Prescient Therapeutics Limited (PTX) Earnings Call Transcript & Summary

Okay. Good afternoon, and welcome to Precinct Therapeutics Investor Briefing. My name is Patrick Nelson. I'm the MD at Reach, and I'll be facilitating the webcast today. I'm joined by Steven Yatomi-Clarke, the CEO of Prescient. Thank you for joining us today. The purpose of today's session is to give -- for the company to provide an update and explanation of the progress of Prescient towards their vision to be a global leader in bringing personalized therapies to cancer patients. And to provide an overview of its diversified and cutting-edge project pipeline. We expect the session to take around 35 to 45 minutes and will include a Q&A session at the end of the presentation. If you've got a question, please put it into the chat box, and we'll do our best to ask them as we go. Otherwise, we'll get to all questions at the end of the presentation. Any advice contained in today's presentation is general only. It doesn't take into consideration your circumstances. The information is for self-directed investors and educational purposes. But we would encourage you, if you have a question, you use the opportunity to ask Steven questions directly. Prescient is taking the cancer compensation from fight to cure with its next-generation CAR-T therapies. The company's clinical trial progress in next-generation CAR-T therapies places it in the forefront of the fastest-growing area in cancer treatment. Our next-gen CAR-T platform, OmniCAR is seeking to take advantage of CAR-T or taking -- seeking to take CAR-T therapy to the next level and has been doing so with high-profile collaborations, including the Peter MacCallum Cancer Centre, all right? So today, Steven, the CEO, Steven Yatomi-Clarke. Steven took over as CEO in 2016, has overseen its progression from start-up phase and manages a team in Australia and U.S., and has been instrumental in the strategy and business development. He's been a collaborator on various immunotherapy research projects. Steven, I'll pass things over to you, you should have control of the presentation.

Thank you very much and pleasure to be speaking with you all again. This is a high demand one in the last couple of weeks. I know we did one a couple of weeks ago. And I also realize that this session was focused for current shareholders. If you would have heard my voice many, many times before, we were seeing of these slides before. I'm going to dive down a little bit deeper into some of these and take the time to provide a little bit more context on certain slides than others. So again, by popular demand. So for those who are new to the story, hopefully, there's enough background information so you can keep pace with this presentation. Again to remind ourselves on the investment highlights here, what we stand for, and it's a very simple license from the best and work with the best. You would have heard of University of Pennsylvania and Yale and other such Ivy Leagues and a little university called Oxford university. So license from the best and work with the best over 100 peer-reviewed publications on our technologies. Peer review publications means that you don't think it's -- it's not what you think the data as you published for what it is, it gets rigorously reviewed by peers in -- what is a very competitive industry that I try to prior calls in it, pass all of that gets published and that's had another 100 times. So a real sleep at night factor with the science. We don't live in a world with guarantees by any stretch, but in science, you really want to make sure that you can -- you have the best of the best, try to rigorously stretch and test that are we are and we at that time and time and time again. So that's what we stand for. Lots of shots on goal, as you guys know, with a deep pipeline, we have 2 drugs in the clinic right now, as you know, PTX-100 and 200. We only need one of these horses to come home, and I think we're doing very, very well. And we'll spend a bit of time on OmniCAR, which many of you will know all about and next-generation technology in a new modality called cell therapy using leading cells as a medicine and really taking that to the next level. We've got 3 in-house programs. I don't have slides on each of these programs, but I will spend a little bit of time on each of them explaining what they are and how they're different, and also the ability to use this platform for third parties, people who might be in CAR-T or not to get into CAR-T and want to make their therapies safer and controllable. Again, we can work with them a lot as many external fights as we can where it makes sense. And bring in a lot of basically been validation that way and the potential to monetize an asset much sooner than would otherwise be possible. Corporate snapshot. We've rebounded since the volatility of the last couple of weeks, thank goodness, but still very good buying at these levels of about $120 million market cap. Cash position just announced last Friday, $14.7 million. Just as a reminder, very responsible custodians of shareholder funds. When we did the capital raising about September 2020, at the end of that, our proforma was $20 million cash. And you can see what we've got left there. So we've gotten a lot of mileage, very responsible custodians of shareholder funds, and a nice tight register. I will probably get questions on shareholder movements and what not. I can tell you that certainly, the top 20 and the top 40 look to be rock solid even in this market, what we're seeing when the volatility shook out in the last couple of weeks. People exiting equities altogether lots of hundred thousand dollar parcels self-managed supervise people exiting altogether. We understand the macro volatility. I can tell you that the core of the shareholder base remains intact and even adding to their position. So I think it's a nice position to be in. So a snapshot our pipeline here, as usual, start with the targeted therapies. PTX-100 and 200 and then we move to the OmniCAR programs. I think the second message on this slide is always, we're not a one-trick pony. There is too many companies on the ASX so I feel that are either single asset companies and/or single project or trial companies. Now there is -- with the inherent risk involved in drug development or what might be very, very careful with situations like that. We take a diversified approach to our portfolio, so that investors need to diversify, not only by cancer type, but by the modality and stage development. So lots of built in risk mitigation and also lots of built-in opportunities for value creation and will these potential fulcrum for uplift. PTX-100 is an inhibitor to targeted therapy and an inhibitor of a very important pathway in cancer called Ras and which drives many, many different malignancies. We put several of these into the basket trial last year and found an excellent safety profile. Even at the highest dose, there was not a single serious adverse event related to the drug, which is very, very unheard of. So safety doesn't seem to be an issue because our people until it is. But I can tell you, you can't move forward unless you have a good safety profile. The good thing about this is that it's a very fragile patient population that we're looking at here, many of whom can't tolerate very overall certain therapies. This looks to be very, very safe. And also has the opportunity if we need to or want to, to mix and match with other drugs in combination. If you've got a good safety profile that allows you to add another drug to -- if both of them are just on the edge of safety is so often is the case, then adding them together often tips it over the scale, combining them is a little bit too toxic. It looks like this has a much larger window to play with other drug. So it's important not just for clinicians, we don't want to mix and match their standards of care with PTX-100 to move the needle for their patients, but also for commercial partners going to enter these as well. So even though it was a safety study, we saw something we didn't expect to see, and that was some responses and quite stunning responses in a couple of patients with a certain type of blood cancer care T-cell lymphoma. And as a bit of background and context on that in T-cell lymphoma precious little works and what does work doesn't work very well. But those who just happen to it work, you see maybe responses to 3, maybe 4 months. So we get 12 months and now it's almost approaching 2 years for that patient number 2. We're quite stunning at unexpected responses. And just speaking the Miles Prince earlier today, first thing in the morning today, actually speaking about some of these patients again in this upcoming study. So where does this leave us? We're doing what's called an expansion cohort. Normally that Phase I, Phase II, Phase III, where each of those can take a very long time. We found ourselves now in this area of unmet need where we can, actually truncate a lot of this. And so what we've got now with the expansion cohort is the ability to do less equivalent with Phase II really. So this is going to be focusing in on T-cell lymphoma. It's 8 to 12 patients. We would have worked with kickstarted the study towards the end of last year. We had some drug manufacturing issues, anyone that's been in a supermarket in the last 4 months would have seen certain items missing. It's just getting going better and better now. But the supply chain issues across the world were affecting ahead of chemistry manufacturing controls in the U.S. decades of experience. And we haven't seen bottlenecks like this in 20 years. So we got bumped. Everyone got bumped. We managed to get back up the queue, which was great, thanks to Mike. But again, supply chain issues, is you supply and supplier, then is waiting for product and whatnot. In a long story short, this is all behind us now. We went through all of this at our AGM, for those who were there, and in our subsequent quarterly. So none of this is new news, but luckily, it's behind us. Miles is wearing and ready to go. And again, just speaking to him this morning, super enthusiastic and looking to complete enrollment of this study this year with hopefully interim readout. Again, we've got, what is life look like on the other side of this trial. It could be a monotherapy. We might want to take sneak peek at this and start to do another round, perhaps in a combination for what might be then in a registration study. So that is all going well and looking forward to announcing that first patient, and I'm sure we're going to catch up on the timetable. So our end date has not moved. It was just that manufacturing issue. A good idea of market opportunity available for us in this indication is pralatrexate, which is -- it's not a very good drug, but it is approved, nevertheless because it's an area of unmet need. So this drug was approved on an overall response rate of only 27%, which is to say, 27% of everyone that took the drug, and only you had a some sort of benefit only 20% -- 27% of the time. Some of them are good benefits, some of them aren't. On average, it was 3 months. So you can see, compared to -- if we can replicate some of the data, we have while we're very excited about this. It's not the biggest market in terms of patient numbers, but in terms of its size by dollar value because it's an unmet need, very high value. You can see how much Folotyn costs per patient per year. So it's a big opportunity. It's a narrow one, which is good because it's accessible, and it's the shortest path to market. The plan for this is to, in the event of success, expand out into other indications. That's the shortest point between here and an approved therapy. So we're ready to go on this one, which is -- or keep going, should I say, on this one. PTX-200. It is progressing now. So with the 45-milligram per meter squared dose. Jeff Lancet leading this study, the first guy in 40 years to get a drug approved in this awful disease. AML, acute myeloid leukemia, a disease of the bone marrow that really is -- it's the cancer that gives all other cancers a bad name. And in this particular setting, average expectancy -- life expectancy of 4 to 6 months. So to have 3 complete responses on this study is encouraging. Looking to escalate this drug. We've got FDA orphan drug designation for this as well, which gives you 7 years exclusivity around this once approved and some benefits beforehand as well. So that is that. So all of these -- both of those are in the clinic right now. And now switching gears to OmniCAR. By now, you would have heard me talk about CAR-T many times. But for those that want a little refresher, it's a way basically harnessing your bodies in an adaptive immune systems. So blood collected from the patient and isolating a certain type of cells in the immune system is frontline soldiers called T cells, which are good at fighting infected cells and infection, but not so good at fighting cancer. So we help that by engineering them outside of the body. You put a receptor on it that can now recognize a cancer cell and you grow, release up and give them back to the patient. So when you hear me talk about CAR-T, it's at step 3. It's a patient's own immune cell that is now engineered outside of the body to express a type of a receptor that it can latch to and kill a cancer cell. And this is moving the needle in cancer like we've never ever seen before. And this time last month, worldwide headlines made when Carl June from University of Pennsylvania and a pioneer of CAR-T, he used the cure word. Now we've never heard that used before in the history of medicine. You talk about shrinkage of tumors. We talk about keeping the disease at bay for a certain length of time. It's called progression-free survival. We talk about quality of life. Never ever, ever has anyone been so bold as to use the word cure until now. And Carl June seeing some of these patients on his initial study, still cancer-free 10 years later, and there's been multiple examples of this since. And so if it looks like a cure and smells like a cure, it's probably a cure. So for the first time in the history of cancer, this mentions we can have curative intent. And I can't tell you what that means. Wouldn't it be great if in the not too distant future, we're speaking about cancer around the dinner table as if we'll go into the dentist. Instead, when you hear a C word mentioned by the doctor, you start making plans for -- making arrangements for your family. It's devastating. For these patients, thanks to the curative intent, it's I have cancer and I'm great, I'm going down, I'm going to get some CAR-T therapy and I'm booked in for next month and it will be under control. So that is where not only we're moving to, but already starting to see. And I'll also mention for those that follow the space, 2 days ago, the FDA granted approval for -- so firstly, the very first one approved was Novartis is Kymriah. That's $0.5 million that bag. If cells there that was pioneered at University of Pennsylvania. But 2 days ago, the FDA approved a sixth CAR-T therapy cells. So it's here and now. And this was J&J and Legend making one for multiple myeloma. And I don't think I've ever seen data submitted to the FDA that looked so bloody good. It's astounding. They had a 97% response rate. We've never seen anything like that. But before CAR-T came along, this exact same population of patients, it was sort of 20% to 35%, something in that range. To come up with a 97% response rate in a pivotal study, absolutely unheard of. I don't think we're seeing data like it. And it's just the start. That's with the first generation CAR-T. That's the great news is that this is using technology that's 10 years old, up to 10 years, I should say. But it is just the start. And in order to bring this to more patients, we need to overcome these obstacles. So these 2 -- so the 6 drugs approved. They are all targeting 2 particular targets on the cancer cell. They were always going to be the lowest hanging fruit. I'm so pleased that they've worked. But really, the whole industry is scratching its head now and saying, well, go, that's great for these types of cancers. It's 2 very specific types of cancer, 2 very specific targets. What do we -- where do we go from here? And these are the things that the whole industry recognizes we need to overcome. Obviously, it's a very expensive therapy to make 22 days and hundreds of thousands of dollars to make that single bag. So the more we can drive that down, the more patients we can access, safety and control because these are living cells. So in order to -- once they're injected, a living cell, 1 cell becomes 2, 2 becomes 4, and they're out of control. Well, certainly, they are unable to be controlled. And we saw no better example of that. Again, those who follow the space would have seen Celyad announcement 2 days ago, devastating for them. 2 patients passed away on their study. They can't switch the therapy off, patients passed away. Tmunity before that, Allogene before them. So again, if people, are you winning at safety, just don't. I mean, it can't be -- it's so important. At the moment, you can only give these CAR-T therapies to the sickest of the sick patients because those are the only patients at the end of their lives where you can justify the risk reward. These patients have to be in an intensive care unit just to receive the therapy, and all the doctor can do in that situation is treat the symptoms. So you need a therapy you can control. If you can have a therapy that's safer and controllable, you can give it to patients who are not as sick, earlier in the disease setting, before they're on death's door. And beyond that, you can give it to other types of cancers, even in non-oncology indications, so it's super important to overcome that. Targets I mentioned before, these 6 -- first 6 approved by the FDA are only focused on 2 targets, but watch you beyond that. Exhaustion means basically, it's a marathon, not a sprint. The current generation of CAR-Ts, they sprint really hard. They generate all sorts of cytokine, the inflammatory and safety issues, and then they get cuffed out. And really, when you're fighting cancer, and especially in solid tumors, in these bigger tumors, it's a marathon, it's not a sprint. You need to get these things to hang around and you need to outlast the cancer. And at the moment, it's tricky to do that. An escape as what happens if the tumor mutates and all of a sudden, it starts expressing a different type of antigen. Because these are very sort of cunning type creatures. In the event of selective pressure, they will change, like antibiotic resistance, like a similar type of thing. The cancer will mutate. And at the moment, you've got -- if you give a CAR-T against the one and that mutates, you've got all the bad side effects of the CAR-T and none of the benefits and you do not want to be there. So it is universally accepted that these are the big issues that need to be solved. The people who pioneered CAR-T, University of Pennsylvania, they came up with this system to deliberately solve some of these problems. And it's a modular CAR system. Again, you would have seen me introduce the mechanism of action here. Basically, it's separating the part that binds to the cancer cell, called the targeting ligand, from the actual cell itself, separated by 2 bits of Velcro invented by a University of Oxford. So you've got the targeting ligand, you've got the cell that comes together with a covalent bond, and this creates a fully armed CAR-T cell. It's ready to go. It's on-demand killing. And the beauty of this is a genuine platform. We can work with any targeting ligand. So there's companies that they're saying, we love this target, this is going to win. We love this target. That's going to win. Good luck, good luck to you all. We can work with any or all of them. And there's other companies out there saying, we think this cell is going to win. We think this cell is going to win. T cell, that's an off-the-shelf cell or it's an NK cell or an iNKT cell or a macrophage. I couldn't give a good goddamn. We can work with all of these. So that's where we are and a genuine platform that can solve all the problems that I mentioned before. I'll just play a quick little explainer video that [indiscernible] would control on Reach play that. But while that's loading, this video will run you through some diagrams of how it works and what it means in terms of safety and control and efficacy and what it allows everything to do. [Presentation]

So hopefully, if a picture tells a thousand words, hopefully, video tells a few more. I will just wait for Reach to load the rest of the presentation. But any -- that's available on our website under the Technology tab for those who are interested. So what does this mean you would have seen this depiction before in terms of current CAR-Ts. So current CAR-T is a soldier fighting cancer, but it's only got 1 map and 1 weapon, you can't redirect it, you can't control it, whereas with our modularity OmniCAR can beyond with multiple weapons at once, multiple maps for multiple deployments can be trained to hit any target, including several at once and full communication and control during therapy during mid-Mission and even send images back. So again, the first iteration of any technology, iPhone 1, the first ever laptop, VCRs, whatever you like. The first iteration is the clunkiest and you can see that we are of the future, we're taking it to the next level. And this platform has given rise. We did a big strategic review and identified 3 areas -- 3 projects that we are carrying in-house. And that is for AML, HER2-positive solid tumors and an aggressive type of brain cancer called GBM, glioblastoma multiforme. And each of these was characterized by, firstly, an unmet need. But secondly, where CAR-T has tremendous potential for really moving the needle in the patient benefit, but where current CAR-Ts were stumbling. And I was stumbling from one of the reasons that I mentioned before on that slide, to aggressive the therapy or the tumor now takes too quickly and escapes or it doesn't persist for long enough. So some of these problems are preventing CAR-T from working where we heard that would have shown promise. And that's where OmniCAR can help overcome where the others are stumbling in areas of unmet need and also where the competitive landscape was very favorable for us as well. But above and beyond that, we can work there in the green, we can work with third parties regardless of their targets, regardless of their constructs or cell types where you can collaborate with them and by modularizing what they have, we can make their therapy safer and more efficacious at the end of the day. So I'm just going to present a couple of data slides, some of which you've seen before to illustrate some of the features that, that video showed. And one is control dose-dependent lost-dependent cytotoxicity. So you'll see on the left there, the mice -- you'll see when you give the cells alone, the tumor just keeps growing, the cells aren't switched on. But as soon as you give a little bit of binder, the therapy switches on and starts killing the tumor and the more bind you give, the more the, the better the cells kill the tumors and the longer the subjects live. So you get dose-dependent cytotoxicity. In traditional drug development, pre-CAR-T, this is what you would expect to see. The more medicine you give the stronger the effect up to a certain point of toxicity, it's called a dose response group. That doesn't happen in CAR-T. But this is combining like the unparalleled cancer-killing properties on a T cell, but you're giving it the control and the predictability of a regular medicine. So this is exactly where you want to be controlled like a remote control being able to control the activities of these cells in obedient and predictable manner, which is fantastic. And this was some world first data we presented a couple of months ago or a few months ago now, where we can reno one's done this before. So we got some OmniCAR cells, armed them against HER2. And you can see a nice curve there in the green that started killing these tumors in goldilocks manner. You don't want that curve too steep or too flat, you're at a nice low control curve. And we can get a steepen flat one if we want it, but we can control that and given the exact curve that we wanted. So that's wonderful. But here's what we do. This is where we need. You get these same cells and you wash them a new rest of them so that they're naked, if you will, that's just got their one half the Velcro again. And then you armed them again. And something amazing happens is that not only do these start killing the cancer again, but it kills it in the exact same way and to the same level and the same kinetics as they do preowned. So what does this mean? Not only can they cells be rearmed but it doesn't matter whether it's rearmed or preowned, it kills in the same the predictable level, not only the level but the kinetics of that killing. So flexible and predictable killing. And this was the -- well first. Another world first and bear with me because this is a little bit geeky, but to show redirection here is it's never been done before. So brain cancer is one of these awful cancers where there's not just one type of antigen on the service of the cancer cell. It's like a soup of different cells with different types of antigens on them. And 2 of the common ones are HER2 in the green and EGFRviii in red and so we put a soup of these 2 types of brain cancer into these cells and into these walls. And we added an OmniCAR. So an OmniCAR cell that was pre-armed against one of them, the red one EGFRviii. And what did we see? bang rapid killing of those brain cancer cells. Interestingly, the ones expressing HER2 were left alone, completely unharmed until at 20 hours, we did something that we didn't expect to see the results of this so dramatically. [ Our 20 ], all we did was dropped in another binder this time against HER2, note there are no new cells being added. We just dropped in the binder and bang, something amazing happened. We got redirection. So it's stopped killing one and started killing the other one, almost immediately. And so for the very first time being able to say, not only by dropping in a binder, we're switching its redirection and by redirecting it, we're actually -- it's sniffing up and killing these cancer cells without any new T cells added no new cells added. So just by switching out the binder, we can redirect this thing to [ Snipe at Cancer ]. So what does this mean in a real world? Well, as -- again, as the tumor mutates at the moment, current CAR-Ts are call flat-footed. You can't do anything that's bad luck. But with super aggressive cancers, especially GBM is one of them, AML is another one, you can chase it down and you don't need to wait 22 days for another manufacturing run if the patient still allow you drop in another binder and you can redirect this therapy to chase down that cancer even if it mutates with the aim of curative intent each time. So super exciting. Now another aspect of OmniCAR which is maybe a bit closer to home for those following general industrials is one of COGS. So conventional CAR-T, very expensive to make each time you make one it's several hundred thousand dollars in 22 days. And if you wanted to make a multivalent CAR-T, so a CAR-T that created -- you wanted to address it against many different antigens on the cancer, you would have to do it like this. So if you want to persistently give it in a solid tumor in order for it to work it out to do 1, 2, 3, 4, 5, 6 different runs, each of them has gone across hundreds of thousands of dollars. Each of them is going to take 22 days from vein to vein. You can't redirect them. It's prohibitive. Yet, we've seen in some investigator-initiated studies that are having to get huge grants of millions of dollars to do this in 1 patient or 2 patients. We can see that this sort of works is just prohibitive. But with OmniCAR, we do the hard work once, making the cell is the hard work, you do that once. And then for each subsequent time, all you're doing, you're making and binders. And that is much, much, much cheaper. It's a fraction of the cost. It's done all the time, all day every day by many, many companies around the world right now, right now. So subsequent administration of the binders is cheap, and there is no delay. And here's the thing. We're the other ones where you have to -- you can't redirect it against another target with this one you can redirect it, as I showed you in the previous slide as the tumor mutates. So a fraction of the cost. So you got the expensive part you do once, which is making your cell and then you just do the binders. And this will be the case even if they're off-the-shelf cells, the economics would still stack up. So that is the -- so the end game, we all know what Apple did with their ecosystem of consumer electronics and online services, making them integrated and creating a whole ecosystem for the consumer. Well, if you can do this for a consumer, it's not a shame that in throughout the medical history, we've not done this in medicine. We think OmniCAR is uniquely placed to do this for the very first time, a patient-centric ecosystem of personalization with OmniCAR at its heart. So we see a world in the not-too-distant future where a patient goes into the clinic as their biopsy or a blood sample. And they run sort of pathology on that determines the mutational profile of the cancer. And this happens already and has been happening for a few years. So this is a routine right now in any developed country. This already happens. So a doctor will look at this patient profile and say, okay, I need binders against 1, 2 and 5. And you can pick off the shelf, these [ spike end ] binders, plug them into the cell of your choice, whether it's a T cell, an NK cell, it doesn't matter, and then you got a plug-and-play approach. A patient is getting a world-best therapy that happens to be bespoke for their exact tumor profile. Now normally, personalization comes at the expense of efficiency. Think of like a bespoke suit versus one off the rack. Well imagine if you could get a bespoke suit that was off the rack. That's basically what this is. That's a plug-and-play approach. We are progressing our 3 in-house programs, AML, HER2 positive and GBM, make no mistake about that. But that is going to be the beachhead for this ecosystem. And if you like, we're developing the first apps in the app store. But above and beyond that, anyone developing a binder, we can tag their binders and put them in the app store. Anyone developing a cell waiting their cells is going to win. We can tag that and put it in the app store. So this is going to really be -- again, this is only possible because of the unique covalent modular features of OmniCAR that no other system can do. So it's incredibly exciting. It's very ambitious. Make no apologies for that. And the good thing is we are hitting there anyway because our first 3 programs are going to be the first in the app store. So that is where we are really on. Just to summarize, OmniCAR, you just heard me prattle on about that and why I'm so enthusiastic this platform that's given us to 3 programs, but really there's a whole bigger play here. And you've heard me talk about targeted therapies in the clinic now. Drugs made, patients ready to go, 200s already being treated at 45 mgs, all producing data this year. So sort of the enhancements in the middle currently in stealth mode for patent and commercial reasons. That is due to come out of stealth mode in the coming months. So please look out for that. And as the name suggests, is a way of enhancing current generation of cell therapy to make them -- basically make them work better. And if we get it right with that, with the current generation, it will also be applicable for next-generation cell therapies as well. We are doing that with Peter Mac. Data is being -- we've been looking at that very, very closely with them, designing all the studies, running the studies with them and due to come out of stealth mode in the coming months. So lots of catalysts this year, as you'd expect from a pipeline like this. So again, ready to go. First cap off the rank is this study in PTCL. That is imminent. We're not awaiting drug delivery now. It's been made and been shipped. So that's fantastic. Spoke to Miles Prince, ready to go, super enthusiastic. Cannot believe the responses you're seeing in a couple of its patients, giving us updates on those patients, continue to do very, very well. AML results this year, cell therapy enhancements coming out of stealth mode. OmniCAR AML, OmniCAR HER2, OmniCAR GBM, all of that is this year, and that's not -- and that's just the tops of the waves types of things. So very exciting full year for us. So again, a reminder, world-class pedigree. We've got a very deep pipeline with lots of shots on goal. 2 targeted therapies in the clinic, from blue chip institutions spinning out data, and it's all about OmniCAR for the future and couldn't be more excited. And I'll finish with this slide, which I've gotten a lot of feedback on actually from last week. And that is in a market like this, especially when there's a lot of macro movement, what do you do? Very hard to pick a winner from a bottom-up point of view. Top-down is very different. You look at what sectors are more resilient to macroeconomic uncertainty. Well, certainly, health care is the beneficiary there because regardless of geopolitical escalations, regardless of inflation, people aren't going to stop taking medicines, especially life-saving medicines. So you look at health care. So what's the biggest market within health care? Well, hands down, by a factor of 3, it's oncology. Oncology is 3x bigger than the next biggest health care sector. And you look, okay, within oncology, what's the fastest growing area, not the biggest area because some of those big areas can be diminishing. What's the fastest-growing area in this biggest health care market? And without that, you only need to be able to read headlines to see that its cell therapy and CAR-T in particular. Why? On the back of unbelievable data, data like Carl June just spoke about a month ago, data like J&J and Legend released 2 days ago. So it's on the back of real world data, not hype, not promise. Real data that is making this the fastest growing area. And then you think, okay, of this fastest-growing area, who's at the front? Well, I can tell you, at the front, and you know this makes sense. It's someone that can do this at scale. Someone that can make these therapies controllable and predictable like a regular medicine, people who can address any target in any immune cell. Why? Because it's too early to pick winners? And who satisfies all of these? Well, it's Prescient, and we're uniquely placed. I can't think of another company that's as well placed as this from a top-down perspective. So incredibly exciting. You add to this our collaborations. You add to this our leadership and talent in-house. You add to that our fiscal responsibility and whatnot. And you can see it makes a lot of sense. So from a top-down approach. So I'll end up there. Thank you for indulging me, and I look forward to your questions.

Thank you, Steven. Quite a few questions have come through. And I might start off with Matthew's question, the data on rearming, resting, switching and lower immune potentially immune potential looks promising. What are the other specific preclinical milestones you are planning to undertake and test before reaching the clinic?

So yes, good question. It is -- there are 2 buckets, if you like. One, can we get them to work the way we think they're going to work, and that's some of the data that we've shown you there and continuing to do that. Looking at different variants of what we have, so we can optimize the system. This is all the stuff that's necessary, and it's exciting to nerds and people in the industry, people who look at this with a fine-toothed comb. And the other bucket is making these -- getting these regulatory packages in shape for the regulators, for the FDA and the TGA. And that is on manufacturing. That's on safety, that's on reproducibility. It's on immunogenicity. So we're doing all of these things in parallel and running good speed on those.

Thank you. A couple of questions around is, is OmniCAR the same as [ IMU's 1 kinetics ]? And then also referenced back to mRNA and other cancer treatments. I mean I'm just going to broadly wrap this into one question and say, how are you -- is there competition? Do you see there being competition? And then how do you stack up against the competition and or deal with or working with competition?

Yes. So that's the great thing about being in our position. And I understand like a small market like there some companies say some things about others. I can say this about imaging. Well, first of all, imagine on a CAR-T company. They don't have a CAR-T. They have an oncolytic virus that can infect cancer cells and make them express CD19 so that you can use one of those first-generation CAR-Ts, okay? So I can imagine every -- given that, that race is running on with CD19, I would imagine that the people wanting to collaborate with imaging are people who considerably behind the current leaders. I'm talking about Gilead, BMS, Novartis, and want to play catch up and apply their technologies give them a space to plan, and they're the people I would have mentally want to play with imaging. So imaging don't have a CAR-T. If they did, guess what, they would want to speak to us, and their collaborators should want to speak to us. Why? Imagine your whole body, you've got big solid tumor masses all laid up with CD19. Do you really want to give these patients a therapy you can't turn off? No way. There's no way. And what happens if the tumor mutates? So bottom line is, in our position, it's so enviable because we can work with anyone. Why? Because they're not competitors, they're customers. Anyone with a CAR-T can come to us and we can make their therapy safer. We can make it controllable, and we can make it flexible. So that's the great thing about the position we're in. Bring them on. The more people in this space, the better. They're all potential collaborators and potential customers. Insofar as mRNA, that is -- that's a completely different area. That's not cell therapy. That's -- it's obviously its first utility, as many would know, is in vaccine development. That's fantastic. They're very, very short-lived. They're very unstable, which is why Pfizer's vaccine and Moderna's vaccine have got to be shipped very, very, very low temperatures with strict content logistics, but they're not cancer therapies today, and they're not CAR-T today and a long way from that. So again, that's probably a bit of a red herring and is not where the field is at now. People might use these to actually make the CAR-Ts, but they're not going to supplant CAR-Ts, certainly not yet, not in the foreseeable future and if ever. Hopefully, that answers the question.

Yes. No, thank you. And it kind of led into the next question a little bit. It's not [indiscernible] this is from John. There are not many Australian listed companies in this field. How does Prescient Therapy, its Prescient Technologies differ from Chimeric Therapeutics, which is also working on CAR-T therapy?

Once again, they have a -- they've got one of those first -- a variation in the first generation CAR-T. So they're de novo constructs. They're not modular. They're not controllable. They're not adaptable. They're not redirectable. So Chimeric kind of targeting a type of -- that's -- I don't even know what they are targeting exactly, but they're using a coral toxins it's something derived from a scorpion, I believe, and we're using that to target 1 thing on GBM. So once again, I wish them all the best, but it really is a particular customer. Do you want to target more than 1 thing on GMB? Do you want to make your therapy safer? Great. Come talk to us. So that's how they differ, they've got -- again, once again, I don't want to sound like a parrot, but we're not in the business of picking winners with respect to 2 targets. Other companies don't do that. Fantastic. We can work with you. Other companies like Arovella on the ASX want to champion a certain type of cell. Fantastic. I hope we will win. Why? Because they can work with potential customer.

Question on PTX-100 from Tom. Once the PTX-100 TCL trial, once enrolled, how long is the treatment, please?

It depends how long they respond. So the treatment, it typically, it can be -- these patients normally progress either immediately, which is sad. And we had in our study, depending on the malignancies, some of them are like that as well. So it can be anywhere from -- those who respond tend to respond for normally 3 to 4 months. So that's how long the treatment can go for each patient. And then you get some spectacular responses like we got 1 at 12 months and 1 now at 24 months. So that's how long the therapy can go for each individual patient whereafter saying a dozen patients. The good news is we don't need to -- if we -- I hope that we're at the end of this study, and we've got still got patients that are still on therapy, that would be unbelievable, but you don't need to wait until so we're aiming for full recruitment this year. It doesn't mean that the patients would have stopped therapy this year. In fact, I think it will be good for us if it wasn't, right? I mean they're staying on therapy for longer.

Thank you. Maria, it's Steve. With Joe Biden calling for massive investment and finding better treatments and potentially curing some cancers, can Prescient take advantage of this massive investment? And can we get our name exposed with the people leading this drive?

I would love to. It's -- so Joe Biden -- for those who don't know, Joe Biden lost his son to brain cancer. And when he was Vice President, he pioneered what's called the Moonshot program. And I applaud that this -- we'll leave politics out of this. But I applaud the ambition, which is instead of incremental benefits in medicine, which we've seen in cancer right up until now. It's all incremental benefit, okay, 6-week survival, let's make that 8-week survival, great. Let's make that 12-week survival. Who cares? So Joe Biden said, let's swing for the fences. Let's go for the Moonshot. And as we all know brain cancer is obviously very close to his heart. So I welcome this with open arms because we are also swinging for the fences. Cell therapy is swinging for the fences, and we're right at the front of that queue. So I don't actually know how we get. There's no details on this initiative yet, but you can bet we'll be looking into it. That it would be nice.

Thank you. All right. Owen, does this application for B-cell blood cancer -- does this have application or B-cell blood cancers?

The short answer is yes. But that first generation, like the Novartis, Gilead, BMS, they were on B-cell malignancy. Some of these stunning responses were in B-cell cancers. So if you know someone that has B-cell cancers, the great news is there's therapy is approved and subsidized right now, CAR-Ts. They're the first generation of those. We -- there's 2 schools of thought. And when we first got this technology in our hands, do we say, should we be fast followers? Shall we do the exact same disease and try to improve on it? Or should we go where no one else is now and where they're really struggling? And there was a good debate, and it was a multifaceted debate. We eventually decided we shouldn't play fast followers because that race is largely one and done. And look, if you're getting sort of 70%, 80%, 90% response rate, how much more improvement can you possibly make on that to get the commercial outcome there? So broadly speaking, pharmaceutical companies, they want to either make it safer, make it cheaper or make it more efficacious. We think we can do all 3 of those, but we think we deserve our -- would be better off putting our efforts where no one currently is making a dent rather than hoping to improve on a really excellent data.

Thank you. And Owen is asking, is there any ponytail application for Parkinson's disease?

No, that's trickier. And again, are being touched by loved ones with Parkinson's, awful disease. That is not so much created by aberrant cells getting out of control, if you like. It is a deficiency in the cell creating something called dopamine largely. So it's more a degenerative disease rather than a disease of malignancy. I think cell therapy will play a role there, there's no doubt, I think. But I don't think it's where you're trying to eliminate some badly behaving cells so much as we are looking to replace them with cells that are doing the right thing. So I think that will be an area for cell therapy and regenerative medicine rather than there might be applications in CAR-T. If I can find a target that's problematic in Parkinson's, what we can get there and make a dent, but I'm unaware of one. It's not the lowest hanging fruit for us now. And I wish it was.

[indiscernible] asks. My only question would be PTX-100 shipment in previous briefings that was mentioned, the shipment is imminent. Is there any indication as to how much longer?

It's weeks now. And again, no one's more frustrated than myself or other than the clinician. But again, this was largely out of our hands. It's on our way. And it's not like you can make it and then ship it just so -- just so people appreciate. You make it, and then once you finish making it, you have to do a sterility study on this, a purity study on that. So that means you have to make sure that no bacteria is growing in that before they release it. So when you finish making it, you then have to test its sterility. And that sterility is finished, and only when that is finished, you don't want these things growing bacteria in it and then injecting sick patients with it, right. So that's being done. It has been now released and scheduled for shipment in imminently, I mean any day now. And then it comes to cold storage here in Australia and then we're ready to go. So that is, once again, -- it's a shame that it took this long, but it's -- luckily, it's behind us now.

Matthews. It seems great to have differentiation in current in-house programs. It also potentially low-hanging fruit in to develop an OmniCAR version against CD19 that is controllable and safer versus existing approved first gene therapies.

So I think that goes back to...

There is, and it's probably -- I'll just reask the question again, sorry. Is it also potentially that there is low-hanging fruit to develop an OmniCAR version against COVID-19 that is controllable and safer versus existing approved first-generation therapies?

So did you say COVID-19 -- or CD19? They're very different.

Yes, CD -- oh, sorry, yes, let's go CD19, sorry.

Yes. Very different. Yes. I think yes, there's no reason why we can't do an anti-CD19 OmniCAR. Absolutely, we can. Absolutely, we can. And you know what, I would love to do this off balance sheet and work with someone who has it. What I'm saying is when they get it, it would be -- there'd be no B cell plays no long-lasting bad side effects of having a permanent therapy, get the job done and let these cells become dormant in case you need them again 1 day, hopefully, you don't. But having something that's controllable, safer and then you can switch off once the job's done, will be a much better to be a first-in-class CD19 therapy. But I would rather give that to someone with a vested interest in CD19. It looks like, as I said, the CD19 looks one on one, but it is validated, but there's -- it's -- there are more -- there are so many CD19 trials out there. I just don't know how they're ever going to find oxygen, all of them to find oxygen. But when there's already excellent data out there. So yes, we can make one, absolutely. I'd rather make it for someone else and do that off balance sheet so that you, good shareholders, aren't wearing the risk. They are. And I'm not talking about scientific risk or clinical risk. I'm talking about commercial risk.

Thank you for that. I'm currently suffering from COVID-19. So maybe I've got it on the brain. So John asks, melanoma cancer must be included in PTX offer. So I think that's a question. Just be a statement.

John standing what is demanding it. But the thing about melanoma is it is very treatable. There's -- melanoma is -- has lots of neoantigens. Neoantigens lend itself very, very well to basically things like Keytruda checkpoint inhibitors. There is -- you don't need a CAR-T for melanoma because there's already existing therapies that work really, really well in melanoma. There might be a space for neoantigens where people might have relapsed against checkpoint inhibitors. But it's not like 7, 10 years ago when people were terrified of melanoma, like now there's -- people get a really, really good survival out of melanoma without any CAR-T therapy. That said, could we work with melanoma? Yes, we could. It's just, again, from a competitive landscape point of view, I'd rather it be someone else because it's a pretty well-served market right now and without CAR-Ts. So where -- it's the really the wrong question, what people should be asking is, where are no other therapies working very well where CAR-T holds really good promise. That's the question people should be asking. Not can you do a melanoma study.

Understood. All right. Look, I think it's got 2:00. So we've sort of used the allotted time for the presentation. And Steven, thank you very much. Really enjoyed the presentation and the updated runway, and look all very, very promising. And congratulations to everything that you've achieved over the journey in more recent times. I think we got some great questions today. We really appreciate everyone's participation. If there are any questions that I haven't asked, I tried to sort of observe what was subsequently covered as the questions came through in the presentation. But if there's anything further there, put it in as you leave in the survey, and we'll forward it on to Steven, and my team will coordinate answers where needed. And otherwise, Steven, I'll leave it for you to finishing comments.

I just think whether we left that final slide, the biggest market in health care, oncology, fastest-growing, CAR-T, who's at the front of that? Well, I think we are. And you added on our -- our other great qualities of our in-house programs, the ability to work with others, our being financially astute, good leadership, good collaborations, it makes a lot of sense. So thank you, everyone, for their support, and looking forward to cracking you.