Good morning, ladies and gentlemen, and welcome to the Annual General Meeting of Alterity Therapeutics. Excuse me one moment. We'll just let some more people arrive into the meeting. I'd also like to welcome shareholder and guests joining us via webcast. My name is Geoffrey Kempler, and I am the Chairman of the company. Can I please ask everyone to place their electronic devices on silent? I'm advised that the notice of meeting has been properly dispatched and that a quorum of members is present. Accordingly, I declare the meeting formally open, and thank you all for your attendance today. I'm pleased to introduce my fellow directors, Mr. Lawrence Gozlan, Non-Executive Director, and Mr. Peter Marks, a Non-Executive Director and Chair of the Remuneration Committee, who's joining us via Zoom. Mr. Brian Meltzer, a Non-Executive Director and Chair of the Audit Committee, has provided his apologies for this meeting. Also present is Mr. Jon Roberts, our audit partner at PricewaterhouseCoopers, and the team from the company share registry, Computershare, who will assist in polling votes. Thank you. Our Company Secretary, Phillip Hains. The order of events for today's meeting will be as follows: I'll first say a few words about the past year of Alterity. We'll then proceed with the formal business and the resolutions of the meeting to consider any questions on the resolutions. Then we'll hear from our Chief Executive Officer, Dr. David Stamler, via Zoom from San Francisco. So we're very much looking forward to his comments. I'm pleased to share with you my chairman's address for our financial year 2023 annual general meeting for Alterity Therapeutics. We're hosting this meeting in person, in Melbourne, and virtually, to ensure all of our shareholders, employees, and corporate partners are able to join us. We've had a strong year at Alterity, with progress on many fronts as we move closer to our goal of improving outcomes for people with Parkinsonian disorders, including Multiple System Atrophy, or MSA. Let me start by discussing our clinical progress. Most importantly, we successfully completed enrollment in our ATH434-201 phase II clinical trial, a double-blind, placebo-controlled study for participants with early-stage MSA. This is a significant milestone for Alterity as we move one step closer to bringing a new oral therapy to people living with this devastating condition. Because MSA is a rare disease with no approved treatments targeting the underlying pathology of the disease, the interest in our trial is extremely high, and we consequently exceeded our enrollment targets. Study treatment will conclude in the fourth quarter of 2024, and the results from that trial, from the trial, will clarify the path forward for potential approval of ATH434. The trial is being conducted at over 20 sites in the U.S., Australia, New Zealand, and Europe. Physicians across the board have received the trial enthusiastically as they implement Alterity's novel methods to diagnose, evaluate, and treat early MSA. In July, we passed a critical catalyst in the trial when we received feedback from an important data monitoring committee, who reviewed clinical data from an initial cohort of study participants. The committee expressed no safety concerns and recommended that our trial continue without modification. During the year, we also commenced a new and separate phase II clinical trial, known as ATH434-202. This open- label biomarker study will allow us to assess the efficacy of ATH434 in participants with greater MSA severity than in the double-blind study and will give us valuable information for the next phase of development. Because the trial has the same key biomarker endpoints used to assess efficacy in the double-blind study, it may give us an early indication of efficacy. Clearly, clinical measures important in MSA will also be assessed. And finally, our BioMUSE Natural History Study is helping to improve patient selection and identify appropriate biomarkers that will inform clinical trials in MSA, including our own ATH434-201 study. The study continues to generate valuable information by assessing a diverse set of biomarkers to augment clinical criteria for MSA that will greatly improve the diagnosis of this devastating disease. Data presented also demonstrated that wearable sensors can quantify impairment in MSA patients that is not captured by neurological examination, an important component to those living with the disease. We also continue to generate promising data on our lead asset, ATH434. Earlier this month, we presented new data indicating that ATH434 can preserve mitochondrial function after oxidative injury and exert direct antioxidant activity independent of its iron-binding properties. While we have long known that ATH434 is able to reduce labile iron. The demonstrated mitochondrial protection may reveal additional mechanisms that augment its ability to slow disease progression. Our research team also continues to produce novel patentable compounds covering several neurodegenerative diseases. In August 2023, we secured a new composition of matter patents in Europe, providing broad protection over a new class of iron chaperone drug candidates for treating major neurodegenerative diseases, including Alzheimer's and Parkinson's disease. In March 2023, we licensed the use of a separate patent family of more than 100 compounds, along with our product candidate, PBT2, to Professor Colin Masters, to advance the compounds for the treatment of Alzheimer's and related diseases. Professor Masters' research on the beta- amyloid protein that forms the cerebral plaques in Alzheimer's disease has laid the foundation for extensive research on the disease and recently approved treatments. Our collaboration with Professor Masters broadens the opportunities for our clinical development efforts, and I'd like to thank Professor Masters for being here today. I'd like to thank our CEO, Dr. David Stamler, and his executive team, as well as our scientific and operational staff, for their work and dedication to advancement of our development programs. To our shareholders, thank you for your support as we gear up for another exciting and productive year for Alterity. We look forward to updating you on our progress for fiscal year 2024. Thank you. That brings me to the end of my comments. We'll now move to the formal business. I notice that the notice of meeting has been appropriately dispatched to all shareholders and other persons entitled to receive it within the notice period. The matters requiring consideration today are outlined in detail in the notice of meeting. The notice will be taken as read. Alterity Therapeutics' financial statements for the 2023 financial year and the auditor's report are in our annual report, which is available on our website. Resolution one is a non-binding resolution that requires at least 75% of votes cast by shareholders to be in favor of the resolution to pass. Resolutions two to four are ordinary resolutions that require more than 50% of votes cast by shareholders to be in favor for the resolution to pass. Resolution five is a special resolution that requires more than 75% of votes cast by shareholders to be in favor of the resolution to pass. Today's voting will be conducted by way of a poll on all business items. If you have not already voted or wish to change your vote, please submit your proxy cards to Computershare representatives at the end of the meeting. Proxy votes submitted prior to the meeting will be set out on slides shown for each resolution. For context, Alterity currently has approximately 2.4 billion shares on issue. Proxy votes cast during the meeting will be counted after the end of the meeting, and the results will be published on the ASX and on Alterity's website. Shareholders have appointed the chair of today's meeting, myself, as proxy voting, either for, against, or with discretion for all resolutions, and as indicated on the proxy form and in the notice of meeting, my intention as chair is to vote all discretionary or undirected proxy I hold in favor of each resolution. The first item is to receive and consider the company's annual financial report for the financial year ended the 30th of June 2023, together with the declaration of the directors, the directors' report, the remuneration report, and the auditor's report. The company's auditor from PwC is available to answer any questions concerning the conduct of the audit, the audit report, the company's accounting policies, or the auditor's independence. Are there any questions in relation to the financial year 2023 annual report or of the auditor or management? There are no questions at this time. As there are no further questions, I hereby table the accounts, and we shall move on to the resolutions. The first resolution is to adopt the remuneration report, and I'll take the resolution as read. The proxy results are available on screen and will be determined by poll at the conclusion of the meeting. Are there any questions related to resolution one? There are no questions. Resolution two is the re-election of Director, Mr. Peter Marks. The proxy results are available on the screen and will be determined by poll. Are there any questions with regard to this resolution? Well, sorry I couldn't be there. I've just got a cold and sort of flu. Didn't want to be coughing on everybody, so I thought it was safe to be offline than be here. Okay. Thanks, Peter. Thank you. Next resolution is the re-election of Lawrence Gozlan as a director. The proxy results are available on the screen. Are there any questions with regard to this resolution? No, no more questions. No questions. Thank you very much. Next resolution is with the ratification of prior issue of shares. The resolution appears on your screen. I'll take it as read. The proxy results are available on the screen. Are there any questions with regard to this resolution? No, no questions at this time. Thank you very much. The last resolution is the approval of the 10% placement issue. The Resolution 6 approval for the additional 10% placement capacity available under the ASX listing rule was set out in the notice of meeting. I'll take it as read. The proxy results are on the screen. Are there any questions in relation to this resolution? No questions in relation to the resolution. Thanks. Thank you very much. So we now have an opportunity, prior to hearing from our CEO, to see if there are any general questions that are not related to the resolutions that our shareholders have asked. Moderator, do we have any? I'm sorry. We have none. Okay, so as there are no questions, are there any questions in the room? As there are no questions, I'd like to thank shareholders for your participation today and your ongoing support for Alterity Therapeutics. And it includes—this concludes the formal business of the meeting. Please submit your proxy forms to the Computershare representative now. The final results of the polls will be released on the ASX as soon as they are available, and I now declare the meeting closed. I'll now hand over to Dr. David Stamler to make a presentation, to provide an update on the company's research and development activities. Thank you, David. Well, thank you, Geoffrey, and it's nice to speak with you again about the great progress we've made over the last year. As with Peter, I'm very sorry I can't be there in person, but I'm definitely there in spirit, and I'm excited to tell you about the great things that have happened over the course of the last 12 months. As I bring up my presentation, I'm gonna wait and to make sure it's loading properly. I will now move it to... These are our forward-looking statements. I encourage you to review anything about our risks in our 20-F filed with the SEC or the Australian equivalent. Okay, as many of you have heard before, Alterity is an English word that means a state of being different, and it really captures what our mission is, which is to change the state for people living with these terrible neurodegenerative diseases. And our goal is really to modify the course of their disease through our development of disease-modifying therapies. Our lead product is called ATH434, which I will refer to just as 434. And this is our novel drug candidate for targeting proteins that are implicated in neurodegenerative diseases such as Parkinson's disease and related disorders. One of those related disorders is referred to as Multiple System Atrophy, or MSA, which is a Parkinsonian disorder. But it's a rare disease, and there's no approved therapy for it. It is an orphan disease and has the designation for orphan status from both the U.S. FDA and the European Commission. We've made excellent progress over the last 12 months with our phase II program, and we have 2 ongoing phase II trials. One is the randomized, double-blind, placebo-controlled study that Geoffrey referred to in his address, and the other is a biomarker trial in more advanced patients. I'll be updating you on these trials in greater detail. We also have made continued progress in our patent portfolio with filing and approval of new patents. As we have progressed through our development of this compound, I've been very happy to have participation from our head of nonclinical development and our head of clinical development, who with me have achieved success in bringing 3 neurology-related drug approvals through the FDA. Now I'll be talking about Parkinsonian disorders, which represent a very significant unmet need in many diseases. Parkinsonism is a syndrome of motor symptoms that we've all seen in friends or family members. And this includes the slow movement, stiffness, or tremor. And it gets its name from Parkinson's disease. That's why it's called Parkinsonism, because Parkinson's disease is the most common cause. And it is a major source of disability, especially as the disease progresses. Now in addition to Parkinson's disease, there are other disorders that have the same motor manifestation. That's why they're called Parkinsonian disorders. One such disease is our lead indication, Multiple System Atrophy, MSA. They have prominent motor symptoms, but they also have prominent non-motor symptoms I'll tell you more about. And importantly, they have a limited response to available therapies. therapies. These therapies that are available do not address the underlying pathology of disease, and that's really what we're hoping to do with our treatment. This is a snapshot of our portfolio. The first two trials here are the trials I've told you about. The double-blind trial in early-stage disease, 201, and then the 202 study, which is the trial in more advanced patients. We've also continued to reap great rewards from our BioMUSE Natural History Study that we've been conducting since 2020. We will be presenting soon some data on the evaluation of 434 in animal models of Parkinson's disease, in a primate model of Parkinson's disease. This is an investigation that was conducted in collaboration with Michael J. Fox. Lastly, we've continued to make excellent progress with our drug discovery efforts to date, as mentioned, with our patent filings. Talking about a little bit about the biology of the diseases that we're treating. Our biologic target is this protein called alpha-synuclein, which may be a mouthful for some of you, but it's a very important protein that's present in all neurons. It really helps these neurons communicate with one another. To do so, it exists in this unfolded state that you see pictured in this cartoon on the slide. However, in diseases like Parkinson's disease or MSA, the protein aggregates, therefore it can't do its function. Nerves don't communicate well with one another, and you get neurologic symptoms associated with that impaired communication between the nerve cells. So our strategy is to really prevent that misfolding and aggregation of the protein that you see pictured in the bottom part of the slide. We address this by targeting the excess iron that is increased in areas of pathology in the brains of these patients. Now, this is a study, an autopsy study, looking at the brains of patients with both Parkinson's disease and MSA. And what you see is a comparison of affected areas in the brain of patients in blue versus controls of the same age in green. And you can see in Parkinson's disease, there's elevated iron in these areas of pathology. And in MSA, we see similar increases, but as the name implies, we have multiple systems or multiple brain regions that are really affected, and it's just excess iron that we're really targeting with our therapy. Now, if you fast-forward about 25 years, there's been great advances made in MRI techniques so that we can actually look at this iron in the brain of a living patient. And what you see at the tip of the orange arrow is the excess iron that we're measuring in the autopsy study that I told you about a minute ago. That dark red staining material actually is, the increased iron. This is important for two reasons. Number one, this helps us identify patients that we want to come into our clinical trial. So it improves our selection of patients. It also represents our key endpoint in our patient studies, really the change in the iron in these brain regions. Iron itself is critical in disease pathogenesis, and both, iron and that protein I told you about, alpha-synuclein, are strong contributors to the pathology. The iron itself, promotes that misfolding and aggregation or clumping of the alpha-synuclein protein, and it's also the root cause of oxidative stress. If you take a look at this, a diagram on the right side of the slide, you get a sense for what's actually going on. So in the center of the circle, you see the misfolding and aggregating protein, the alpha-synuclein protein. This iron imbalance you see on the right side really contributes to generation of these free radicals that you see pictured. And that oxidative stress actually injures intracellular components like DNA or lipids, and that leads to the host trying to clear that abnormal response and inflammation. So what we're really trying to do is to break this vicious cycle. And in essence, we're by targeting the excess iron in the central nervous system, we're aiming to reduce that protein clumping or aggregation, reduce the oxidative stress, ultimately with the aim of rescuing the normal function. The aim is by rescuing these neurons, we want to modify the course of disease, slow the progression, and help patients, live more, a more functional and productive life. Let's turn a little bit to talk about ATH434, which is our disease-modifying drug candidate. This is a small molecule drug, which is important, meaning it's a tablet that people can take at home. They don't require an infusion or any, injection into their body. It's an oral drug, and it acts as an iron chaperone, which means that it binds the iron in places where it's in excess, and it helps move that iron outside of those cells, so that it can be put to good use. And the drug we know is readily absorbed and reaches the site of action in multiple animal studies as well as in man. And I don't have time to review all the animal studies, but we've shown in animal models of Parkinson's disease, animal models of our lead indication, MSA, multiple different types of studies that we've seen very nice efficacy.... I've mentioned that we have potential to treat various Parkinsonian disorders associated with increased iron. And as mentioned, we do have Orphan Drug designation in the U.S. and European Union, and we've had numerous discussions over the years with the FDA as well as with various regulatory authorities in Europe. So turning to Multiple System Atrophy, I want to tell you a little bit about the disease, if you're unfamiliar with it. It is a rare disease. It's highly debilitating, and unfortunately, it's rapidly progressive. The clinical impairments are summarized here as well as in the diagram on the right. So we've talked a little bit about the Parkinsonism, that's the slowed movement the patients get. Patients also have impaired balance and uncoordinated movements that contributes to increased falls, which can cause serious injury in patients. As mentioned before, patients also have impaired autonomic function, which really means the autonomic nervous system controls things that we don't think about, our blood pressure, our respiratory rate, and the like. So these patients actually have reduced ability to maintain their blood pressure. They have impaired bladder function, sometimes leading to urinary incontinence, requirement to catheterize. They have impaired bowel function, which can lead to protracted constipation. So these, these are not trivial symptoms that really impair patients' qualities of life. Now, what you see on the right is kind of how patients manifest. Initially, with these nonspecific symptoms, then they tend to come to the attention of a neurologist when they have parkinsonism or the uncoordinated movements governed by the cerebellum. I mean, then they ultimately progress to requiring a wheelchair in more than half of patients. And unfortunately, patients have a median survival of 7.5 years. So we really hope to slow this progression and really preserve function. These are the patients we're really aiming for, the patients who have the motor symptoms, but don't yet require these walking aids. Now, one other thing I'll show you in a subsequent slide is that the excess brain iron that we see in these patients, both we've shown this and others have shown it, does correlate with disease severity. So it really supports our approach toward targeting the excess iron in these brains, in these patients' brains. Now, we successfully completed phase I a couple of years ago, where we achieved drug concentrations associated with efficacy in the multiple animal models that I've told you about. We've also had a very nice safety profile. There have been no serious adverse events in this phase I study or adverse events leading to withdrawal. They were all mild to moderate in severity. There were no findings in the ancillary tests, like laboratory procedures or on clinical labs or ECGs. So now I'd like to tell you about the natural history study, which I think is an aspect of our development program that distinguishes us from most other companies that are working in this area. As mentioned, we started this study a couple of years ago, with the aim of aiding in the design and the de-risking of the phase II trial that is now ongoing. And the goal is to really identify biomarkers to use in the end, in this treatment study, as well as to fine-tune our protocol to make sure we're getting just the right patients. So we targeted the same patients we're targeting to. We observed them for 12 months. We looked at multiple biomarkers, imaging biomarkers, fluid biomarkers, the wearable sensors that Geoffrey mentioned in his presentation, and then all the clinical endpoints that assess the impairments in these individuals. And that's with the aim of understanding what we could expect in the clinical trial. So these are kind of the summaries of kind of what we wanted to do. We wanted to optimize patient selection in subsequent trials, learn how to assess these endpoints and improve the precision with assessing those endpoints, and then pilot clinical measures to make sure that we could detect abnormalities in a patient population that we're targeting, so that if we have something abnormal, we can actually improve it. So regarding optimized patient selection, these are the advanced MRI methods that I showed you before, but these are now in early-stage patients. And we showed that we could identify an iron signature in the early-stage patients to use as our endpoint. We also showed that we could distinguish between MSA patients and Parkinson's patients in the natural history trial, which really allowed us to optimize the patient selection in the phase II study. And now our collaborators at Vanderbilt University that have great expertise in this area have been helping us develop a new MRI template to implement for measuring the iron in specific brain regions with great precision. And we have been looking at various methods for quantifying the iron in these affected areas. I'll show you in another slide on this a little more detail in a moment. Then, as mentioned, these are the clinical measures, some of the symptoms of MSA patients that look at the one over day in an individual patient, and you can see that there's a very clear change. Then also, we have secondary symptoms. So we took these measures, the natural history study, and felt confident about implementing. A little bit about that phase II study. Looks very similar to the natural history study, except now this is a treatment study. And it's a randomized, double-blind, placebo-controlled study, really the gold standard for demonstrating efficacy and characterizing safety in these patients. Again, we're looking at early-stage patients, those that are ambulatory, don't require walking aids, and that do have biomarker evidence of MSA. We targeted 60 patients, but as Geoffrey mentioned, due to the great interest in our trial as well as our molecule, we enrolled a total of 77 patients in multiple regions, as indicated here. Patients were randomized to 12 months treatment, with 2 dose levels of ATH434 or placebo. As I've referenced before, our primary endpoint in the study is a change in iron content in the brains of these patients, as measured by the specialized MRI method. We obviously looked at clinical endpoints in the study as well, those that we would hope to see and expect to see some change in clinically to demonstrate the benefit to patients. This is a diagram of the two treatments versus placebo treated for over 12 months, and this is some of the data supporting our choice of the primary endpoint, which is the change in brain iron on MRI. Here, from our natural history study, where we looked at the iron content on the y-axis compared to the clinical symptom severity, as measured by something called the Unified MSA Rating Scale. It showed a very nice correlation, which really supports our approach to prevent or reduce the iron accumulation in the brains of these patients to try and improve their symptoms. I mentioned these methods that our lab at Vanderbilt are developing. This is a nice depiction of this. So, we've learned from the natural history study that the brain distribution of increased iron varies from one patient to the next. You can't really apply a one-size-fits-all approach towards measuring the change in brain iron. Otherwise, it might be too insensitive. What we've done is we've really taken the patient's individual age and their MRI, and then we plotted the amount of iron they have in their brain, and we compared it to control patients of a similar age. And that helps us generate a patient-specific map, where you see in this color scheme areas of increased iron. The dark red material is the strong, strong increases in iron, whereas the blue-green areas are moderate increases. And this allows us to look at changes within these different regions with great precision. The other thing that's really important is that every patient, because every patient has their individual map, we're going to be able to look at change in the brain iron in those regions for each patient. And that's gonna give us the greatest precision of measuring this change in iron. Now, just pivoting quickly to our second phase II trial. This is our biomarker trial. This is a single-arm, open- label trial. So even though it's a treatment study, there's no placebo. We did this for a couple of reasons. We wanted to understand target engagement, again, like, like in the double-blind trial. We also wanted to get a sense as to whether or not patients who are more advanced than those in the double-blind trial also saw a clinical benefit, and if we could see reductions in iron. The target population is more advanced than the other study. It's referred to as clinically established MSA, but they also have to have biomarker evidence. We're targeting a total of up to 15 patients, again, treating them for 12 months and looking at the same primary endpoint. As Geoffrey mentioned in his address, we think this can give us a good insight into what we can expect from our double-blind trial because this endpoint, even though this is an open-label study, is an objective measure with no opportunity for introducing bias when assessing it. And that's why we think we can get an early look at what we can expect from the phase II study. We have continued to look at the commercial opportunity. Many companies that are interested in MSA have come and gone over the last couple of years. There's just a few of us left. And the clinicians that we've talked to over the years recognize the substantial need based on the fact that we're targeting the underlying pathology of disease and not just symptomatic treatment. They have a strong intent to prescribe. They like the fact it's an oral drug and it's not a monthly infusion or bimonthly infusion. And based on updated orphan pricing and current prevalence numbers, we now estimate potential peak sales in the U.S. of well over $1 billion, and that's just for MSA and just in the U.S. So rest of world would obviously augment that substantially. So just in summary, we are targeting an orphan disease that has no approved treatments. We've got two very nice phase II trials ongoing. We've got a very strong development team that I'm really pleased to be working with. They are really my partners in drug development. It is a true team effort. And we're very confident in the progress that we've made and our potential for future success. Regarding cash balance. We last reported AUD 16.7 million at the end of the month, and many of you know, we've recently undergone a capital raising of AUD 4.8 million. And we have announced a securities or share purchase plan at the same time as that cap raise. That will be subject to a shareholder approval towards the end of December. Clinical milestones are depicted here on the right. I won't go through all of these, but as Geoffrey mentioned, we do plan to conclude enrollment, I'm sorry, treatment in the fourth quarter of this year, and we'll be working our best to bring the study in as soon as possible after that last patient finishes. As I'll mention on the next slide, we do expect to have preliminary data from our natural history study. I'm sorry, from our biomarker study in the first half of next year. So these are the key milestones that we're aiming for. I did mention the enrollment completing. We've recently presented BioMUSE data at a scientific meeting, and we will be presenting in December data with ATH434 in a primate model of Parkinson's disease. We're very excited about these results. And then these are the two milestones I mentioned. Preliminary data from the open-label study should be available in the middle of the year, and then we expect enrollment to complete by the end of the year. I'm sorry, not enrollment, treatment. Anyway, thank you for your time and your attention. Thank you very much. I appreciate the presentation, and also, it's an exciting year ahead with these milestones coming up, and it's congratulations to you and the team, David, on a tremendous amount of extremely complex work that's been done to get us to this point. With that, I'd like to close the open part of the meeting. Once again, thank you for your presentation. Thank you, everyone, for attending either here or online, and we look forward to communicating with you again as we progress. Thank you.