Hi, good morning, everyone. Thanks for joining us for our 45th Annual Healthcare Conference. I'm Vishwesh Shah, an associate on the biotech team here at TD Cowen. It's our pleasure to introduce Dr. Christopher Missling, CEO of Anavex Life Sciences. Thank you very much for the very kind introduction, and thank you for inviting us to this conference. I'd like to share with you Anavex Life Sciences. Since we're doing a forward-looking statement, I'd like you to read this. "We are dedicated to pushing the boundaries of scientific discovery with novel oral small molecules tailored to potentially offer hope and relief." I'd like to share with you the worldwide direction of Alzheimer's disease pathology, which is increasing in some areas almost exponentially. It's important because probably these numbers are underestimated. A recent paper came out pointing out that minorities are probably underestimated in this entire estimation. This is also across the globe that these numbers might actually improve. It will increase, actually, which is not good news for the overall population for Alzheimer's. It means we need really a treatable, easy-to-administerable solution for this horrible disease of dementia. Since we're able to address many diseases these days, hip can be replaced, kidney can be replaced, and cardiovascular diseases are addressable these days. The only area where we have an unmet need is the brain right now. That's what I'd like to address. With our small molecule approach, which is upstream, I'd like to share with you the mechanism in more detail. Let me give you an overview of where we stand. We're now in a submission stage. We submitted to EMA with a market authorization application since November, which was accepted a month later in December. We're also in the process of meeting with other regulatory bodies around the world to share with them the data we have. We're also in a comfortable cash position. We have run about four years of cash and no debt at this point. I'd also like to point out in terms of putting this in perspective, blarcamesine's Alzheimer's data, phase II-B/III, we have demonstrated numerical superiority of the efficacy as well as safety compared to the currently in the U.S. approved antibody, which are injectable drugs, Leqembi (lecanemab) and Kisunla (donanemab). We also demonstrated a reduction of neurodegeneration, which the antibodies have not demonstrated yet. Again, this gives us a good platform to work from with our early once daily, convenient and scalable potential treatment with good AIP protection as well. I point out the importance of early available treatment options, especially in areas like the Midwest or in Europe, in Poland, Romania, and other areas of Eastern European. There's just not enough MRI centers or PET centers which are required, for example, for the identification for the beta level for the antibodies and/or for the administration safety observation, which is mandatory since the antibodies received black box warnings, and that made them also hard to implement and scale in the larger regions. An oral once daily treatment, which does not need those complex logistical challenges, is probably more favorable to address these unmet needs. We also have other indications confirmed. So we're talking about a platform within Anavex with the approach of upstream activation of restoration of homeostasis. We have demonstrated data in Parkinson's dementia. We're planning a Parkinson's study as well. We also have a rare disease franchise with a liquid formulation, which is different from the oral once daily formulation for Alzheimer's disease, which is targeting unmet rare diseases like Rett syndrome. We're also moving forward after very encouraging data, preclinical data in Fragile X, infantile spasm, and Angelman in these indications. At the same time, we also have other compounds in the pipeline that includes oral solid available ANAVEX 3-71, which is a completely different molecule and has demonstrated very solid data in preclinical animal models of FTD and Alzheimer's disease. It's running right now a phase II study in schizophrenia, which I will talk more about in a minute. I'd like to highlight now the precision medicine approach of the mechanism, which is really focused on upstream restoration of neural homeostasis via sigma-1 activation. The most interesting target of this beneficial effect is the autophagy restoration. In a nutshell, what happens in the body naturally is to restore balance or homeostasis. This is done through this protein, which is called sigma-1 receptor. We all have that. If you have chronic manifestation of a pathology, and that's not limited to one indication, that's why we mentioned here, for example, Alzheimer's or Parkinson's, it's been shown that the sigma -1 levels are reduced. It's not because they don't want to be there. They want to be there, but the activators, which are endogenous sigma -1 small molecule endogenous activators, agonists, are depleted because of constant requiring them to be available. What we can do now from the outside, we can now send in the activators, small molecules like blarcamesine or ANAVEX 3-71 into the system and increase again the level of sigma -1 proteins to counter the pathology, which then leads to beneficial therapeutic effect to the patients. That's described in the autophagy restoration, which is a compensatory therapeutic intervention in Alzheimer's disease, which is not only challenged by the presence of a beta or tau pathology, but also general aging to survival of the brain cells. The current treatment paradigm, the most advanced, is the antibodies, which, however, have the disadvantage to be injectable and come with a safety challenge as well. They only are also downstream only. They're able to only remove beta amyloid. You have to have a patient with a beta amyloid level. Without that, you cannot even approach this treatment approach. Compare this to our blarcamesine approach, where we give the drug once daily, and it not only removes the beta and tau pathology, but also it's more upstream beneficial to the autophagy restoration, is removing and also repairing and regenerate and building resilience in the system in a holistic way. This brings the approach of neurology to another level. I'd like to now move to what's ahead of us. It's a long list of accomplishments we already have accomplished, and many of these features we already accomplished this year. For example, we submitted a fully regulatory package, which, by the way, is more challenging than in the U.S. because you have to have the package complete for EMA submission. There's no rolling submission, and it was accepted in December, as I mentioned. We also have provided a publication of the phase II/III data, and just recently was in January. Everybody can see, and very nice to see the details of the study, how it was executed. We are now ahead of us to provide details of the already provided top line data of the attention AD study, which is the extension study open label of over three years in totality, four years if you include the placebo-controlled part. That leads to the top line data, additional data to be shared at the upcoming conference in April at the AD/PD 2025 in Vienna. At the same time, we're now expecting data readout of our ongoing schizophrenia trial for ANAVEX 3-71, which is moving very nicely. We are enrolling patients swiftly, and so we expect to read out in the first half of this year. We're also expecting to initiate, we are getting ready for a Parkinson's disease study. We are fine-tuning the design. Parkinson has gotten a lot of challenging outcomes recently. We want to really make sure that we are falling on the right side of history and making sure that all the I's are dotted and T's are crossed to make sure that we have a very good chance of increasing the chance of success of such a study. We are moving forward with the rare disease franchise, we have a Fragile X study ahead of us, and also are now in the process of planning the additional Rett syndrome study. You will see more publications showing up. Last but not least, I also want to mention that we also have demonstrated with our compounds, both ANAVEX 2-73, blarcamesine, as well as ANAVEX 3-71, long-term benefit in terms of prevention of the pathology in preclinical animal models. It is important to demonstrate the therapeutic intervention area or time point of the drug, but also looking into the future and seeing what could it hold up in terms of potential prevention and regeneration medicine comes to mind here as well. The overall picture is really of a promising pipeline with potential progress towards commercialization. We have several studies already executed, completed. Additional studies are planned or ongoing. It is really also a balanced portfolio with different molecules in the pipeline, with all share one common trait, which is upstream small molecule oral activation to help the body to help himself and provide benefit to patients. Clinical milestones ahead of us. To give you a background of what we have accomplished so far in Alzheimer's disease, we have completed a phase I study for blarcamesine and a phase I study for ANAVEX 3-71. We completed a phase II- A study in Alzheimer's disease and a phase II/III study in Alzheimer's disease. We have now an ongoing dialogue with the regulatory bodies at EMA this year, and we expect a review of this by the end of this year. We are planning also to move forward eventually with ANAVEX 3-71 in Alzheimer's disease. I think it's like important to also take a quick snapshot of the future. Potentially, blarcamesine could be used prophylactically in order to prevent the loss, what I refer to as reduction of sigma-1 levels, and what we have seen beneficially to be the case in animal models of the disease. This could be something which has been demonstrated preclinically, and blarcamesine significantly prevented a beta-induced cognitive deficits, which confirms the significant biomarker response in an animal model of Alzheimer's disease. It was also demonstrated dose-dependently, which shows the prevention of a beta pathology, and it correlated with a cognitive improvement with the drug, resulting in future blarcamesine treatment options, which are an orally convenient and scalable potential treatment. To Parkinson's disease, we completed the phase II in Parkinson's dementia, where we basically looked at both the feature of the drug in terms of its approach or ability to address the impairment of the movement disorders, which is the Parkinson's part, as well as to confirm if the drug also in other pathologies beyond Alzheimer's disease would be able to demonstrate improvement in cognitive features. That was accomplished, both of that with a proof of concept study in 132 patients, placebo-controlled. We demonstrated in both domains, we saw benefit both in the cognitive domain as well as in the Parkinsonian domain. We were planning now for that reason to move ahead into a larger study in Parkinson's disease, given the unmet need, and also requests from physicians and advocacy groups to do that, given the unmet need, and also eventually to plan ahead with a Parkinson's dementia study in that regard to confirm what we saw in the phase II. Regarding the Rett syndrome paradigm or program, we demonstrated a really encouraging in three studies in different age groups, both adults in two studies, as well as in one study in pediatric patients, a signal of efficacy of the drug. We have now realized that we know much better now what to do now in a future study, which is like identifying the right dose and the right paradigms of the study. That's very encouraging to have accomplished already with these studies a very strong support also from patient advocacy groups. As a matter of fact, all patients in these studies have accepted or requested actually to go on compassionate use after the open label studies, which were 48 weeks in addition to the studies which lasted up to 12 weeks. The feedback from these compassionate use programs demonstrates some potential for real-world evidence where some parents reported, and I want to share with you that patients with Rett syndrome cannot speak, they cannot walk, they're very impaired, and it's a horrible disease that they have to sustain. There are around about 10,000 patients in the U.S. alone. We saw very intriguing and encouraging feedback that a patient has apparently, the feedback was we did get a surprise once with the mobility. We heard a noise from the family room. The next we looked, Madeleine had climbed 12 steps upstairs to her bedroom by herself, again with movement impairment and wheelchair bound. Jayne reports with a week of starting the Anavex open label extension study, she only had one seizure, and then she went three months without seizure. These are additional stories which you can look up in the website at RSAA website. I would like to also point out there was a high switch from the open label into the compassionate use program. Some patients are now over four years on the study drug and apparently would not do that if they would not feel well about it, both from a safety and efficacy point of view. I would like to switch over to the Alzheimer's disease study, which is the 48-week study where we tested the blarcamesine against placebo in 508 patients. The key endpoints are ADAS-Cog13, ADL, and CDR Sum of Boxes. I would like to first share with you what is really common sense, and it is expected to be very intuitive that Alzheimer's disease pathology describes itself clearly as shrinking of the brain, enlarging of the ventricles, which are the holes in the middle of the brain. A normal brain has much voluminous brain matter. We looked at the changes from baseline to end of trial of the placebo arm as well as the active arm. This is what we noticed in almost all regions of the brain. That is the whole brain, the total gray matter, the parietal lobe, the temporal lobe, the limbic lobe, insular cortex, and frontal lobe showed a significant delay of the shrinking of the brain and respective enlargement of the ventricles. Very encouraging to see this biomarker of effect, which is within the ATN biomarker spectrum, represents the N neurodegeneration spectrum. I would like now to move to the attention AD study, which read out, and we provided top line data recently. You have to think of this as the placebo-controlled studies finishes. Some patients, after some little break, sometimes different patients took longer to stay on a break because there was also during COVID time that this was not possible to get them right away, the drug in the open label study. In a way, however, you could measure now what happens to patients from the very beginning, who had the benefit of the drug from the very beginning to the end of the open label study, which is a total of 192 weeks, which is around four years. Compare that to the outcome from those patients which were first on placebo, which did not get the drug right away, but got delayed with getting the drug by 48 weeks later. What would be, if at all, the difference between these two arms? That is referred to as the delayed start analysis. You compare the continued blarcamesine arm early start group versus the placebo to blarcamesine arm, the late start group. This is what we found as an outcome. First of all, there were no safety challenges over four years that includes also in the which are of concern. There were also no deaths related to the study drug in the entire study, which is also important because if you remember, the antibodies both have a black box warning, which says you can die from this drug, and that's happening, unfortunately, the antibodies have that problem. The efficacy output is very intriguing and encouraging because it shows clearly that the effect of the patients which were early starters had an improvement delta to those who started later of minus 3.83 in ADAS-Cog13. In the ADCS-ADL, which is function, of plus 4.3, it's the opposite. ADL, like ADAS-Cog13, improvement is minus for ADAS-Cog13, improvement for ADL is plus. Both are clinically meaningful and shows really like you do not want to delay the initiation of treatment if you know you have Alzheimer's because you lose significant function and cognition if you do that. The earlier blarcamesine treatment is suggested in order to have a continued long-term benefit therapeutic event effect. Also, last but not least, I would like to point out that the scores are considered clinically meaningful. That means the patient notice, the caregiver notice, as well as the physician notice that a paper recently pointed out that a score of ADAS-Cog13 or ADAS-Cog of larger than two points is considered clinically meaningful. This is the paper I was referring to. It It came out in January. Please take a look at this open access, but demonstrates oral administration of blarcamesine, novel target, which novel mechanism of action, which impacts positively neurodegeneration and with promising clinical results. You see on the right side, that's how the capsules actually look like. Now I'd like to move to the preparation we are doing right now. I'd like to mention since JP Morgan, it was also the right the time around when the paper came out, we started getting a lot of inbound calls from pharma companies, and that has actually accelerated recently. I think that's possibly also because of the paper came out, and that's encouraging because it's clear that Alzheimer's disease is a very large indication, which you need a partner to execute and implement the marketing for that. At the same time, we're also engaging with payers already and with a patient advocacy group to raise the awareness of blarcamesine and its potential, given its orally once daily impact and its nuanced efficacy and safety features. The whole picture of the targetable, addressable market is, of course, significant for Alzheimer's, both in the U.S. as well as in Europe and rest of the world. We're talking about 6.9 million patients in the U.S. alone, 7 million in Europe and Asia 23. Similarly, Parkinson's disease and schizophrenia, very large markets. Schizophrenia is 1.6 million patients in the U.S. and 3 million in Europe and 9 million in Asia. So are the rare diseases of relevance for you to be able to make calculations, your own calculations. I would like to now talk about the patent protection, which is very important. We were recently awarded a patent for composition of matter for blarcamesine up to 2039. We really have worldwide tried to be really mindful of building a very good patent portfolio worldwide in Europe, Asia, Pacific, and the U.S. in all our compounds. Last but not least, I'd like to give you a snapshot of our financial situation. We have run about four years of cash. We have no debt based on the last year cash utilization rate. These are the calculations. We also like to thank partially the reason for this is for certain support groups, which I'd like to mention here, the Michael Fox Foundation, which was supported very generously for Parkinson's disease, as well as the Rett Syndrome Foundation. This allows for a sustainable cash runway due to disciplined operations and non-dilutive cash sources. I also like to point out we have a strong team with background in large pharma and execution. I'd like to especially highlight Kun Jin, who came from the FDA with 27 years of experience as the lead statistician. He knows the inside out of that agency, of course, which is good to have. We also have strong support from key opinion leaders relevant for the indications and very supportive. You might recognize some of these names. In summary, I'd like to point out what is really important, what could drive neurology to another level with oral once daily solutions. For indication, really requires a simple solution without complex logistical challenges. This is really the scalability of blarcamesine. We also believe that we're able to overcome the diverse population challenges and hence maintain a sustainability maybe, which is challenges in the global healthcare system around the world, not only in the U.S. With that, I'd like to thank for your attention. If you have more need for information, please come to visit us at anavex.com for more details and information on the website. Thank you very much.