Okay, welcome everyone. We've started with a showcase, and can I say welcome to the Peak Asset Management Monsoon Communications Biotech Showcase 2025. I'm Rudi Michelson of Monsoon Communications. We've organized a special showcase today. Every company we've invited, we either already back or rate very highly investable. We've been overwhelmed with the interest in this showcase. Within a couple of days of the invitation going out, we already had a couple hundred RSVPs and we had to close it down. We've got an audience also on Zoom of a couple hundred, and we expect many hundred more to watch the replay on YouTube later on. I want to congratulate you all for being biotech investors. It's a risky yet noble thing, and I hope many of you scored big time. I hope you've invested in Neuren and Telix and Pro Medicus, and that's the name of the game. When you invest in biotech, you're investing not just for the returns, but these enterprises are striving to substantially advance human welfare. Just think of Neuren, a company that only develops and commercializes new therapies for rare diseases suffered by children. Neuren exists because of investors like you, and of course, many years of research and trials by the company. There are about 175 listed life sciences companies on the ASX, and it's the third biggest biotech or life sciences exchange in the world. It all started back in 1985, when Circadian was the first life sciences company to list on the ASX. Circadian held patents covering the use of melatonin for things like jet lag and sleep disorders. Circadian's Managing Director was the great man of the biotech, Leon Serry. In those early days, though, Leon had a problem. His patents were being infringed. He was the first Aussie biotech battler, and in 1987, got on a plane to the U.S. to engage lawyers to sue Eli Lilly & Co. for $182 million. The figure was 9x Circadian's market cap. Leon Serry won, settling out of court. He got $4 million and described it as an excellent settlement. It was reported in 1999 as being the equal cost to running Circadian for 14 years. Now, how do you like that for a low cash burn rate? Leon Serry died a year ago, September last year. Beyond decades at Circadian and many spin-off investing companies, he remained a champion of Australian biotech. Leon loved personally investing in biotech, and he mentored a lot of young CEOs. That's enough for me for the time being, because I also want to introduce Niv Dagan, Co-Founder and Executive Director of Peak Asset Management, who's going to say a few words first. Thanks, everyone. Now, look, a fantastic lineup, and I just want to say thank you very much for everyone here, and also Monsoon Communications and FB Rice as well. Peak, we're a boutique investment manager and corporate advisory business, Melbourne-based. Our model is all about co-investment, so we only put things in front of investors unless we're co-investing our own balance sheet behind it. We are sector agnostic, but probably our biggest wins have been in the biotech space, and we're lucky enough to back Neuren when it was $1. I still remember John coming into the office, and we gave him a pretty hard time after that. That did fall from about $3 to $1, if you recall, and we rode it all the way up to an ASX 200 company. Same with Dimerix, we had Nina in the room, and she will be presenting a bit later on. We underwrote, put about $1 million of hard capital when the stock was around $0.08. Ali from Peak that you've met at the door is probably a major investor there as well. Some really notable names here today. I want to say thank you very much to the presenters and the speakers. Today's a little bit of networking and catching up with everyone and meeting like-minded investors and CEOs. I want to say thank you very much for attending. Just some housekeeping things. We'll try and keep it to schedule. Toilets just right up at the back. There'll be an afternoon tea as well for about 20 minutes, 25 minutes. There'll be some drinks and canapes. Today's all about networking and catching up. I want to say thank you very much and welcome. We'll hand the microphone back to Rudi. He'll introduce our first presenter. Thank you. I wanted to point out FB Rice is sponsoring this event, and we're very grateful to FB Rice. I've got a few words to say about FB Rice. Proud sponsor of this event, reflecting their commitment to a strong biotech ecosystem that supports the growth and sustainability of biotech startups and companies. Over 75 years of experience, FB Rice is Australia's leading independent intellectual property firm and home to the largest life sciences patent team in the country. The team offers deep expertise across an entire IP lifecycle, from patent searching and protection to cost savings through the R&D tax incentive program and support for commercialization goals. Thank you, FB Rice. We're very grateful. Now, we have three sessions today, and the first is convened by the CEO, Dr. Rebecca McQualter, CEO of the very promising CAR-T company, Chimeric. Please welcome Rebecca. Thank you so much, Rudi. That's very kind. No one's ever called me that this week. As Rudi mentioned, my name is Dr. Rebecca McQualter. I'm the CEO of Chimeric Therapeutics. We're a small little Aussie battler. Can I say that? That's fair, right? We have novel cell therapies targeting different types of solid tumors, namely colon cancer is our main focus. I'm delighted to be chairing today's session, and we've got such a great lineup of speakers for you today. What's going to happen is each speaker will have 15 minutes, and then we'll have five minutes for questions. Get those questions ready. Our first presenter comes all the way from the United States, and it's very late over there, actually. My team have gone to sleep from Alterity Therapeutics. This company is advancing a first-in-class therapy for multiple system atrophy, which I'm really delighted David can explain that to us and what that means. They have FDA fast-track designation in the U.S. and EU orphan designation with very robust Phase II efficacy results with a clean safety profile. You can't ask for much more than that. Please join me in welcoming Dr. David Stamler, the CEO of Alterity Therapeutics. Hello. I don't know if you can see my slides, but perhaps someone could let me know that. All right, great. Let me put it into slide mode. Good afternoon, everyone, and thank you for hearing an update on Alterity Therapeutics. We've had an exciting few months. The last six months have been very exciting, and we think the next six will be equally exciting for us. Sorry, we jumped ahead. These are our forward-looking statements. As Rebecca mentioned, about six months ago, we disclosed robust, positive Phase II data from our first phase two study in multiple system atrophy. This is a Parkinsonian disorder with no approved therapy. I'll tell you more about that disease in a moment. Our lead asset has large market potential for treating various neurodegenerative disorders because many important diseases, such as Parkinson's disease, do have the same overlapping pathology as our lead indication. Our molecule is orally administered. It is only one of a handful of drugs in development and the most advanced asset that is orally administered. Many therapies are antibodies or direct injections into the brain. Lastly, I'm fortunate to lead an experienced development team that has three CNS approvals under our belt in the neurology area in front of the FDA. This is our portfolio in a snapshot. I'll be focusing mostly on the first three lines, the clinical trials in multiple system atrophy, both the 201 and the 202 study. We just recently released positive top-line data from that open-label study, the 202 study, about a month ago. Our development program actually began several years ago with a natural history study, which I won't have time to tell you too much about, but that did help us design and de-risk our program in multiple system atrophy. As mentioned previously, we do have potential to target other orphan diseases, as well as other major diseases. Now, I'd like to tell you a little bit about how we are targeting the underlying pathology in these Parkinsonian disorders. Before I do that, I really need to explain some normal aspects of physiology and the central nervous system. At the center of our target is a protein called alpha-synuclein that you see pictured on this slide. This is present in all neurons and regulates neurotransmitter release from synaptic vesicles. Accordingly, it's really important to enable neurons to communicate with one another. In diseases, unfortunately, this protein misfolds and neuronal communication is impaired. The other aspect of our treatment that we target is imbalanced iron. This is pictured on this slide. I don't know if you can still see my slide. Perhaps someone could just confirm because I see the Biotech Showcase logo on my screen. In any case, iron exists in two forms within the central nervous system. It's critical for energy production and for the activity of many enzymes. It's also important for neurotransmitter synthesis, as well as synthesis of myelin, which is the fat sheath around neurons that enables neuronal communication. On the left side of the slide, we can picture the pathology that is ongoing in these diseases. Number one, we see this is alpha-synuclein aggregation on a brain scan, specifically a PET scan, which you see at the tip of the red arrowheads on the pictures on the bottom, both in Parkinson’s disease and in MSA. On the right, we see elevated brain iron on autopsy. This is from patients who expired from either Parkinson’s disease or multiple system atrophy. We see the patients in blue have elevated iron as compared to their age-matched controls in areas of pathology. This is really the iron that we are targeting and that we're trying to reduce the accumulation of. The way we do this is by chaperoning iron. This is a rather complicated slide, which I won't go into, but the table on the right summarizes the key aspects of the mechanism of action of our lead compound, ATH434. It redistributes iron within the central nervous system. It does it by either effluxing it from the cell, increasing its storage in normal storage proteins, or buffering that extra iron inside the cell. All these mechanisms actually reduce the amount of reactive iron that is really the driver behind the pathology of these diseases. To summarize our approach, we are really redistributing the excess iron that is in the central nervous system. In doing so, reducing the aggregation of the alpha-synuclein protein, as well as reducing the source of oxidative stress and oxidative injury. The goal there is to preserve neurons and preserve their support cells with the overall goal of improving function. I should say that before we got data from this trial, I was clearly of the opinion that if our drug works, it's because we are really preserving neurons and modifying the course of disease. ATH434 is our lead molecule. It's a small molecule, which is important because that means it can obviously be orally administered, which is preferred by patients over other available therapies that are in development. We've shown it nicely crosses the blood-brain barrier and can address pathology inside the cell. Because it targets iron that's involved in many neurodegenerative diseases, it has broad treatment potential. As mentioned at the outset, we have orphan designation in the U.S. and Europe, as well as fast-track designation, which gives us many benefits in the United States. Now let's turn a little bit to the development program. Multiple system atrophy, or MSA, is a highly debilitating and rapidly progressive disease. It is rare, it affects up to 50,000 patients in the United States. The diagram on the right side of the slide really depicts the typical natural history of the disease, where people can present with nonspecific symptoms such as urinary problems or difficulty maintaining blood pressure. They can progress to developing motor symptoms, which is when they come to the attention of a neurologist. Following that, their symptoms progress to the point where they can require a walker and ultimately a wheelchair. The autonomic symptoms can be quite disabling. As you can see by the progression and the timeline, more than half of patients require a wheelchair within five years of diagnosis. These patients only have a median survival of 7-8 years after symptoms first appear. Really very aggressive. As I mentioned at the outset, our development program in MSA actually began about five years ago with this natural history study that we did in the U.S. This is a study where we just observed patients that we wanted to study in our Phase II program. It was with the aim of trying to improve the specificity of patient diagnosis coming into our clinical trial. It was strictly an observational trial with no therapy other than standard of care. It actually helped us de-risk the phase two program such that we could identify biomarkers, both a fluid biomarker and a neuroimaging biomarker that could help us identify patients with MSA. As mentioned, I'll tell you the results of these two studies you see on the right, the 201 study and then the 202 open-label study. The 201 study is a randomized double-blind placebo-controlled study where we enrolled about 75 patients with a clinical diagnosis of MSA, but that also had elevated brain iron on MRI. That was one of the important things we learned from the natural history study. Elevated levels of plasma NFL, which is a CSF protein that is a marker of axonal injury. Patients were then randomized to either 75 mg or 50 mg twice a day or placebo, treated for 12 months. We assessed the various endpoints you see on the right side of the slide. The key clinical endpoint is called the UMSARS Part 1, and that's a mouthful, but that stands for the Unified MSA Rating Scale. The key items on this scale are shown in the right lower corner of the slide. You can see that these are the areas that are largely affected in this disease, things that can have a profound impact on quality of life, such as speech and swallowing, fine motor skills that affect handwriting or dressing or cutting food. They also affect things like walking, falling, and, as mentioned, blood pressure symptoms, the lightheadedness that comes with low blood pressure. These things are quite profound in terms of their impact on patients' quality of life. These are the baseline characteristics from the trial. There are a lot of numbers here, but what I can say is, in general, the groups were well balanced at baseline and typical for an MSA population, about five to ten years younger than a Parkinson’s population. The notable exception on balance among the dose groups is this last line, severe orthostatic hypotension. This means when people go from a sitting to a standing position and their blood pressure drops more than 30 mm, which is quite profound. You see there was a quite significant predominance of that in the 75 mg dose group. That's important because that's a marker of rapid disease progression. We think that explains, in part, the differences between the two dose levels, which are summarized on this slide. This is that Unified MSA Rating Scale. You can see the scores are on the Y axis and the time is on the X axis. The gray line is the placebo, which increases by, on average, eight points over the course of a year. If you look at the two active dose groups, the 50 mg and the 75 mg, the 50 mg declines by 48% or 3.8 points lower than the placebo group. The 75 mg dose group declines by 30% less than that 8.8 point decline, or 2.4. Those are both clinically significant because a treatment effect of 1.5 points has been shown independently to be clinically meaningful. Another cardinal symptom that I've talked about a couple of times is orthostatic hypotension, which causes profound disability in these patients. It's one of the most important symptoms. We can see that the placebo patients over the course of a year deteriorated by six points, whereas both active dose groups stabilized or actually improved slightly. This can have a big impact on whether or not patients can actually take care of themselves or have any functional activities around their house. In addition to that orthostatic hypotension assessment, we showed that 434 actually preserved patients' walking in the outpatient setting. We assessed this with this pendant that you see on the right side of the slide. It was a wearable movement sensor that they wore for two weeks at baseline and then at every three months thereafter. We looked at the change in their activity at the end of therapy compared to baseline. If you take total walking time in the top right part of the slide, you see that the placebo patients lost on average about 25- 28 minutes of walking over the course of a year, whereas the active treated patients lost just about half that time. If you think back on that natural history and the progression of the disease, that inability to walk and require a wheelchair is really quite profound. Anytime you can maximize for these patients to keep walking is really important. Now, regarding adverse events, as Rebecca mentioned, we did see a very clean safety profile with similar adverse event rates overall, similar adverse event rates for the most common adverse events that are listed there in descending order. There was no signal in terms of severe adverse events or serious adverse events. I would point out that none of those serious or severe adverse events were related to study drug. To turn quickly to the open-label study, this was a study that looked at the high dose that we studied in the double-blind study. We targeted an advanced MSA population. What we saw was in the open-label portion of the study that you see in the first data column that patients declined by an average 3.5 points on that scale, which compares favorably, slightly better than what was observed in the double-blind study. We also saw on global measures of change from both the clinical and the patient perspective that we saw a similar rate of stability. Finally, when we compare the change in brain volume between the two studies, we saw that the change, the decline in brain volume was similar. I would point out, although I didn't have time to show this in the 201 study, that the decline we saw on active treatment in the double-blind study was less than placebo, indicating that the drug actually is demonstrating a trend towards preserving brain volume. I would mention in this study also that there were no serious adverse events related to study drug, and the AEs, like the double-blind study, were consistent with the underlying disease. In summary, regarding the phase two study, the double-blind study showed that we had clinically significant efficacy slowing disease progression at both dose levels, along with evidence of target engagement and reduced iron accumulation in MSA-affected regions. I didn't have time to show you those data, but those are available on our website. In the open-label trial, we did show similar efficacy in advanced patients, as was observed in the double-blind study, with a good safety profile. We have achieved many significant milestones in the last 6-8 months with the positive data from these two studies, the fast-track designation from the FDA, as well as oral presentations so far. In the upcoming several months, we do have another platform presentation at the International Congress on Parkinson's Disease and Movement Disorders, other presentations later in the year. We are targeting an end-of-Phase II meeting with the FDA for the end of this year, where we aim to finalize our design for Phase III or subsequent studies. With that, I will pause and thank you for your attention and happy to take any questions you might have. Oh, jeez, I can't hear. Or is it still Rico? Hi, Rebecca, I just heard the tail end of that. I didn't actually hear the question. If you could maybe. Who makes up your register? Is it the majority retail or are there any stores? No, we have quite a substantial institutional register. I think our only over 5% that is on our register is Rico, but we do have several other long funds that have come in with our recent cap raise. We did raise $40 million after our Phase II data in February. Another question in the front here. Hey, Leah Mann, Alterity Therapeutics. I wanted to just know why you went with the 75 mg dose for the open label? when it looked to me from the data that 50 mg seemed to be giving slightly better results. Yeah, so when we started the open label study at the same time or shortly after we started the double-blind study, we didn't have the result. I do want to point out that the response at 75 mg was largely affected by that baseline severity of that orthostatic hypotension. As mentioned, that was present in about 25%- 30% of patients in that dose group. That is a predictor of rapid disease progression. If I were to bring up the slide again, which I won't, I'd show you that 75 mg was actually superior to 50 mg at the 26-week mark. What we think happened was we think because of these baseline differences that. I don't know how to finish his answer because he's frozen. He's back. You're back. Keep going, Dave. Yeah, anyway, the short story is we think that the 75 mg dose group is really fine, that it's a population issue, not a drug issue because we didn't see any evidence of toxicity. Actually, when you do account for some of those baseline differences, the efficacy signal at 75 mg does strengthen quite a bit. I think we'll leave any other questions, not for the afternoon tea break, but you can email David and send your questions there. Thank you so much, David, for joining us all the way from the U.S. Have a good night. Great, thanks for attending, and thank you, everybody. Bye-bye.