Good morning, everyone. The clock has just ticked over 11:00 A.M. now, we will get started on today's call. My name's Alfred. I'm from Syntara's Investor Relations team. Today we're joined by CEO Gary Phillips. As many of you will have seen this morning, there's been some new interim data released from Syntara's skin scarring trials in collaboration with UWA. This is one of the trials we get the most amount of questions for. If anyone does have questions throughout the presentation, feel free to type them into your Q&A box. If you're on a computer, your Q&A box is on the left-hand side of your screen. If you're on a smart device, it's at the bottom. Once we get through the brief presentation, where Gary will talk through the data, we'll open up to Q&A from those in attendance and anyone that's emailed questions through already. Gary, I'll hand over to you. Thanks very much, Alfred. Thank you to all of you who've dialed in, coming in over the internet this morning, at relatively short notice. As Alfred said, we put out an announcement earlier this morning, releasing interim data from our skin scarring study that we're doing in collaboration with the University of Western Australia and Professor Fiona Wood. I've got a few slides just to frame the results that we're gonna talk about, and then very happy to take your questions. For those of you who perhaps aren't familiar or just need a reminder, Syntara is a clinical-stage development company. We develop small molecule drugs that are either first-in-class or best-in-class. We target fibrosis and cancer indications. We're a global leader in a particular enzyme called lysyl oxidase, which we'll spend most of today talking about. The results we're seeing today are the result of a multi-year research program. We've done that leveraging it with a lot of external collaborations, of which the one with Fiona Wood and Mark Fear in UWA is perhaps one of the longest lasting and most productive ones. We have five studies that are either recruiting now or will start recruiting next year to lead to real value for shareholders in the company. SNT-5505 is our lead asset, an oral pan-LOX inhibitor that's in a rare bone marrow cancer called myelofibrosis. That's more than 50% recruited now. A liver cancer study with the same drug, which is due to start recruiting in this quarter. 6302, our trial in scarring, which we've got the ongoing study in established scars and another one due to start recruitment at the beginning of next year. Finally, a neuroinflammation drug that we recently had a deal with Parkinson's U.K., who gave us AUD 5 million to do a study in a sleep disorder, which is prodrome or leads to development of Parkinson's. Quite an exciting pipeline, all reached a clinical stage, which, you know, gives us many shots on goal at delivering value. Just going on to the lysyl oxidase, and just before I dive into the results, just a reminder of the way that these enzymes work and their role in fibrosis or scarring. The chart that you're seeing on the left-hand side here shows what happens during the process of fibrosis or scarring. We all have within our cells types of cells in our bodies called fibroblasts. When these the body is injured, either through a mechanical injury, a chemical scarring, metabolism, or genetics, then these fibroblasts become activated and they start producing a substance called collagen. Collagen, when it's cross-linked together into a close-knit mat, gives us the scars that we can see on our skin. It also causes the scarring that we don't see, which is in our organs, which can cause long-term damage. Now, the process of that cross-linking is called by an enzyme called lysyl oxidase. That's a family of enzymes. In the skin, it's lysyl oxidase itself and lysyl oxidase one that are the key enzymes that cause the cross-linking and therefore cause the scarring. This is a normal process in the body and is a perfectly healthy one. But if you get too much collagen production and too much lysyl oxidase released, then you get excess scarring. That in turn leads to very stiff and hard tissue. And that mechanical stiffness of the tissue, in effect, gives mechanical stress that causes feedback loop back to the fibroblast, which will then release more collagen and more LOX. It's a feedback loop that can get revved up and go into excess. That's when we see scarring, which can be problematic, both in organs and in this case we're talking about is on the skin. Now, 6302 is the drug that we're talking about today. That's given, it's a pan-LOX inhibitor, but it's given in a topical form. It's given in a cream which is applied to the skin. Like a lot of our drugs, these are very recent patents. They're 100% owned by Pharmaxis. They're not licensed in from anybody else. There's no lien on them anywhere, so we don't have to give away any royalties or anything as we develop it. A patent was filed with a priority date of 2019. This is a product with a long life ahead of it. We've got strong preclinical evidence in models of skin fibrosis and scarring. I'll touch on that in just a minute. We've already gone through Phase I, showing we had a safe and well-tolerated drug when given to healthy volunteers. Scarring, in particular, hypertrophic and keloid scarring are the sort of two areas which we've really focused in on. The number of patients who have problematic scars every year is huge. You know, it's 100 million patient that gets scarring from elective operations or operations after trauma or burns. These hypertrophic scars or keloid scars are ones where that scarring process that I talked about go into overdrive and cause excess scarring, that can and that's driven after you have the injury. These scars are both a cosmetic problem in that they often stand out, and we've all seen examples of these, I'm sure, in people that we know or even ourselves. They also cause functional problems as well, depending on where they are. They're often stiff, they're not very pliable. They can restrict movement, and cause a lot of harm to patients in terms of their wellbeing, both from a mental health point of view and a physical health point of view. Now, we started our work with UWA several years ago, and in fact, the researchers there, Dr. Mark Fear and Professor Fiona Wood came to us when they heard that we were developing a LOX inhibitor and said, "Look, we think this enzyme is really important in skin." They embarked on a series of preclinical work in several skin models of skin scarring. We were quite frankly, you know, we had some really great results. The results of those studies were actually published at the end of last week in Nature Communications. You know, a high value journal, the first time that this data's been released. I can just summarize it there with that quote from Dr. Mark Fear. You know, the models of scarring, and there were several that they ran, found that the topical application of our drug reduced collagen deposition. We talked before about the amount of collagen that was going through and cross-linking, and improved scar appearance without reducing the tissue strength. That's a really important point in scarring. Obviously, we want to reduce the excess scarring, but we don't in any way want to damage the ability of the skin to heal itself. He said, you know, he sees this as being a unique way of modulating what's that critical stage in scar formation. There are very few other treatments available for scars. A lot of them are quite physical in their approach. You know, surgical revision or laser therapy are very commonly used. Corticosteroid injections into the scar are sometimes used, but are quite temporary fixes to the thing. The idea that you could have a pharmacological approach to scarring and actually reduce the scarring process and manage it would be a real breakthrough for these patients. We've had, you know, as I said before, the clinical evidence from our phase one in healthy volunteers showed good tolerability and full inhibition of lysyl oxidase in the skin. The drug looked promising. The total market here is very large. Depending on which one you're going for, but even the subsegment of keloids and hypertrophic scars is worth several billion dollars per year in treatments that are currently used. Just going on to the study that we're reporting on today. This is a three-month placebo-controlled study. It's being done in adult patients with an established hypertrophic scar. The scar has to be of one-five years of duration. We're not looking for people with new scars. These are people with established scars, have to be over one year old, less than five years old. We've tried to restrict the group here to certain types, so the scars have got to be more than 10 cm², so a significant scarring area. It excludes patients with acute skin conditions or a history of keloids. We're really focusing on hypertrophic scars in this case. Now the study was split into two parts. The first is Cohort 1, which we're reporting preliminary data from today. Now, that was eight subjects that were treated for 12 weeks. The objective there was to confirm what was the level of drug that we could measure in the skin, and what was the level of inhibition of the lysyl oxidase enzyme in the skin we could measure in biopsies taken of those patients' skin after 12 weeks of therapy. That was done to confirm the doses that we saw to be effective in the healthy volunteers that we did in the study before this. Once we had those eight patients all on active treatment, open label, unblinded to see, we then progressed into Cohort 2. That's 42 patients. Again, they're being treated for 12 weeks, with the objective there, again, to confirm the PK/PD, but also look for safety and efficacy of the dose that we selected in that Cohort 1. You know, primary endpoints were safety. Secondary endpoints, there are some several lots of different ways of physically and assessing the physical and visual appearance of the scars. That study started to recruit earlier this year. I, you know, I'm pleased to say is progressing really well from a recruitment perspective. Moving on to the results. The results today are just coming from the first cohort. That's important to note. The second cohort of patients who are placebo-controlled, so out of those 42 patients, 21 of them are gonna be on active and 21 on placebo. We've already recruited 24 out of those 42 patients. The total study is more than 60% recruited and UWA are doing a terrific job with that. They're screening lots of patients all the time. The results from the first cohort of the open label, these patients all received a definitive dose of the drug through a special applicator that was put onto a defined area of skin on a daily basis. The skin biopsies we got showed excellent skin penetration and a very high inhibition of the lysyl oxidase enzymes, as we had predicted. We were able to take those biopsies and then look at the biomarkers of the scarring process. If we're having an impact on the scar, then what we should see is a reduction in the amount of collagen that's present in the scar, and also a reduction in the amount of lysyl oxidase enzyme sitting in the scar as well. In fact, we see a reduction in both of those measures. Based on the work we've done preclinically in animal models, reducing those two biomarkers suggests a drug which will have a disease-modifying effect. We're all really excited by this process. We also saw some patients experience some redness, and a couple of patients with itchiness at the site of application, that resolved when the treatment was taken away. As a result of that, and the very high inhibition we were seeing of the lysyl oxidase because the drug accumulates over a period of three months, we've modified the regimen in the Cohort 2 to reduce the frequency of the dosing. We've gone from a daily dose to one that's applied 3 x a week. I'm very pleased to note that we haven't experienced any episodes of redness or itchiness at the site having reduced the drug exposure. We're still very confident that we're seeing enough inhibition of the enzymes to have a treatment effect on these patients. Professor Fiona Wood, you know, many of you have known of her and have read her articles and know of her work. She's noted positive changes in appearance of the scars of the patients that were all on active drug. Also a change in the pliability. If you roll the scar between your fingers, you can actually sense a change in the stiffness of the scar. Those results now need to be confirmed by the placebo-controlled phase. This is a, you know, and I think a really nicely designed study. We've learned a lot from the first cohort of eight patients, and that's allowed us to go on confidently with the second cohort. We appear to have resolved the side effect issues that we had with redness at the application site, and we now have to wait and see the results so we can see a difference between the patients that are on active and the patients that are on placebo. We're really excited by the stage we've reached and the continued collaboration with the group in Perth. Just to finish up, you know, this is this one study is part of a number of studies that we'll be reporting in this quarter, that's you know we're just entering into now. We will hopefully report the first patient joining the liver cancer study. We expect to have interim data from our myelofibrosis study. That's a big deal. You know, that's 24 patients in an open-label study with the first patients that have completed six months treatment. We hope to have some data from them to share with the market later in the quarter. Hopefully fully recruiting that study by the end of the year. Some publications still to come on that drug from key opinion leaders and the collaborations we had with them. Following into next year, we expect to see the top-line data from the study that we've talked about, interim data to date, and starting the second study with the group in Perth. The neuroinflammation study should start recruiting. Later on in the year, we'll see the 5505 reporting, and the 4728 recruitment continuing. With that, I'll stop, and I'm very happy to take any questions that you have. Excellent. Thank you very much for that presentation, Gary. We have had a few questions come in already, so if anyone does want Gary to answer your questions, type it into your Q&A box, left-hand side of your screen, computer, or bottom from a smart device. First question, Gary, comes from Ian. "Of the four patients which withdrew, how quickly from commencement was the skin reaction seen typically? We saw them all within the first month of treatment, which is why we're confident now because we've got a lot of patients in the second cohort that have progressed past that one-month point. We don't see any of that redness any longer. We think it was just a dosage-related issue, and fortunately, we think we've got a quite wide margin in terms of efficacy with the drug. You know, dealing with patients and scarred skin is you know is it's not a straightforward thing. You know, each patient has a different type of scar, often different type of skin, you know, based on their racial background that, you know, they'll have different structures. It really is a I think Fiona Wood has talked about the amount that we've learned from the first eight patients going through the cohort there, and the learnings of that now being applied. Also, you know, what we hope to learn from this study will go into the design of the second study, which we'll start with them next year. Thanks, Gary. Following on from that, just one that came through email. Have any more patients pulled out since those initial four pulled out? I have to caveat that slightly in that our information and discussion. This is an investigator-led study being run by Fiona Wood in UWA. Our information isn't absolutely current all the time as it would be with a study that was being run directly by Pharmaxis. To my knowledge, we haven't had any patients withdraw from the second part of the study. As I say, I think you know the learnings from the first part have been very useful. Thanks, Gary. A question from John: It seems to take a long time to recruit. Can you please comment? I think actually this study recruited pretty quickly. I mean, it started in the first quarter this year. We're, you know, just approaching the fourth quarter now and third quarter. In six months, they have put a lot of patients onto drug and through. I think the clinicians are also learning as they go. They started off with a fairly narrow entry criteria in terms of the patients that they were looking for. The patients were required to be extremely healthy when they came into the study. They found that actually a lot of patients who have these larger burns actually have quite a lot of comorbidities. They've modified the protocol slightly, widened the thing to allow more patients in, and I know that they're screening a lot of patients each week now. We're still comfortable based on our information that the study will fully recruit this year. Fantastic. A question from Mark. How consistent was drug penetration and inhibition of collagen and LOX in each of the 8 patients? I think from the data we've got, I mean, this is data from a small number of patients, so it would be wrong of me to over give a too high a level of confidence to what we've measured. What I would say is from the data we have, we are confident that we're seeing a very good average level of LOX inhibition over the whole week for, say, patients that are receiving it three times weekly. Yeah, it's probably too small a data set to go into give it, you know, precise numbers and variability and that kind of thing at the moment. That will be obviously a key report that comes out of the study when we finish the completion of the placebo control part of the study. Fantastic. All right, Gary, it looks like you've gotten through all the questions that have come through in the Q&A box, so we might wrap it up there. Hang on a second. We've had one more. Are there any photos available showing the efficacy of PXS-6302 drug? If not available, can you comment on the visual change further that was provided by Professor Wood today? Yeah. I think we don't have photos available at this time. The reason for that is that, you know, these patients have just received active drug. I think in order to really make a judgment on the impact, we need to see the effect of the drug versus a placebo so we can see changes. What we're going on here is Professor Fiona Wood and her extensive experience in this area. A lot of the patients that she recruited are very well known to her, and she's known them for many years, in fact, having treated them for their often burn injuries at the very beginning. We're going off, you know, her assessment at the moment is that this drug is making a difference. We are seeing changes in appearance and the pliability, the stiffness of the scar. The more hard endpoints will have to wait until we see the comparison with the placebo-controlled arm, which we expect to have in the first quarter next year. Fantastic. All right. We might wrap it up there, Gary. We know you've got quite a few meetings for the remainder of the day. If anyone does have any more questions, feel free to email them through, and we'll get a response to you from Gary or someone at Pharmaxis or UWA directly. Gary, on behalf of all the shareholders and attendees today, thank you very much for your time.