Thank you for joining us today. I'm Robert Burns, a managing director and senior biotech analyst at H.C. Wainwright. I'm joined today by Chris Behrenbruch, the CEO of Telix, and David Cade, the CMO of Telix. Gentlemen, thank you for joining us today. Thanks very much. Good to see you, Robbie. Awesome. Why don't we just dive in? For those who may be unfamiliar with Telix, can you give us a brief overview of the company and give us a recap of your 2025 earnings that led to a strong year-over-year growth, as well as the disease areas that you're focused on? Yeah, thanks. We're a fully vertically integrated radiopharma company specializing in oncology. We have a portfolio focus in urologic oncology and neuro-oncology in particular. We're a commercial stage company. This past year we did just over $800 million in sales, primarily around our U.S. prostate cancer imaging franchise. We have two FDA-approved products in that space. You know, very active product portfolio on the therapy trials, which I'm sure we'll get to at some point as well. In terms of commercial performance, we've just put out our guidance for 2026, targeting the mid-$900 million in revenue. Really reflective of, I think, a very solid growth in the prostate cancer imaging space globally, but particularly the U.S., as well as the launch of our second prostate cancer product, which got pass-through in October of last year. That's putting a fair bit of momentum into our commercial operations as well. I'll pause there. Hopefully, that's a good snapshot. Yeah, no, it definitely was. I sort of wanted to hone in a little more on the revenue guidance that you provided. I know it's around $ 950 million- $970 million in revenue for 2026, with roughly a 25% growth in the Precision Medicine business unit. You know, when we think about the growth opportunities for the PSMA franchise, you know, where do you see significant upside for that agent, as well as the new launches in brain and kidney cancer, specifically Pixclara and Zircaix? Well, our guidance doesn't include any unapproved products, so it's. So when we get approval for Pixclara, which we've just resubmitted just this past week, and Zircaix is not too far behind. As you recall, we had a CRL for both of those programs last year. We will revise our guidance accordingly. We still expect to resubmit Zircaix, obviously this year, and hopefully launch it this year as well. That product has a breakthrough designation, so pending the review of the CMC issues we had with the FDA, we, you know, expect to get that program back on track. For the prostate cancer area, I would say there's sort of three drivers for the business. First of all, you know, there's the inherent growth still in PSMA. You know, we think that's 5%-7% a year based on the fact that there's still white spaces in the market. There's still referral urologists that are getting up to speed on the value of PSMA. It may surprise you to know it, but CTs and bone scans are still prescribed and obviously practice of medicine has changed. Maybe David can elucidate a little bit more, you know, how that practice is changing. We also see urologists taking more and more of a front line interest in PSMA imaging. So we're seeing. I think in the steady state, call it, you know, three to five years out, you're gonna see 25%-30% of the market for PSMA imaging actually directly controlled by urology. I think that's an emerging sort of category of PET scanner user/owner /stakeholder. I think the second tailwind on the PSMA landscape is really around having a second product that's got pass-through. You know, Gozellix is a very innovative product. It offers some real clinical and distribution benefits. By having a product segmentation or market segmentation strategy for prostate cancer, we really target commercial and OPPS payers very differently. I think that gives us a commercial advantage that will translate into revenue. I think the third one is we have a significant phase III trial running this year, which is the BiPASS trial. This is an opportunity to significantly grow the TAM. The BiPASS study stands on the shoulders, obviously, of great work that's been done in academia, particularly PRIMARY2 study that was recently presented. We actually wanted to take that study to the FDA. Lost you. We actually took that study to the FDA. No, please wait a moment. Did. Sorry? We lost you for a second there. Oh, I'm really sorry. Can you hear me now? I can hear you, right, Chris? Yeah. It might be Robbie. Okay. That's super weird. It might be Robbie. Am I back? Can you hear David Cade? No, it's coming in and out. Can you hear David? David, can you speak, please? Can you pick up on the, Yeah. Robbie, how's my reception? Robbie, I can hear Chris perfectly fine. Oh, okay. Yeah. I guess it's on my end then. It might be. All right. My apologies. Let's continue. I'll continue for a second, and then we'll just pause and do an audio catch-up. Awesome. Basically, PRIMARY2 study, we actually took that study to the FDA, and it does require some tweaks for it to be a label indicating study. You know, there's a very important education process that's going on in the process of executing that study, and I think that builds further momentum into where prostate cancer imaging can be used. I'll pause there. Hopefully, you got some of that. There's a lot of, you know, to look forward to in prostate cancer imaging in 2026. One of the things I'm curious about is, you know, if the BiPASS study actually succeeds, you know, what does that mean for the market expansion potential in terms of number of scans that you might be eligible to garner? Yeah. Dave, why don't you have a chat about the clinical consequence and maybe what that means in TAM? Yeah, sure. Robbie, it's a very important question, and it was really brought to us by our clinicians themselves. Essentially, in the United States, if we just focus on the U.S., you know, there's north of 1 million biopsies done to try to establish the diagnosis of prostate cancer a year. I emphasize the word try because a very significant proportion of those, somewhere between, you know, 750,000, maybe 800,000 of those, don't yield tissue that can be decisively ruled by a histopathologist as either being prostate cancer. The yield from the biopsy is low, and as a consequence, there's a very significant number, maybe 250,000 men, that actually decline a prostate biopsy when they probably should. There's a lot to improve. The way it's usually done is with an MRI scan, and I won't bore you with all the details, but the MRI scan is scored according to a five-point scale, which is called the PI-RADS system, you know, 1, 2, 3, 4, 5, where 1 is a very normal scan. You know, typically we don't get a lot of PI-RADS 1s in the men in the age group that we expect to have prostate cancer. That's like a very normal scan. PI-RADS 5 is prostate cancer. There's an area in the middle, PI-RADS 2, 3, and 4, particularly PI-RADS 2 and 3, which is a very significant group where the MRI is unresolved, and it doesn't indicate to the urologist where to biopsy from. We typically end up doing what we call a template biopsy, which is sort of, you know, a row, 4, 4, 4. Basically somewhere between 12 and 20, maybe 12 and 24 needle cores for the biopsy, and even yet it doesn't yield a result. There is a huge opportunity to do, and the results of this study, this BiPASS trial have already shown this, is that with a gallium PSMA PET scan added to the MRI, it can either direct, you know, using that imaging, where the biopsy should be taken. Instead of doing 24 core biopsies, it can be image-guided and one needle core can be taken, or, on the other hand, if the gallium PSMA PET scan is negative, no biopsy needs to be taken at all, and the patient can be reassured and put on to active surveillance where their PSA is monitored, and they'd come back and are simply non-invasively scanned at a later date, six or 12 months' time. For laypeople, and this is not a lay audience, but for the laypeople, I explain it as either one and done or none and done, which is a major de-escalation of what we typically do today, which is very unsatisfying with that low yield of diagnosis. You can see with that utility, that opportunity is very significant, as Chris described, and that's probably an explanation of why this BiPASS trial is enrolling so rapidly, possibly even ahead of plan, which as you know, doesn't happen with trials all that often. Just to summarize, you know, we're talking about a sort of an estimated 750,000-800,000 scans with the way that clinical evolution takes place. What it also does is it affords the question to be asked in the future, should PET follow MR, or in fact, should PET lead MR. That will be something that will come out as there's more experience with clinical practice and combining the two modalities. Yeah. You know, at least for me as a male, it seems like I would definitely prefer to have, you know, the added-on diagnostic imaging rather than having to take these numerous core biopsy samples, which are frankly onerous. Yeah. Well, also, I think it's a cost issue. I mean, if you look at the health economics of replacing biopsy, not just the cost of biopsy and the practice demands, but also the morbidity issues associated with it, you know, it's gonna clearly save the healthcare system money and, as you know, you know, it does. Patients care about this and, in fact, it's hard to know the exact number, of course, 'cause it's an estimate, and literature varies fairly widely. You know, there's estimated to be 200,000-250,000 men that simply don't participate in the process because just don't want stuff near their nether regions and, you know, if we can I'm putting that as diplomatically as I can. You know, I think that if we can make patient compliance better, and patient engagement better, that's gonna have a big consequence on detection rates, so I think it's very positive. I would certainly agree with you there. Why don't we move on to your therapeutics pipeline now? You know, you recently reported initial data from Part 1 of the ProstACT Global trial, which is your phase III trial in mCRPC. You know, can you provide an overview of that trial design and remind us what you reported in terms of, you know, safety as well as dosimetry, and what impact that it has on Part 2? Sure. Look, when we took the protocol to regulators, you know, not all regulators had the same viewpoint on it. You know, we had a number of sophisticated regulators that were quite okay based on the data that we had of going straight into ProstACT Global, which is a randomized phase III trial across three different treatment cohorts. It's a standard of care plus versus a standard of care alone, randomized study. The three different treatment arms are enzalutamide, abiraterone, and docetaxel combinations. We've selected those because those ARPI switches and taxane reflect sort of consistent global standard practice in first and second line metastatic prostate cancer. When we went to the agency, they felt that we were a little bit light on the combos with the ARPIs comparatively. We went in with the view that enzalutamide and abiraterone are a class, and we had some, you know, data to support that assertion, but the FDA wanted to see a bit more. That's where the genesis of the Part 1 study came out. It's really to reinforce that there's no particular delta between the different treatment arms, particularly the ARPIs. I mean, we had some combination data with docetaxel. We showed that it was tolerable in combination with docetaxel, but we were a bit lighter on than the FDA wanted with the ARPIs. That's why we've done this additional study. We've, as you note, just put the results out. Maybe I'll make an initial comment, and then David, if you wanna chime on anything. The purpose of the study, as you know, was safety and dosimetry. We were really looking on a cross-cohort basis. There's always been a lot of speculation around the asset, around safety and particularly hematologic AEs. What we hope that the data shows sort of fairly definitively is that these are well-tolerated treatments. They, TLX591 lays very nicely on top of those different combinations. What the data shows is that we do have hematologic toxicities. It's the main toxicity associated with it, but it's transient and self-limiting and reverses very rapidly, even when the adverse event is a higher grade adverse event. That's counterbalanced by the fact that the patient-centric AEs are very benign, because we don't have salivary gland, you know, exocrine gland uptake. We don't have renal excretion. We think on the balance that it represents a very compelling risk-benefit. That's what's demonstrated in the safety data. Now we'll be taking that combined with the dosimetry, which is again, very favorable, particularly compared to, you know, current solutions that are in routine clinical use. You know, we'll take that to the agency with the expectation that we'll be able to move to Part 2 and dose patients into Part 2 in the United States in the fairly near future. Awesome. Thank you for that. You know, one of the things I'm sort of curious about as well, you know, what are the next steps in terms of opening up enrollment within the U.S.? Yeah. I mean, we did recruit patients in Part 1 in the U.S., so we do have sites that are sort of in the program. We will of course be adding a bunch more that are particularly focused on the Part 2. It is a global study, so we have regulatory approval, I think now in seven or eight countries. We are actively recruiting patients in Canada, Australia, New Zealand. We've got U.K. just coming online. We are you know rolling out the program globally. I expect that we'll get U.S. patients subject of course to what the agency says you know into the study around mid-year, maybe early Q3. We expect about 20% of the study to be recruited in the U.S. Yeah, obviously it's critically important to get U.S. patient experience for the study. You know, it's a high priority study. We're really pleased with the data. You know, I think it sort of finally benchmarks once and for all the profile of the drug. Unfortunately, when we deal with targeted radiation, cytopenias are a common side effect. The fact that the management of those AEs are so straightforward, you know, that was the clinical experience, gives us a pretty clear platform for discussion with the agency. I don't know, David, do you wanna add anything, you know, just from a medical perspective? Dave? I think he may have dropped off. Yeah. We did a lot of homework. We took a lot of patient input into the design of the trial, a lot of FDA input into the design of the trial. I think, you know, fundamentally, the Part 1 results do demonstrate the feasibility of integrating TLX591 with a contemporary backbone of different global standards of care, as Chris mentioned. You know, just what the prevailing practice is in the United States, which is predominantly ARPI switch, but also outside of the United States, both Europe and in Asia, which is primarily moving from an ARPI to docetaxel. It really is, as the name of the study says, a global trial. We would see, you know, should the trial, you know, meet its primary endpoint, that it would lead to simultaneous filings, not just in the United States and Europe, but ultimately Japan, China, South Korea, and so forth. That's why we designed it that way. I think it's a very pragmatic trial. As Chris mentioned, the next step is to take those data. They're exactly what the FDA asked for. We'll present it to the FDA seeking an IND amendment to start to put U.S. patients into Part 2, which is already enrolling elsewhere. Yeah. Very exciting. Talking about Part 2 of the trial, you know, what is the sort of enrollment trend that you're currently seeing for that portion of the trial? Yeah, I mean, I can initially comment. So the trial is certainly picking up steam compared to the Part 1 study. The Part 1 study took a long time because it was a very technical study. It required a lot of SPECT imaging, a lot of patient visits, so we had limited it to a limited number of sites because of its technically demanding nature. Now we've added, of course, a lot more sites for the Part 2, and so that's a natural accelerator. Also the protocol of Part 2 is just much more streamlined. You know, there's a single time point PET imaging for patient selection. It's much more like a clinical treatment protocol for, you know, conventional PSMA RLT therapy. We do expect to see a pickup and obviously having some data out as well from Part 1 is quite motivating, I think, for investigators to kinda get on with the study with a sort of clear understanding of what they're dealing with and how they manage patients going forward. We've seen good pickup. The goal this year is, we have based on an event-driven process, obviously, on 25% of events, so around 80 patients, we expect to report out a futility, an interim futility. We discussed that with a number of regulators, but particularly with the FDA. We don't have, obviously, because it is event-driven, we don't know when that's exactly gonna drop, but we would imagine sometime around Q4 or Q1 next year, and that will be the next sort of milestone on the study, as far as the Part 2 randomization goes. Well, I'm certainly looking forward to that data. One of the other questions I also have, you know, I note that you also have TLX592, which is, you know, which utilizes an alpha emitter, versus the beta from TLX591. How are you thinking about the sequencing of those two agents, within your portfolio and the treatment paradigm specifically? Yeah, look, we're exploring a number of things on alpha. We haven't locked down finally what our PSMA strategy is really gonna be in alpha. TLX592 is a fairly you know, very early stage asset. We have done some human studies with TLX592, but they were done with PET imaging as a surrogate. As you know, actinium is quite tough to image in humans. It can be done, but it's not sort of that straightforward. So what we did is we did targeting and biodistribution studies with copper-64 as a surrogate. Not that we have the intention to develop it commercially, but to get a sense in a benign way of really what the pharmacology of that agent's like, and it looks quite promising. We are getting ready now to do the first in human actinium studies with that agent. We're you know starting off in very late stage patients that have typically progressed on lutetium therapy. That's where we'll get initial clinical experience with that. The value proposition of TLX592 is really twofold. First of all, it doesn't have exocrine gland uptake. One of the real challenges with small molecule delivery of alphas has been salivary and lacrimal gland ablation, and not typically transient, usually fairly well more serious, I would say, in terms of grade than what we typically see with a beta emitter. Then secondly, you know, we've had discontinuations of programs recently for renal you know toxicity with renally excreted alphas. Again, that will vary from program to program, but generally speaking, alphas don't have much business ending up in your kidneys. The liver is a far more radio-resistant organ, and so the attraction of TLX592, it's somewhat derived from TLX591, hence the sort of naming convention, is that it is also hepatically excreted like TLX591. It has very little renal excretion, and so the expectation is that it's a better suited moiety for targeting alpha emitters, and I guess we'll find that out in due course. We, of course, dabble in small molecules. I mean, we wanna understand the field. We have a fairly active R&D program looking at alpha emitters with small molecules as well 'cause, of course, the advantage with smaller formats, and, you know, we look at small molecules, we look at small proteins. We have a protein engineering team in Los Angeles that looks at smaller formats. Of course, the advantage is that as we move into earlier lines of therapy, and I think the sweet spot for alphas is honestly not treating late stage advanced bulky cancers. It's not really what the radio biology of alpha is optimal for. I think alpha will have its sweet spot one day in targeting that very low burden of disease in the early metastatic, perhaps even hormone-sensitive, space. That's where alphas will be fantastic, and then tumor penetration is really gonna matter. But also those patients are gonna live for a very, very long time. You know, we've got to be confident that when we're parking an alpha emitter, particularly with respect to clearance organ, that we are not creating something that's gonna be a major downstream, you know, multi-year risk for the patient. I think that's where the field has quite a bit of evolution to still undertake. Yeah, you know, when you think about the alpha emitter space, obviously, you know, you have actinium as well as 212 Pb or lead. You know, there are a few players within the lead space. Obviously, ARTBIO is one of them, Perspective Therapeutics. You know, how are you thinking about the utilization of lead specifically with the small molecule components? Yeah, I mean, look, there's sort of a heuristic in radiopharma that your pharmacologic half-life and your radiobiological half-life should somehow be similar. Of course, you know, we also ignore that heuristic quite often. I mean, lutetium PSMA products that are out there today in commercial use or even in late development are obviously violate that. You have a small molecule that has some hours of residence time, and then you put lutetium on it, which has a multi-day half-life. We're obviously not very dogmatic about it in practical reality. I think that the challenge with the short half-life alpha emitters is really when you're dealing typically with a small molecule, you're dealing with something that's under the threshold of first pass renal clearance. You know, you have to manage the design of your molecule very carefully around kidney metabolism. If your alphas end up, you know, in sort of prolonged glomerular retention, you're not going to really have a great outcome for the patient. You know, you want those decay events to happen quickly with a small molecule because typically, you know, it's not targeting the lesion for very long before it gets washed out. On the other hand, you also wanna make sure that those events are not taking place in your kidneys. We've seen in the last few months discontinuations of programs because that balance between, you know, imparted energy to the tumor and excretion, you know, is not really, you know, balanced. No, I completely agree with you there. You know, when we think about the mCRPC space more broadly, obviously there are a few other modalities that are targeting PSMA. T-cell engagers are a great example of that, and we've seen data from Genix as well as, Amgen. You know, how are you thinking about the deployment or physician preference for a radiotherapy over a T-cell engager? Yeah, I think it's a really important question, and I sometimes feel that the nuclear medicine community, we sort of ignore these questions at our peril. Part of the answer to that is how we've tackled TLX591, which is really, you know. Because it's a short duration of treatment, it's much more appealing for a medical oncologist to refer a patient. You know, they're not handing over a patient to an authorized prescriber in nuclear medicine or in radiation oncology for, you know, 40 weeks of therapy, right? It's more. You know, in fact, if you look at the global design, what we're trying to do is really layer TLX591 on top of, you know, kind of routine standard of care so that the patient management dynamic sort of stays status quo. You know, we've seen nuclear medicine products fail in the past because there hasn't been, you know, putting clinical efficacy aside, there hasn't been, you know, adequate motivation for a referral physician to just hand over a patient to another specialty. I think that is, particularly in the U.S. context, I think that is a real kind of just practical challenge. Yes, we forget kind of, you know, ignorantly that the med onc has a lot of opportunities to prescribe innovative new drugs to patients. There's a lot coming down the pathway. You made a couple of great examples. We're seeing next generation androgens, we're seeing PARPs, we're seeing all kinds of other things impact standard of care in prostate cancer. I think that the short answer to your question is really that radiation is incredibly valuable as a pillar of therapy, of durable treatment response in metastatic prostate cancer, and you have to think about radiopharmaceuticals as a sort of, you know, migration from a box, you know, from traditional LINAC-based approaches to systemic approaches. It's really the evolution of radiation oncology. I think that, you know, managing prostate cancer, as we all know, it's about therapeutic drugs, it's about surgery, and it's about radiation. I think that PSMA-targeted radiopharmaceuticals have a very natural role alongside potentially other immunomodulatory strategies in prostate cancer. I think they're actually complementary. You know, we see radiation as a driver of immune response in all kinds of cancers. We haven't seen a lot of success stories on the immunology front in prostate cancer so far on the immuno-oncology, and I actually think that radiation can drive more success in that space. Yeah, there's a lot to think about as the field evolves. No, I completely agree with you there, and thank you for those insights. Why don't we shift gears now to TLX101, which is currently being evaluated in the IPAX BrIGHT study, which is a phase III trial, in brain cancer. You know, can you talk a little bit about how that trial is designed, what the status of it is, as well as the market opportunity there? Dave, you wanna talk about IPAX BrIGHT? More your wheelhouse. Yeah, sure. Maybe I'll open, Chris, you could add some comments. But Robbie, IPAX BrIGHT, as you say, it's a phase III trial of our iodine-131 demonstrated meaningful tumor control and some extended survival. I'd caveat that because these are phase I trials, but you know, survivals from time of diagnosis you know in the range of 23-32 months. These are meaningful survivals you know given the median survivals typically of the order of nine to 15 months in that population. Essentially, IPAX BrIGHT is our phase III trial. This study again has a part 1 and a part 2. I won't bore you with all of the detail, Robbie, but Part 1 is a Bayesian design which aims to optimize the dose of TLX101, and to optimize the dose of lomustine, which will be the control arm. There's two agents, and the FDA requires us and other sponsors to spend a fair bit of time at the front optimizing the dose magnitude and the dose schedule. That's Part 1, optimizing the dose of TLX101 together with lomustine, and there's a Bayesian design that does that. Once we get to the optimized dose, there'll be an expansion cohort. We get to the exciting bit, and it's a familiar theme, you know, Part 1 and Part 2 of ProstACT Global we talked about. IPAX BrIGHT has a similar schema where Part 2 is a randomized phase III design where we will randomize patients to the conventional therapy, which is typically lomustine. That's in the guidelines like NCCN guidelines versus lomustine again, which is having TLX101 layered on top. The question that is being asked in this trial is can we take A conventional standard of care and add a radioligand therapy on top of that to improve upon the standard of care. In this setting, it will be overall survival. These patients have a limited duration upon recurrence. This population is patients with recurrent glioblastoma, and overall survival is the primary endpoint of this trial. Again- Can I just make a quick chime in? Yeah, sure. Please do. We've been getting monotherapy data, IPAX BrIGHT. IPAX-2 study was monotherapy data. We have done a dose escalation study, just to be clear. We have an idea of what we're targeting in terms of dosing regimen. It's, as David noted, it's about layering that now on top of standard of care, where the extra run-in piece is required. We've done prior studies, including quite a bit of compassionate use experience in Europe, patients have typically been receiving whatever standard of care is available. Whether it's temozolomide, lomustine, adjuvant radiation therapy, additional surgical. I mean, it's been the whole heterogeneous Hail Mary of recurring glioblastoma research, or clinical management. Now it's really about locking that down into a slightly more constrained study. That's really what that run-in part of BrIGHT is. It's not about to validate dosing because we've done that, but it's about really ensuring that the dosing assumptions that we have on top of standard of care and on top of a prescribed standard of care, you know, hold up as we go into phase three. I have to say, Dave's team has done a phenomenal job from a KOL engagement perspective. You know, we've got a bunch of sites in Europe now that have been working with the asset for a long time, have done a lot of patients, have a really positive, you know, temperament towards the asset, and have seen really good disease control and treatment responses even in some cases, which we don't see in this patient population very often. So it's a very gratifying. You know, to have so much investigator momentum and interest in this study, and from, you know, top-tier European neuro-oncology sites is very gratifying. We're really looking forward to rolling this out to U.S. patients this year as well. You know, one of the interesting assets that I also find fascinating in your pipeline is TLX 250, which is being evaluated in clear cell renal cell carcinoma. You know, I'm curious. What's the status of that trial that's ongoing and, you know, from an early site activation perspective specifically? Yeah. I'll make a few comments, and then Dave perhaps you chime in. I have to tell you, this program has been very challenging, because of the constant change in standard of care. I mean, kidney cancer moves so fast. You know, it's actually really gratifying to take a step back and look at the field overall. We've made huge strides in kidney cancer over the last decade. It's become a very immunotherapy-centric study. We are seeing new combination therapies evolve that are providing, you know, fairly, incremental but steadily in the right direction, survival benefit for patients. I think the two cornerstones today as we see it evolve is really the immunotherapy combinations, whether that includes or doesn't include things like, TKIs or cabozantinib or whatever. On the other end of the spectrum, we've obviously seen the emergence of belzutifan in the last-line setting. What this has done is we've been developing our sort of phase II strategy around this asset. We've been taking multiple approaches. We've been looking at combo immunotherapies in first- and second-line setting and how to layer in kind of more traditional treatments. We continue to do research in that area. What we have decided is that there still remains an unmet need in last-line, you know, rapidly progressing patients. We don't feel that. I mean, belzutifan has emerged as a new standard of care in that setting, but it's not. I don't think anyone believes that it's a very overwhelming solution. I think while it's good to have a new option in that patient setting, and there are a lot of patients that progress off immunotherapies, I think we can do better. What we learned from this initial work that we did in this space is that we can resensitize patients back to immunotherapy to an extent with radiation. What we have done is we've gone back and said, we're gonna do a, call it a VISION trial style study in last line progressing metastatic patients, and then start to work upstream in parallel with the immunotherapy combination. We have, for example, a study that's open, at the moment that's combining, immunotherapy, your checkpoint inhibitors with targeted radiation that's being run at MD Anderson. We have these sorts of studies which are really about, you know, preempting and planning a little bit what happens when we move upstream from that monotherapy, you know, advanced metastatic signal. That's the current plan today. That's what the Lutetium trial is designed to do. It's to really, to look at that last line setting, where there really isn't a lot of treatment options. It's a traditional place for nuclear medicine to be. Once we get that monotherapy efficacy confirmation, 'cause we have some pretty nice data that shows disease modification and stabilization in that patient population, progression-free survival prolongation, then there's an opportunity to move up into the earlier lines with combination immunotherapy. Dave, do you wanna add anything? Thanks, Chris. Robbie, you'd be familiar with this, but yeah, I just wanna highlight the need. You know, we've had a major advance, you know, with immunotherapies over the last decade, and if those patients who enjoy a response, you know, that's great for them, but it's only a, you know, it's a 30%, maybe 40% of the population that you expose to an immunotherapy agent in advanced, you know, kidney cancer that get a response. There's a large group that, you know, when I talk to patients about this, they often say things like, you know, "What if I blow through and just go straight through because I'm not one of the responders?" They're the ones that are really worried about needing something else. There is a large subset that end up in the treatment refractory end of the journey very quickly, and that's why we need assets like this to be developed and so on. Well, also why we need the imaging as well. Yeah. Just the same way as we're seeing PSMA playing a huge role in patient selection and longitudinal patient response assessment in prostate cancer, we already see the same demand for renal cancer. There's no doubt that the Zircaix product, which we, you know, we still expect to launch this year, that's the true companion imaging agent to TLX250. You know, it's actually the same targeting agent. It's actually, we are able to do predictive dosimetry with the zirconium agent for the lutetium product, which is really exciting. That's the first time that we've had that in our portfolio because, as you know, prostate cancer imaging has really centered around small molecule imaging. But with renal cancer, for particularly for primary staging, we wanna keep the ureters nice and clear. We don't want bladder, we don't want kidney, we don't want anything basically from the belly button downwards. We don't want any of that. We don't wanna see any of that. That's why a hepatically excreted agent's very compelling for imaging. Ultimately, that asset is not gonna get just used for, you know, indeterminate renal masses and primary staging and maybe evaluation of recurrence, but ultimately, it's gonna get used for looking at treatment response, and to try to determine, as David says, when is a patient, you know, really truly progressing, and to try to get ahead of that, and, you know, not subject the patient to prolonged toxicity from immunotherapy, if there's something that or cabozantinib or belzutifan, if there's something that you can do, if you can move them on more quickly and still preserve some capacity to respond. Thank you for that. One of the things I'm also sort of curious about, you know, 'cause I know we're running up on time, so I'm gonna make this succinct. You know, when we think five years down the road, five, 10 years for Telix, into the earlier stage pipeline, how are you visioning the mixture of validated targets versus more novel nuanced targets, as well as beta versus alpha emitters, and what do you think is the most underappreciated aspect of Telix? All of it's underappreciated at our current market cap. I think we're trading at a paltry multiple of our commercial business, but I think you'd be disappointed if the CEO didn't say that, so I'm just meeting my obligations there. I think at the end of the day, look, I'll be the first to admit, you know, some of our portfolio has fairly well-trodden targets, like everybody does, but we think we're taking a differentiated approach from a pharmacophore perspective. You know, our focus on biologics is quite unusual, mostly because biologics are harder, you know. But the selectivity and the engineering that you get on a protein is, gives you all kinds of strategies for PK modification and changing your biodistribution. You know, it is more complicated, it takes longer, but it also gives you a lot of really great control and flexibility over where you steer radiation. I think one of the things when you look at Telix's pipeline, whether you like our targets or you don't like our targets or whatever, is we choose the right radionuclide for the biological problem that we're trying to solve. I think that that's really important. We do have the appetite to say, "All right, you know, this is the cancer biology we're dealing with. This is the radiobiological mechanism of action we're hoping to achieve, and here's how we're gonna steer it," you know, within time and energy constraints. This is how we're gonna steer that radioactivity to that, with that particular goal in mind. Now, we are, as you noted before, we do work in lead-212, we do work in actinium, we do work in astatine. You know, if you wanna get something across an intact blood-brain barrier, chelators and radiometals are pretty challenging. You know, charge matters. Pretty tough to do, but radiohalogens have lots of potential. We have, for example, a near-term first-in-human study with an astatinated amino acid, which is for looking at leptomeningeal disease. That's a, you know, really beautiful example of where you have a widely disseminated, small, relatively small metastases. It could be a great opportunity for an alpha emitter, but you still need to have things that have a more favorable CNS biodistribution. You need to think about your radiolabeling strategy there as well. You know, those are the sorts of thoughts that we have as we develop the earlier stage pipeline. You know, some of our first generation products were either small molecules that people relatively well understand or antibodies, full-length antibodies. I think that the sweet spot somewhere in the middle, where we're dealing with smaller formats potentially that have better tissue penetration, but are still steerable to more radiation-resistant clearance organs. You know, internalization still matters, even with alpha emitters. You know, receptor-mediated internalization is different than binding to the substrate of a receptor and having some transient on/off effect. You know, I think there's a long way to go. I think what we really see now is the first generation of pharmacophores. You know, we've had some great successes for the field, but there's a lot more that we can do to optimize the pharmacology of radiopharmaceuticals for the types of isotopes that we're interested in delivering to patients. I think that's the science lens of the company, and fortunately we're in a great position where through some M&A and through some, you know, organic investment, we've been able to build new capacity. In fact, this year you will see the beginning of a couple of very novel targeting agents, including with novel targets that will, you know, come out and go into first in human studies where you'll see the fruits of that labor, you know, materialize. Well, I'm definitely looking forward to all of the innovative science and data that's gonna be coming out of Telix both this year and in the future. Gentlemen, thank you for taking the time to have this insightful discussion with me today. Yeah, thanks. I'm sorry about the audio. I hope it came through reasonably well, but always appreciate the opportunity, and you always ask great questions, Robert, so thank you. Awesome. Take it easy, Chris. Thanks. Nice seeing you again, David. Thanks, Robert. All right. Bye-bye.