All right, so we'll continue here with Perspective Therapeutics. Thijs Spoor, CEO, will present, and then we'll take some questions. Thank you, guys. Good afternoon, and I want to thank Guggenheim for inviting us to present here. I love telling the story about Perspective Therapeutics and where we're going, and part of it is where we come from. So Perspective, stock ticker is CATX. We were formed initially from a merger between Viewpoint Molecular and Isoray. And so the I in the logo are Isoray and Viewpoint. We use SPECT imaging for what we do. And so the Perspective name sort of naturally evolved on its own. What we've recently done is divest ourselves of the legacy brachytherapy business that Isoray was in, and now we're exclusively focused on the radiopharmaceutical side of the company. And because we are publicly traded, I encourage everyone to read every word very, very carefully. I'll wait 20 minutes for you can write it all down. So really, what motivates us? It's really changing a patient's life. We always say if we can change one patient's life, then it makes all the difference in the world and makes our job worthwhile. This is the first patient that ever received our drugs. So the first drug that we did is targeting SSTR2. This poor patient has a neuroendocrine tumor that started in the pancreas and now metastasized into the liver and other parts of her body. If you look at the image on the top left, you'll see the patient scan four weeks before the first dose of our drug. Then if you look at the middle column, you see what happens eight weeks after the first dose. Then on the far right, you see what happens after three doses of our drug. So absolutely extraordinary what we can do. If you look at the ACTH levels on the bottom, you see the patient's hormonal status was resolved. It was normalized. Internally we say, you know, she went back and became a productive member of society. She's an investment banker, so some argue with that statement. But she was able to resume her life and actually get back to spending time with her family, going on vacation, and literally getting her life back. We transformed this woman's life, which we feel very grateful for. So I'm surrounded every day by incredibly talented people. Mike Schultz and Frances Johnson formed the Viewpoint Company back in 2015 with this unrelenting belief that they could make better pediatric drugs in the neuroendocrine environment. That's what started the whole concept. Jonathan Hunt came over from Isoray, brought Amos Hedt with a background in radiopharm development. Markus Puhlmann came over from Seagen. And when I recruited him, I said, "Listen, these are like ADCs except they actually work." And I thought, "That's kind of a strong statement to make from someone with a background at and Bayer and Amgen and Merck." But if you look at his form for us, he does believe it. He's been buying our stock in the open market too. And the advantage we have is that unlike ADCs, we don't have to internalize, release a payload, and let the payload have some other derivative effect. We can actually target the tumors and blow them up directly. If we target them with a peptide, we can actually have very rapid accumulation out of the bloodstream within 30-60 minutes. We will tune the peptide depending on what we're going after and optimize it in animals. If needed, we can adjust the length of the linker. We also then attach to it our proprietary chelator. One of the limitations we often get asked is why there's so much energy in actinium and not in lead. The answer is that back in 2015, when the company was founded, there wasn't a good generator available for Lead-212, and there wasn't a good chelator available. So like all good scientists, we invented both of those. We're able to sort of move things forward with reasons that we think actually make a lot of sense. If we look at a lot of the constructs that are in radiopharm right now, they tend to use DOTA as a chelator or DOTAM or TCMC. One of the limitations we see for these is that they have a charge on them. A plus charge or a minus charge, we think it slows down the ability to clear the drug through the kidneys, right? So kidneys love picking up charged proteinaceous species. And so if you can have a net neutral charge, you actually get rid of an extra barrier for retention inside the inside healthy tissue. One of the other things this does is make for easy labeling. And also the first daughter off of lead is bismuth, which gives the alpha. And we've actually designed this chelator to hold both the lead and the bismuth together. One of the panelists in the first thing this morning had questions about how this works. And the answer is you can actually design a chelator to hold both. And we did that. So both the lead and the bismuth are held tightly together with our chelator, less than 2% leakage, unlike about 20% or so with DOTA. So when we reduce this to practice, I think at this point, hopefully everyone in the room can agree that, you know, alpha particles hitting a tumor is desirable. Alphas hitting healthy tissue like a kidney is undesirable. And so we really want to skew that ratio as much as we can. The more we get on tumor, the better. The less we get to kidney, the better. And if you look at the side-to-side comparison, you can see about an 8-1 improvement. Some of the improvements from the peptide, some of the improvements from the chelator, some from the linker, they all contribute together. And we often get asked, well, what's the best isotope or what's the best in radiopharms? And there's no absolute statement there. All these have to work together to get your best possible clearance as far as you can predict in a human model. So when we actually compare versus standard care, in this case, we looked at a neuroendocrine tumor model. And in this model, you're looking at a xenograft, in mice. And the top left, you're actually seeing what happens if it's untreated. Versus in the top right, you see Lutathera. And so you see about a 23-24-day shift. That correlates to about a two-year PFS that you do see with Lutathera in humans. And on the bottom left, you see a single larger dose of our drug versus on the bottom right, you see four fractions. We like to fraction, a little bit just to avoid any risk of bone marrow toxicity. The one side effect you cannot predict with imaging is bone marrow. And so to avoid that risk and mitigate it, you do fractions. But if you look at the top right and the bottom right, so Lutathera versus ours in mice, hands up anybody who cannot see a difference between these curves. Okay, no, thankfully you can see it. When we went to the FDA, we said, "Hey, we want a fast-track designation, second line like RayzeBio has, in SSTR2, drugs, tumors, excuse me." And the FDA came back with the best letter ever. They said no. They said, "You guys get fast-track first line." So instead of Lutathera. And so not many of my colleagues get that kind of response from the FDA. They said, "It'll actually first line in all SSTR2-expressing tumors, not just, you know, just GEP-NETs." So that's been very, very encouraging. That's led us to pursue our imaging work. The reason I joined the company with a background in nuclear pharmacy and having seen many, many drugs in cardiac, have challenges is the unrelenting, unforgiving image that you get on a radiopharm. It doesn't matter what you want to have happen. You can see the in vivo fate of every single molecule you inject. And what you don't see here is just as important as what you do see. You don't see brain. You don't see lung. You don't see heart. You don't see liver accumulation. You just see liver mets. You don't see kidney accumulation. You see kidney clearance. And, you know, the next day, you get a very similar biodistribution pattern. Any drug that rolls off a tumor is going to get dumped in the bladder or get picked up by other tumor. So that gives you very, very strong predictive potential of what's happening with this therapy. The nice thing about nuclear medicine too is you can actually visualize before and after. You can do these three 3D portraiting images and really see what's tracking through. When we actually look at the serial slices, we get these kinds of series in a patient. There's two ways nuclear medicine looks at a patient. They look at something called PERCIST or they look at something called RECIST. So most people are familiar with RECIST. That's a radiological change. But PERCIST is equally interesting. PERCIST shows what's happening functionally with the tumor. So if you look at that top left and the top middle column, that reduction in the tumor uptake, that's a PERCIST response. Any radiographic change will always be preceded by a biochemical change. And so the tumor just doesn't all of a sudden decide to just collapse on itself. There's, you know, pathways within the tumor that are changing. And nuclear medicine likes to look at those and predict them in advance. Whereas if you look at the middle bottom versus the far right bottom, you see a reduction in that tumor volume. That's a RECIST change. So PERCIST is on the top. RECIST is on the bottom. Radiographic versus functional changes. We did have some data come out at the European Nuclear Medicine Congress. This was an investigatorship trial. If you look on the far left, you see four patients in here were actually pretreated with Lutathera. So it's a "second line environment." The other patients were Lutathera naive. And this data came out last October from a data cut-off in September. We expect at the SNMMI conference coming up in Toronto to have an update on these patients. The abstracts have allegedly leaked out there already. We haven't received formal notification about these abstracts. But Dr. Sen has told us she expects to present a further patient series, sort of all 12 patients, that she's been studying, a mixture of first and second line and a mixture of medullary thyroid and GEP-NETs. So we're actually enrolling a first line trial right now. So this is patients that are Lutathera naive. We cleared through the first cohorts very, very quickly for safety and efficacy. Excuse me, for safety. Now we're tracking efficacy. And we expect to have a readout on both of these in the second half of this year. And this is in the Lutathera naive environment. There's also an investigator-initiated program in the post-Lutathera environment that's happening as well. But we also have a much broader pipeline than that. We've got a differentiated agent, we think, for melanoma. We have a really interesting compound for FAP targeting. We've got some great clinical images there. And as we kind of move forward, you know, we think melanoma is a really interesting target. I don't need to explain what melanoma is to this audience. But what really excites us is about what we actually see, if we do a scan. So on the far left scan, you'll see an FDG PET scan. FDG is reactive sugar. It goes to any sugar-hungry cell in the body will pick up FDG and is and will light up what's metabolically active. And so that's brain and a lot of tumors. If you look on the right-hand scan, this is all the cell cells that on their surface express MC1R. And so melanoma is a very heterogeneous tumor type. We don't actually get this in all melanoma patients. The literature says 50%. And the beauty of this sort of matched isotope pair, Lead-203, Lead-212, you can image with 203 and identify patients that can work with 212. So the degree of concordance here is extraordinary. If you look in the patient's shoulders and their groin, you see all these tumors that light up with both. And so this gives you a high degree of confidence that if you inject the patient with the Lead-212 alpha-emitting version, you should be able to get quite a bit of activity onto that, onto those tumors. If you look at the power of molecular imaging too, you can see exactly why this is so compelling. I'd argue this is an inoperable tumor. It's so close to the esophagus, you would never want the surgeon going in there and trying to remove it. But you also can hit not just deeply embedded tumors, but every tumor. And where the clinicians are hoping we can get to is micrometastatic disease, which is a really tough one to try to image and prove, but we'll see in the long-term data readouts how that manifests. We've also got an amazing ability in a heterogeneous tumor to actually use combination therapy. This is absolutely extraordinary data. We got an additional $2 million grant from the NCI to study this. Because if you look at that top right image there, you see the black line is untreated. You see what happens if you treat this melanoma model with a Zelboraf. And in contrast, add one dose of our drug to the Zelboraf, and you get this extraordinary right shift on that curve. And that was in a, you know, immunocompromised mouse model. In an immunocompetent model in the bottom, you see the dark line is untreated. The light blue is Ipi/Nivo. The interrupted line is a single dose of our drug versus the dark blue line is combination, our drug plus checkpoint inhibitor. And that you get this extraordinary response. So even with a 45% response rate, 75% of those animals could not grow a tumor again on re-challenge. So we tried reinjecting them with tumor, and we could not grow again. So absolutely amazing benefits for what may show up there. We actually announced an agreement with Bristol Myers Squibb to look at nivolumab in melanoma patients post-second line. But trying to take advantage of the fact that we can actually use a, we think, is really interesting MC1R targeting agent and combine that together with a compound. So we actually get a, you know, a dose escalation in monotherapy, but rolling into a combination study as well. The advantage here is that we'll be able to practice and see what happens in humans with a synergistic effect. The first two dose cohorts, we expect to have readout on safety and efficacy at the end of the second half of this year. We actually did disclose some of our initial safety data at our analyst day in March. That data looked very, very compelling. We're not seeing a lot of safety signals showing up at all. So really what we want people to look at is what happens on the efficacy side. We don't know yet. We haven't, you know, the patients haven't been followed through. And we're just as excited as everyone else is to see how that plays out. We're also excited about what else we can do in our lab. We have an amazing group of chemists that can actually do some pretty extraordinary things. FAP is a really cool target. Rather than going after just sort of one particular tumor type, what's beautiful about FAP is you can actually look at multiple tumors that express this any sort of epithelial cells. And so in things like sarcoma or cancer unknown primary, some of the advanced breast cancer patients, all these are really interesting because they start to have FAP- alpha expression. And in some cases, the expression is on the tumor itself, in some cases on the stroma. So the tumor gets large enough to form its own scaffold, you can then attack it directly. And what's beautiful here is that the nuclear medicine community has already shown lots and lots of tumor types where this can be interesting. So in terms of what we can do, we'll actually iterate through various programs in-house. And so if you look at the sarcoma in this mouse model, in the tumor, you see, you know, in the first iteration through, you actually got activity in the tumor, and then the center, you see the kidneys. This is a fairly typical biodistribution pattern early on where you get tumor and kidneys. But we've already established we want more in the tumor and less in the kidneys. So we changed the peptide construct a bit. Now if you look at that two hour scan, you see a lot more in the tumor and a lot less in the kidneys. So I think this is actually really, really compelling. And, but wait, there's more. We went a couple steps further. When you look at these images, it really is extraordinary. We actually get incredible tumor uptake. It's not sticking in the kidneys. It's going right through the kidneys to the bladder. So the ability to actually image just tumor and get very little background activity to us says, it's not great as a diagnostic agent necessarily, but it's fabulous as a therapeutic because it's just hitting tumor and stroma and showing you where you could actually treat the patient. When we actually go into head-to-head with animals, we did some work and showed, you know, phenomenal response rates versus FAP-2286 lutetium. But getting into humans is really where the rubber meets the road. And this is an osteosarcoma patient. If you look at their FDG scan on the far right, you see that you're seeing activity in the bladder. You're seeing a lot of brain activity that's classic with an FDG scan. And you're also seeing this extraordinary activity in the shoulder. And this is an osteosarcoma where there's very few treatment options available for the patient. If you look at our scans, one hour, four hours, and 21 hours post, you see exactly what will happen if this patient gets a Lead-212 version of our drug. In that case, you're getting incredible accumulation just at that one site. You're not seeing a lot of background activity. And this also points to the beauty of peptide imaging. Peptides accumulate within about 30- 45 minutes. So the one hour scan, you can see that you've gotten rid of pretty much all the background and blood pool kinds of issues. If we zoom in on these scans, you can see beautiful resolution of what actually is in the joint itself. Is it in the tumor, or is it inflammation? In this case, it really looks like it's tumor. We actually looked at a neuroendocrine tumor that had devolved so much that he actually had started some sort of stroma showing up and some scaffold proteins. And if you look at a comparison here of the FDG scan and a FAPI scan versus our drug, you can see we can actually light up a whole bunch of the tumor types that we actually want to address directly. And we actually look and zoom in on some of these lesions, we have great uptake. And a lung adenocarcinoma. Here, this poor patient, we're looking at a posterior view. You're seeing all these tumors throughout their back and across, across their whole thorax. And you see a lot of, uptake. Again, that one hour, four hour, 18 hour shows if you give a Lead-212 therapeutic, all these tumors should get a very, very healthy dose of of alpha particles, which we think should correlate to a better outcome. And we think that they should, there's a very low likelihood of of major toxicity issues because we're not seeing a lot of off-target uptake. So when this goes into clinic, we'll probably want to dose a bit more frequently, you know, and split into fractions to make sure we don't inadvertently get any kind of bone marrow activity. And looking in at these images, the beautiful part of molecular imaging is you can zoom in and see exactly what's happening. Where is your resolution? Are you getting tumor? Are you getting stroma? Are you getting joint? In this case, we feel very, very comfortable that we're actually picking up all these tumors that are really sort of tight with various tissues. As a publicly traded company, we do have to report out quarterly, on the 15th. So in two days, we'll be filing our 10-Q. People can come back into a bunch of these numbers, and our cash position is actually very strong. We did a financing with the street. We did an option agreement with Lantheus where they invested in the ability to negotiate with us for rights to our lead asset. So there's no obligation for them to license with us, but they have a first crack at it, and they also have the ability to co-invest in our prostate program if they choose. We also acquired a facility from them. And people who watch the stock very carefully could see that there's probably some cash taken down from the ATM at some point. But across the board, our cash position is probably well north of $200 million. Our current burn rate is about $4 million. And so if we do nothing and just operate as we are, we've got a long cash runway. We do expect to invest pretty heavily in our infrastructure and our clinical programs. We expect come the fall, we'll know a lot more about what expansion cohorts will look like. And so we do expect our burn to increase, going into the fall once we see how things are progressing there as well. So to try to tie all these sort of themes together, one of the things I hope you've taken away from today is that, you know, it's not this radiopharmaceuticals are big. The more important concept is that radiation oncology is big. You know, and targeting tumors with radiation is not a new concept. No one at this conference has pioneered that idea. The whole goal is, can we actually get the radiation to only the tumor? And so I think you'll see a shift and hopefully see much more of a shift from external beam to, I'm not calling it internal beam, but the, you know, treating cancer from the inside out. If you can deliver that radiation to just the tumor and avoid the healthy tissue, you've got a phenomenal way to actually go and treat these tumors directly. And in all likelihood, there's going to be combination therapies that keep building up. It's so difficult to treat all these tumor types. But thankfully, there's so much innovation in the field that we think there's a lot more coming. One of our competitors in the space at the World Theranostics Conference was asked, is this a bubble? Has all innovation really happened here? And they said, no, only 7% of tumors are being addressed right now with Lutathera and Pluvicto. There's still 93% of tumors that are decent candidates for radiopharmaceutical therapy. There's still can deal with innovation and evolution in the field. So lots of things we can go across bonus or pause here for questions. All righty. Any questions? No, maybe just one. So going back to your study, SSTR2 study, and I may have missed it, a lot of moving parts, but so the investigator-sponsored study, right? So you had presented data on 10 patients, I believe, and some of it now, an update of that leaked. Can you just remind us what is now publicly out there and what else will be presented from the SSTR2 program? Yeah, so, in June at the SNMMI conference, we expect the investigator to present all the patients that she's treated. She has told us that she's treating 10 GEP-NET patients and two medullary thyroid cancer patients. The data cut that was in the abstract, that we think got leaked, was probably where she was in January with her study. And so what she often does is do a data cut right before an actual presentation. So we expected to have much more data on all these patients and a bigger kind of read-through. So there are four second-line patients here. There's six kind of first-line patients, and we expect, wherever the investigator is with safety and efficacy in all 12 patients, in June. So it's 12 up from 10 and then more follow-up on those. Okay. Gotcha. And I think you said so you have a company-sponsored phase 1 in naïve treatment-naïve GEP-NET. Is that correct? Yep, that's correct. That's this design here. And so we actually have announced previously what some of the initial safety data looked like. And I think the clinical term is nothing burger. It was very, very clean profile. The patients really tolerated the drug well. Now we're looking to see what does the efficacy signal look like with just a few patients. We escalated it very quickly into that 5 millicurie dose cohort. We expect to have data from both the 2.5 and the 5 millicurie cohorts in the second half of the year. Okay, and do you have a sense of where the effective, the minimal effective dose is for this? So that's a great question. We have a lot of internal bets right now. We know if we jack the dose up to 10, 15, we can start to induce side effects. That's not in our interest. We really want to see what does the effective dose look like. And Dr. Sen's investigator initiated a trial. She did an average dose of 2.9 millicuries. Her patients are also really small. They tend to trend about 40 kilos in weight. And so Western patients tend to be about almost twice that. We're not doing weight-based dosing, but we think that we're pretty close to the range where if we're actually patients starting to feel better, if we actually, if we don't see any safety issues, we'll then want to look at the scans to look for radiographic evidence of slowing down disease. Okay, and then, yeah, what will, when will you be able to present this data? So we said in the second half of the year. Gotcha. So we're waiting for the patients to go through, receive all their doses, and track them through. As a reminder, the Lutathera package insert says a 13% ORR. When we look at these circles, for example, we see a lot better than 13%. So we're hoping that we'll see something in our U.S. trial as well, which will give us a great reason to talk to the agency. And so just to confirm, so this trial will compare to the approved Lutathera indication, not the first-line study that no one has seen? So Lutathera is effectively first-line. Right. And so we think the benchmark the agency will look at will be compared to the historic, what's presented with that in the PI. Gotcha. So there's no control arm in the study. We're dosing the patients and we're looking for response rates. Okay, great. Then, yeah, I just had one more on FAP, where there's, I think, four, at least four programs ongoing. And yeah, I'm just curious, is an alpha emitter, you know, the best choice as a payload just given the way the targets express in a tumor stroma, not necessarily on the tumor in all cases, do you need a greater distance for the payload, you know, to be active at And then also, what, how do the different FAP programs differ? Are there differences that are important as you think about the competitive landscape? So first, I'll take that as an inference then that it's a good target to go after. And we think it is. You know, FAP is really, really interesting. If you can knock out the scaffold and the stroma, we think that's really compelling. We've actually done a lot of our own internal comparisons. Every time we innovate, we do synthesize all of our competitors' known agents in our lab and do the head-to-head comparisons. We compete against them and keep iterating till we get a lot better. And then we do a head-to-head efficacy in our labs as well. So if you look on the right of the screen, we see some published data with FAP-2286 with lutetium. In that case, you've got four out of 10 responses at 40 days. Our data shows in the same sort of model against sarcoma, we got 100% survival at 90 days. And so we feel very, very strongly that we get good data and not just good, but great. So having this kind of effect in animals is really encouraging as we all know animals don't pay and they don't say thank you. But we want to sort of look at what happens in humans. Do you actually have to get, you know, sort of deep penetration all the way throughout? Probably not, right? If you're actually looking at what you're targeting, in the stroma versus the tumor itself, sticking anywhere near that tumor, you've got that two-cell zone of destruction. So betas will give a 200-cell zone of damage. The difference with alphas is you get a two-cell zone of destruction. And so if you're completely knocking out, with alphas, anything that's tumor associated, that can only be good for the patient, we think. Great. And then, yeah, how are the different? I mean, obviously you have a lead payload, but I think any other differences compared to the other FAP programs out there? I think there's some imaging data from Novartis Clovis is available, but yeah, it's sort of, yeah, in terms of some of the other physicochemical properties of the molecules. Yeah, so really want to make sure we get good tumor accumulation. We don't get background. Our first clinical images show that this molecule does do that. So we know where the energy is going to be delivered. It's everywhere that's dark. You know, the bladder is a very alpha-resistant organ. And so therefore, having that extra alpha damage going to the osteosarcoma in this case, we think is beneficial. The images across the various FAP conjugates look quite interesting. Some people are trying to look at developing a new diagnostic for cancer staging with FAP. We applaud that, because I think any way to identify more patients for us to treat is quite welcome. Great. Awesome. Well, with that, we'll wrap up. Thijs, thank you for the presentation, and we'll continue here in a few minutes with Convergent Therapeutics. Thank you. Thanks for your time.