Perspective Therapeutics, Inc. (CATX) June 8, 2026 Conference Transcript

Okay, we'll continue with the next session. I'm Paul Choi, and I cover the SmidCat biotech sector here at the firm. It's my pleasure to have perspective here on stage with us. And what we'll maybe do is what we've done in the previous sessions, and we'll kick it off maybe with some high-level comments, if you will, on just sort of what your strategic priorities are for the remainder of the year and going into 27, and then we'll go into questions.

Terrific. Thanks, Paul. And thanks to Goldman Sachs for hosting us here. So Taste Forum, the CEO of Perspective Therapeutics, I have to say this has been an absolutely extraordinary year for us. We're doing an amazing job at pretty consistent execution. And when I say pretty consistent, we're regularly treating patients around the world. In the U.S., we regularly enroll in our clinical trials. We're building out our manufacturing network. We have a great cadence for bringing in best-in-class, first-in-class molecules to humans. But we've had a really fantastic time really making a difference in patients' lives. We've been able to produce 400 of our generators that are used to actually create the isotope. We've made sort of several hundred doses of our products. We've treated over 100 patients in the U.S., another 30 around the world, across now four programs in clinic. So it really feels great that everything we've done over the past several years, we're executing consistently, flawlessly, and really sort of going on a very steady cadence of data and patient management. Great.

The radiopharmaceutical space is very diverse with lots of approaches, lots of technologies. Can you maybe briefly provide an overview of what perspectives, sort of background technology is in terms of your platform and how you think about how it's positioned or differentiated versus some of the other competing platforms?

Thank you. So it comes down to targeting cancer. And as we target cancer, if we find the molecular target on the cancer cell, we know we can target it directly. When I think about how the radiopharmaceutical space has evolved, I have to do a bit of a humble brag here and say we're playing in a different league. When you think about some of the early programs that are now actually commercial and are out, very interesting programs using the TCM-177 to target PSMA and SSTR2. We've really amped things up. we've taken a different approach. We use an isotope called lead 212. Lead 212 is an alpha emitter or gives rise to an alpha emitter. It was always considered interesting, but there wasn't really a good way to to make the isotope. There wasn't a safe way to chelate it, and it lacked new targets. So three big gaps which we've solved across the board. We have our proprietary generator system. We've, as I said, we've made hundreds of these generators we ship around the world to Asia, Europe, across the U.S. Our proprietary key leader is actually translating into what looks like best-in-class patient safety profiles. And so it's undeniable. A targeted therapy, if it kills a cancer cell, you kill a cancer cell. A targeted therapy, if it hits a healthy cell, will kill a healthy cell. And so we want to make sure we really open up as broad a therapeutic window as possible. And our key leader allows that as well. And then to go from in a different league, we're actually now innovating with best-in-class PEPTA. And so we have the ability to target directly. We have a built-in enrichment strategy just by the nature of how we actually develop our medicines. So we'll use the drug itself as a way to target if the patient could ever respond. So we're not just sort of guessing. And really what that means in oncology is we've always had four major approaches in how we treat patients with cancer. Surgery is pretty clear. If it's a small enough tumor, if it's clean enough, cut it out. If we get into chemo or targeted chemo like ADCs, That's great. That's one mechanism of action. If we can get the body's immune system to kick in, that's a fantastic model as well. And lastly, radiation has always been a great way to address cancer that's different than the other three. And the nice thing about precision radiation is that you're going from an external beam, which irradiates a lot of healthy tissue at the same time, to what we say, treating cancer from the inside out. What that means means we actually hit the cell surface and actually target it absolutely And all these things are synergistic with each other. In the same way that chemo and radiation evolved into really interesting chemoradiation approaches, we think our medicine in combination with targeted therapies like ADCs or in combination with the immune system will lead to really good synergies and potentiation of the potential effects.

You have a great seat at the industry table in terms of looking at the broader radiopharma landscape. And so as you think about the industry and how much it's changed over the past couple of years, There were many acquisitions, a little bit of sort of, you know, quote-unquote, consolidation, but you may speak about, you know, what is the level of enthusiasm, I guess, from your seat as you talk to clinicians and other developers for using sort of and developing next-generation radiopharmaceuticals here.

So I think it's been an extraordinary time of creation in the field. We've got, I think, at the last count, I saw over 75 different companies looking at just on the peptide side of things. You've got another sort of 20 to 30 in the isotope game and the CDMO game. There's been a lot of push and a lot of capital to try and take advantage of the fact that these markets exist. And for pharma, it's not a zero-sum game. Any advances in the radiopharmaceutical business are synergistic to their existing markets that they have for treating patients with cancer. So as we look at how the industry goes, there's a lot of seed capital and there's more coming in all the time. We've had some companies close down. And we've had some technologies that have tried and haven't quite worked. I think what was missing in the field was that there wasn't a lot of true innovation and taking things into it differently. And I think the early guesses or attempts to go generic SSTR2, generic PSMA, and actually doing sort of various combinations thereof. At one point I looked at the landscape map and I saw about 30 companies with some variant of a PSMA. And that makes sense. a lot of men have prostate, have a prostate. A lot of men that have prostates will get prostate cancer. So it's a readily built market. But in order to differentiate or disrupt an approved drug, you need to be differentiated enough and actually show some better effects. When we look at the capital that's going in, there's been a lot of great ideas, and they're all worth exploring to a certain degree. But then it's going to come down to what makes sense. There's been a very fragile isotope ecosystem. When we look at an industry where you only have one or two suppliers, that doesn't feel healthy. We need to have a more competitive landscape. We need multiple players, but all able to be sustainable. And that's been a challenge on the supply chains, too. Thankfully, what's happened is that with the investment that's come into the field, it's been sort of a virtuous circle. We've had this sort of reinforcing group of expansion of indications with some of the earliest drugs in the space like Zofigo. so radium-4 prostate cancer, expansion of indications for Pluvicto and Lutothera in PSMA expressing tumors. And that whole sort of virtuous circle means that more people are going to come in. And now, for example, on the lead side, it used to be only the Department of Energy. DOE made a lead generator the third Tuesday of every month. Now you've got seven commercial ventures trying to make lead 212 generators.

Okay, great. Right. Maybe turning to the regulatory side, can you maybe comment on how your interactions with the FDA have been going? How are you finding the agency, or what is its stance towards development of radiopharmaceuticals, maybe specifically for you, and as you think about the industry broadly?

So, I mean, I won't be able to comment on ongoing dialogue we have with them, as we said publicly, we're trying to get into, and we're getting ready for a registrational trial. But the agency overall has been very willing to learn, and we think has been a terrific thought partner in terms of really working out how to actually bring these new technologies forward. There are several programs that we've been accepted into. For example, we got a FastTrack designation with our first program, trying to get into, we thought about getting into the post-Ludithera space, and we were encouraged to get into this sort of Ludithera-naive space. There's also the CDRP program, which is like a fast track, but on the manufacturing side. We actually wanted to go through all the previous barriers that existed for radiopharmaceutical therapy. And two years ago, the FDA actually had a joint FDA and Nuclear Medicine Society workshop to say, how do we dose higher, what's a thoughtful approach? And what they suggested, for example, is that there is a limit for how much dose a kidney can get based on historical external beam data. And that 23-grade limit was considered a concrete ceiling that no one could go past. We actually had submitted our data to the agency to allow or to ask if we could dose 20% higher on the SSTRT program. And what would that do for the mean dose of the kidney going from 37 up to 45-grade? We showed a lot of data, and the agency agreed with our approach. We showed them our calculations, And we also published all of our calculations. I think it's important to space, publish your work, show what's there. The FDA then published guidance to the industry that basically laid out a whole case for here's how you show with a clinical profile, with better data, with consistent data, and overall patient safety. Can you actually increase things beyond what were previously thought to be as limits? So we found a very, very receptive agency that really wants to learn. There are multiple things that kick in. There's groups that are involved with radiation management. There's groups with radiation safety. There's the usual CMC groups. As a peptide, we follow within CDER and not CBIR. But across the board, we found the agency very willing to engage and that they really want to learn, and they've been working with us to really help bring advancements out there earlier.

Great. Maybe turning to Perspeca's platform, can you maybe comment on how do you develop an early view on a candidate or a construct using your dosimetry work, and then when do you decide it should be advancing to the clinic? What are sort of the key steps you look at?

Thank you. So we have many, many programs that are active. The company spun out of the University of Iowa. And so in Iowa, we actually have a core discovery team that looks at innovation that's internally driven. We also look for external partnerships when relevant and appropriate. The internal team, any external teams, we have to go through some pretty hard filters. What we follow relentlessly is by distribution. And that feels almost obvious, right? You'd always want to follow by distribution. But the way we design our medicines, using lead-203 as an imaging surrogate, and then its elemental twin lead-212 for the therapy, we can actually do multiple iterations and rounds in animal work without sacrificing the animals to really see, can we change our biodistribution? So we can actually get very, very high binding affinity to a receptor. And in our corporate web presentation, you'll see we show images of how we iterate that through on the animal side where we can bind in those images we show, for example, fap alpha very high levels but in the early images and the early candidates in the field we looked that we looked at we saw an awful lot of off target we saw a lot of kidney retention and we try and avoid that we know we can tune our peptides to skew things away from kidney or towards kidney we can skew it away from liver towards liver and obviously with a medicine you want to have you don't want kidney retention or liver retention you want any unbound drug to leave the body as fast as possible, which is usually through the urine. So we follow that biodistribution pretty relentlessly in animals. Once we can know we get a fantastic imaging agent animal, then we'll try treating animals. And if that works, then we'll image humans. And once that works, then only then will we start to treat humans. What this means is that we have multiple programs in development. So we only name our candidates and identify them into the street once we have good first in human imaging, showing really, really good biodistribution. And so we just rolled out this year our latest candidate that we're pushing to clinic targeting CCK2R. And that target was very, very interesting because we could show fantastic accumulation of patients with medullary thyroid cancer and almost no other organ retention. Okay.

You know, investors focus on a lot of different agents, but ultimately, how did you choose land on lead-212 as sort of your go-to here?

So we like to say we're isotope agnostic. And we actually live that. In our labs and our discovery centers, we use lutetium or actinium or iodine or lead. What we found is that for all the constructs we have and all the tumors we're going after, we get the best safety window or therapeutic window when we're using lead-212. What we like is the really hard, fast punch of lead-212, and we like the fact that it disappears. And if it disappears, then actually the body's own immune system can actually kick in and not be damaged. External beam with a lot of fractions has shown limits to how much you can actually help a patient, because if you're always damaging the tills, you don't get enough chance for the body's own natural mechanisms to help the patient or the animal resolve the tumor. So we think it's important to have times where the body does not have any radiation, so it can heal. And at times we get these bursts of activity that are even more valuable if you get a neoantigenic storm. So the really exciting thing about alpha particles, it's such a violent destruction of the cells. You get this neoantigenic storm that's going to create all these fragments that can then help present to the immune system to move forward. We also like with lead-212 is that it has its elemental twin, lead-203. lead 203 is a gamma emitter only the gamma emitter the pure gamma means that you can image you can image with very very high quality with the drug that you expect to use and therefore embedded in that you have a self-enrichment strategy where we can actually identify in advance if a patient should ever respond to that therapy and we had a great um case study that that was just shown at asco where we showed a patient that was positive for the mc1r receptor as a melanoma patient 50 percent of patients have that 50 percent don't and we can see in advance if they're positive that patient had the receptor we could treat them and have incredible amount of disease burden go away and so with several doses in we're seeing more than 60 percent reduction that patient served tumor volume which is absolutely extraordinary and it's one of the things that really allows us to use lead 212 we could actually use other isotopes we just haven't found combinations between isotope chelator, ligand, tumor type, that all together give us a better profile, but we're open to it. Okay.

You touched on something that's key in development in this category, which is safety, and specifically kidney toxicity, where you can see quite different outcomes, even when you're using the same isotope, depending on the construct. And so can you maybe walk us through why these outcomes might be so different from a toxicity perspective? And relatedly, what other things are you monitoring for as you advance your program in the clinic? Sure.

So thinking back to a little bit of drug 101, you take a drug that's systemic. It's either going to go to the liver and stay there, go to the liver and wash out through the GI system, go to the kidney and stay there, or go to the kidney and be dumped out through the bladder. And we always like that last choice. Go to the kidney, quickly dump it into the bladder so it can leave the patient's body. It's also important in radiopharms to look at not just the initial drug that you've developed, but think about an analogy like toxic metabolites. What's downstream?

What happens next?

And with any isotope that decays, there's inevitably a daughter. That daughter may be radioactive or not. If it's radioactive, there'll be another radioactive daughter or stable daughter. You have to follow that cascade all the way down. What we have found with lead-212, it's first emissions of beta, and then it creates bismuth 212, which is where the alpha comes from. So we have found an imperative to make sure that our chelator holds that bismuth as well. So you can either think of it being bismuth, the ultimate drug in the lead is the pro-drug, or you can think of the bismuth as being an active metabolite. But in either case, you need to know where's the lead, where's the bismuth. Our chelator approach holds that daughter captive as well. So wherever our initial lead drug goes, that very, very active daughter goes as well. and we hold that on to tumor. I think we've seen some situations using the same isotope where that may not be the case. And using a different chelator like DOTA or DOTAM, we've shown in publications that those leak that active daughter. And if that leaks, it's going to be a leakage of bismuth, which tends to go to the kidney. What we also find is the initial biodistribution of the drug, you want to make sure it's going to tumor. And if it's going to kidney as it clears the body, it doesn't just go to the kidney and stay there, it flushes through. And so most of our medicines we make sure have a net neutral charge, whereas we've seen some other programs with a net positive or net negative charge. That really matters for clearing a drug. If the protein has a charge on it, the kidney will pick it up and hold on to it. So we try and do everything we can to make sure that the kidney spends as least amount of time as possible with that drug on board. And if it doesn't have that drug on board or the active isotope on board, it has a better chance of not getting damaged. And we've shown some very, very good data now this year where we actually believe with our SSTR2 program, we've dosed 46 patients at a dose that we think is one we want to take into a registrational trial. And we've shown at ASCO a week and a half ago a very, very clean safety profile. We still have not seen any grade 4 or 5 adverse events, and we've not seen any dose-limiting toxicities. So the ability to create a very broad therapeutic window with a lot of safety data, especially in vulnerable organs like kidney and liver, I think has been absolutely critical.

You actually brought up what I was going to ask next, which is the investment community went to Chicago for ASCO last week where you did provide an update. Can you maybe recap for us what you showed there and just sort of what the implications are and learnings are from your data there?

So with two of our programs in clinic right now, our SSTR2 program and our melanoma program, we gave updated information on the posters. At ASCO for our SSTR2 program, we showed that we get a consistent deepening of responses over time. Patients, when they get dosed, they get dosed over a 24-week period with four doses of the drug, and then we stop treating them because they've received the dose that we want to give them, and then we observe them over a period of time. And what we've found is that in some cases, even 60 weeks post-initiation of treatment, we'll still get responses where the tumors shrink. There'll be much earlier changes that are seen initially with the tumor morphology, but they don't start to hit resistant criteria until quite a bit of time has passed. So broadening and deepening of responses. We also show that across other dosing cohorts, so a total of 20 millicuries, a total of 24 millicuries. We aggregate all that safety data. We've not seen any major issues show up yet, and across the board, we feel we have a very, very safe candidate that we're bringing forward. We also showed with our melanoma program that now in monotherapy, at what we think is a very compelling dose of 3 millicuries, that the majority of patients have disease control for well beyond their expected natural history. Melanoma patients that are post-second line plus, meaning they try check-1 inhibitors, They try to be a RAF inhibitor if that's suitable or not. So they're expected to have a two- to four-month window before they get severe progressive disease again. We extend this out to up to a year in some cases, and we've had several responders now show up. So having this almost impossibly-to-treat group of patients where we get responders and, just as importantly, disease control, we think is really, really compelling.

I want to go through these two programs separately and maybe just starting with Nat. do you feel like you've gleaned enough information from what you've learned so far to advance the program and just sort of what other tweaks or modifications do you think you would do based on your learnings from this data?

So with the NET program we're looking at patients who are newly progressing with a neuroendocrine tumor. Often times these patients will start on the semantastatin therapy to manage their symptoms and they'll live that sometimes years. And then when they start to progress again and they need some kind of therapeutic intervention. In patients that hit that profile with gap nets, so gastroenterotic or pancreatic net neuroendocrine tumors, we can actually start treating those patients. What we found is that the 5 millicry dose given in 4 times 4 is giving a very clean and effective profile. That is a dose program that we'd like to bring forward into registration. So the whole organization is getting ready to initiate a registrational trial in that space.

Would you look at other doses or schedules? Do you think before advancing to registration, or do you plan to go directly to your next study and then maybe potentially add some other variants of dosing or scheduling?

So the 5 millicres times 4 we think is absolutely appropriate for bringing to registrational design. In parallel, though, we are also exploring a few other dosing scenarios to try and pick apart is there a differentiating signal if there's a minor tweak? So rather than doing four doses of five millicuries, what if it's four doses of six? So 20% higher dose, what's the downstream implication of that? We're also testing a slight front-loading shift. So rather than doing each dose being five millicuries, the very first one is six, and the last one is four. And in doing that slight shift, we've already shown that can be very, very safe, but we're wondering can we get an earlier or a deeper response in the tumor if we load a bit higher right when the tumor is the most receptive, right? And so when it's most like a sponge, if we give it a little bit of a front load, can that help? Neither of those two studies interfere with our going full steam ahead, knowing that a 20 millicurie dose should be suitable for registrational trial. We love that profile. We think it's very, very strong. It's giving clear signs of efficacy. It's a fantastic safety profile, and we want to move that down a registrational pathway. If there are other learnings along the way, then we'll have to assess that data as it comes.

What in your mind would be clinical success or evidence of differentiation? How are you guiding investors to benchmark this data that might be coming up in a pivotal study? Are you comping it against, let's say, TKIs that are approved in this area? Just maybe help us frame how you're thinking about this.

So I think for a lot of clinicians, the default setting is that they may go for Lutathera. So the TCM-labeled SSTR2 analog. And the package insert for that shows a 13% response rate in GI tumors and a certain PFS metric as well with a reasonable safety profile. We think we have a more compelling clinical proposition there. We're getting pretty high ORRs right now. from the last data cut that was presented at AACR. We showed a 50% response rate, which we think is very compelling for these patients. That's in tumor reduction. The patients feel better. And so with such a high response rate and without showing any major safety issues, this is very important for clinicians to look at. What we've seen with our program is that the clinicians are coming into our program with great enthusiasm. And I say that meaning we keep opening these sites. And the last time we opened up a cohort, it filled not instantly but almost instantly with patients that the clinicians really wanted to have experience with our drug as well.

Maybe one more before we turn to the melanoma program, which is there are also a number of competitors working on generics or basically equivalents of Lutathera here and just that could theoretically increase availability of that approach for lutetium. And just how do you think about that market dynamic down the road versus your clinical development plans?

So I think that with the approved medicine and with generics coming in, they all use the same payload. It's a beta delivered via lutetium. And there's going to be natural limits to how much a beta can do. Beta particles are fundamentally different than an alpha particle. An alpha particle is 7,000 times as massive as a beta. A single alpha particle will only go about two cells, and a single alpha particle hitting a cancer cell will kill it. Betas, you need about 1,500 particles to kill a cell. They'll travel about 200 cells. And it's a very, very different tool. If you can have an ultra-sharp scalpel, like an alpha particle, it can be that much more potent if you can target it explicitly at tumor and not target other cells as well. So I think generic luteesum agents coming in will be interesting for the market. It's natural evolution and natural maturation. But at the end of the day, if we can identify, if we can deliver a much more effective alternative, still keeping safety in mind, that's a lot more compelling.

Great. Maybe turning to melanoma now. You mentioned earlier there's a well-established treatment paradigm where checkpoint or immunotherapy is typically front line for patients with BRAF mutants. Those targeted therapies are typically used. radiopharmaceuticals doesn't often come up in the treatment of melanoma outside of potential external radiation that you talked about. So maybe can you talk about the logic, first of all, of developing a more specific approach here?

So I think there's never been a radiopharmaceutical that could target cleanly. And this is where we love the ability that we can differentiate and, more importantly, innovate. We've looked at a receptor called MC1R that shows up in about 50% of metastatic melanoma patients. And we can tell those patients in advance by doing the screening test. And so that's been very, very interesting to actually highlight those patients. I have seen a few other programs targeting MC1R that have struggled to reach a therapeutic window, but they also haven't been able to screen for MC1R positivity. And so in this case, we actually have the ability to go in earlier. What's really compelling here is that we can actually get, you know, my vision for this field is that any time you're getting a checkpoint inhibitor, there's an opportunity to also give a targeted alpha therapy to really help create a lot of neoadjudins for that tumor microenvironment. You have the potentiation. And the first time a checkpoint inhibitor is given, there's a lot more chance to have cold tumors turn hot. There's a lot more opportunities for the whole system to actually have its ability to address the tumors directly. So we think the fact that no one has really been able to bring something into the clinic yet with a broad therapeutic window highlights our innovation and is providing a great opportunity for these patients.

Great. In terms of next steps, what do the data support in your view? And then I guess just maybe frame for us what is the regulatory pathway? I think the investors in Wall Street community know sort of what the path looks like post a checkpoint inhibitor, but how does your candidate fit in here?

So one of the things that we want to identify no matter how the drug ultimately gets used is is there monotherapy activity? There's very, very clear data from the preclinical side that there's combination activity as well. But in humans, we need to identify monotherapy activity, monotherapy safety, combination safety, and then ultimately combination efficacy. So as we think through those boxes there, we've shown we've done some dose finding now with that monotherapy environment. We show that at 1.5 millicuries, we start to get some signal. At 3 millicuries, we did a very strong signal. And going up to 5, we tended to roll off. And that tells us that 3 is really the right way to go on the mono side. A monotherapy indication where if we're hovering around a 30% kind of range for response rate looks very interesting in that field, especially for patients where they've exhausted all other therapies and if we can get that disease to be stable and, as we say, frozen in time. So to take a patient that's newly progressing, post-second line plus melanoma, and freeze their tumor in time for a year plus is absolutely fantastic for those patients and lends the way for a monotherapy approval or registrational pathway. And so if we identify that pathway, that's very interesting. Once you identify that monotherapy activity, it feels obvious that you'd then want to try to use that earlier in the patient's disease progression. So you can then go earlier, and in combination with that, you also want to look at combinations with other therapies to see how they play together, and you also want to prove there's no contribution of components to a safety profile that would make clinicians adverse to using that instead of a standard of care. So in classic oncology drug development, we want to sort of take a therapy that we can show is safe and effective on its own, and then showing it's also safe, then find the right sequencing to get that to be used in other combinations.

We've been talking about fairly specific tumor types, like PSMA, where there's a very clear biomarker, same is true of NET, but the dream, I think, is to develop a sort of pan-tumor radiopharmaceutical here. And can you maybe talk about your efforts in that area?

So I love the idea of a pan-tumor concept. And I think there is a kind of a pan-tumor imaging agent, right, FDG for PET scans, that still doesn't quite work in all tumors because tumors are so different depending on where they come from. We have a program that targets FAP-alpha, which we think could be one of several pan-tumor agents. FAP-alpha shows up in all solid tumors when they get large enough and they start to form their own stroma, their own sort of vasculature. It also shows up on some tumors directly on the tumors themselves. We just had an agent, CCK2R, that shows up on an awful lot of tumors as well. And it gets expressed at various levels. There are certain broad tumor markers that we do not go after. And it's a good strategy that says what you say no to. For example, we have not gone after RUR as a target because it tends to express on healthy tissue. So we're so relentlessly focused on that safety and therapeutic window, we're not going to go after things that express unhealthy, and we want things that only show on tumors, which is such a tough nut to crack because tumors come from healthy cells, and so it's really hard to kind of define that. But we think that FAP-alpha could be one of those pan-tumor agents. There are several others we're targeting as well. And we also think that some of the new targets we're going after really will blow open the field of targeted radiopharmaceuticals because we're going after these almost ubiquitous cell surface markers that we want to chase if they have a high enough receptor density that they're suitable for a target. In things where there's only a few copies per cell, it gets trickier with a peptide target. Once you get multiple copies in the cell, we can then self-enrich by doing the scans and using that enriched patient population then get very, very effective therapy.

We're coming up on time here, so I want to maybe address a little bit about your supply chain and manufacturing capacity, can you maybe talk about where you are from a capital position to build out some of your planned facilities and just sort of what the goals are there? You also recently acquired a facility from one of our other companies, Lantheus, and can you maybe just talk about the status of integrating that facility into your company?

So I'll take the second half first. So the Lantheus facility is a terrific site. The FDA has regularly inspected that site. It was previously commercial. It took us about six months from taking over that facility to have it operational to make our programs in a way that is consistent. We regularly produce product there that we ship all across the U.S. in our current clinical trials. It's been a great success because our team is very, very good at making regular radiopharmaceuticals. Balance sheet, as of our last quarterly filings, showed $271 million. A lot of our cash shifts around on the balance sheet. We'll spend money to build out a new manufacturing site, And so it shifts from cash to PP&E. We have a flagship site in Chicago that's coming online at the end of this year and a site in L.A. that will be coming on beginning of next year. So we have invested in infrastructure. We think if you're in the radiopharmaceutical business, you must have a network. And we're building now one of the largest networks across the U.S. that's purely dedicated to alpha therapies, and that's going very, very well. We've secured all the upstream materials that we need in order to actually produce the lead-212. We have a strategic stockpile of the thorium-228 precursor that's so important. It's got a two-year half-life, so we have a lot of that material on hand. And we're able to actually produce drug every single day at our multiple manufacturing sites, and we deliver across almost the entire United States right now. So we actually have realized the network is important. We have multiple nodes in that network. We keep adding to it, and we keep investing our capital to expand that network.

Great. Maybe in our last minute here, you're obviously pursuing a lot of things here. Can you remind us on the status of what your current cash runway is?

So from our last quarterly filing, it showed we had $271 million cash on the balance sheet. We've shown that runway will last us until late 2027, assuming all of our programs keep delivering at very, very good speed and we keep building out our network. So we'd expect investors to look at updates It's a crossover programs for clinical readouts across our BMT AlphaNet, NETS program, our melanoma program, our FAP program, getting our sites qualified on the manufacturing side. And we also expect to have interactions with the FDA. Well, on that note, my thanks to Taysen Perspective for joining us today. Thanks so much, Paul. Appreciate it.