Conference Transcript - CATX 2026-09-16

Speaker 1

Good morning, everyone. I'm very happy to be here with my friend Tace Spohr, the CEO of Prospective Therapeutics. I'm really happy you're here on the third day of the Morgan Stanley Healthcare Conference, so thank you for joining us, Tace.

Speaker 2

Well, Kelly, thank you for you, the team, and Morgan Stanley for hosting us. We're pretty excited to tell the story.

Speaker 1

Great. It's great to have you back. I'm just going to read a quick disclaimer. Please visit morgansanley.com slash research disclosures for our research disclaimer for anyone following along. So before I get into any of your programs, Tase, I want to just start at a high level in thinking about the radiopharmaceutical industry. You know, despite all the advances we've made across the oncology space, metastatic disease remains very difficult to treat. So what is the fundamental unmet need you believe radiopharma has the potential to meet and also that conventional oncology treatments cannot?

Speaker 2

Thanks, Kelly. It's a great question. We think about cancer and how we treat it. And because cancer cells are so similar to the human cells they come from, it's really hard to target just them and not healthy tissue. And we think about the growth of chemotherapy using chemicals that try to take advantage of cancer cells growing a little faster. We think about things we try to do with the immune system to recognize only a certain kind of cell and not others. We think about external beam therapy and external radiation and all the other healthy tissue that hits as well. We have a really interesting opportunity here, especially with alpha particles, to use one of the most powerful mechanisms in the universe, atomic particles smashing into cancer cells to destroy them. And I think that opens up a lot of opportunities used to have a different way to treat a cancer cell that we don't want. Where it gets really interesting for the pharmaceutical business as an industry is that this is the first time you've taken a modality like radiation and made this a therapeutic drug, right? So we can actually turn what used to be a device-based business of external beam that damaged a lot of healthy tissue and take it as a drug and a pharmaceutical inside the patient's body. And the mechanism of action, the side effects, they're all orthogonal to each other. And so you don't expect things to compound on the safety side, but you also expect in multiple approaches to do everything they can to actually hit the cancer cell. We talk about chemo, chemoradiation. Chemo got more targeted with ADCs. Now radiation is becoming targeted with radiopharmaceuticals. So targeted chemoradiation we think is a big plus.

Speaker 1

And then within radiopharma, Perspective was one of the first to use lead-212 as the payload of choice. So why did you choose lead? What do you think are the most important differences between lead and other isotopes being developed, particularly versus lutetium and actinium?

Speaker 2

So it's a great question. And we think about when the company started as a spin-out from the University of Iowa. And so back in 2015, the company founders, Dr. Schultz and Dr. Johnson, We're focusing on a safer way to treat kids with pediatric neuroblastoma. And so everyone's familiar with the periodic table. But there's something called the gray chart. And the gray chart shows all possible isotopes and what could exist. And they looked at that and said, you know what? Lead looks really interesting. Lead has a short enough half-life that you can give a hard, fast punch to the tumor. It's got a long enough half-life that it can exist for a period of time. If your isotope exists for seconds only, you can't make it. If it exists for thousands of years, it's going to be really tricky on a safety level. And lead also has an elemental twin, lead-203, so you could actually image with the same chemical entity as you're treating with, and that opened up a lot of possibility to help prescreen kids for potential therapy and prescreen adults for potential therapy. But the challenge with lead-212 especially was that it wasn't available, And you could only get lead-2-12 at that point from the U.S. Department of Energy, and it would be the third Tuesday of every month, and it was really difficult to do any kind of research. And the other issue as well is that lead didn't have a specific chelator, a safe way to take just that lead, hold its daughter bismuth as well, and have both of those release their energy onto the tumor. So like all good scientists, our team invented both of those. We have a proprietary generator that we've shipped around the world, We've actually made over 400 generators to date with our company. We've treated over 120 patients in the U.S. We've treated over 30 patients outside the U.S. And so the ability to bring a really hard-punching isotope is great. And what's extraordinary is in the past year, we've now seen the first in human images of lead T12. So this is the first time we actually literally see the therapy as it happens in the patient's body and calculate the symmetry.

Speaker 1

So on that note, let's get into your lead program, VMT-AlphaNet, that you're pursuing in neuroendocrine tumors. Can you tell us where you sort of envision the therapy fitting relative to existing treatments in the NET space, such as Lutathera?

Speaker 2

I want to give a great shout-out to Novartis and the teams at AAA for helping develop Lutathera into a medicine that's now, I think, approaching about a billion dollars in its own revenues. It's a beta emitter. It's done, it's been a lot better than nothing, right? Patients, their only choice was failing a somatostatin analog and treating symptoms was really limited to some chemo options. And so Lutathera is a very interesting medicine with a beta emitter. We think that an alpha emitter will actually have a lot more potency. And most importantly, if we can do it safely, that's when we can actually bring, we think, a really compelling choice for patients. We've had a lot of physician engagement. I think the Lutathera over response rates are interesting. The disease control rates are interesting. The question is, can we do better with a more potent payload? And we really think we can.

Speaker 1

So when you look at the data that you've generated to date, what gives you confidence that you may actually be able to differentiate, whether it be on PFS or response rate?

Speaker 2

So I'm going to cite some unpublished data, but that we show in our corporate presentation. And we do a lot of the work in animals. And so we think through the cascade and radiopharmaceuticals. You start with an image animal, and then you treat animals. Then you image humans, and then you treat humans. And the early animal work, we showed that the beta particles were mostly, call it tumor static. We saw that the tumors wouldn't progress. They'd stay level, and eventually they would progress. Whereas we saw that using lead T12 in the mouse model, we could actually completely get rid of the disease. So getting kind of complete response rates. And a lot of that data is what we presented to try and get a fast-track designation in the space. And we actually looked to go into the post-Lutthera space, but we were actually driven to the alternative Lutthera space. Instead, we have a fast-track designation in this that the FDA granted us. And more importantly than that, we have an extraordinary amount of physician engagement as the docs really want to look at establishing this in patients as an alternative.

Speaker 1

So then when you think about that data set maturing, how do we think about response rate versus PFS? What ultimately matters more in sort of determining whether VMT Alphanet is going to be meaningfully better than what's already on market?

Speaker 2

So it's always a great thing to look at in cancer. There's so many different metrics that you can score. Do patients do better? Are the patients responding? Is it safe? Is it effective? How is it tracked through? Overall response rates are a fantastic early marker if you actually get the tumors shrinking. What's interesting about the neuroendocrine tumors is that there's a delayed effect before the tumors start to shrink. And we can show on images, for example, that the patients will have had a benefit. They feel better. They tell their docs they feel better. The tumors themselves will form these almost like crusts, but they don't change in their diameter or their volume. And until that volume change kicks in, you don't get an overall response rate technically by resist. the approval endpoint we think is probably going to be more disease control, so a PFS-type kind of number. And we want to really sort of look at those numbers as well. So should a patient and a clinician and investor feel comfortable that you get an overall response rate? We've shown some fantastic data now in an sort of all-comers approach or even with a narrow filter that we're in the sort of 40% to 50% overall response rates with the data that we've shown. And disease control, that's a very, very long period of time. which tells us this could be a terrific medicine for patients if the safety is okay. What's great about what we've shown so far is that the safety has been terrific. We have, across our programs, we've not had a single grade 4 or grade 5 adverse event. We have not had any dose-limiting toxicities. We've not had any discontinuations due to the medicines. And we really endeavor to make the best-in-class molecules from a safety and efficacy, the therapeutic window that everyone's trying to chase. And we think that our data so far has shown this could be very compelling medicine.

Speaker 1

The safety point you raise is really important. And just talking about the therapeutic window, I mean, you're exploring multiple dose cohorts even as you prepare for the phase three. So is that just about finding that therapeutic window, or could the data still influence sort of future development and dose selection?

Speaker 2

The interesting challenge for us, and I think for every drug developer, is that perfect is the enemy of good, right? And in our case, perfect is the enemy of great. We've got really, really great data. the more you get into personalized medicine the more you try and really fine tune exquisitely a medicine for a patient we have the luxury of a very broad therapeutic window which means we can do more broader approaches to how we enroll who we include, how we exclude how we treat, how often we treat and having a really broad therapeutic window means you have a lot more latitude to develop a medicine that's more broadly applicable it will also incumbent upon us to learn as much as we can So one of the things we've looked at is a cumulative dose of 20 millicuries, and that's four doses eight weeks apart. That data looks terrific. We often get asked the question, what if it was seven weeks apart or six weeks apart or four weeks apart? All interesting questions, but at this point, not necessary for us to say we don't have an approvable drug. The same question for given how clean our safety profile is, could we go 20% higher, 50% higher, double the dose? And we're really nervous about radiopharmaceuticals having the potential for long-term safety, toxicity issues. We're not trying to follow a project-optimist approach. You know, the fear there is that patients are being overdosed. If we get a really good therapeutic response at a certain level, we want to be very mindful of what's possible, what could show up later, what could be detrimental to patients. And so we want to learn a little bit, cautiously test some limits, try dosing a little bit higher. One of the things we're exploring also is that the total 20 millicuries, if we give it a little bit more up front when the tumors are more sponge-like and then just, like, kind of taper down at the end and still get to a 20 millicury cumulative, all those things get very interesting because they actually help us learn what could be best for a patient. But none of that changes what you actually would expect a C4 is 20 millicuries given sort of four doses, eight weeks apart, good. And the answer is, it's really good. So we always want to learn. We always want to try and establish what else can we do. But it doesn't deter us from the fact of what's the fastest way to get this drug to the market with the current indications and the formulation we have.

Speaker 1

So, Chase, you're going to have some updates around the corner, the first being at ESMO from the VMT Alphanets program. What are the most important questions you're hoping that that data set will answer?

Speaker 2

Well, we want to give clinicians and patients and investors confidence that this is a medicine that could be approved. And we don't necessarily need to learn a lot more things across everything. We know there's a lot of other tumor types that SDR2 positives could be relevant. It could be shown in, you know, small cell lung cancer patients, in breast cancer patients, meningioma patients. But we're focusing right now the neuroendocrine tumor patients as a very fast path to a first approval. What we always show is more data on safety. We've been very transparent about showing all patients exposed to the drug and all the safety for all patients known dosed at a certain time. We also want to make sure that we are driving towards a registration study. And so we'd want to be able to communicate what it would look like and give patients and clinicians confidence that we could enter a registrational trial and get that concluded quickly and well.

Speaker 1

Speaking of the registrational path, I know you are now engaging regulators and targeting Phase III site activation around year-end. So can you give us a sense of sort of the key topics being discussed at the FDA, what you're kind of working through with them?

Speaker 2

So without getting into sort of detailed discussions and communicating with an ongoing discussion, there's a lot of engagement that happens with the regulators as we get closer to a Phase III study. We're making sure that internally we're ready by the year-end to begin a registrational Phase III kind of study. A lot of the questions that the FDA asks and wants to be informed about are usually expected as it relates to your clinical pharmacology, your safety, your manufacturing processes. There are many, many parts of the FDA, and we want to make sure as many as need to be are comfortable with what we do, how we do it, and how we move forward. Ultimately, we want to get to a point where we feel comfortable that we've taken risk off to initiate a registrational study.

Speaker 1

And how are you thinking about the control arm in that study? I mean, is it going to have to be a head-to-head?

Speaker 2

So I think we're certainly in this modality. We're past the days where we could have a placebo control. That certainly wouldn't make sense. The FDA position appears to be they want your control arms to match your label and also real-world practice in U.S. patients. And so if we went to a jurisdiction where the standard of care, you know, sort of was a glass of water every day, that wouldn't be an act of control. to be reasonable for what's happening in the United States. And so we want to make sure that we would like to see that the physician's choice, but for the study, what would happen to the patient, and therefore we can take a matched number of patients and say what happens to them if they receive our medicine and compare those to each other and say is there a net benefit from having patients have this as an option.

Speaker 1

And do you see ultimately the opportunity mostly in radio-naive patients, or could this also, you know, sort of serve an important role after lutetium-based therapy?

Speaker 2

So I think it's a really important question for people to think about, which is that these therapies are appropriate in every patient where the receptors are expressed and where the receptors are expressed on cancer cells. So you don't want to give a targeted receptor-based therapy against patients where those receptors are only showing on healthy tissue that would get destroyed. It doesn't matter if a patient has their first radiopharmaceutical or their second or their third or their fourth. If they have those receptors, you know the drug will go there and deliver the radiation to those tumors. We haven't done any company-initiated or sponsored assessment in patients that are post-glutathera. There have been investigator work that has been done in the U.S. and in Europe, and that data shows as well if patients present with receptor, they can get a very good response if they receive a radiopharmaceutical therapy. So our initial data that we've been sharing with the FDA and the company-sponsored trials has been Lutathera-naive. We've certainly seen evidence from investigator-initiated work and from first principles, if the receptor exists, it's going to work, that would support its use in the post-Lutathera space as well.

Speaker 1

Okay. Just thinking beyond your lead program, You've also begun exploring VMT-AlphaNet in SSTR2-positive meningioma. So we're, and by the way, there's no approved therapies, systemic therapies in that space. So what led you to expand there, and how broad could that opportunity be?

Speaker 2

So we were actually really excited when the clinicians came to us, and we met with some really interesting world-leading experts in meningioma, And they said, we've got data that shows that you have SST2R expression in meningioma. There is no good therapy there. This could really work. And in response to clinician demand, we would love to bring a new medicine into this area. Meningioma is a really tough one to treat. And what's interesting for us as we look at the numbers is this could effectively double the market size for how SSTR2 agents are currently being used, just with that one indication alone.

Speaker 1

Okay. Very helpful. Why don't we shift gears a little bit and talk about VMT01 and melanoma? Melanoma is a very different disease with effective immunotherapies available in market. So, you know, why is MC1R an attractive target for radiopharma in melanoma?

Speaker 2

So MC1R can be an attractive target if the patient expresses it. And this is one of the interesting things about that versus SSTR2. SSTR2, you have a slow-growing tumor where almost all tumors express SSTR2. Melanoma, you've got an incredibly heterogeneous tumor type that's hyperaggressive. So you're really looking at both ends of the continuum for how tumors can actually grow and represent and present in patients. With melanoma, the literature tells us that MC1R, melanocortin receptor type 1, shows up in about 50% of melanoma patients, though not necessarily in all tumors. And we've actually seen about that rate of screen failure in our study where we'll screen patients that are, in this case, post-second line plus. So if they've seen a BRAF inhibitor, if they're eligible, they've gone through multiple lines of checkpoint inhibitors, everything that we can look at, there's not a lot of choices left for these patients. And we're actually seeing some pretty remarkable images of response rates and also patients who lives are radically transformed for the better with this medication. And when we think about my own family, we have a sort of northern European origin or highly prone to melanoma melanoma has touched my family members and the ability to actually have something where we can tell in advance if the patient has a receptor or not. So we're not going to give the therapy to a patient that is receptor negative but we think we can give a really good chance to a patient if they are receptor positive and we can image with the drug ahead of time.

Speaker 1

Okay, that's good context.

Speaker 2

So there's one other thing if I can just add to there which is YMC1R. We want a receptor on a cancer cell that doesn't express on normal tissue. And we could ask this question before. Do we see other MC1R-positive cells in the body? And not any kind of a copy that we see in a tumor cell. And so we want to make sure we can get it to receptor-based therapy to a cell if there are multiple copies and enough copies of the receptor that we can actually get accumulation.

Speaker 1

Okay. Thanks for kind of setting the stage on that. I mean, if you look at this drug in a potential combination with NEVO, what's the biologic rationale for combining the alpha radiation with checkpoint inhibition here?

Speaker 2

So a lot of things kick in, and I think back to these sort of first principles for how do we treat patients with cancer? We use chemo, we use checkpoint inhibitors, we use surgery, or we use radiation. In melanoma patients, the surgery one feels pretty obvious. If you see a mole or something, you're going to try and cut it out. If you have an isolated area, cut it out, and that's got very good response rates. It's when you go systemic, but you have to think about a systemic therapy like chemo or radiation or checkpoint inhibitor. Checkpoint inhibitors at some point will start to fail. Different tumor environments will be hot or cold. You get different kind of response rates. What's pretty amazing is that an alpha particle smashing into a cancer cell causes a neoantigen storm. So all of a sudden you've given all this new information for the immune system to try and do something with that it may not have had before. Attempts to actually kind of match checkpoint inhibitors with external beam therapy, radiation, have not worked. And the general consensus is that it's not going to work because these tumor-infiltrating lymphocytes will come into the tumor microenvironment, and if the external beam is hitting it, you're killing the helper cells that are trying to get rid of the cancer. For that reason, we don't see checkpoint inhibitors combinations working that well with longer-lived betas or alphas either. If the residence time of that medicine and the tumor environment is sort of a 7-, 10-day half-life drug, then the tills are coming into a hostile zone. What's nice about lead T12 is you get about 80% of all possible emissions within the first 24 hours. It will decay away and leave the area clean, so the antigen-presenting cells will come in, see all the kind of debris that's been created or the new information that's there, and by the time three to five days later when the tumor infiltrating lymphocytes come into the tumor environment, they're not coming into a radiation hostile zone. They're coming into an area where they can actually help. We've seen fantastic data in mice. As everyone knows, there's always challenges to think about how to scale from mice to humans, but that being said, the data is very compelling, and we now have the opportunity to actually look at these effects in combination. knowing that the safety risks from a checkpoint inhibitor versus an alphameter are different from each other, and we can then start to look at contribution of components.

Speaker 1

So Chase, will you talk a little bit about your next major update from this program and sort of what you would need to see out of that combination cohort to sort of justify a larger development program going forward?

Speaker 2

So there's two things in parallel that we're looking at. One is the efficacy and the monocide and the safety. and there may be a path to an early approval in a monotherapy. We're getting such strong efficacy with a very clean safety profile. Again, all of our programs have incredibly clean safety profiles. In combination therapy, we need to understand then contribution of components. Can we demonstrate that these can be given together safely? And that sounds like an obvious question, but you have to be able to demonstrate that. And then looking at what's the right sequencing in order to get the efficacy to work and really thinking about the rhythms, fundamentally, of the immune system. When do you want the checkpoint inhibitor on board? When do you want the alpha emitter with what frequency? And tracking it through. The nice thing there is that once that gets established, there's a lot of reasons to go very, very early into lines of therapy for patients. So the first time they see a checkpoint inhibitor, we would love to have those patients also have the potentiating impact of a targeted alpha therapy to really give the immune system the best possible chance. So, you know, why wait for patients to fail checkpoint inhibitor when we can actually give it much earlier?

Speaker 1

Okay, that's great context around VMT01. I just want to turn quickly to your FAP program. This is a much broader target expressed across the tumor microenvironment of many solid tumors. So why, maybe you can just describe, you know, how could FAP represent an important target for expanding RLT beyond tumor types where this modality is already sort of established?

Speaker 2

So FAP's been a really interesting target. It's been known for quite a while, but it's one of those almost undruggable targets. It's been really hard to figure out how do you target FAP with an ADC, for example. And so you kind of think through where is FAP showing up on a cancer-associated fibroblast. It's really hard to get an ADC to bind, and what would it internalize to? What would it release a payload into? There's issues with tumor permeability for ADCs as well. So if you've got a structure like stroma that forms, which helps protect the tumor from the human body, but it's covered with these receptors and things that we can target directly, we can then destroy something that doesn't have a functional purpose. It's not really a passenger or driver to any kind of activity, and we can go in there and bind to it. If it exists, we can destroy it. And that's unique to radiopharmaceuticals. Treat what you see, see what you treat. That means if you can identify it, you can scan the patient, you can do an image, and if they are fat positive, you can then treat as well. We've shown some remarkable images in humans where after one hour injection, we get an extraordinary amount of accumulation of our drug at the areas where the fat is supposed to be. In some cases, that's on the stroma. In some cases, that's on the cells directly. But that tells us then we can deliver an extraordinary amount of energy into those tumor cells, into that tumor environment, into the stroma, all of which are going to be interesting. There's been a lot of published data now showing FAP expression across almost every kind of solid tumor. And initially, the research for FAP was looking at imaging drugs and trying to turn them into therapy drugs. And imaging drugs are designed to have an optimal peak, usually at four hours post-injection, where you get a really clean image. And then you don't really matter where the drug goes afterwards. With a therapeutic like ours, you want it to go to the tumor site, stay there. and you want it to go there, stay there for at least two to three half-lives. So in our case, if we can prove that we can actually bind to the tumor and stay there over a day and a half, two days, then we have a very strong potential for a therapy.

Speaker 1

So just given how broad this target is expressed, how do you think about which tumor types to prioritize and the opportunity you'll actually pursue?

Speaker 2

So we actually recently announced an agreement that we have looking at pembrolizumab as well. and a collaboration to actually study that drug in patients in combination with FAP. In that case, we're actually looking at a lot of patients with some of the lung cancers, some of the colorectals, patients with sarcoma, also highly expressed FAP. But any solid tumor, when it gets large enough, tends to express. And so we're not going to do every single cancer type at once in the phase one. We're going to dial in pretty quickly to things that we think will get us a faster initial approval pathway.

Speaker 1

Okay. Just thinking about your platform, and you referred to lead 203 as sort of the elemental twin to lead 212, how important is this theranostic pairing for you guys?

Speaker 2

So we think the theranostic pairing helps an awful lot. We can actually go and screen patients. There are other ways to image patients. You can use gallium-68, you can use fluorine-18, copper-64, lots of different ways to image. What's different about all those metals is They're all different metals, and therefore they're going to have a different biodistribution. If you actually look head-to-head, if you just change one thing in a radiopharmaceutical, change the metal, you will change some of the biodistribution. So as soon as you get differences, you've got differences, right? And that means that you're not going to get a perfectly correlated biodistribution or dosimetry plan. So what we really like is the fact that with lead two or three, we can do these perfectly predictive scans. We can tell if patients should benefit. it, we can calculate dyssymmetry in advance of the patient receiving the exposure of the therapy, and then also give everyone a lot more confidence that the medicine could work.

Speaker 1

Maybe just thinking about the competitive landscape and taking a step back, where do you think perspective has the greatest sustainable advantage? Is it the isotope and your argument around lead? Is it targeting molecules, chelator chemistry? Sort of what sets you up for success in this competitive space?

Speaker 2

So I guess it's too easy to answer all of the above, but not to be trite about it. But we have over a decade of engineering to really address all these issues. If we could have easily purchased lead into our facility and had chelators off the shelf, we'd have loved to have done that. But we didn't have that luxury, so we've invented best-in-class chelation chemistry. We've invented best-in-class lead separation. We think best-in-class can be defined by a lot of metrics, One of those, can you go commercially scalable? So we don't want to invent a medicine that can't be given to patients in a broad commercial fashion. So we have invested, we've got hundreds of patents now on file that get issued that show that we have one platform, which is our ability to manufacture the product at commercial scale to a lot of different sites. We have another series of technologies that show that we can scale that up and provide the isotope on demand. We have another series of technologies that show we can chelate and actually hold things to make the safest possible medicines. And then those medicines themselves, which have their composition of matter for a drug, each of those has a distinct therapeutic window and strategic advantages. So we've got enabling platforms and what we think are differentiating drugs.

Speaker 1

Clearly manufacturing and isotope availability are critical components of the radiopharma business model, but they have historically been viewed as sort of bottlenecks in some businesses. So you guys are building out a regional manufacturing network, and your own led to 12 generators. How confident are you that supply and distribution can scale from where you are today to actual commercial product distribution?

Speaker 2

So the nice thing about isotope scale-up is you're not taking leaps of faith. It's engineering work, right? You know that if you can actually look at separation of resin and separation of chemistry at a one scale, you have more predictable paths to scale that up. Right now, we're treating patients from Washington State on the sort of northwest of the country to Florida and the southeast. So we can cover this country very well, provide access to patients. We're investing in new facilities that bring the drug production site closer to the patients. We think that's important to take risk off the supply chain and to make it cheaper to produce these medicines. But when we actually kind of look across the whole space, we know we've invested in the scale-up, And we think in the isotope supply business, we actually have a luxury of having a stockpilable isotope. So one of the challenges of lutetium actinium and iodine-131 and fluorine-18, all these elements need to be made on demand. And there's upstream from there, you have unstable components. So you have to make on a daily or weekly batch the actual isotope itself involving accelerators or reactor time or cyclotron time. The interesting thing and the beauty or elegance of the thorium-radium-lead cascade is that through that cascade, you can stockpile various components. We can have radium-224 at our manufacturing site with a weekly frequency, and we can have thorium-228 sitting with sort of an annual frequency of supply. So we have enough thorium-228 on hand to cover us for many years now. I still remember my first day in the nuclear medicine industry, this grizzled old chemist in the U.K. said, You know, the easiest, cheapest, simplest, fastest way to make any isotope is do nothing. Natural decay. So start with the right upstream precursor and let it just turn into what you want for free. Just do nothing, just wait. And we do that. Thorium-T2-8, if you do nothing, it will turn into radium-T2-4. The radium-T2-4, if you do absolutely nothing, will turn into lead-T2-12. And then it becomes a chemistry process to separate one from the other.

Speaker 1

Okay. You ended your second quarter with about $237 million in cash, which gives you runway into late 2027. How are you thinking about just managing burn in the business going forward and capital allocation across programs, particularly as you think about rounding the corner on this year and getting into a registrational trial?

Speaker 2

So I appreciate the question. I don't want to be cute on definitions, Kelly, especially to an experienced investment banker, but we try and split out the difference between burn, spend, and investment, and how we allocate our capital. So I think the question is, on capital allocation, we have been investing in our manufacturing sites. These are durable PPE assets that sit on our balance sheet that position us well for the future. We have an ongoing, there's a corporate burn, and there's also then spend in the clinical trials. So when we look at all those things together, some of the cash is moving to a different part of the balance sheet. with our PPE need that gets put in place, and some of the cash is converting into data which advances the programs forward. At some point, we'll need to think about what comes next. We have a lot of unmonetized capacity in our system. We've built world-leading facilities that can handle any possible isotope. We've had multiple inbound calls from people looking for access to our network of what we're building. We've also had a lot of interest in out-licensing our assets to various players. So we look pretty carefully and see what makes the most sense for our business. How do we monetize the engineering investment that's been made? Do we have things that we can look at carefully? When it's appropriate, we may always look to the capital markets as well.

Speaker 1

Speaking of what comes next, I'll just ask you one last question, which is why should investors be excited about perspective today, and what are you most looking forward to in the next 12 months?

Speaker 2

So I think investors can look at a company where we've got three programs in clinic. All of them are expected to have data readouts over the next 12 months. We've got one of the largest manufacturing networks for radio farms in the world that's being developed and built to handle any isotope with an exquisite focus on lead-212. We've got multiple programs that are coming out of our discovery team that are best-in-class or first-in-class medicines for known targets with incredibly large addressable markets. And when we look at all this sort of virtuous circle of engineering talent and innovation, we actually end up with a series of platforms. We have a scalable platform of discovery. We have a scalable platform to deliver the medicines and all that goes into really large unmet medical needs. So for investors, you have a chance for pure play into one of the most exciting parts of oncology research. The ability to actually treat a patient with a medicine and treat cancer from the inside out. So bring the alpha particle to the cancer patient's cells and not or minimize damage you're giving to the rest of that patient.

Speaker 1

Some very exciting updates ahead. We're looking forward to hearing them, and thanks for joining us, Tase.

Speaker 2

Great. Kelly, thank you for hosting me.