get into the brain, bind to the target. And this is, as I said, the only data that any 11-beta-HSD1 inhibitor has been able to show at this level that it actually engages the target in human brain. So the first step is, does the drug get there? Is it doing what we think it's doing? The answer is yes. Next, please. Next is, is it having any indication of benefit in patients?
This is the study also that's been published that looked at the group of patients that had elevated p-Tau 181 with a clinical diagnosis of Alzheimer's disease. What can one see here? On the y-axis is the CDR Sum of Boxes . This is a universally accepted endpoint to measure severity and progression in patients with Alzheimer's disease. As it goes down, it means a patient's disease is progressing. The y-axis shows the CDR Sum of Boxes change. The x-axis shows time. What you see here, the placebo patients have about a one-point decline over three months, whereas the patients treated with Xanamem have a substantially less decline, lower level of decline. This is in a modest group of patients, only 34. The p-value here is 0.09, but if we had had a larger number of patients, this certainly would have been significant.
This delta of this magnitude of effect of 0.6 units over three months of time is much more robust than any of the other data, for example, from the monoclonal antibodies studies that have shown a much more modest change over time, which I'll show you in a minute. Next, please. And so this is the trial then that we're now conducting that we've enrolled 246 patients. And so the key.
Hang on, Dana. I think you skipped a slide. I think Michael may have skipped a slide. Sorry, Michael.
Can we go back one then?
No. Next, number four. No, go forward. No, go back. I think someone's deleted a slide. Anyway, not to worry. That was just the depression data, Dana.
Yeah, so the depression, what we saw in depression, and I'll just describe it verbally then, is that the drug had a divergent improvement in depression compared to placebo starting at six weeks and then magnifying as we went out to 12 weeks. And to remind you that that study was conducted in patients who basically have treatment-resistant depression. So those are patients with pretty severe depression, multiple episodes of severe depression in the past, 80% of them were on background antidepressant medications, and still had substantial residual depression. And so that's a tough group of patients to treat, and the drug had a beneficial effect in that.
Now, all of these factors together, the basic science, the PET scanning, the initial study in Alzheimer's disease, the depression data, then really increase our level of confidence that this trial is shown here schematically has a very good chance of being successful. So what are we doing? We're taking patients that have the NIA-AA criterion of clinical diagnosis of Alzheimer's disease, also have elevated blood p-Tau 181. This shows the patients, A, as I mentioned, have Alzheimer's disease, but importantly also for our trial, it means they're more likely to progress over our 36-week observation period. The primary endpoint is the CDR Sum of Boxes . As I mentioned, this is universally accepted by all the regulatory authorities and the clinical community as the meaningful endpoint in Alzheimer's disease. We have a number of important secondary endpoints, cognition test, and importantly, an Amsterdam Activities of Daily Living.
This is an ADL scale that determines how independent is the patient. Can they make their own breakfast, for example? Self-hygiene. These are very important things that indicate the functional level of the patient. Now, this study is being done in Australia and the United States. We've also mentioned that it's fully enrolled. There will be a futility interim analysis in late January in about two months' time, month and a half time, and it really will be looking at, and I'll talk about it a little bit in a slide or two ahead, as a futility, so we're not going to be declaring victory. We will be simply looking at whether or not the trial is headed in the right direction, and the final results then will be available in November of 2026. Next slide, so this interim analysis then will be conducted late January.
The Independent Data Monitoring Committee will do this. This is made up by experienced clinicians that's chaired by a neurologist who actually developed and got a drug for Alzheimer's approved a number of years ago. He's an expert in this field. It will be conducted by that group separate from the company. We will not be privy to the data. They will be looking at the data, and they will tell us whether or not the trial is sort of headed in the right direction and whether it's a futility analysis. We will not be spending any alpha, so to speak. With that decision, which we feel pretty confident the trial won't be futile, but we will see what the interim analysis shows, we will continue on to complete the trial.
The other big activity coming up relatively soon, which will be in the end of Q1 next year, is the open-label extension. This is very important. It helps attract patients to trial, but it also gives us a very nice long-term safety. And if we keep this somewhat blinded, we can also look at key efficacy endpoints. In this open-label extension by its very nature, there's no placebo control group. The placebo patients will be crossed over to 10 mg active. We will maintain the blind, though, so that the investigators and patients will not know during the open-label whether or not they had active drug in the first portion of the trial. But all of the patients will be receiving active Xanamem 10 mg during the open-label extension. Next, please. And I think, Steve, maybe I hand it back to you at this point.
Yeah, that's fine, Dana. Yeah, I'll go a little bit faster just so we have enough time for questions, but I think it's very great to spend a little bit of time on the interim analysis and the open label because I think those particular issues are important for investors, and we already have a couple of questions about that, so just in brief, thinking really commercially about what is Xanamem as a product. I mentioned earlier the anti-amyloid immunotherapy infusions or subcutaneous really don't work very well. And we have a slide on that. Xanamem is being developed with a much better risk-benefit profile as a safe and effective, once-a-day, easy-to-use product that potentially goes straight to the first line of treatment once it's approved ahead of amyloid antibodies and essentially everything else. It can be used safely with the old drugs.
And the desired benefits we're looking to bring out in the Xanamem program include not just slowing progression dramatically, as we saw in the pilot data in p-Tau elevated patients, but to have a potential benefit on multiple aspects of cognition and life functioning, as Dana mentioned. Ideally, and the most common outcome in the pilot data was that we did see Alzheimer's decline halt completely. And that was the most common outcome. We would love to see that in this trial. But we have made the trial considerably bigger on the assumption that that would be an extremely good news story, and we can't necessarily count on that huge in effect size. So the current Xanamem trial is definitely a catalyst for both commercial and partnering interests. We do have active parties under discussion. But we're not going to do a deal unless the deal terms are right.
And that remains to be seen. Next slide. We've shown this slide before. This is just showing you in orange the modest benefit of the solid active line versus placebo over 18 months. At three months, just to compare to the data Dana showed, it was only 0.1 difference between active and placebo, whereas we saw a 0.6 difference at 12 weeks. If that were to be extrapolated, we would be 6x to 8x better than the Eli Lilly drug shown here in orange. So drug targeting mechanisms other than amyloid are clearly needed, and Xanamem is leading the pack, as I explained. Next. And really what we want to see is that the purple lines are the active Xanamem trial. We would love to see the commonest outcome be the horizontal, in other words, complete stabilization of patients. That may be overly optimistic, but I hope that's not.
Basically, having a result where, compared to placebo in the orange dotted line, we see a dramatic slowing in the purple lines there. That's what we're going for. That would be a much, much bigger effect than any other drug has ever shown on slowing disease course progression. Next slide. Importantly, I mentioned safety long-term now in 36 weeks of treatment in this study. So far, the drug continues to be super well tolerated, no serious adverse events related in the whole program, and we've now treated about 500 people in total. Key secondary endpoints that we looked at in the interim analysis and also at the end include various measures of the ability to think or cognition and the activities of daily living important in everybody's lives. Next slide. What do we know about the commercial opportunity?
The market is huge and growing and unsatisfied. Andy led some work with 100 everyday working neurologists with large treatment populations in Alzheimer's disease. And they love the idea of the Xanamem profile as a safe and effective oral. Indicated uptake would be rapid in the first year. In fact, 80% said they would prescribe it in the first six months, which would be an amazing product launch. And Xanamem could easily move into first-line therapy and is easily combined with other molecules in the field and also the many different medications that elderly people are typically taking on an everyday basis. We have multiple partners looking at our data, and we are planning for one or more regional partnerships only if the deal terms are favorable and increase shareholder value, of course.
And final results in November next year that excite multiple global partnership bids and enable regulators to seriously consider sort of a rapid or expedited approval. And that's extremely optimistic. But if we do have breakthrough groundbreaking results, we will certainly be asking the question of regulators as to how we can bring this important drug to patients earlier than would otherwise be required with a new trial. Next slide. So in conclusion, we're building momentum towards our final results. And November next year is just around the corner, literally. We have an experienced team with proven track records. We know what we're doing, and we've been delivering on our goals. We're on track with the trial. We've talked about the interim analysis and the final results. The market research is extremely positive about the product profile for Xanamem.
We've got good FDA agreement on streamlined development and expect the same from the EMA. We've got good intellectual property strengthened with multiple newer patents, including manufacturing patents. There's a lot of partnership interest and data and activity, and we're well funded beyond the middle of next year, as we've said before, so with that, I'm going to open the floor to Q&A. If we go to the Q&A, oh, sorry, then one last slide, which we can come back to. There's multiple near-term milestones in the coming year, including the publication in a peer-reviewed journal of our depression trial, various meetings with business partners and analysts and so forth, conferences, and of course, the final results next year. Next slide. As a reminder, the questions can be put in the chat button in the bottom right-hand corner.
Hit the send icon or enter, and we will take those questions as they come in. So there were two questions before we started, pre-submitted, which I'll go to first. Alan asked with the interim analysis, "Why is it that you can't have two bites at the data, if you like?" In other words, "Why can't you peek at the data?" So Alan, if the company itself looks at the final primary endpoint twice, you do take an alpha penalty, as Dana explained. There's no way of getting around that. However, to be clear, the Independent Data Monitoring Committee does see the two different groups on a graph, and they can see to what extent Xanamem is beating placebo. We trust and hope. However, they cannot stop the trial because of perceived efficacy at that time.
As a result, the company doesn't spend alpha and doesn't need to have a change in the statistics or the size of the number of patients in the trial. If we did have two peaks, you'd need nearly three times as many patients in the trial to have the same P less than 0.05 significance at the end. And so that's why it's set up this way. But importantly, the committee also looks at the safety in an unblinded fashion as well to make sure that the general safety monitoring of the two groups mixed up together doesn't obscure some other safety signals. So a positive outcome of a recommendation from the committee to the company saying the trial should proceed does take away some of the negative downside of the drug obviously heading in the wrong direction or of a safety issue.
But even if it was good enough to stop, for example, if the data were as good as the pilot data, then probably looking at 100, 120 patients and halfway through the trial may well be statistically significant already. The committee cannot recommend that we stop. The trial is also a medium-sized trial on Alzheimer's, so it's advisable to do that. Jerome asked, "Interim analysis, January or February?" We covered that late January as the guidance, and that's exactly when it will happen. But also asked where the depression trial is up to. And essentially, what we've done with depression is really park it for now. We've met with the FDA and clarified the path forward to an approval in depression. However, we're focused on putting all our resources on the Alzheimer's trial.
Part of the reason for that is that the path to approval is probably a bit faster in Alzheimer's disease. The unmet need is huge in Alzheimer's, much greater, I would argue, or we would argue, than in depression. As a result of value-based pricing, it's very likely that Xanamem would be better priced and better positioned as a product in the Alzheimer's market first. We may well get to a new depression trial in the future. It's certainly a very good backup indication. Xanamem is a unique mechanism of action. Drug developed for depression in and of itself would be a great program. The Alzheimer's program has priority. All right. We have five more questions in the chat. Let me just go to the top here. Matt asked, "How selective we've been in choosing the patients that enter the trial?
What percentage of initial applicants made it through into? So basically sort of a screening success. So Dana, would you like to answer that one?
Yeah. So we've used p-Tau 181. And like many other companies that are doing studies, they're now using p-Tau 181 or p-Tau 217. And the screen fail rate on that pre-screen criterion is 60%-70%. So we screened about 1,100 patients to come up with 246 that are eligible. Now, once the patients get through that pre-screen on p-Tau and their diagnosis, then they go into a full screening. And the full screening, screen fail rate has been very low. It's really that p-Tau initial pre-screen which calls out a lot of the patients.
Yeah. Another question related to p-Tau is from Johnny. Is the elevated p-Tau in patients accepted by the TGA or the FDA as a clear indicator of Alzheimer's disease?
Yeah. So the FDA has issued a guidance on this and has said that these p-Tau species can be used to establish the diagnosis. Previous to that, one where patients were getting amyloid PET scans, they were getting CSF analysis. And this is both expensive, laborious, invasive, difficult. And the field clearly is rapidly moving to p-Tau species as the confirming biomarker to establish the diagnosis of Alzheimer's disease. That's becoming de facto what is done. And importantly, when we proposed to the FDA what the additional trial would be, we said we would be using p-Tau as an indicator. And this trial we're doing is using p-Tau. The FDA had no pushback on that. They said that was fine.
Thanks, Dana. Alex asked, "Dr. Hilt, is there any causal evidence around cortisol increasing symptoms of depression or Alzheimer's?" Or is it still all association? Would your trial effectively be the causal evidence?
Because, I mean, I think probably Alzheimer's disease is multifactorial. Okay? When you look at where this enzyme is expressed in the brain, it's predominantly expressed in glial cells in the brain, microglia and astrocytes. And these in patients with Alzheimer's disease become activated, and they secrete cytokines and other molecules which lead to neuronal dysfunction. So I think that Alzheimer's disease is really multifactorial. And clearly from the data I showed you and the vast literature, elevated cortisol is associated with the condition.
Yeah. Thanks, Dana. And I look at it, yeah. And I would say I would add the randomized prospective trial we did in depression did show that inhibiting cortisol had a clinical effect. And thus, we believe that that trial in particular has proven the cortisol hypothesis as a causal part of depression, at least.
If you.
Our Alzheimer's data is certainly going towards proving that it is relevant in Alzheimer's as well.
If you simply Google cortisol in depression, you'll get many, many references. This goes back decades about elevated cortisol being associated with severe depression.
Yeah. Thanks, Dana. Alex asked, "For the open label, will all the patients start on the active drug straight away in January or February, or will they roll onto it individually after each have been in the trial for the full 36 weeks?
It will be individual so that after the patients finish their course, then they'll be eligible for the open label. Now, we have many patients who are finished the 36 weeks already. We're going to allow those patients to actually roll into the open label as well, so patients will come into the open label to some degree with some variable length of a drug holiday, if you will, between the end of the blinded randomized portion and the open label phase, but we will be following the patients in the open label in a blinded way. In other words, we will not know what treatment those patients in the open label had in the first portion, but they'll all have active in the open label portion.
Yeah. Thanks, Dana. Johnny asked about the primary endpoint of the Clinical Dementia Rating Scale sum of boxes we're using. Is it the same as was used by the company in the XanADu Phase IIa trial? And the answer is no. While the CDR Sum of Boxes was a secondary endpoint, the primary endpoint for that trial was a cognition measure called ADAS-Cog and a combination endpoint of several different things called ADCOMS. So the endpoints there were different. However, the data Dana showed you in the positive p-Tau biomarker patients was CDR Sum of Boxes . And part of the reason we like CDR Sum of Boxes , it seems to be a very sensitive endpoint for our particular drug when we look at these data. Somebody asked about perhaps a misunderstanding about the last slide about whether is there a 1,500-patient trial.
Now, the 1,500 patients refers to the FDA and ICH requirements that will also be for the EMA. For a drug like this, you need to study 1,500 persons in open-label studies and randomized trials with active therapy, at least 100 of whom have been treated for 12 months. So that's just the standard ICH guideline for a small molecule like our once-a-day Xanamem pill. And so it refers to the total number of people in the various different trials in the program, not a new trial. Peter asked, "What is the funding runway? And is there a capital raise envisaged within 12 months?" So we have funding through beyond the middle of next year. We have other sources of funding available to us potentially that are non-dilutive. We also have some option exercises.
But now that the stock price is well above the AUD 0.0375 for the unlisted, which is about AUD 6 million worth of stock that could be exercised and paid to the company. And then there's more than AUD 20 million in the listed options, which are AUD 0.05 listed options. And some option holders have chosen to exercise those already. We may also do a regional deal, as we've talked about, and that would bring in an upfront payment that would be non-dilutive. And so at this stage, we certainly are not raising money. We are well funded, and we have a number of different options, including additional funds from the tax credit rebate to fund us through to further into the next part of next year. Mike asked, "Can you report data from the open-label trial as it progresses?" Indeed, you can with an open-label trial.
The great thing about it being open is that, yes, everybody's on active Xanamem. Patients know that. We know that, and the doctors know that. There won't be that many people with a lot of data ahead of the November 26th final results of the randomized section. So it's a bit hard to say at this point whether we'll have any meaningful data we could report. But we will be keeping a close eye on that. And if there is something we think is meaningful and material to investors, we will tell you about it. All right. All right. And I think, everybody, I think that's the full list of questions that I can see here in the chat. We're almost right on time, 45 minutes past the hour. So I think let me just see if there's any last questions from anybody present.
So if not, I think we will say thank you very much for your attention and for many of you who have been following and investing in the company for a long, long time. Our story is very well understood now by people all around the world. We're leading the pack for a safe and effective oral. We're just around the corner from final major results of an intelligently evidence-based design clinical trial that has a high probability of success. And we very much look forward to bringing you that kind of success as early as November next year. So thanks, everybody. Thanks to the presenters. Thanks, Dana and Andy.
Thank you.
Thanks. Actinogen. And we look forward to talking with you all soon.