Good morning and welcome back to the third and final day of the Bell Potter Healthcare Conference. My name is Thomas Wakem, and we have an exciting final day of presentations across a range of companies today. Before we get into those presentations, I'd just like to take a moment to run through a few housekeeping items. Firstly, the conference is interactive for all participants, and we encourage you to submit questions to the presenters. Simply type your question in the chat box on the right-hand side of this video and press send. The agenda for today can be found below the video, and presentation slides can be downloaded using the link next to each presenter. Thirdly, if you do miss a presentation, don't worry, we will be sharing the video recordings after the conference finishes. If you do have any technical issues or questions, please contact our technical support using the number provided on this webpage or reach out to your Bell Potter advisor. Thank you once again to all you listeners and viewers for joining us today, and we hope you enjoy the final day of our conference. To kick things off in this first session, we're going to hear from several drug developers looking to improve outcomes for patients across a range of different cancer types. Unfortunately, cancer remains a leading cause of death here in Australia and is responsible for about 30% of all deaths in the country. With that context, I'm really pleased to be welcoming the first of our companies presenting today, and that is Syntara. The ticker for the company is SNT. Joining us from the company is CEO Gary Phillips. Gary, thanks very much for joining and presenting today. Welcome to the conference. Thanks very much. Pleasure to be here, Thomas. Great. I am going to do a brief introduction, and then we will pass it over to you for some slides. Syntara is a clinical stage biotech company with a broad pipeline of four novel drug candidates. Over the last 12 months, since Gary was presenting at our conference last year, Syntara has reported some impressive clinical data from its lead drug called Amsulostat in myelofibrosis, which is a rare form of bone marrow cancer. In addition to myelofibrosis, the company has drug candidates treating other forms of blood cancer, skin scarring, as well as a sleep disorder condition. Those in the audience may be thinking blood cancer, skin scarring, sleep disorders sounds like a pretty diverse area of focus. The common theme is Syntara's unique expertise honed over several years from their facilities here in Sydney, focusing on what's called amine oxidase chemistry, which plays a key role across each of these conditions. It is very exciting times, plenty of clinical studies underway. I am going to pass it over to Gary to run you through some slides, and then we will go through some Q&A afterwards. Thanks, Gary, and take it away. Great. Thanks, Thomas. Great introduction. Good morning, everybody. It's my pleasure to be here and presenting at the Bell Potter Healthcare Conference. Again, for the number of series of years I've done this, and as Thomas said, we've made great progress since this time last year. I'm just going to give you a couple of highlights and then a few slides on some data that we've presented in the last month or two, and finish up with a slide showing the news flow and the number of opportunities for value appreciation that are coming up in the next 12 months before handing it back to Thomas for some Q&A. At this particular point, why should you be paying attention to Syntara as a potential investment opportunity? I'd say that there are three key things that make us stand out from the crowd and make us a particular thing that should be on your watch list at the moment and thinking about an investment. The first one being, we are not a virtual company. We are a real-life biotech with labs based in French's Forest just outside Sydney. The implication of that is that we have control over our own pipeline. We haven't licensed anything in. We have multiple shops, so several different opportunities to generate value for shareholders with long IP because it comes from our own invention and full control over that. At the same time, you would not be the first investor into institutional shareholders. Many of them are specialist healthcare investors. Many of them have made money in the lead indication that our drug is in myelofibrosis before investing in Syntara. Smart money is already in the stock. Lastly, building on that pipeline that I talked about, in the next 12 months, we have five different studies that are going to deliver efficacy and safety data to the market within the cash runway that the company has. That is unprecedented that a stock with the valuation that we currently have under $50 million has that number of opportunities from phase one C or phase two clinical trials delivering data. Any one of those could lead to a significant appreciation in value, which is why I say now is a good time for you to be thinking about an investment and whether it makes sense in Syntara. Just to back up that statement I just made about cash, the company had over $14 million in cash at the end of September. That cash takes us through to the end of next year, beginning of 2027. That is the length of time that the cash lasts through which we've got these milestones coming. As you can see there, the amount of institutional ownership north of 40%, including some significant specialist healthcare investors who've done a lot of diligence on the company before getting to this point, and coverage from four different banks. There is plenty out there to read if you want to, along with Thomas's excellent analysis he's done on the company as well. If you look at the share price graph on the right-hand side, you can also see why now might be a good time. We lost a lot of value in the middle of the year when we announced that the FDA had suggested and proposed to us to do a phase 2b study next for our lead asset, Amsulostat in myelofibrosis. The market was expecting that we might go straight from our phase 2a study that we've completed through to a phase 3 study. We got a slight slowdown from the regulator. This was not a clinical trial failure. This was just a regulator posing an alternative way forward for the drug. Still, which gives us lots of opportunities for value operation, actually leads to a smaller amount of investment to get to the first of those value appreciation points and still leads to multiple points for partnering as well. Whilst the market reaction was understandable in terms of disappointment, we believe that the amount of knockoff in the value leaves a real opportunity at the moment for investors thinking about us for the first time. The main disease that our lead asset is in is myelofibrosis. As Thomas said, that's a cancer of the bone marrow. The bone marrow becomes fibrotic. The bone marrow is your blood production unit, which is used to produce red cells, white cells, and platelets. Patients with myelofibrosis have a life expectancy of about five years from when they're first diagnosed and given their first treatment of a JAK inhibitor. These patients suffer from cytopenias of dropping red cells, white cells, and platelets, enlarged livers and spleens, and constitutional symptoms such as night pain, night sweats, bone pain, fatigue, more infections. These patients do not live a happy life. The only drugs available at the moment for treating them are JAK inhibitors. These are drugs which are myelosuppressants. They hammer on the aberrant cells that produce those enlarged spleens. They are good at reducing spleen size, improving some of the symptoms. In doing so, they also kill some of the good cells that are left behind that are still producing red cells and platelets in particular. These patients eventually come off of these drugs because they get dropping levels of blood cells. They cannot stay on them any longer. Despite only being symptomatic, these drugs sell about $2 billion a year of sales. There is a huge unmet need here and a great commercial opportunity for a drug that will work on top of these drugs to improve the status of these patients. We have done already one study in patients that had failed on JAK inhibitors. We reported that in 2023 at the American Society of Hematology. It showed that we reduced the fibrosis in the bone marrow of patients with our drug, which is an oral drug given twice a day when they were treated for six months. The FDA then allowed us to go on and do a further study with our drug on top of the JAK inhibitor. This study lasted for a 52-week or one-year period. We reported that interim data at the American Society of Hematology last year. The final data from that study will be presented next month at the American Society of Hematology in Orlando. We presented it earlier in a media release a month or two back. What did that data show us? First of all, it showed us that the drug was extremely safe. We have no adverse or serious adverse events that are related to the drug. This stands out in vast contrast to other drugs in the area, which do produce still a lot of side effects when they're used to treat patients on top of a JAK inhibitor. We think we have a first-in-class drug, best-in-class drug when it comes to treatment and safety of the tolerability profile. The patients we treated were still pretty sick. They'd been on ruxolitinib, the lead JAK inhibitor, for about three years. Despite that, they still had enlarged spleens and significant symptoms. We relieved both the symptoms and the spleen volume. In this case, we had almost 75% of patients who were on the drug for six months or more had a 50% or more reduction in their symptom score. These patients come in with a symptom score that's out of 70. Say they came in at 40. More than half of them had a reduction. We've gone less than 20 in this case. The chart on the right-hand side shows patients in the gray bar what they got at six months, and those in blue were the patients beyond six months as they continued to improve. This is an outstanding reaction to the drug. It's a best-in-class response, we think, in symptom control compared with competition. It's backed up by also improvements in spleen volume as well. As well as those improvements in symptom score, we saw patients have about half of them get a reduction in their spleens of about 25% or more. Again, a really reassuring efficacy signal on top of a very good safety profile. We're now looking at the next stage of these studies, and we have appointed an advisory board of experts to help us, including clinicians. They were on the right-hand side, Claire Harrison, Gabby Hobbs, and John Mascarenhas, but also on the left-hand side, some advisors to the Syntara board, including Adam Craig, who was the CEO of CTI Biopharma, a company which itself developed a JAK inhibitor and then exited the space for $1.7 billion three years ago. That's a good segue to the fact that there is a huge amount of interest that still remains in companies who have assets in myelofibrosis. These are the last deals that were done in myelofibrosis. The two columns on the right-hand side were for JAK inhibitors. Me Too drugs, drugs that are a little bit different from the lead drug ruxolitinib in myelofibrosis, pacritinib, and momelotinib. Those drugs sold for just under $2 billion. CTI was the company that was where the CEO was Adam Craig, who is now an advisor to our board. The two ones on the left-hand side are for drugs which were used on top of a JAK inhibitor. The MorphoSys drug sold to Novartis, the one in the middle there, was sold for $2.9 billion at the beginning of 2024. When added on top of ruxolitinib, that drug in phase two studies, very similar to the ones that we've reported on, produced results which are still, I think, from a safety perspective, not as good as our drug. I think spleen volume, they did as well as we did. We still think our symptom control was possibly has an edge on that drug. You can see this is what happens when you get the drug to the end of phase three. Very, very valuable commercial opportunity. The column on the left-hand side, the Kairos drug bought by Takeda, that's more analogous to where we are now. This was a drug that was sold at the end of phase two. The upfront was $200 million and a deal value of $1.1 billion. This just indicates the level of commercial attractiveness of the market and the willingness of companies to enter into development at different stages. It does not have to wait until the end. I will finish up and then hand over to Thomas for questions after going through our pipeline. I said at the outset that Syntara was a company that was a bit different from others on the market. We have a number of studies in a number of different assets on the way to market at the moment producing clinical trial results, which gives opportunities for value appreciation within the cash runway that the company has. From the top, there are lead asset Amsulostat in three different studies. The top one already been reported. The next step for that is we are in discussion with the FDA now. We're expecting the first half of 2026 to have an approved development plan for the next study in myelofibrosis, a phase 2b plan, and also to be engaging with potential partners in that process as well. A big news ticket item coming in the first half of 2026 for that drug as it advances to the next stage and potentially partnering. That same drug is also in two different studies, both of them of a disease called myelodysplastic syndrome. This is another blood-related cancer. One of them is in high-risk patients. The other one is in low and to intermediate-risk patients. Both of these studies are funded by external non-dilutive cash, and both of them due to produce interim results by the middle of next year. If either of those studies produce even a sniff of a positive result, it somewhat doubles the value of the asset because it's already shown its efficacy in myelofibrosis. If we can show it's got efficacious in two different blood disorders, then that really increases the attraction of the asset to both investors and potential partners alike. Same technology, but formulated as a cream, is being used in skin scarring. We've already reported a long-term collaboration with Fiona Wood in Perth at UWA of how our drug can reduce the amount of collagen in scars by more than 30% after three months treatment with a cream on old scars. We're now repeating that study in keloid scarring, a particular kind of scars where there's a really high unmet need, and also in hypertrophic scarring where we've got a new asset, SNT-9465, which we believe has an edge on the first drug in terms of its tolerability. That study, we're due to start reporting data from that this quarter. Quite soon, you will see an update from us on the status of that product, which study it's in, and the study that is about to go in, which is going to show efficacy and safety in hypertrophic scars. We're really excited about that program. The commercial opportunity in skin scarring, as you can imagine, for a drug which can relieve scars in patients is enormous. We are working with world-leading experts in this area to try and bring what is still the only pharmacological treatment in early-stage clinical development for scarring, a huge opportunity globally. Last but not least, a drug in a sleep disorder. Again, as Thomas said, the indication is not linked to the cancer in skin scarring above. It does come from the same chemistry platform that we have used to get to the others. This drug is in a sleep disorder where most patients develop Parkinson's. That study is well on the way to being fully recruited. It is a double-blind, placebo-controlled phase two study, three months in length. We expect to report that study in the first half of next year, likely to see the last patient complete in quarter one and a result in quarter two. A real opportunity here. Please think about adding Syntara to your watchlist. Multiple opportunities for value appreciation in the next 12 months and a cash runway that covers that. With that, I'll hand back to Thomas for any questions. Great. Thanks, Gary. Very good run-through there. I want to start on your lead program in myelofibrosis. You've obviously reported some really good clinical data in that phase two trial. One thing I just want to try and highlight for the audience here, this TSS endpoint, total symptom score, can you just elaborate to us what that means in simple terms? I mean, you had two patients that were completely resolved of all their symptoms. Can you give us an idea of what that actually looked like and what they ended up like at the end of the trial? Yeah, it's a confusing thing. I understand. I mean, in many cancer studies, we often talk about complete response as an endpoint. I think people kind of understand when you've got a tumor that's gone. We don't have that in myelofibrosis where these patients have a fibrosis in the bone marrow and a lack of healthy cells producing vessels and platelets to monitor their improvement by the impact of actually measuring the cells in the blood or measuring their symptoms. The symptom score, which is the primary endpoint that the FDA are likely to use in any pivotal study going forward, is scored out of 70. There are seven different domains scoring from abdominal discomfort to pain, a number of different avenues that you can go down. The patient is the patient-reported outcome. The patient fills that in on a regular basis. If they're anything over a score of 20 out of 70, it's considered to be very clinically significant. You can reduce their symptom score by maybe 2. They come in with 20, and you can reduce them to 18. However, that wouldn't be sufficient for us to sort of call them a responder. I go back to my analogy of the complete response that we see in sort of tumor types. The FDA required these patients to have a symptom score reduction of 50% or more in order for them to be called a responder. Those two patients you mentioned who went from a symptom score of around about sort of they could have been 10, 20, and they would have gotten either complete resolution back to 0 or 50% back to 10, those patients are now living a much more normal life. One of the key things in this area is fatigue because of the lack of red cells. Often, your blood is not as well oxygenated, so you get tired more frequently. If you can reduce symptom score by more than 50%, you've made a material difference to these patients' lives. All the endpoints within the symptom score are measuring things which are important to the patients about their daily lives they go about. Very good. All right. Thanks, Gary. That kind of leads into another point I just want to elaborate on, which is your engagement with the FDA. You've touched on a meeting planned for the first half of next year to discuss the path forward in myelofibrosis. Can you tell us a bit more about what you're expecting or hoping to achieve from that meeting and the clarity that that will give you moving forward with that program? Yeah, it's just fairly straightforward now. We submitted our data, or maybe with a couple of data points missing earlier in the year, and asked them for guidance on the clinical development path forwards. They came back and said that they wanted to see a phase two B study in a control population with a placebo involved to get a very clear idea about what both the efficacy and the safety profile of the drug was. Our next step is to submit a study which fits in with the guidance that we've got. Whereas before we were going back with questions, including our data and asking questions about the pathway, this time around we're going back with an actual protocol addressing the issues that they raised in their last advice to us and looking for them to agree with the protocol we're giving or give us comments that allow us to finalize the protocol. We expect a response back from the FDA to our protocol to have resolved any issue from that response within the first half of next year. Great. Okay. Let's talk about how you're planning to progress that program through that phase two B and beyond. You've obviously in the past, one of your assets did a big deal with Boehringer Ingelheim. How are you thinking about partnering in light of the cash balance and everything else that's going on with the company in the pipeline? If we decided to do the phase two B ourselves, we would need to go back to the market and raise money to do that. The potential outcomes that there are at this point, Thomas, are on the one end of the bell-shaped curve, you've got one where we raise the money from our shareholders. I mentioned that we have large institutional shareholder base. Many of them have made money in myelofibrosis from backing companies through to phase three where they've exited for multi-billion dollar deals. We do believe that that is a realistic option for the company to do that. At the same time, we are receiving quite a lot of interest from companies in this space who are trying to add assets to their franchises in blood disorders and hematology cancers in particular. We have enough data to interest them. We have, with the engagement of the FDA, a clear way forward and development plan that it's quite possible that we could do a partnering deal with the asset where a third-party company could take over the development or possibly engage and collaborate with us and help us to do the phase two B study. That's sort of you've got the two extremes and the one in the middle in terms of how we might go forward. We are going to the American Society of Hematology in three weeks' time in the U.S. We are meeting with many of the companies that have shown an interest and talking to them about our data and the plan with the FDA and engaging with them at this point. Great. I assume plenty of those prospective partners would also be interested in the other indication of that program, myelodysplastic syndrome. Basically, it is similar clinicians. It basically gives more optionality from the one product and doubles the commercial opportunity there. Could you just remind us? [crosstalk] Sorry, Gary. If anything, myelodysplastic syndrome is a bigger indication than myelofibrosis and has a larger unmet need. Yes, your statement is absolutely correct. If we show any data in that, it is going to be big news for those partners. Right. The data that we're expecting in that MDS or those two MDS trials next year, can you just quickly remind us what we can expect in terms of the size of the trials? Yeah. Both of those studies are eventually going to be kind of 40-patient studies in phase two, looking at the addition of our drug on top of a hypermethylating agent in patients with myelodysplastic syndrome, and they'll be treated for six months and more. The data that we'll see by the middle of next year from both studies is the first stage of those studies, which is a dose escalation where the drug is used in combination for the first time at the first dose, which allows selection of the dose going into the phase two. In both those cases, we'll see patients on drug in combination for longer than three months. We believe that will give us an early indication both of safety and of efficacy before the patients go on and spend longer on the drug in the phase two. Great. Okay. One of your other programs, this is in the sleep disorder behavior program. You're running a phase two trial here in Australia, in the U.K. It's randomized. It will be quite an interesting readout where you've got half on placebo, half on your product. What are the key endpoints that we should be looking at at that top-line data readout next year? These are patients with a sleep disorder, which means they act out their dreams. It's caused, we believe, by inflammation in the brain. The study itself, which runs for three months with a drug that's taken once a day, Oxford and Sydney being the two clinical trial centers, we're looking at two things. The first one being their quality of sleep because these patients suffer severe sleep disturbances. That'll give us a clear readout. If positive, gives the drug a commercial opportunity in sleep disorders. These patients have no treatments other than melatonin at the moment. Secondly, we're also looking at PET scans of their brains using a radio-labeled ligand. That allows us to look at inflammation in the area of the brain, which is implicated in Parkinson's. If we can show that this drug reduces inflammation in that area of the brain, there's a commercial opportunity for this drug to go on and be studied to see whether it can slow or even stop the progression of patients with this disorder to Parkinson's. The majority of these patients with this sleep disorder all go on to develop Parkinson's within a five-year time period. It is a big opportunity and a high unmet need. Great. All right. We've just got about a minute to go here, Gary. To wrap things up, I'll pass it back over to you. I know you had your slide with the pipeline and the different catalysts, but why don't you just remind us? Obviously, myelofibrosis, you're engaging with the FDA in the first half of next year. Can you just remind us again, what are some of the other key events we'll be looking out for next year? Yeah. Investing in biotech is a high-risk area. It's important that you spread and mitigate some of your risk by looking at a portfolio of assets that you're interested in. In Syntara, you have a company that has mitigated some of that risk. We are not a company where you're putting everything on black or red on the roulette table. We have five different opportunities for value appreciation. Start with the myelofibrosis study, getting approval from the FDA to go forward in that disease, and opening up opportunities for partnering with that drug the middle of next year. You can see that drug around the middle of next year going forward into the next study. Secondly, that skin scarring program, two different assets, two different disease areas. Watch out in the next month. We will be coming back to the market and talking extensively about the next clinical trial design in that area that we're going to be starting in the next month, which centers we're opening up, how the trials are designed, giving an opportunity for investors to listen to key opinion leaders talk about the unmet need in scarring and why they believe the technology behind our drug has a lot of opportunity going forward. Lastly, the drug we just talked about in sleep disorder. I think that's a little bit under the radar at the moment, but that is a placebo-controlled double-blinded study, three months in duration, with the top key opinion leaders in the area. It's fully funded by Parkinson's UK, showing the amount of interest in that from the community as well. That's a real one that will blow everybody up, I think. If that one comes through positive, it will be, I think, a real flip for the stock and investors and patients alike. Great. All right, Gary. Thanks so much for your time. Plenty going on. We'll be watching closely across all those clinical and regulatory events over the next 12 months or so. Thanks again. All right. Thanks, Gary. For our audience, please hang right there. We'll be back in a couple of minutes after a short break. Thank you. Hello and welcome back to the Bell Potter Healthcare Conference. For our second session this morning, we are joined by the CEO of Immutep, Marc Voigt. Marc, welcome. Thanks very much for joining us today. How are you going? Thomas. Thank you for having me again. Very good. We are going to have a bit of a fireside discussion today, which I am very much looking forward to. Before I get to some questions, I will just provide a brief introduction for our audience. Immutep is a clinical stage company with its lead drug candidate in phase three clinical trials for lung cancer, as well as having a second asset undergoing trials for an autoimmune condition. Under Marc's leadership, Immutep has reached a point that only few peers on the ASX have achieved in the past. That is to take a drug through its early discovery activities, conduct initial phase one and then phase two clinical trials, speak to the regulators at the FDA and EMA, get alignment there, and then finally conduct a large phase three global trial in hundreds of patients. It is this final clinical stage that Immutep is now in, with its lead drug candidate called eftilagimod being evaluated in a global phase three trial in patients with a type of lung cancer. That is my intro summary spiel, Marc. Thanks very much again for joining us. Why do you not just, to kick things off, start by reminding us about how eftilagimod works through its LAG-3 pathway and how you are aiming to improve outcomes for cancer patients here in general terms. Thanks. Yeah, thank you, Thomas. Indeed, eftilagimod is a unique approach, a unique drug. We are activating the immune system specifically, very broad and very deep. If you have cancer, of course, you would like to have an active immune system and overcome practically cancer with fighting the cancerous cells with your own immune system. Eftilagimod is using LAG-3 as a tool to activate the dendritic cells, if you like, the generals of the immune system very specifically. This leads to a very broad immune reaction so that we have more CD8 T cells, if you like, the soldiers who are actively fighting cancer, providing the right information, see more CD4, more natural killer cells. It is a unique approach. Very good. Let's drill into that lead program of yours. The most advanced trial that you have underway is in non-small cell lung cancer. Unfortunately, that remains the number one killer in terms of types of cancer. I think here in Australia as well as the US, there are many patients that unfortunately have this. Can you just, I guess, describe to us what that means in terms of the addressable market size, how many patients there are, and how many dollars are being generated by drugs in this therapeutic area today? Yeah, as you said, unfortunately, we are talking here about the leading cause of cancer death. It's globally the largest market, also in terms of dollar terms. As we speak right now, for those specifically addressable by anti-PD-1, the most modern immunotherapy you have marketed, it's round about up to $25 billion annually. And it's believed to reach more than $40 billion by the early 2030s. Unfortunately, it's a deeply increasing market and a high unmet medical need. Despite all progress we saw in the past decades where you had new therapies approved, but unfortunately, the median overall survival is much below two years. Okay. Very good. We'll come to the phase three trial that you're running in a moment's time. Before we get there, I just wanted to recap for the audience. You've already done some phase one and phase two clinical trial work in non-small cell lung cancer.