Anavex Life Sciences Corp (AVXL) 2025 Q4 法說會逐字稿

(audio in progress) 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.

And 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 ANAVEX 3-71 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 extending 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 reexamination of the CHMP opinion upon its formal adoption based on feedback and continued guidance from the CHMP, EMA and the Alzheimer's disease community. EMA procedures adopted by the CHMP allow an applicant to request reexamination 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 advisers, 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 a clinical trials documents, facilities, records and other resources to ensure compliance with GCP guidelines.

We're looking forward to working closely with the 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 US 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 of iScience ascertaining the precise autophagy mechanism of sigma-1 receptor through blarcamesine activation titled Conserved LIR-specific interaction of Sigma-1 receptor and GABARAP. A publication or blarcamesine Phase IIb/III 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, ABCLEAR3, consisting of early Alzheimer's disease patients with confirmed and progressed pathology taking 30-milligram once-daily oral blarcamesine demonstrated barely detectable decline. This was comparable to minimally perceptible decline in prodromal, which is pre-dementia 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 intent-to-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 at ADAS-Cog13 total score of minus 2.68 points.

Over the course of the open-label extension study at [10.96] weeks, these two groups further diverged sharply with statistical 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 -- 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 ANAVEX 2-73-AD-004 randomized trial. Also, newly identified precision medicine gene, Collagen 24A1 with over 70%, 7-0 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 ANAVEX 3-71 in October, Anavex announced positive top line results from its placebo-controlled Phase II clinical study evaluating ANAVEX 3-71 for the treatment of schizophrenia in adults on stable antipsychotic medication. The study successfully achieved its primary endpoint, demonstrating that ANAVEX 3-71 was safe and well tolerated. The safety profile was consistent with previous studies of ANAVEX 3-71 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, ANAVEX 3-71 represents, therefore, 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, ANAVEX 3-71-SZ-001 revealed very encouraging data in patients suffering from schizophrenia. Following successful Phase II results from the SZ-001 study, while confirming the excellent safety profile of ANAVEX 3-71, the study demonstrated reduction in GFAP and YKL-40 neuroinflammatory markers. GFAP is a structural protein of astrocytes in the brain represents apparent 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, a key pathogenesis mechanism in schizophrenia.

This positions ANAVEX 3-71 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 ANAVEX 3-71 to potentially achieve disease modification claims beyond symptomatic treatment, representing a paradigm shift in neuropsychiatric drug development.

And now 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 am pleased to share with you today our fourth quarter financial results for our 2025 fiscal year. Our cash position at September 30 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 noncash 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. And lastly, we reported a net loss of $9.8 million for the quarter, which is $0.11 per share. Thank you.

And now I will 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 all administration. I would now like to turn the call back to Clint for Q&A.

(Event Instructions)

Michael Obodai, H.C. Wainwright.

So I'll be asking the questions on behalf of Ram Selvaraju from H.C. Wainwright. I have a couple of questions for the management. And 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? And the third question is, what initiatives does Anavex plan near term to pursue blarcamesine approval in regions beyond the European Union and the United States?

I appreciate the questions. So 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 with also with anti-tau injectables. So there's a lack of upcoming pipeline certainly.

We also understand that the evoke semaglutide GLP-1 finding highlight the complexity of Alzheimer's disease biology and the challenges of expecting the metabolic pathway alone to meaningfully alter neurogenerative processes. But Alzheimer's is more complex, involves impaired proteostasis, autophagy dysfunction, synaptic failure and multiple converging mechanism. So 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, significant amounts, in some cases, over 50% with an acceptable safety profile with no ARIA and as demonstrated in the Phase IIb/III study. So 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.

Second question is about timing. So we provide, as we stated, updates what will follow-up in the initial discussion with the US regulators, and we'll provide updates as we receive them. But we're very excited about the initiation of these discussions. Regarding the third question, we are continuing to now explore other regulatory geographies as well as moving forward where we can see fit to address open questions. So I trust this addresses the question.

Yes. Thank you very much for the clarity and transparency.

Thank you.

Tom Bishop, BI Research.

From the press release, the CHMP seems to have given you some guidance about the additional information they need to see, for example, biomarker. But can you elaborate what this includes?

So we want to proceed with the reexamination because we owe it to the patient and we get the feedback also from investigators that the unmet need is very high. And we -- it boils down to demonstrating to the CHMP the benefit away the risks of the drug to be on the market. And that discussion includes all available data. And it might be to make the glass half full that additional correlation or information about objective biomarker, which are not subject to influence might be helping in getting to that point. So that is the background of biomarker, including biomarker assessments.

Well, there was no particular biomarkers that you hope to bring up.

We have communicated and it's been published that we have a very strong biomarker of the pathology, which is the analogy of oncology where tumor growth and 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. And the same is in Alzheimer's disease is the brain shrinks. So the brain gets smaller, the brain mass shrinks, and we can measure that as well. And it's a very objective marker of neurodegeneration. And 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. And 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% to 86% slowing depending on the gene biomarker or combination. Was this -- I guess this was not considered by the CHPT as it came out MP because it came out kind of late. But can this be included for consideration on reexamination?

So it's a good question. So we like to emphasize our focus is on each individual patient affected by Alzheimer's. And 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-I, that is the Quality of Life, NPI-Q, MMSE in all the measures, ADAS-Cog13, CDR Sum of boxes, ADCS-ADL in all this ABCLEAR2 and three populations, we see a clearly clinically meaningful and significant improvement. So we would like to also point that out. And that is really a good data set to have and to put this forward.

And also 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 7-0 in the trial. That means the Quality of Life is better after one year than at the start of the trial. And that's very impactful because that's what is really impacts the individual patient.

Okay. If the 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's really not -- it's 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's a huge significant unmet need for a drug with these features today, and we pointed out the recent pipeline failures. And also, I want to point out that between '20 and '25 this year in 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. So 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.

Well, 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?

Yes. So we pointed out just in this call that one of the key things we are focusing on now is expanding the corporate development partnership activities. And we mentioned that we are presenting at the most important conference every year, which takes place in San Francisco in early January, and we are presenting company on Wednesday on -- at that conference itself and that allows for more meaningful discussions, which is the hotspot for business development activities at this conference, and we will make sure we are present in that regard.

Okay. Well, 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 -- and the risks are so low and it's oral that I just can't fathom that it wouldn't get approved, but that's just me. I wish I had a vote.

We would agree. Thank you for your vote as well.

Tom, are you there?

Yes. As long as I'm still on, is there a mechanism of action for COL24A1?

Yes, there is. And this will be now published in a peer-reviewed paper. But in summary, I can say that Collagen 24A1 is the ingredient -- key ingredient of the extracellular matrix called ACM. And when you look at pictures of brain neurons or astrocytes, you always see this very nice connections or network like a web -- spider web description or pictures. And in the background, it's always like pitch black.

And you're wondering this is how the brain looks like. And of course, it doesn't. It does not. And this background is actually the extracellular matrix, and that's where these neurons and astrocytes are sitting on in your brain. And 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 better in tau. So it's further upstream, closer to the origination of the pathology of Alzheimer's, if you like, that is impaired. And for that reason, we found that patients with a wild type with not mutated collagen genes, they respond extremely well. And we see effects of in ADAS-Cog13, minus 4.7 in the patients with that effect with that wild-type gene. And in the CDR sum of boxes, the scores go up to 1.4, minus 1.4.

And these are really very unprecedented effects of benefit. And we pointed out that, that means patients are actually almost not declining or declining less than prodromal patients, which are less impaired. So that's quite impactful. And so this is really intriguing science, and it will be published in a major peer-reviewed paper very soon. So extremely intriguing and also consistent with the mechanism of blarcamesine.

Great. Okay. Well, that's it for me. I'm just excited to see this ABCLEAR data get examined by the CHMP as well.

I appreciate it. Thank you.

Thank you for the question, Tom. The next question is going to come from Jesse Silveira with Spirit of the Coast Analytics.

Can you hear me all right?

Yes, you're fine. Go ahead, Jesse.

This is Jesse Silveira from Spirit of the Coast Analytics. Some of these questions you've kind of addressed a little bit earlier, but hopefully, you can maybe provide some additional color on some of them. Yes, just to reiterate kind of one of your previous points. So my first question is sort of an assumption, though I think you got at it earlier. But 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 the reevaluation?

That's correct. That's correct.

Okay. Got that. And perhaps adjacent to that conversation, do you think you can give more detail on a statement that was found in the 14 November press release that stated the company intends to request a reexamination 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?

And is that some of the data that you may or may not be presenting to the EMA?

That's accurate. So the advantage of the biomarker is that the biomarker endpoint is objective and it cannot be influenced by a patient, by the caregiver or the physician or anybody else, as a matter of fact, because it's objective. And 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 and while, for example, the clinical effect was not yet significant. And that is something which we like to point out that the analogy is in Alzheimer's, the clear pathological shrinking of the brain, which is one of the first features Alzheimer himself actually identified in his patients with Alzheimer's, the first patient he assessed. Subsequent later on, when he looked into the brain, he found this additional apparent features of proteins then identified as a better plaque or tau.

But the first thing he identified was really that the brain shrinks and the holes, the gaps widen in the brain. And that's really the pathological logical consequence of a declining brain, less functional brain and it's like a lemon which is drying up. You cannot squeeze anything out of it. And that is really a strong objective biomarker and biomarker endpoint for demonstrating an objective effect of a drug, and that was demonstrated with blarcamesine. So we just want to make sure that gets visibility.

And part of this is also a correlation analysis that we are able to find that not only that there's a shrinking -- 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 ADAS-Cog13 subdomains, for example. For example, learning and reading and writing is in one area of the brain, that is improved in the clinical trial for the patient in that same region of the brain responsible for that, that also is less impaired in the active blarcamesine treatment arm compared to placebo. And if you can find this, this further confirms the true effect of the drug, and that will be convincing in our opinion.

Yes. I think that's really interesting. I'm definitely looking forward to that. And I think kind of related in light of the semaglitude failure is that they reported that the drug had improved biomarkers, amyloid, maybe tau, I don't recall about tau, but -- the improved amyloid, but had no clinical effect, no improvement on CDR Sum of Boxes. And 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.

But moving along kind of on September 9, the company PR really impressive ABCLEAR3 comparisons to prodromal populations and had a detailed follow-on analysis of ABCLEAR3 and ABCLEAR3 subpopulations in a GWAS preprint a little bit later. ABCLEAR3, in particular, appears to showcase an effective functional cure in early Alzheimer's patients. And you covered the mechanisms of these earlier. But can you give further color on ABCLEAR1 versus ABCLEAR3 and ABCLEAR3, specifically, whether they were prespecified or exploratory and how regulators may or may not view these subpopulations in light of being exploratory or being prespecified. Is this something you can talk about?

Yes. So the definition of ABCLEAR1, which basically is the wild-type sigma-1 gene, which was identified already in the beneficial effect of that gene in the previous preceding Phase IIa study, which was published 2020, where we identified that patients with the sigma-1 wild type, which represents 70%, 7-0 of the population had a better response to blarcamesine than those with the respective mutation. It's a point mutation, and that's how biology is 30% of overall population, that's not patients, but overall population has a point mutation, RS180866 and this one mutation changes the confirmation 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 blarcamesines through sigma-1 activation as its ultimate effect. And so the patients with the wild type, the fully functional non-mutated gene respond better. So this was identified in the Phase IIa.

So we prespecified the analysis of the primary endpoints as well as the secondary and exploratory endpoints with this in mind, how would patients do in the Phase IIb/III study with the wild-type sigma-1. And that was prespecified, and we now define this as ABCLEAR1. And we did indeed demonstrate, or it was demonstrated that indeed, that was confirmed blarcamesines increased effect of patients with that 70%, roundabout the number of patients, 7-0, which improved better than the patients with the mutation. And that is improving. So now ABCLEAR2 was the result of a preplanned in the trial, we did a whole genomicome analysis.

That means we looked at all patients in the study and analyzed their genes and genes expression and response to the drug based on the genetic profile as well. That is the DNA of all patients. And in this analysis, which was preplanned, we found to our surprise unexpectedly, one gene showing up as an extremely strong driver of efficacy, and that gene turned out to be the collagen 24A1 gene. And that gene, I explained it just before, is involved in the buildup of the extracellular matrix. And that's really, really intriguing novel science and underappreciated or overlooked up to now by the -- in the field because everybody always looks at the neurons or the astrocytes or the areas of active involved in the brain.

But the extracellular matrix is where all these neurons and astrocytes are residing or sitting on. It's like a pavement, like a street. And if that street is not smooth, like a highway or like a pavement, then these neurons cannot function well. And we were able to find them because the patients with the mutation of this collagen in this extracellular matrix did not respond so well to blarcamesine, representing that they're not as viable as the respective wild-type carriers. And the good news, though, is the collagen wild-type represents 71% of the overall population.

And that was also found in our trials. We had roundabout 70% with patients with this collagen wild-type gene. So very intriguing new data, and that was, as a consequence, was preplanned in the study, of course, not prespecified because we found it in the analysis of the Phase IIb/III study.

Okay. And it's my understanding that Leqembi and Kisunla were both approved after a CHMP reexam, and that subpopulation data enriched their filing by conferring a more desirable like safety efficacy access. Is that true? And is this any way relevant to Anavex's current position with some of this data, the ABCLEAR2 and ABCLEAR3 data?

It's correct, both lecanemab and donanemab, and these are run by large pharma companies. They had been, although prior approved in the US reached the same point as we did just as we communicated a few weeks ago, and they underwent the same reexamination and we're able to get approval. I don't 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 reexamination process. But what it boils down to in the assessment of lecanemab and donanemab was the assessment and the judgment of benefit needs to outweigh the risk. And our drug has safe safety, has no ARIA, and we talk about the efficacy, which we just discussed. But we cannot anticipate, of course, an outcome of the regulatory review.

Okay. Understood. And moving forward, will you be immediately refiling for the EMA reevaluation? To my knowledge, it took about 3.5 to 4 months for the CHMP to give Leqembi and Kisunla their next opinions, respectively. So maybe we could see something around April. Is that about what you're projecting?

That's correct. We will immediately ask for the reexamination as soon as possible. And again, while there's never certainty to obtain approval from regulators, we remain highly excited about the science and the data.

Okay. And 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's Europe and even the US Alzheimer's Association kind of put together persuasive arguments for the CHMP to consider during the Leqembi and Kisunla reevaluations. 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's really not for us to make that move. And the community is aware of our drug, and we let them basically do what they think is appropriate. And what we only can do is point out the data, and this is a process, and we are committed to this process. But also very importantly, with this process, we gain also confidence with the regulators. We are doing this in a partnership. We are doing this in an open discussion. And we are also getting the -- 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. Well, I see that we're nearing time. So 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 and the efficacy has been absolutely unprecedented in these megalithic effect sizes were achieved in a really small population, which should theoretically make it more difficult to do. So I think it's a clear win for patients, caregivers and payers. And I think part of the problem the first time around may have been that it was sort of piecemeal analysis and you're introducing analysis as you were going.

But now that you have all analysis at your disposal and a clear narrative, it's my hope that the company will use the reexamination to tell blarcamesine story and earn the approval it deserves. So I hope you have a good rest of the day.

We appreciate the kind words. And our expert advisers advises us also to proceed and so do the patients and investigators, they also advise us to proceed, and we remain committed to do our best. Thank you.

Yes. Thank you, Jesse. And Dr. Missling, I don't see any further questions at this time.

Thank you. So we are thankful for your continued interest and trust in Anavex and wishing you a happy and blessed Thanksgiving. But 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's patients with a clinically meaningful efficacy profile of slowing cognitive decline by more than 30% and sometimes even higher for certain populations and its acceptable safety profile as demonstrated in the Phase IIb/III program. Thank you very much, and 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.