Thank you so much. My name is Peter Lawson. I'm one of the Biotech Analysts at Barclays, and really pleased to have on stage with us, Thijs Spoor, the CEO from Perspective Therapeutics. You know, I guess my initial questions for everyone have been, you know, the impact of tariffs and how that could potentially impact supply chain, and if there's anything we should be thinking about, whether it's industry-wide or company-specific. Sure. No, thank you, Peter, and thank you for hosting us here at the conference. It's always a relevant question on everyone's mind, when you think about the supply chain and the precursor materials. The amount of actual peptide that we use in our programs is pretty small and is produced in the U.S. Really the big question on everyone's mind, independent of tariffs on this radiopharmaceutical supply chain, is where does the isotope come from? To cut to the chase, thorium-228 is the ultimate precursor for what we do. Thorium-228 is found relatively abundantly around the world inside reactors and things like that. There is a U.S. supply through the U.S. Department of Energy. There are sources in Russia, in the U.K., the Netherlands, Australia. We predominantly source from the U.S. Department of Energy. Our precursors are not dependent upon any tariffs that may show up, in terms of what we're trying to do. Gotcha. Thank you. The FDA potential cuts, your fear of cuts, has that changed in any way the communication pattern with the FDA? Has it delayed things? Have you noticed any changes? No, so any potential cuts and change of the FDA, we have not seen any impact on how we engage with them. We found the FDA to be consistently very supportive of innovation and new therapies, and a really, you know, dedicated group of professionals trying to help bring new therapies forward. We have not seen any acute impact from anything that we've done at this point. Gotcha. The next final macro question would just be around NIH funding, cutbacks there. I mean, clearly, it could have long-term impacts on biotech industry as a whole. Are there any kind of near-mid-term effects that you worry about, even if it potentially trickles down to university funding and? There are some really drastic acute impacts from NIH cuts. As we look at a lot of our clinical trials, you know, we're doing work in oncology. A lot of the university and academic centers that do work in oncology are major recipients of NIH grants, and that has a direct impact on their operating budgets. Our clinical sites are feeling systemically the impact from their institutional budgets being drastically cut and really scrambling to try and find out how they provide integrated cancer care to their patients. Every institution that we deal with that does research is impacted by these cuts. The read-through is into patient care pretty acutely. It's number one on people's minds as we speak to our clinical trial sites, as we look to see how they can operate. Thank you. Thanks. Really great insight. As we think about your own company and, you know, manufacturing, you know, I wonder if you could kind of talk through where you are for the building out of manufacturing. That is clearly an important part for the radio-pharmaceutical space. No, thank you. The supply chain, if it's radio-pharmaceuticals, is going to be dependent upon your product shelf life and how much time you have and how far you're trying to get the product. With the Lead-212 isotope, we can think of product shelf lives being up to about 24 hours. The isotope is a 10-hour half-life, but the effective product shelf life is about 24 hours. That means we have ideally same-day distribution or potentially overnight. There was a recently announced deal between Sanofi and RadioMedix to distribute their compound centrally in the US from one site in the Midwest, which certainly seems very feasible. As we look at the currently approved radio-pharmaceuticals that Novartis distributes, odds are that any product injected today, for example, into a patient was probably made yesterday. The sort of the slightly longer-lived isotopes, like the Lutetium and Actinium-225, rely on about a 48-hour or so shelf life. How we think about our programs, we have a site in Iowa that's currently producing material for the clinical trials, has been for several years now. We can get product from Iowa, across the entire U.S. right now. We just opened up, in October, a facility in Somerset, New Jersey, that we acquired from Lantheus. That site we acquired in March and started shipping doses in October. That site is commercial-ready and can ship product by ground across the East Coast, and obviously by air across the whole U.S. As we look at our published expansion plans, we have acquired a building in Houston, a building in Los Angeles, a building in Chicago. We are investing in manufacturing sites there as well. With these manufacturing sites, being actually pretty efficient to operate, given that they, you know, the capital requirement for each of these sites is under $40 million, to produce a facility that can support quite a large number of patient doses. In order of magnitude less than some other manufacturing programs, we have the luxury of not needing to create the isotope on-site, from a, you know, linear accelerators and cyclotrons and nuclear radiation. We have the benefit of all of our isotope comes through chemical separation. There is a very interesting separation technology that we've developed just for Lead-212, its parent Radium-224 and its parent thorium-228. On-site purification or separation by washing a column is much easier technically than having a cyclotron or a reactor on-site. Gotcha. Thank you. Maybe you've kind of touched upon it, but just the differentiations of your platform versus others and, you know, why Lead, why Alpha? Mm-hmm. When we think about our platform, we've leaned in pretty hard on Lead-212. We think Lead-212 is in that sweet spot. Not too long, half-life, not too short. We can distribute it, but also is able to irradiate the tumor with a hard fast punch and then disappear so that the body can respond. The tumor microenvironment isn't being irradiated. We're not damaging tumor infiltrating lymphocytes that may be recruited into the cause. Lead-212 has an elemental twin, Lead-203. This allows us for early work in drug development to do perfectly correlative dosimetry using the same composition of matter, the same chemical at a dosimetry level. We like those isotopes of Lead-212 and Lead-203. The big enabling piece for our platform is actually incorporating those into a proprietary chelator. We have intellectual property around this chelator as well. The chelator is like a chemical cage. It holds the metal in place and then drags that metal wherever the rest of the moiety, the rest of the peptide linker wants to go in the body. All of our programs so far take advantage of the fact that we can have this proprietary chelator. The chelator plus any physical linkers plus the targeting peptide together form the composition of matter that we actually also file IP around. That overall targeting entity, the molecule with the chelator, the metal, the peptide, the linker, all those things together are what differentiate. We develop new programs with novel compositions targeting unique targets. If we have target expresses on the tumor and doesn't express in a lot of normal tissue, then we'll look at that pretty actively as a candidate. We will actually use this and develop assets that we take into the clinic. One of the nice things about a platform is that by using our expertise in things like peptide chemistry, we can tune biodistribution. We can tune the pharmacokinetics of the drug during discovery and try and optimize for biodistribution. We lever our experience in making these programs, scale them up, do proof of concept imaging in animals, therapeutics in animals, imaging in humans, and then move from there to treating in humans as well. Yeah. It's an interesting dynamic where you can kind of visualize and treat. No, it really is powerful. The see what you treat, treat what you see, it's not just a great tagline. It really means you can run your, you can do test runs in animals or humans without damaging them. The ability to actually go, if so for a patient with melanoma, for example, 50% of patients with metastatic melanoma should express MC1R, a target that we like. A non-invasive way to identify if that target exists is to actually give the patient the drug that they'll be getting as a therapy, but only as a diagnostic. You can do a dry run in that patient and get perfectly predicted dosimetry for a follow-on dose. If a patient is injected with a diagnostic and they're MC1R positive, then we know that they could be candidates for the therapeutic. If they don't express the target, don't treat. That's a really nice way to go where we can actually do these things. Also, looking at biodistribution, we de-risk every step. Imaging the animal is great. Treating the animal proves, you know, localization. Imaging in a human is a phenomenal de-risking point because then we can actually really see, do we get tumor accumulation or do we get off target? What's the time between, so if you took that idea and if you can essentially image the patient, and then could you treat them the next day, or how would that work? Depending on the receptor and depending on the patient type, it can be as quickly as next day. Some receptors have a very, very high turnover ratio, turnover rate, and there's so many of them that there's no issues of occupancy. We're doing pico molar levels of activity, and so it's almost impossible to saturate all these receptors. Logistically, though, you want to make sure that the patient is screened. In theory, a patient with a positive scan could even be treated the same day. For most sites, they want to wait the next day and make sure the drug's available and ready. We try and treat patients within a week or so of a positive, confirmatory scan showing that they have the receptor that we target. Gotcha. Thank you. I guess if we move on to the SSTR2 targeting molecule, just if you run through the current standing of that, of that data and now dive into, you know, the FDA feedback you've had so far. Sure. When we actually were developing this program, it came out of the University of Iowa. We wanted to develop a better drug for pediatric neuroblastoma. We wanted to design a safer molecule for kids that ended up having, we think, you know, ideally a safer product for adults too, safer meaning a broader therapeutic window. By looking at some of the preclinical data, we sent that to the FDA and asked for a fast track designation in that post-lutetium treated patients. They came back to us and said, "No, we could have a fast track pre-Lutetium there." In the PRT naive space, that was very exciting for us both with the one condition that we meet with them after our first few patients are dosed at 2.5 and 5 millicuries. We planned in advance a dose escalation design, the mTPI-2 design. We can iterate through and see where the data takes us. However, the FDA said, "Please pause after those first few patients are dosed at 5 millicuries so we can understand what the safety and efficacy looks like and then have a dialogue with you." That was predetermined two years ago. We enrolled patients into the trial at the 2.5 millicuries last December. We decided very quickly that we could actually, sort of a year and a half ago in December, escalate to the 5 millicurie dose. Those patients were enrolled, the first seven. Initial results from that study that we intended to submit to the FDA were presented at the NANETS conference in November. Since then, we've had an update on therapeutic results at ASCO GI. Tracking these patients forward, what we've told the street is that once we have clarity in terms of what we're telling the investigators about those types of escalation, we'll then tell investors as well. It is really a matter of making sure that we develop medicines that everyone considers to be within reasonable therapeutic ranges. Gotcha. How does it stand for like a cohort two, cohort one data sets? I think you were waiting for FDA feedback for cohort three. Yeah. Once we get FDA clarity on what we're telling the investigators for cohort three, we'll then be disclosing that. We prefer not to, sort of, you know, kind of comment on discussions in progress. The cohort two, the 5 millicurie level, the Data Safety Monitoring Committee recommended that we reopen that cohort and we could dose up to an additional 40 more patients. The physician interest in that has been extraordinary. Prior to the NANETS data and post, we had a lot of interest. We disclosed that as of December 31, 11 more patients had come in on that reopened cohort two. You can run through and see how long it takes for them to kind of see results. That was between August and December. We are committing to doing regular updates on enrollment. We will see as the data matures, we can track the patients through. You know, we can't do a two-year follow-up on a patient that only got enrolled a year ago, obviously. We are watching patients all the way through and seeing how the follow-up goes and when reasonably appropriate at medical meetings. We'll be giving updates to everyone about the progress. Gotcha. Because what, there's two unconfirmed PRs within that? What we disclosed at the ASCO GI conference was two unconfirmed PRs, and then whenever the data is updated at a medical conference, we'll be able to disclose the next, you know, what happened with those patients. Okay. The one, the one confirmed response and two unconfirmed, was what we disclosed at ASCO GI. All those patients are available for follow-up, is it? Yeah. These are patients where if you think about patients with neuroendocrine tumors, it's a very long, slow-growing tumor. For a while, they would have been treated with somatostatin until they started to progress. Once they started progressing, they would have come into the study. Right away out of the gate, eight out of nine patients had disease control. That gives the physicians confidence that they can actually monitor them as they would normally. As part of the study, the patients do come back every eight weeks or so for follow-up and for routine, reasonably clinically relevant scans to assess their disease status. Is there a good venue for the next update? Presumably that could include cohort three or how do you? Yeah, we want to be really careful about not front-running conference materials and things like that. As we're allowed to with the various conferences, in terms of commenting if abstracts have been submitted or accepted or what will be produced, we'll be communicating that. We do like medical conferences because at the end of the day, we're trying to inform physicians and clinicians about how this could impact their patients. We like that setting as a way to have data come out. Perfect. Okay. I do want to give a caveat though, which was anything that's going to go in an abstract will, will almost by definition obsolescence itself by the time, you know, that the data gets presented at a conference. Gotcha. Of course. Okay. It's, there's a long lead time with these abstracts that you're thinking of. Correct. Okay. I guess MC1R, I guess why that and, you know, we've got some follow-up questions around. Yeah. I mean, melanoma, as everyone appreciates in this room, is a very, very tough disease. I think the recent, if you look at the SEER database for metastatic melanoma patients that are on diagnosis of being stage four have a 50% mortality after one year. It is a pretty tough disease to try and interact with a lot of energy in the space. What we like about the MC1R target is that about 50% of patients express MC1R with metastatic melanoma, 50% do not. Therefore, it is absolutely appropriate to try and do a screen. What we like about this matching isotope combination is that you can actually screen the patient with the potential therapeutic to assess if they have enough receptor positivity to warrant treating with the therapy. There is a clear unmet medical need in melanoma. If we look at the expected PFS of the patients that we've been enrolling, we're enrolling patients in that post-second line plus setting when on average they'd had five previous therapies that had been tried and not worked enough. The patients were progressing. With the expected PFS of two to four months, we were thrilled that in our three millicurie dose cohort, all three patients went well past that timeline. At nine, eleven, thirteen months post, we still had stable disease. To take a rapidly progressing aggressive disease like melanoma and turn that into stable disease, and I'll quote our Chief Medical Officer in the audience here. He said, "It's like the disease has been frozen in time." That's an amazing thing to do if you're treating a patient, to have that disease frozen in time, versus a reasonable expectation of rapid progression. The fact that we have clear signs of activity and efficacy within what we think is a very good safety profile to actually freeze that disease. In fact, one of those patients turned into a confirmed response about a year post. Perfect. Thank you. Where are you for the, in that dose escalation? Yeah. It's dose finding more than dose escalation. What does that mean? That's a subtle nuance, which is that we can go up or down with the design based on safety and efficacy trade-offs. What we found is that if we were dosing at 5 millicuries, what we think happened then is that, you know, we took this incredibly complex system called the immune system. If that gets out of balance, you know, the disease goes unchecked. We did not want to interfere with the immune system, which we think happens at higher doses, and get that optimal slightly lower dose at 3 millicuries that did have a beneficial impact for the patients. The preclinical data says that if possible, we can get a much higher response rate if we combine with a checkpoint inhibitor and an alpha-emitting therapy. The idea of actually going into combination therapy has been our development goal from out of the gate. We did not feel comfortable going into combination therapies without isolating the safety and efficacy profile of the individual components. In our case, we have an agreement or collaboration with Bristol Myers Squibb with Opdivo. That has been well characterized. What is not known is what monotherapy looks like with our drug, the alpha-emitter. Now that we have a sense for what that safety and efficacy profile looks like, to avoid stacking safety signals, we are taking that 3 millicurie and lowering it down further to 1.5. The animal data really supports lowering doses as well. We are now actively enrolling patients in that 1.5 millicurie cohort in either monotherapy or combination with Opdivo. Okay. Thank you. Did it was, I believe, kind of some renal accumulation of the drug. Is that something that? You get normal expression of MC1R in the kidneys as well. The kidneys tend to be the path for, for any, for almost any drug to be cleared from the body, right? It's either going to be through the hepatobiliary system or through the renal system. You do want to monitor kidney exposure very carefully. We are starting to hit some calculated thresholds at the 5 millicurie dose level, that would make us really be thoughtful about watching those patients through. Lowering the dose lowers the overall kidney exposure. We did see that there was a calculated kidney dose, but we did not see anything manifest clinically acute or chronic to imply that there is any damage to the patient's kidneys from this. Okay. I want to be really careful about that because there's a nuance there. These are, there's calculated limits for kidney exposure that are based on historical external beam data. Taking a different energy form and trying to extrapolate what that could mean from a safety perspective. In this case, we didn't see anything show up on any of the biochemical markers to imply any issues with the kidneys in these patients at all. Yeah. I assume as you kind of explore lower doses, any of those worries or concerns or points of monitoring will kind of diminish. We have a, you know, strong attention to making sure we look at everything very carefully, potential, you know, heme tox, kidney tox, cardiac tox. We look at everything across the board. Lowering the dose of the radioactive material really lowers those theoretical calculations for kidney as well. We found in the animal models that there are, it's, it's more sort of parabolic shape response curves where you want to find the right part of the curve so you can actually get enough of the neoantigen exposure, or generation to actually let the immune system do its job. You don't want too much radiation to overload either the immune system or to cause theoretical kidney damage. Finding that sweet spot by lowering the doses down follows the animal data from an efficacy hypothesis while having less burden and less potential load on the patient. Okay. When should we expect the next data set? What's the right path for success in these patients, whether it's the monotherapy or the combo? It's a really tough field, in melanoma. We know what the PFS data looks like in the post-second line plus setting. We would love to see if we can actually explore dosing patients earlier in the disease progression to allow a much greater potential potentiation of the immune checkpoint inhibitors, give the immune system something to grab onto by having these neoantigenic, you know, generating alphas on board. When we actually think about where we're trying to get to, the fact that we took patients with, you know, really short expected PFSs and have them extend out so far is always a big plus. We see that as a win. We'll follow the data wherever it takes us. What we are committed to doing is giving regular enrollment updates, at our quarterly earnings. Then have people track through the, the melanoma program has three doses of the drug, eight weeks apart, whereas the neuroendocrine program has four doses eight weeks apart. There is a slightly different kind of range of time that we look for. Perfect. Let me move on to the FAP target. It was a really interesting target. How do you differentiate versus the other players within that space? I appreciate we just have a minute left here, but, you know, FAP is a really interesting target. The stroma that forms when cancers get big enough, they have to form their own infrastructure, is a really complex structure. There's the competing hypotheses if it helps or hinders the immune system's ability to go and address it. At the end of the day, no one thinks that stroma is good or beneficial in the fight against cancer. It seems to help the tumor out. Taking out the stroma at the end of the day and also any tumor associated with the stroma, and the stroma forms almost a web and a sponge-like structure within the tumor. Getting an alpha-emitting therapy into the whole complex tumor structure is a big plus. What's really different about our approach is that we've actually targeted, not just the stroma, but optimized the molecule so we don't get accumulation in other tissues. Prior FAP targeting agents have had, you know, different, you know, initial biodistribution. At the four-hour mark, they've kind of peaked in the tumor and then they sort of moved out. Those have been really interesting imaging agents, whereas we've designed ours to go into the tumor right out of the gate and stay there over the, over the, the half-life of lead. Designing a therapy means hit the tumor hard and fast, have it bind, and have it stick. Perfect. With one second left, thank you so much. It was a pleasure, Thijs. Likewise. Thanks, Peter.