Greetings and welcome to the Perspective Therapeutics ASCO GI investor call. At this time, all participants are in listen-only mode. If anyone should require operator assistance, please press star zero on your telephone keypad. A question-and-answer session will follow the formal presentation. You may be placed into question queue at any time by pressing star one on your telephone keypad. As a reminder, this conference is being recorded. It's now my pleasure to turn the call over to Annie Cheng, Vice President, Investor Relations. Please go ahead, Annie. Thank you, Kevin. Good morning. Welcome to the Perspective Therapeutics call to discuss the VMT-α-NET clinical data being presented at the 2025 American Society of Clinical Oncology Gastrointestinal Cancers Symposium, ASCO GI. During the call, we may make forward-looking statements that are subject to risks and uncertainties. Factors that could cause actual results to differ materially from our expectations are detailed in our SEC filings, including in the risk factor section of our most recent annual report on Form 10-K, quarterly report on Form 10-Q, and our other SEC filings, which are available on the investors' section of our website. These forward-looking statements apply as of today, and we undertake no obligations to update these statements after the call. Today's call is being webcast and can be accessed on the events page of our website. The call will be archived and available there for a period of time after the conclusion of this call. Today's call will start with prepared remarks by our Chief Executive Officer, Thijs Spoor, Chief Medical Officer, Dr. Markus Puhlmann, and lead investigator of the study to be presented, Dr. Richard Wahl. The call will then be after their prepared remarks. We will open the call for questions. With that, I will hand the call over to Thijs. Great. Thank you, Annie. And thank you, everyone, for joining the call. So we're really excited about what we're doing here at Perspective Therapeutics with the next generation of targeted therapies. And rather than going into our whole corporate presentation, we really want to highlight we think we have really disruptive platform technology. We're really excited about the various programs we bring through. We design our molecules to hopefully have the broadest possible clinical potential. We're really trying to develop the next generation of medicines that we think can actually have a major impact on patients' lives, especially with the ability to sort of kill these tumor cells both directly. And we also think it may help with the immune system across the board in helping address how patients manage their disease. We have a broad pipeline we're developing with incredible potential leveraging off of this platform. And we've also been making investments in our manufacturing infrastructure to really allow the best possible medicines to come to patients at the right time. Next slide. One of the things that we really do try and focus on is trying to think through how do we get a broader therapeutic window. And we do this by designing the molecules upfront. We've taken what we think is the ideal isotope for the tumors that we're targeting. We've made sure we've chelated it very, very carefully within a chelator that's proprietary to us that we think is optimized for overall body distribution. We want the drug to go to the tumor. We don't want the drug to actually go to other organs of interest or to minimize those as best as we can. And if we can optimize the peptides and how they target, then all these things together, we think, will make a very interesting medicine. And we hope to broaden the therapeutic windows compared to other available treatments. Broadening that therapeutic window hopefully means we can go higher doses and actually sort of treat the tumors more directly. With that as our core premise, we actually have a very exciting pipeline on the next slide, which is really addressing several tumors that are out there. Our VMT01 program is now in human clinical trials for melanoma. We're excited that we opened up our combination arm as well as a monotherapy arm for that program. We previously discussed results of the SITC of melanoma research. We're really excited about our VMT-α-NET program that we'll dive into a little more today. And also, we have our FAP targeted agent that we hope to initiate in human clinical trials by the middle of this year. Behind that, we've got an interesting set of compounds that we're focusing on. And we really are trying to get those a broad pipeline out to the market. We hope that these radiopharmaceuticals will actually change oncology treatment. We think targeted therapies and the ability to internalize a radiation source, treat cancer from the inside out, does an awful lot, not just in the initial indications, but hopefully has broad potential in other solid tumors as well. With that, I'd like to turn the call over to Dr. Markus Puhlmann to talk about our neuroendocrine tumor program. Thank you very much, Thijs. Good morning, everybody. I will present next slide, please. Thank you. I will present a short refresher about the neuroendocrine space. Next slide, please. The most common somatostatin receptor, SSTR2, is most commonly presented on all neuroendocrine tumors. It is mainly presented at the gastrointestinal indications, but also widely expressed in other tumor indications such as SCLC, small cell lung cancer, breast cancer, meningioma, head and neck cancer, and others. Despite the regulatory approval of Lutathera, there's still an unmet medical need for new therapies based on the low objective response rate of only 13% per the US PI and the lack of overall survival. For our own program, we have already received fast-track designation for our VMT-α-NET program from the FDA based on our stellar preclinical results. Our ongoing company-sponsored therapeutic trials are currently ongoing. These trials are dose-finding and enroll PRRT naive patients throughout the U.S. Next slide, please. We are aware of other SSTR2 targeted programs. This slide is included in the deck for your comparison and peruse. Next slide, please. At this point, I would like to introduce the speaker for the next session. Dr. Richard Wahl is a professor at the Mallinckrodt Institute of Radiology at the Washington University in St. Louis. He has been the director at this institution from 2014 to 2023. And he is well known for his work and the development of the PERCIST response criteria. Dr. Wahl. Yeah. Thank you, Markus, and good morning. This is a multi-center study. I'm reporting the data, but there are patients from other institutions. You see the title here. Next, please. These are my disclosures, and as you know, this is not an FDA-approved agent. This is being used under an IND in a clinical trial. Next slide, please. This is an overview of the study design and its background. Some of these data were presented at the NANETS meeting in November in Chicago, but it's a dose escalation. The patients are advanced or unresectable or metastatic neuroendocrine tumors with progressive disease on prior therapy. They have not yet received radiopharmaceutical therapy, and they have to be positive on a PET scan for SSTR2 receptor expression. The dose escalation is an mTPI-2 design, and dosimetry studies were performed using Lead-203 in cohorts one and two. So the main goal, of course, is to look at safety and look for dose-limiting toxicities following a single dose and then the repeated doses to determine the MTD or the recommended phase two dose. And, of course, exploring tumor response is something we also have looked at and duration of response. And dosimetry data will be presented later. Next slide, please. These are the patients. These are the first nine patients on whom data are available. Six were non-pancreatic neuroendocrine tumors. Three were pancreatic neuroendocrine tumors. Six were grade two. Three were grade one. And their prior systemic therapies are noted here. The patients were mainly ECOG 0. We had one ECOG 1 patient. And the tumors were not insubstantial in burden. The RECIST median sum of target lesions was about 6.7 cm. Next, please. A high-level assessment of the safety is that this was quite safe in these patients. No dose-limiting toxicities were observed in either the 2.5 or 5 mCi cohort. No grade four nor a grade five or serious adverse events were observed. I'll show you in a moment that there was no decline in renal function. Hematologic adverse events were few and low grade. We observed no dysphagia, no difficulty with swallowing, and no treatment discontinuations due to adverse events have occurred. And our dose escalation has occurred per the protocol. Next, please. This is a little busy, but I think what's notable is that any adverse reactions are typically grade one and grade two. The grade three reactions were actually modest, but they were a decreased—excuse me—a bit of diarrhea in one patient. And one patient had a brief episode of syncope. No more serious reactions. Next, please. Here's an example of the renal function before and after. The baseline eGFR on the bottom and most recent on the top. You see that these lines are well correlated. No decline in renal function identified. These are data through January 10th, 2025. Renal function well preserved. Next, please. These are the data we presented at NANETS. In our presentation, no one in this group had, by tumor size, enlargement of tumor over 10%. At this time, we had one patient with a 57% reduction in some of the dimensions of the tumors by RECIST. You can see that was a cohort two patient. One thing probably worth mentioning and it's relevant to the next slide or two is that these tumors sometimes have relatively slow growth rates. In assessing neuroendocrine tumors, it's often recommended that one not make too early a conclusion on efficacy of the therapy because the tumors can continue to shrink because of the nature of the cell division and of the radiobiology. It's important that follow-up images be performed and to assess for response over a period of time. Next slide, please. I think these are quite exciting and perhaps not completely surprising given the biology of these tumors. What we have observed and which will be presented in the ASCO GI poster today are that several of the patients converted to what appears to be by RECIST measurements of partial response. We obviously want to confirm that on follow-up. It's called unconfirmed, but significant reductions in tumor diameters in several of our patients. Several of the other patients who had responded also had some modest deepening of their responses. So these were notably patients who received the 5 mCi sequential dosing. But this was a substantial ongoing reduction well after the treatment had been concluded. Next slide, please. Here's the data we presented before swimmer's plot on the duration of disease control. I think you see we were able to present out to a year here. There was one patient you see at the bottom who had progressed early. The rest had been doing well, but they were pretty early in the treatment course, just getting the first post-treatment scans. Next slide, please. The data have matured to some extent. Now we go out. This is weeks. The X-axis is weeks. But here we see it goes beyond one year. And the patients we have treated continue to do well without progression. And what we see, at least with these yellow triangles, is that the first response was seen a bit later after the conclusion of the therapy in a couple of the patients. And those, I think, are interesting and exciting data. So again, the durability of these responses appear promising with a little more follow-up. Next slide, please. These are data we showed at NANETS in 2024. And again, you see that there is evidence of tumor shrinkage in several of the patients, but before their therapy had been evaluated, longer after the treatment had been given. So just sort of make a mental map of this. And let's look at the next slide. We see that with several of the patients that the responses have continued to evolve after the therapy has been given and have converted to size changes consistent with partial response. And this is, again, a delayed response after the treatment. So this really is not chemotherapy. This is radiopharmaceutical therapy. It's a different class of therapy. And some of these responses in this tumor type appear to occur later. And this certainly is supportive of this. And it's exciting and encouraging. Next, please. Here's an example. You see the arrow here, but this is a patient of ours who started with a fairly substantial tumor. The white thing in the middle is the aorta, the kidneys and back. And the arrow is pointing to the tumor. But here we're seeing, after each cycle, a continued reduction in tumor size in this measurable tumor. That size there is getting to be sufficiently small that it's approaching a size criterion that, on its own, by RECIST would be approaching a complete response. That has to be assessed in the context of all lesions. It's a very encouraging and substantial response occurring ongoing and well after the treatment has been completed. Those are the data that will be presented later today. Next slide, please. Thank you. Thank you, Rich. And thank you, everyone. We're really excited about what this means. As we previously disclosed, we had intended to submit this data to the FDA in 2024. And when we look at the initial trial design that we wanted to go through, we would hope to be able to dose-escalate further because we think the safety criteria would warrant exploring higher doses as well. If we go to the next slide. As we look at overall profile for VMT-α-NET, we believe it was very well tolerated. We did not experience DLTs in the studies that have been performed so far. No grade four, grade five AEs or SAEs. We've not seen any significant decline in renal function. And as far as we look, as far as we can tell, no treatment discontinuations have happened due to any adverse events. We do think we've seen some appreciable activity with one confirmed objective response and two unconfirmed objective responses. We feel very, very excited about where things are going with this program. So the Safety Monitoring Committee has recommended dose escalation and reopening of cohort two, which we've done. We've previously disclosed last week that an additional 11 patients were dosed in cohort two as of December 31st, 2024. And we're very excited about ongoing investigator interest in our program and where this goes forward. Hopefully, in the future, we can also look at potential expansion into other SSTR2 positive tumor types. So with that, I'd like to open line for question and answer. Thank you, and now begin the question and answer session. If you'd like to be placed in the question queue, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. We ask you to please ask one question, one follow-up, then return to the queue. Our first question is coming from Jeff Jones from Oppenheimer. Your line is now live. Good morning, guys, and great update. Thanks for taking the question. Just want to confirm the two patients with unconfirmed PRs are continuing to be followed and timing for next scans, and then in follow-up, can you give any updates on how you're thinking about your strategy for dose escalation for cohort three? Thank you. Markus, can you take those? Cool. Thank you very much, Jeff, for the question. Currently, the patients for the first half year scanned eight weekly. We are following up every patient for several years, at least three years. We will have very definitive and sound data packages for long-term safety and efficacy. In regard to how we proceed with the next cohort, we will indeed continue once we get the go-ahead from the FDA with a flat dose that will give us a very broad spectrum of patients, probably with different body weights. We don't know yet whether body weight may actually be the ultimate determinant, but we will generate a very broad and rich data package that we hope will give us a very sound and reliable way to determine the recommended phase II dose. Appreciate that. Thank you very much, guys. Thank you. Next question today is coming from Gregory Renza from RBC Capital Markets. Your line is now live. Good morning, Thijs and team. It's Anish on for Greg. Thanks for the updates this morning. Just a few questions from us. Firstly, with the patients enrolled thus far into cohort two through year-end 2024, how are the distributions of weight, age, and tumor type shaping up as compared to the original nine patients enrolled? And as an add-on to that, with the data today, how might that be shaping your latest views on a weight-based dosing regimen or alternatives? And lastly, just one more, if I may. Given the safety has been relatively clean, what other gating factors do you believe regulators have on the radar prior to the opening and dosing of cohort three for the NET program? Thanks so much. Thanks for the questions. There's lots in there, so we'll try and just sort of tease out the main theme there. So in the ongoing patients that have been enrolled, we have not disclosed their statistics, but it suffices to say that they are within the range of the inclusion criteria. So these are all patients that should be consistent enough on their initial presentation from these patients presented here, both NANETS and ASCO GI. In terms of individual patient weights, we have not disclosed that either, nor have we applied a filter to that yet because we do want to look at a sort of broad-scale approach. In terms of the other concept, what's in the regulator's head, we really don't want to speculate there. Our job is to generate really good data, high-quality data, looking at safety and efficacy, and present that with our request. Thank you. Thank you. Next question today is coming from Nicole Germino from Truist Securities. Your line is now live. Thank you. Good morning. When do you plan on presenting kidney dose symmetry data from these patients? And what can you share from other ISTs that would support being able to dose up and still be under that 23 gray kidney limit? Sure. So, Nicole, thank you for the question. It's a great question. As we look at overall dosimetry, there's a few things that we want to just try and remind people who are new to the field, and we love the interest in the field and dosimetry. Dosimetry results that are obtained in a patient scan are really only applicable to that patient only. We presented previously some tumor kidney ratios at the NANETS conference that showed there's huge ranges across the board for what could be a tumor-absorbed dose and a kidney-absorbed dose that's calculated in that patient per se. All this data together is combined to allow both the investigators, the company, and as well as the agency to determine what could be dose-limiting and what isn't, so as we look at this data, we collect it real-time. We do analyze everything. But to answer your question explicitly, once we have the methodologies presented at a peer-review conference, we'd want to be able to have every or any and all investigators be able to reproduce our dosimetry work. And so we intend to have that presented at a later date. Great. Thank you. Thank you. Next question is coming from Yuan Zhi from B. Riley Securities. Your line is now live. Thank you for taking our questions. What are the gating factors to expand into the small cell lung cancer patient population? Is that included in the current IND? Thank you. I'll let Dr. Puhlmann answer that one. Yes. So thank you very much, Yuan, for this question. So based on the IND, obviously, we are able to explore indications for initially, I think, for NETs, but also for other SSTR2 expressing cancers. Thank you. Thank you. Next question is coming from David Dai from UBS. Your line is now live. Great. Thanks for taking my questions. And congrats on the update. So maybe just two questions from me. One is just around the deepening of the response we're seeing here. Maybe you can just help us understand what has sort of driven the delayed response. That's one. Second question is maybe for Dr. Wahl. You've just laid out how this data compares to AlphaMedix and Lutathera. And what type of efficacy would you want to see from a VMT-α-NET to get you excited about using this drug in your patients? So thanks, David, for the question. I'll actually turn both of them over to Dr. Wahl. But Dr. Wahl, with whatever you're comfortable commenting on. Okay. Well, first of all, in terms of the tumor response, the radiobiology of a relatively slowly proliferating tumor is such that you can have with double-strand breaks, you can have cell death, reproductive death, the inability of a cell to reproduce without the metabolic death of the cell. So even the NANETS recommendation for assessing patients post Lutathera suggests not assessing for perhaps six months after treatment to see if effect is sufficient. It's known that these tumors can have a more gradual kind of response. And it's related to their radiobiology. It differs from chemotherapy, and it also is related. These are grade one and two tumors, so their proliferative rates aren't incredibly high. So I think it's unusual maybe when looking at it compared to other chemotherapeutic agents or some immunotherapies, but this is a way radiation can work. So I don't think this is completely surprising, but it's very encouraging as well. So what would it take? I mean, if you look at it, it's really difficult for me to put these completely into context. I mean, there was a slide in here that showed the different trials. I would simply say that the side effect profile of this agent has been quite favorable. I think I'm certainly comfortable with this proposed dose escalation. And it appears that we're seeing. These are small numbers, probably a higher response rate at the higher dose. So these are robust responses, which I think are greater than we typically will see with a beta emitter in a relatively low proliferation tumor. So I think these are encouraging data balancing the efficacy versus safety at this point, but it's early days. Thank you so much. Thank you, Dr. Wahl. Very helpful. You're welcome. Thank you. Next question is coming from Christopher Liu from Lucid Capital Markets. Your line is now live. Hey, guys. Congrats on the data update. Just two questions for me. So for the first question, should we expect to see continued deepening responses from the other patients? Do you have any evidence to suggest that could be the case? And for the second question, in terms of the fixed-based dosing with this new data in mind, do you expect the right dose level to be this upcoming cohort three or beyond that? Thank you. Thanks for the questions. As we look at to answer the second one first, we want to follow the data. And we're very focused on scientific rigor and scientific method. And so we're learning as we go with what it means for fixed dosing, what the interpolated on a weight-based dosing could mean. We want to keep collecting data and follow things through. If we look at other programs in the field targeting SSTR2 expressing tumors, often you may wait up to 10 months post-administration to see all possible responses. So for any given patient, we would tell people it's almost like looking at the stock price for any stock. It could either stay the same, go up, or go down. With any given tumor, we don't know in advance if it's going to go up, stay the same, or decrease. And so we want to watch the data and see where it takes us. Got it. Thanks. Thank you. Next question is coming from Alec Stranahan from Bank of America. Your line is now live. Hey, guys. Thanks for taking our questions, and congrats from us on the update as well. Looking at the spider plot on slide 22, you really see kind of three kinetics of response, which I think some of the other analysts have seen as well. Curious if there's anything else beyond sort of the activity of the radiopharmaceutical itself within the cells between these three patients that are in PR, baseline tumor size, or something else that could be driving the different kinetics here? And then just quickly, in terms of go forward, I know that cohort three higher dose is in the study design for the escalation. But what's sort of the openness to an intermediate dose between the proposed cohort two and cohort three doses? And what would sort of be the driving factor for this? Thank you. So thanks, Alex, for the question. And we are really excited about this data. We think it's very encouraging for developing this medicine. To answer the second question first, we have a lot of flexibility in terms of looking at doses by having a liquid dosage form. So we can change the actual dose administered if needed. And our Chief Medical Officer and his clinical team are constantly evaluating what makes the most sense for further development. Markus, do you want to take the first part of the question? Sure. So obviously, the kinetics of these three responders is clearly different. We have one responder that immediately shows a decrease in the tumor burden. The second one has obviously a more gradual and the third one doesn't show a lot of response until after the end of the therapy and then produces obviously a rapid decline in the sum of the longest diameter. So as Dr. Wahl already suggested, these delayed reproductive deaths of the tumor cell is part of the radioligand therapy kinetics. What we may see also is that obviously with higher doses, the kinetics may be a little bit accelerated. But this is something we're obviously trying to elucidate. And I'm not sure there's a definitive answer in the moment for this phenomenon. Thank you. Thank you. As a reminder, that is star one to be placed into the question queue. Our next question is coming from David Nierengarten from Wedbush Securities. Your line is now live. Hey, thanks. Most of my questions have been asked. But I had a question, maybe just taking a look at the tolerability profile between actinium DOTATATE and you guys. I mean, it appeared to be a little bit better tolerated at the moment. But the patients in the actinium study were a little bit or they had prior radiation treatment. I mean, is there anything to think about in terms of tolerability decisions physicians might make as they look at the alpha emitters here in the kind of second-line setting for neuroendocrine tumors? Thanks. Thanks, David, for the question. And we are really excited about this data and what it means. Just before I turn it over to Mike Schultz to talk about some of the differences between actinium and lead, just as a reminder, the actinium data that we've seen so far has been in a post-Lutathera environment, not in a radiopharmaceutical naive group. So I really want to caution against over-comparisons between different enrollment entrance criteria, so between PRT naive versus PRT experienced patients. And I'd really be kind of reluctant to draw any overt conclusions in the data so far, but in terms of the theory, Dr. Schultz, do you want to comment on that? Yeah, sure. Thanks, Dave. Thank Dave. Thank you. And thanks, David, for the question. So I think from the beginning, as we started to understand that peptides and peptide-like small molecules were going to be the preferred delivery vehicles for radiation to the tumor microenvironment, that kind of led us to this idea of using Lead-212 over longer-lived radioisotopes for this application. And that was further evidence that that was going to be better had to do with the complexity of the decay series for Actinium-225. And the fact that Actinium-225 is an alpha emitter, which means that all of those daughters are going to be released in formulation. So at a bare minimum, when you're administering an Actinium-225 drug, you really have two things. You have your radiolabeled delivery vehicle, and then you have a bolus of unlabeled radiometals, most of which are alpha emitters that are going to deliver their dose based on their own biochemistry in the Bismuth-213 in that Ac series and the following Polonium-213 in the Ac series, then are likely to go immediately to the kidneys, where you're going to get an off-target dose that obviously is not preferred. The second thing that we needed to do was to develop a chelator for lead isotopes that had a better profile not only for radiolabeling of the Lead-212, but also the Bismuth-212. You can look at our publications to see that we can keep the Bismuth-212 chelated very tightly, which means that we have a better chance to be able to deliver the radiation to the tumor microenvironment. And the third rationale there is that with the fast PK properties of these radiopharmaceuticals, the radiobiology tells us that we can deliver a high dose of radiation over a short period of time to the tumor microenvironment. And that should give us a better safety profile. And so far, it appears that the safety profile of this radiopharmaceutical fits the theory behind the design. So I hope that answers your question. I'm happy for a follow-on. Thanks, David. Thanks. Thank you. Our final question today is coming from Justin Walsh from Jones Trading. Your line is now live. Hi, thanks. My question is for Dr. Wahl. I was wondering if you could provide some commentary on why you and your patients are motivated to use Lead-212 VMT-α-NET before trying Lutathera. I'm just curious what points of potential clinical differentiation you believe are most meaningful. I guess Lutathera is an approved agent, but many of the patients will ultimately not have an anatomic response, and many patients ultimately progress. So it's clearly a useful agent. But the data with this agent were sufficiently promising and followed the evolution of this for quite a while. I mean, the fact that the single alpha particles emitted and not likely to have significant free daughters going to the kidneys and elsewhere is attractive. So I followed this technology for quite a while and the evolution of it. And the alphas, in general, are capable of double-strand breaks as single-strand are more typical with beta emitters. So the probability or possibility of a safety and potentially greater efficacy led us to be interested in the trial. I think it led the multiple other sites, many of whom are large sites for neuroendocrine tumor therapy, to be interested in this trial as well. Hopefully, that addresses your question. Yeah, yeah. Great. Thanks. Thank you. We've reached the end of our question and answer session. I'd like to turn the floor back over for any further closing comments. Great. Thank you. We'd like to thank everyone for your continued interest in Perspective Therapeutics and also the investigators and patients that allow us to do this work and develop what we hope to be really defining medicines in the field. Thank you so much. Thank you. That does conclude today's teleconference webcast. You may disconnect your line at this time and have a wonderful day. We thank you for your participation today.