I'll be your host for today's call. At this time, all participants are in a listen-only mode. Later, we will conduct a question-and-answer session, and during this session, if you would like to ask a question, please use the Q&A box or raise your hand. Please note that this conference is being recorded, and the call will be available for replay on Anavex 's website at www.anavex.com. With us today is Dr. Christopher Missling, President and Chief Executive Officer, and Sandra Boenisch, Principal Financial Officer. Before we begin, please note that during this conference call, the company will make some projections and forward-looking statements. These statements are only predictions based on current information and expectations and involve a number of risks and uncertainties. We encourage you to review the company's filings with the SEC that include, without limitation, the company's Forms 10-K and 10-Q, which identify the specific factors that may cause actual results or events to differ materially from those described in these forward-looking statements. These factors may include, without limitation, risks inherent in the development and/or commercialization of potential products, uncertainty in the results of clinical trials or regulatory approvals, need and ability to obtain future capital, and maintenance of intellectual property rights. This conference call discusses investigational uses of agents in development and is not intended to convey conclusions about efficacy or safety, and there is no guarantee that any investigational uses of such products will successfully complete clinical development or gain health authority approval. With that, I would like to turn the call over to Dr. Missling. Thank you, Clint, and good morning, everyone. Thank you for being with us today to review our Q4 financial results and quarterly business update. We are fully committed to bringing oral Blarcamesine and oral ANAVEX3-71 to patients. We are dedicated to delivering on the value of our pipeline and maximizing its potential for patients, investors, and our employees. Over the coming months, we will continue to focus on progressing our clinical trials and regulatory actions. At the same time, we're aiming to expand our collaborative initiatives and strategic partnership activities. As previously announced, through our update on the status of the regulatory filing of Blarcamesine in Europe, we expect the CHMP to adopt a negative opinion on the MAA at its December meeting. We intend to request a re-examination of the CHMP opinion upon its formal adoption based on feedback and continued guidance from the CHMP, EMA, and the Alzheimer's Disease community. The MAA procedures adopted by the CHMP allow an applicant to request re-examination of its decision, which would be undertaken by a different set of reviewers that conduct a new examination independent from the first opinion. Our expert advisors, investigators, as well as patients and their caregivers, encourage us in our commitment to continue working in partnership with global regulatory bodies to advance science and potentially new treatment options for patients and their families. As part of the MAA review process, we have successfully undergone a full Good Clinical Practice GCP inspection of the trial data by EMA. The manufacturing package has passed the EMA review as well. A good clinical practice GCP inspection is an official review by a regulatory authority of clinical trials, documents, facilities, records, and other resources to ensure compliance with GCP guidelines. We're looking forward to working closely with EMA and other stakeholders to advance our investigational therapy for early Alzheimer's disease. Importantly, we also announced that we had initial contacts with the authorities in the U.S. regarding our Alzheimer's disease program, and we intend to provide further updates on our interaction with the FDA as they become available. Going forward, we will provide both regulatory and clinical trial updates on Blarcamesine in other indications such as Parkinson's disease, Rett syndrome, and Fragile X. This will include the disclosure of planned future clinical trial designs as we continue to advance our therapeutic pipeline. During the most recent quarter, we announced several new scientific and medical publications, which includes a peer-reviewed publication in the journal Neuroscience Letters titled "Prevention of Memory Impairment and Hippocampal Injury with Blarcamesine in an Alzheimer's Disease Model." This study shows that pretreatment with Blarcamesine prevented amyloid-beta-induced memory impairment and brain oxidative injury, suggesting that Blarcamesine is an attractive candidate for Alzheimer's disease pharmacological prevention. A peer-reviewed publication in the journal iScience ascertaining the precise autophagy mechanism of sigma-1 receptor through Blarcamesine activation titled "Conserved LIR-specific interaction of Sigma-1 receptor and GABA-RAP." A publication, "Oral Blarcamesine phase 2b/3 trial confirms identified precision medicine patient population, significant broad clinical and quality of life improvements for early Alzheimer's disease patients," to be available online as a preprint and in submission to a peer-reviewed medical journal. Anavex announced the latest published scientific results for Blarcamesine on all standard scales for measuring Alzheimer's disease and cognitive decline after 48 weeks. The defined precision medicine population ABCLEAR 3, consisting of early Alzheimer's disease patients with confirmed and progressed pathology taking 30 milligrams once daily oral Blarcamesine, demonstrated barely detectable decline. This was comparable to minimally perceptible decline in prodromal, which is predementia aging with adults. On October 29, we announced additional long-term clinical data for Blarcamesine. This new data demonstrated continued long-term benefit from oral Blarcamesine compared to decline observed in the Alzheimer's Disease Neuroimaging Initiative control group, also called ADNI, a control group established by a clinical research project launched by NIH in 2004. In the intended treat population, significantly less cognitive decline was observed for the Blarcamesine participants compared to the ADNI control group at 48 weeks, with a significant and clinically meaningful difference in mean change from baseline, ADAS-Cog13 total score of minus 2.68 points. Over the course of the open-label extension study at time point 96 weeks, these two groups further diverged sharply, with statistically significant differences in mean change in ADAS-Cog13 total score at 96 weeks of minus 6.41 points. The difference between groups continues to increase at 144 weeks to ADAS-Cog13 total score difference of minus 12.78 points. The results provide evidence of the significant beneficial therapeutic effect of Blarcamesine, which positively separates from the ADNI control group with duration of treatment. This significant beneficial therapeutic effect of Blarcamesine compared to decline observed in the ADNI control group translates into 17.8 months of time saved with oral Blarcamesine, allowing for longer independence of the patients by approximately over 1.5 years. Looking ahead, Anavex will be presenting additional data and scientific findings at upcoming conferences and in publications. These include the direct relationship between cognitive function and reduced brain region atrophy with Blarcamesine, oral Blarcamesine for early symptomatic Alzheimer's, robust effect size through precision medicine, and analysis of the ANAVEX2-73 AD004 randomized trial. Also, newly identified precision medicine gene, Collagen 24A1, with over 70% prevalence, which establishes effective treatment of early Alzheimer's disease with Blarcamesine, and also continued long-term benefit from oral Blarcamesine compared to delayed start analysis and decline compared to natural history studies. With regard to ANAVEX3-71, in October, Anavex announced positive top-line results from its placebo-controlled phase II clinical study evaluating ANAVEX3-71 for the treatment of schizophrenia in adults on stable antipsychotic medication. The study successfully achieved its primary endpoint, demonstrating that ANAVEX3-71 was safe and well- tolerated. The safety profile was consistent with previous studies of ANAVEX3-71 in healthy volunteers, with no serious or severe treatment- emergent adverse events reported in either part A or part B of the study. In addition to meeting the primary safety endpoint, secondary and exploratory analysis revealed encouraging trends in several outcome measures. Our other oral medicine candidate, ANAVEX3-71, represents herefore a transformative opportunity in neuropsychiatric drug development, leveraging its unique dual sigma-1 agonist M1-PAM mechanism to address multiple high-value indications through a unified neuroinflammatory biomarker platform. Further detailed analysis of randomized, strictly double-blind and placebo-controlled clinical trial ANAVEX3-71 SZ001 revealed very encouraging data in patients suffering from schizophrenia. Following successful phase II results from the SZ001 study, while confirming the excellent safety profile of ANAVEX3-71, the study demonstrated reduction in GFAP and YKL-40 neuroinflammatory markers. GFAP, as a structural protein of astrocytes in the brain, represents aberrant activation of astrocytes, the major brain glial cell lineage. Astrocytes participate in brain neural function in multiple ways, amongst them critical modulation of synaptic relay between neurons in neural circuits. Its dysfunction is a key pathogenesis mechanism in schizophrenia. This positions ANAVEX3-71 to advance into pivotal trials with the once-daily modified release oral tablet, enabling once-daily dosing across depression and psychosis indications, where current therapies have failed or shown limited efficacy. In addition to schizophrenia, one high unmet need opportunity would be depression in Alzheimer's disease, with currently no approved therapies. Up to 40% of people with Alzheimer's experience significant depression, especially in early and middle stages of the disease. Depression in Alzheimer's is associated with worse quality of life, accelerated cognitive decline, and earlier onset of dementia symptoms. The neuroinflammatory biomarker strategy positions ANAVEX3-71 to potentially achieve disease modification claims beyond symptomatic treatment, representing a paradigm shift in neuropsychiatric drug development. I would like to direct the call to Sandra Boenisch, Principal Financial Officer of Anavex for a financial summary of the recently reported quarter. Thank you, Christopher, and good morning to everyone here. I'm pleased to share with you today our fourth quarter financial results for our 2025 fiscal year. Our cash position as of September 30th was $102.6 million, and we had no debt. During the quarter, we utilized cash and cash equivalents of $8.6 million in our operating activities after taking into account changes in non-cash working capital accounts. As of today, with the current cash balance of over $120 million, we anticipate that at the current cash utilization rate, our cash runway is more than three years. Our research and development expenses for the quarter were $7.3 million as compared to $11.6 million in the comparable quarter of last year. General and administrative expenses were $3.5 million as compared to $2.7 million for the comparable quarter of last year. Compared to the same quarter of fiscal 2024, we saw a decrease in operating expenses, mostly driven by the completion of a large manufacturing campaign of Blarcamesine and a decrease in clinical trial activities as a result of the completion of our open-label extension studies and our ANAVEX 3-71 phase II study in schizophrenia. Lastly, we reported a net loss of $9.8 million for the quarter, which is $0.11 per share. Thank you. I will now turn the call back to Christopher. Thank you, Sandra. In summary, we are focused on continuing to advance our precision medicine compounds. We are excited to be potentially making a difference for individuals suffering from these diseases by presenting a scalable treatment alternative alongside the ease of oral administration. I would now like to turn the call back to Clint for Q&A. Thank you, Christopher. We will now begin the Q&A session. If you have a question, please raise your hand or enter it into the Q&A box. It looks like our first question will come from Michael Obadiah from HC Wainwright. Hello. Good morning. I'll be asking the questions on behalf of Ram Selvaraju from H.C. Wainwright. I have a couple of questions for the management. The first question is, what is the likely commercial impact of the failure of semaglutide on the outlook for Blarcamesine in Alzheimer's disease? The second one is, when is the next formal discussion of Blarcamesine scheduled to take place with the FDA? The third question is, what initiative does Anavex plan near-term to pursue Blarcamesine approval in regions beyond the European Union and the United States? Thank you. I appreciate the questions. To answer the first question about the impact of the semaglutide results, we understand there's an unmet medical need here, and this is certainly further highlighted by the recent setback by the two Evoke studies from Novo Nordisk and also by other companies, including other large pharma companies recently, also with anti-Tau injectables. There's a lack of upcoming pipelines, certainly. We also understand that the Evoke semaglutide GLP-1 finding highlights the complexity of Alzheimer's disease biology and the challenges of expecting the metabolic pathway alone to meaningfully alter neurodegenerative processes. Alzheimer's is more complex, involves impaired proteostasis, autophagy dysfunction, synaptic failure, and multiple converging mechanisms. Therapeutic effects seen in related conditions do not always translate into cognitive benefit here. However, we have with oral once-daily Blarcamesine, with this upstream mechanism of action, which restores autophagy, which precedes these pathologies I just summarized, and has demonstrated in early Alzheimer's disease patients clinically meaningful efficacy of slowing cognitive decline in significant amounts, in some cases over 50%, with an acceptable safety profile, with no ARIA, and as demonstrated in the phase 2b/3 study. The answer to the question is, this makes it more clear that this is a complex disease and there's a lack of compounds near-term available for patients to address this unmet need. The second question is about timing. We provide, as we stated, updates that will follow up in the initial discussion with the U.S. regulators, and we'll provide updates as we receive them. We are very excited about the initiation of these discussions. Regarding the third questions, we are continuing to now explore other regulatory geographies as well as moving forward where we can see fit to address open questions. I trust this addresses the question. Yes. Thank you very much for the clarity and transparency. Thank you. The next question is going to come from Tom Bishop at BI Research. Tom, you need to unmute. For the press release, the CHMP seems to have given you some guidance about the additional information they need to see, for example, biomarker. Can you elaborate what this includes? We want to proceed with the re-examination because we owe it to the patient, and we get the feedback also from investigators that the unmet need is very high, and it boils down to demonstrating to the CHMP the benefit outweighs the risks of the drug to be on the market. That discussion includes all available data. It might be to make the glass half full that additional correlation or information about objective biomarkers, which are not subject to influence, might be helping in getting to that point. That is the background of biomarker best, including biomarker assessments. There were no particular biomarkers that you hope to bring up? We have communicated, and it has been published that we have a very strong biomarker of the pathology, which is the analogy of oncology with tumor growth. You look at the size of the tumor, which is measurable objectively, can be measured objectively, and it cannot be influenced by a patient or by anybody else. The same is in Alzheimer's disease: the brain shrinks. The brain gets smaller, the brain mass shrinks, and we can measure that as well. It is a very objective marker of neurodegeneration. We demonstrated that this marker of neurodegeneration is significant. The less or even halted in some patients with active oral Blarcamesine, while in the placebo arm, this shrinking of the brain continues, which is the clear definition of the advancement of the Alzheimer's pathology. We like to include, of course, that as well in the discussion. What about the ABCLEAR data? I mean, that was very compelling, with 48%-86% slowing depending on the gene biomarker or combination. I guess this was not considered by the CHMP, as it came out because it came out kind of late. Can this be included for consideration on re-examination? It is a good question. We like to emphasize our focus is on each individual patient affected by Alzheimer's. We see that very clear beneficial signal of cognitive, but also clinically meaningful effect in both cognitive and functional, but also in all the other endpoints, consistent improvement and significant improvement of the clinical outcomes. That is the CGI, that is the quality of life, and PIQ, MMSE, and all the measures out of ADAS-Cog13, CDR-Sum of Boxes, ADCS-ADL. In all these ABCLEAR 2 and 3 populations, we see clearly clinical meaningful and significant improvement. We would like to also point that out. That is really a good data set to have and to put this forward. Last but not least, making the point about the focus on each individual patient, we see a reversal of the negative trajectory of quality of life of the patients in 70% of the patients, 70% in the trial. That means the quality of life is better after one year than at the start of the trial. That is very impactful because that is what really impacts the individual patient. Okay. If approval ultimately came from the EMA, and let's assume perhaps it was conditional, is there a rule of thumb or how long you would have to do a conditional trial? It is really not—it is really hard to speculate about this, but we would like to make sure we want to point out we are motivated and driven by the fact that there is a huge, significant unmet need for a drug with these features today. We pointed out the recent pipeline failures. I want to point out that between 2020 and 2025, this year and 2030, there will be more than $300 billion of large pharma revenue at risk from loss of exclusivity, with over 40% of top pharma sales exposed, creating an estimated $90 billion growth gap even after internal pipeline contributions. That means there's also a huge unmet need not only for this indication, but also for overall pipeline to be filled by large pharma. That's interesting that you brought that up because I wanted to ask about how you're coming with exploring your options if you get approval, for example, large pharma sales organizations and so forth to take Blarcamesine to market. Yeah. We pointed out in this call that one of the key things we are focusing on now is expanding the corporate development partnership activities. We mentioned that we are presenting at the most important conference every year, which takes place in San Francisco, in early January. We are presenting company on Wednesday at that conference itself. That allows for more meaningful discussions, which is the hotspot for business development activities at this conference. We will make sure we are present in that regard. I think it'd be a real tragedy for Alzheimer's patients to not see this drug approved because especially the ABCLEAR data to me is so convincing that the risks are so low and it's oral, that I just can't fathom that it wouldn't get approved. That's just me. I wish I had a vote. Thank you. We would agree. Thank you for your vote as well. Tom, are you there? Yeah. As long as I'm still on, is there a mechanism of action for Collagen 24A1? Yes, there is. This will be now published in a peer-reviewed paper. In summary, I can say that Collagen 24A1 is the key ingredient of the extracellular matrix called ACM. When you look at pictures of brain neurons or astrocytes, you always see these very nice connections or network, like a web, spider web description or pictures. In the background, it's always like pitch black. You're wondering, this is how the brain looks like. It does not. This background is actually the extracellular matrix. That's where these neurons and astrocytes are sitting on in your brain. If you have a mutation of this extracellular matrix, then your response to Blarcamesine is impaired. The autophagy flux, the autophagy restoration, which is the recycling mechanism of the neurons, which precedes a beta and tau. It is further upstream, closer to the origination of the pathology of Alzheimer's, if you like, that is impaired. For that reason, we found that patients with a wild type, with not- mutated collagen genes, they respond extremely well. We see effects in other ADAS-Cog13, minus 4.7 in the patients with that effect, with that wild- type gene. In the CDR-Sum of Boxes, the scores go up to 1.4, minus 1.4. These are really very unprecedented effects of benefit. We pointed out that that means that patients are actually almost not declining or declining less than prodromal patients, which are less impaired. That is quite impactful. This is really intriguing science. It will be published in a major peer-reviewed paper very soon. Extremely intriguing. Also consistent with the mechanism of Blarcamesine. Great. Okay. That is it for me. I am just excited to see this ABCLEAR data get examined by the CHMP as well. I appreciate it. Thank you. Thank you for the questions, Tom. The next question is going to come from Jesse Silvera with Spirit of the Coast Analytics. Hey, good morning. Can you hear me all right? Yes, you are fine. Go ahead, Jesse. Hey, good morning, Clint and Dr. Missling. This is Jesse Silvera from Spirit of the Coast Analytics. Thank you for taking my call. Some of these questions you have kind of addressed a little bit earlier, but hopefully, you can maybe provide some additional color on some of them. Yeah, just to reiterate, kind of one of your previous points. My first question is sort of an assumption, though I think you got at it earlier. Considering the CHMP review is ongoing and a final decision hasn't even been rendered yet, is it safe to say that you can't discuss the reasons for negative CHMP trending or give details on the strategy going into th e re-evaluation? That's accurate. That's correct. Okay. Got that. Perhaps adjacent to that conversation, do you think you can give more detail on a statement that was found in the 14th November press release? It stated, "The company intends to request a re-examination of the CHMP opinion upon its formal adoption, including providing relevant biomarker data based on feedback and continued guidance from the CHMP, EMA, and the Alzheimer's disease community." I think it was Tom that was getting at this earlier, but can you comment any further on the biomarker data? I think I saw in your press release this morning that you plan to publish maybe a paper about brain atrophy and its direct correlation to cognition. Is that accurate? Is that some of the data that you may or may not be presenting to the EMA? That's accurate. The advantage of the biomarker is that the biomarker endpoint is objective and cannot be influenced by a patient, by the caregiver, or the physician, or anybody else, as a matter of fact, because it's objective. I pointed out that in analogy to oncology, where you get drugs approved purely by the effect of the brain measure, sorry, of the tumor measurement, while, for example, the clinical effect was not yet significant. That is something which we like to point out, that the analogy is in Alzheimer, the clear pathological shrinking of the brain, which is one of the first features Alois Alzheimer himself actually identified in his patients with Alzheimer, the first patient he assessed. Subsequently later on, when he looked into the brain, he found this additional aberrant features of proteins then identified as a beta plaque or tau. The first thing he identified was really that the brain shrinks and the holes, the gaps, widen in the brain. That is really the pathological logical consequence of a declining brain, a less functional brain. It is like a lemon which is drying up. You cannot squeeze anything out of it. That is really a strong objective biomarker and biomarker endpoint for demonstrating an objective effect of a drug. That was demonstrated with Blarcamesine. We just want to make sure that gets visibility. Part of this is also a correlation analysis that we are able to find that not only that there's less shrinking of the brain going along with Blarcamesine treatment, but also that shrinking of the brain correlates with each patient with an improvement in the respective regions of the brain's activities of the other ADAS-Cog13 subdomains, for example. For example, learning and reading, and writing is in one area of the brain. If that is improved in the clinical trial for the patient, that same region of the brain responsible for that, if that also is less impaired in the active Blarcamesine treatment arm compared to placebo. If you can find this, this further confirms the true effect of the drug. That will be convincing in our opinion. Yeah. I think that's really interesting. I'm definitely looking forward to that. I think kind of related is in light of the semaglutide acute failure, is that they reported that the drug had improved biomarkers, amyloid, maybe tau. I don't recall about tau, but they improved amyloid, but had no clinical effect, no improvement on CDR-Sum of Boxes. I think that I'm not sure exactly when there needs to be, if there will be a time where regulators will no longer see amyloid equals better cognition or whatever. Moving along, kind of on 9th September, the company PR'd really impressive ABCLEAR 3 comparisons to prodromal populations and had a detailed follow-on analysis of ABCLEAR 2 and ABCLEAR 3 subpopulations in a GWAS preprint a little bit later. ABCLEAR 3 in particular appears to showcase an effective functional cure in early Alzheimer's patients. You covered the mechanisms of these earlier, but can you give further color on ABCLEAR 1 versus ABCLEAR 2 and ABCLEAR 3, specifically whether they were pre-specified or exploratory, and how regulators may or may not view these subpopulations in light of being exploratory or being pre-specified? Is that something you can talk about? Yeah. The definition of ABCLEAR 1, which basically is the wild type sigma-1 gene, was identified already in the beneficial effect of that gene in the previous preceding phase 2a study, which was published in 2020, where we identified that patients with the sigma-1 wild type, which represents 70% of the population, had a better response to Blarcamesine than those with the respective mutation. It's a point mutation. That's how biology is. 30% of the overall population, that's not patients, but overall population, has a one-point mutation, RS180866. This one mutation changes the conformation of the gene, makes it a little bit less viable or effective in its ability to restore homeostasis, increase autophagy, which is the mechanism of the activation of Blarcamesine through Sigma-1 activation as its ultimate effect. The patients with the wild type, the fully functional non-mutated gene, respond better. This was identified in the phase 2a. We pre-specified the analysis of the primary endpoints as well as the secondary and exploratory endpoints. With these in mind, how would patients do in the phase 2b/3 study with the wild- type Sigma-1? That was pre-specified, and we now define this as ABCLEA- 1. We did indeed demonstrate, or it was demonstrated that indeed that was confirmed, Blarcamesine increased the effect of patients with that 70% runabout is the number of patients, 70, which improved better than the patients with the mutation. That is improving. ABCLEAR 2 was the result of a pre-planned in the trial. We did a whole- genome exome analysis. That means we looked at all patients in the study and analyzed their genes and gene expression, and response to the drug based on their genetic profile as well. That is the DNA of all patients. In this analysis, which was pre-planned, we found, to our surprise, unexpectedly, one gene showing up as an extremely strong driver of efficacy. That gene turned out to be the Collagen 24A1 gene. That gene, I explained it just before, is involved in the buildup of the extracellular matrix. That is really, really intriguing novel science and underappreciated or overlooked up to now in the field because everybody always looks at the neurons or the astrocytes or the areas of active involvement in the brain. The extracellular matrix is where all these neurons and astrocytes are residing or sitting on. It is like a pavement, like a street. If that street is not smooth, like a highway or like a pavement, then these neurons cannot function well. We were able to find them because the patients with a mutation of this collagen gene in this extracellular matrix did not respond so well to Blarcamesine, representing that they are not as viable as their respective wild type carriers. The good news, though, is the collagen wild type represents 71% of the overall population. That was also found in our trials. We had run about 70% with patients with this collagen wild- type gene. Very intriguing new data. That was, as a consequence, pre-planned in the study, of course, not pre-specified, because we found it in the analysis of the phase 2b/3 study. Okay. It's my understanding that Leqembi and Kisunla were both approved after a CHMP re-exam and that subpopulation data enriched their filing by conferring a more desirable safety efficacy axis. Is that true? Is this any way relevant to Anavex's current position with some of this data, the ABCLEAR 2 and ABCLEAR 3 data? It's correct. Both Lecanemab and Donanemab, and these are run by large pharma companies. They had been, although prior approved in the U.S., reached the same point as we did just as we communicated a few weeks ago. They underwent the same re-examination and were able to get approval. I do not want to, I would say, make that this is a guarantee for us because every review is complex and we are not able to anticipate or know the outcome of this re-examination process. The body boils down to in the assessment of Lecanemab and Donanemab was the assessment and the judgment of benefit needs to outweigh the risk. Our drug has safety, has no area. We talked about the efficacy, which we just discussed. We cannot anticipate, of course, an outcome of the regulatory review. Okay. Understood. Moving forward, will you be immediately refilling for the EMA re-evaluation? To my knowledge, it took about three and a half to four months for the CHMP to give Leqembi and Kisunla their next opinions, respectively. Maybe we could see something around April. Is that about what you're projecting? That's correct. We will immediately ask for the re-examination as soon as possible. Again, while there's never certainty to obtain approval from regulators, we remain highly excited about the science and the data. Okay. Being a small company with a unique mechanism of action, it's probably difficult for you to garner support from the community. I recall that the European Alzheimer's Disease Consortium, Alzheimer Europe, and even the US Alzheimer's Association kind of put together persuasive arguments for the CHMP to consider during the Leqembi and Kisunla re-evaluations. Does Anavex have any support like this? Are you aware of any organizations, key opinion leaders, or even patients from the trial attempting to persuade the CHMP to reconsider? Do you have that support from the community? It is really not for us to make that move. The community is aware of our drug, and we let them basically do what they think is appropriate. What we only can do is point out the data. This is a process, and we are committed to this process. Also, very importantly, with this process, we gain confidence with the regulators. We are doing this in a partnership. We are doing this in an open discussion. We are also getting the ability to get feedback, which we need to move this forward in what way it takes to help patients addressing this unmet medical need. Okay. I see that we are nearing time. To conclude, for me at least, it's pretty obvious to anyone paying attention that Blarcamesine should likely be approved for early Alzheimer's patients. The efficacy has been absolutely unprecedented, and these megalithic effect sizes were achieved in a really small population, which should theoretically make it more difficult to do. I think it's a clear win for patients, caregivers, and payers. I think part of the problem the first time around may have been that it was sort of piecemeal analysis, and you were introducing analysis as you were going. Now that you have all analysis at your disposal and a clear narrative, it's my hope that the company will use the re-examination to tell Blarcamesine's story and earn the approval it deserves. Thank you for taking my call, and I hope you have a good rest of the day. Thank you. We appreciate the kind words. Our expert advisors advise us also to proceed. The patients and investigators also advise us to proceed and remain committed to do our best. Thank you. Yeah. Thank you, Jesse. Dr. Missling, I don't see any further questions at this time. Thank you. We are thankful for your continued interest and trust in Anavex and wishing you a happy and blessed Thanksgiving. In closing, we'd like to continue to point out our focus on execution as we advance our therapeutic pipeline to potentially improve patients' lives living with these devastating conditions. Oral once-daily Blarcamesine has the potential to address high unmet medical need in early Alzheimer patients with its clinically meaningful efficacy profile of slowing cognitive decline by more than 30% and sometimes even higher for certain populations. It's acceptable safety profile as demonstrated in the phase 2b/3 program. Thank you very much. Again, happy and blessed Thanksgiving. Thank you, ladies and gentlemen. This will conclude today's conference call. We appreciate you participating, and you may now disconnect.