Good afternoon, everybody. Hope you're having a fantastic day three of the JP Morgan Healthcare Conference. My name is Bhavna, and I'm an associate with the Healthcare Investment Banking team. Thank you very much for joining us today for Perspective Therapeutics' presentation. With us, we have Thijs Spoor, who is the Chief Executive Officer, and we have Markus Puhlmann, who is the Chief Medical Officer. We'll leave time in the end for questions. For now, over to you, Thijs.
Great. Thank you so much, and thank you to JP Morgan for hosting us here this year. We're really excited about what we do at Perspective Therapeutics, so I'm going to take time to try and explain what I can to you over the next little while. We are a public company, so I do encourage you to refer to our filings that we keep current with the Securities and Exchange Commission, and we may make some forward-looking statements. We refer to you with what we keep on file. So, talking about radiopharmaceuticals, it's a really exciting space right now. The field has really grown drastically over the past 30 years. We've gone from a mostly imaging-based field to a wonderful theranostic therapeutic field because we can make really big impacts on patients' lives. When we look at Perspective Therapeutics, we look at targeted therapies.
Really, what we're trying to do is go into things with a high tumor specificity. If we can do that, we can cause a lot of damage, but causing a lot of damage with potent tumor cell-killing abilities means we have to be very, very careful about where else that damage goes, and so we have this relentless focus on designing molecules that can actually go to the tumor and not to healthy tissue, and one of the things that we do at Perspective Therapeutics, we have a proprietary chelator, which helps to minimize kidney reabsorption, and so kidney is not the only organ we're focusing on. We're focusing on many, but that's where there's a lot of energy in the field. We have a really broad pipeline. We've actually developed three clinical stage programs that are on track.
We have multiple readouts expected over the next 12-18 months. But really, what we do, really, we de-risk things by looking at theranostic pairs and trying to predict in advance what kind of safety and efficacy signals we may expect and where we expect the molecules to perform in a patient. At Perspective, we also invested in our manufacturing infrastructure. Radioactive supply chain gets really tricky for those that are not used to it, and we're really excited about the innovations that we're making in that field. We know we can actually distribute products across the U.S., and the nice thing about this field is ready-to-administer products. We try and design to make them optimized for patient treatment centers.
Initially, the company started as a spin-out from the University of Iowa, and we had the goal to try and make a safer product for kids with pediatric neuroblastoma. By designing the molecules to actually end up being safer for kids, we had hoped to make them safer for adults, too. Since then, we've actually exploded into a pretty phenomenal company with a great pipeline of programs. Our lead program in melanoma targets something called MC1R. With this program, we actually are enrolling patients now in a monotherapy trial and a combination therapy with nivolumab. Our second program, VMT-α-NET, targets neuroendocrine tumors that express SSTR2. Then we have a third program that targets something called FAP alpha that's going into clinic this year, and we're very excited about that program, too.
Behind that, we have a phenomenal team of discovery scientists that actually keep innovating, and we hope to bring several of these forward into clinic, too. We don't actually formally name our programs until we show human images, but we're very excited to show you the ones that we have defined so far. The radiopharmaceutical space is pretty revolutionary right now. It's an inflection point. Think about how oncology started. You started with chemo, and then you looked at radiation, then chemoradiation, and as the field innovated, you got targeted chemo in the ADC construct. Now we're looking at targeted radiation, and this is really the ultra-targeted precision radiation. We treat cancer from the inside out, and we do that by designing a drug to go straight into where we want to get to.
We've seen in GEP-NETs, for example, with our VMT-α-NET program, that we can actually get into these sort of gastroenteropancreatic pancreatic neuroendocrine tumors that express SSTR2, but there are many other tumor types that also express, and we follow the dogma. If you see it, you can treat it, and so, if we can actually identify lesions on the scan, we'll actually go ahead and treat. VMT01 is currently being evaluated in melanoma patients in that post-second-line plus setting, very, very challenging setting. However, if the therapies work as expected, we do plan to walk them up into earlier in the patient's journey, especially since we can target all the cells that express a certain receptor, and we know before we treat a patient if they actually have that receptor or not through non-invasive means, and this is what really helps differentiate the field.
If I look at some of the other major multinationals in the area, there's so many areas we can get into next. There's a lot of focus on SSTR2. There are commercially approved products for prostate cancer, but beyond that, there's still about 93% of all tumor types that we can still address with targeted radiopharmaceutical therapies, and so things are just beginning now. I want to start focusing on how we actually design these drugs and these medicines and what makes us differentiating from the rest of the field. When we actually look at a target that we like, what kind of targets are interesting? Things that express on cancer cells but don't express anywhere else on normal tissue normally, and we can see that with the scan. We want things that are, we don't care if it's a passenger or a driver.
All it has to do is surface express. If it's on the surface, we can bind to it and then destroy it using radioactive particles. I showed these images to actually walk through how we actually design our medicines. On the far left, you see a mouse model, and there's a sarcoma in the right shoulder of this animal, and that sarcoma, if we look at that, what it actually does is you can see that there's uptake in that sarcoma, but there's also a lot of uptake in the kidney as well, and then our medicinal chemists work. We iterate through, we tune the molecule properties in keeping binding affinity the same. We're then able to actually iterate the compound a bit further, and we can show here sarcoma and kidney, but we don't stop there.
We went even further, and we're able to identify this molecule with sarcoma and kidney. So, putting yourself in the role of armchair drug developer, what makes the most sense? The one with a lot of kidney exposure or the one without kidney exposure? And we're really leaning towards those where we can actually get very, very high tumor uptake because we think that's going to be better for the patient. When we actually nominate a candidate like this one, we'll file our composition of matter IP, and once that's been done, we'll actually try and do first-in-human imaging. Before we treat patients, we can see what's happening. This is a pretty phenomenal image of a patient with colorectal cancer, and this patient had all these lesions that lit up throughout their body, all that expressed FAP Alpha, and so the molecules I showed you before, they target FAP Alpha.
We're able to validate that in a tumor model in animals. We're able to treat animals. And then, jumping one step further, we can now look in patients to see where does this express. Because we use either the same molecular entity or something very similar for imaging as well as treating, we can predict in advance if we'll actually get uptake. So, we have a pretty innovative platform that we're very proud of with our team. When we actually move things forward, we're big fans of alpha emitters. Beta emitters travel about 200 cell diameters. You need about 1,500 betas to kill a cancer cell. You need about one or two alphas to kill a cancer cell. So, the alphas are so much more potent, but they also travel a much smaller distance.
We like using a lead-203, lead-212 pair for something called dosimetry, which means we can predict in advance if the tumor will retain the tracer, and if so, then we can then calculate the relative impact on healthy tissue versus diseased. One of the things we do is we use a proprietary chelator. This is a chemical cage that drags the metal to the target, and we actually like to use engineered peptides to actually act as a targeting vector. Peptide clearance is very, very rapid, and by bringing a peptide and a chelator onto the tumor, we're actually able to really get a very fine targeting and really look at what's happening in the kidneys. In radiopharmaceuticals, it really comes down to therapeutic window. There have been several companies that have tried and had challenges.
If they could not get a therapeutic level before they got limiting toxicities, and we also know if we go high enough on any molecular structure with a radiopharm on it, we can induce damage and dose limiting toxicities. So, our challenge is to identify and widen that therapeutic window as much as we can. Without jumping too much into it, we love lead-212. There's others in this room that love that as well. When you think about the origin of the space, things started with iodine-131. Iodine was really powerful, but it tended to also go to the thyroid if you wanted to or not. So, for thyroid cancer, iodine is great. Challenges with the chemistry have evolved and not allowed to go too much further.
Lutetium-177 came in as an interesting way to sort of chelate, hold the lutetium intact, bring the betas to the tumor, but not have a lot of off-target impact. And that had trade-offs. I mean, on the plus side, it's developed phenomenal products from Novartis with Lutathera and Pluvicto that can be used for patient management. But the scientific community said, "Well, can we go better? Can we switch to an alpha? Be a lot more powerful?" In which they could do, same chelators, but we felt that there are some trade-offs on potential daughter toxicity and other things that may not make actinium the perfect isotope for what we do. We prefer Lead-212. It has incredibly high potency from both its initial beta and its alpha decay. We think that the off-target chance goes much smaller with such a short travel length of those particles.
We think that the daughter isotopes actually are in its favor. The initial alpha and beta decays end up with a stable product that's not radioactive. The half-life is really advantageous for us. With a 10-and-a-half-hour half-life, we actually hit the tumor hard and fast, and then it completely disappears, and what that does is that preserves the tumor microenvironment to actually let the immune system do its job. We know if we cause damage to a cell, we have these phenomenally powerful neoantigenic events, so the alpha particle is smashing into a cancer cell, and when that happens, you're going to activate the immune system that's both the innate and the adaptive. Those will come in three to seven days later, and if that background tumor microenvironment is radioactive, that can impede the ability of the body to repair and to help the patient heal.
We do have a line of sight on production. We regularly supply product across the U.S. that's labeled. We are building out new manufacturing sites, which I'll touch on as well. But for the clinician in the hospital, you're having a drug that goes in the patient hard and fast. It disappears very quickly, and then afterwards, you're not dealing with a lot of radioactive waste either. When we think about the mechanism of action, the initial portion feels intuitive: cytoreductive. What does that mean? You're smashing into a cell with an alpha particle. If it breaks apart the double-stranded DNA, it can never heal again, and that actually does a lot to damage the cells. But what's really interesting, too, is that neoantigenic storm that created actually can activate then the immune system.
If you present all these antigens to the immune system, then your antigen-presenting cells can then activate the T cells to come in and really help clean things up. So, in some cases, we think it's the cytoreductive mechanism of action that's important. In other cases, it's the immunostimulatory. But in either case, if we can actually help the body destroy the cancer cells or destroy them directly, we think then the patients really benefit. So, just to dive into how we actually do this and the secret sauce that's here, we actually have developed our own chelator. And so, there are generic chelators, DOTA and TCMC, that are available. These give a net charge to the protein. And so, with a net negative charge or a net positive charge, you then change the pharmacodynamics inside the patient. The kidneys do their job really well.
They pick up charged proteins, and they love charged proteins, and they'll hold onto them longer than they will a neutral protein. So, by actually optimizing this chelator, you can see on the design of the molecule here, we actually have changed around the charge, and that change in the charge helps with radiolabeling. What's very important is that the first decay from a beta turns into a bismuth-212. That Bismuth-daughter is also kept tight inside the chelator, and so we've published that you get less than 2% leakage of any daughters from here. So, everything that we're trying to target to the tumor hopefully stays on track with that tumor. The other advantage of Lead-212 after you chelate it is that you can actually use Lead-203 to image. So, this is an elemental twin, chemically identical, same composition of matter.
It's going to have identical biodistribution, and Lead-203 and Lead-212 are literally the same chemical structure. The difference is one gives off a gamma, the other gives rise to an alpha on the tumor, and that's very important to actually look at what's happening in the patient. My own sort of diligence on the company when I looked to join was, "Show me some human images," because the human images tell you an awful lot. Here, we see a patient with an osteosarcoma. It's blindly obvious which shoulder has that osteosarcoma in it because you inject the drug, it's going to go to tumor, or it gets dumped out through the bladder. And so, we can see before we treat patients if they are suitable and how things can work. You can go one step further beyond peptide targeting. You use pretargeting with antibodies.
I don't want to touch on that too much during the time I have here, but the great premise for pretargeting is you can use known antibodies to actually target a tumor. You modify those antibodies with something called chelator. These are little sort of hooks on there that you can then paint the tumor with. And so, if you cover the tumor with these antibodies that have all these binding sites, you can then use a peptide chaser to go in and actually target every cell that's been painted with antibodies, and our scientists are doing some extraordinary work to actually move that program forward. We get asked a lot of questions about supply chain and what this means for manufacturing infrastructure. The nice thing about what we do with Lead-212 is it's got a very, very clean way to actually produce the isotope.
And so, for fair disclosure, I was a nuclear pharmacist 30 years ago. I've been in the field for ages, and what they told us when I first graduated was the easiest, simplest, cheapest, safest way to make any isotope is to do nothing. Let it decay from something else. So, if you can find the right parent, you can then produce those daughters for free if you just sit there and watch. We access thorium-228 from the Department of Energy. They have an awful lot of it in stock that they keep. It's a waste product from other processes. We've located offshore supplies of thorium-228. It exists in monazite sands from various sort of mining activities. There's a lot of thorium-228 out there. If you have it, you can control it, and then if you do nothing, the radium-224 will come off the thorium-228.
And the radium-224 you can isolate and then load into what we call in the industry a generator. And having radium-224 on board means you actually ship it. And so, radium-224 will actually give rise to Lead-212. If you put that radium-224 onto a resin column, the columns are about this big. They're absolutely sort of easily transportable. If you do nothing and watch that column for one day, some of that radium-224 will turn into Lead-212. And because the chemistry is so elegant, if you can actually have different elements with different chemical properties, you can wash this column and pull off Lead-212 on a daily basis. So, if you have thorium-228, once a week, you can pull off radium-224. You can ship this around to your manufacturing sites and then produce Lead-212 chloride on demand as needed.
We have successfully shipped this generator to sites in Asia and Europe, across the U.S., all of which know how to sort of manufacture the product, and then you can actually have a finished dose that you give. So, the nice thing about a Lead-212 manufacturing site is we don't need a cyclotron. We don't need an accelerator. We don't need some of these other ways to create an isotope. We can actually just through straightforward chemistry and resin separation pull off the isotopes as needed. At Perspective Therapeutics, we're investing in our infrastructure. When you think about distribution of isotopes, it's really important to think about the shelf life of the isotope. So, while the isotope will have a half-life, the drug has a shelf life, and the shelf life of lead products tends to be up to about 24 hours.
Some of the lutetium-actinium drugs out there have a shelf life of up to 48 hours, but really not too much past that. And so, having a very kind of knowable shelf life, you can then set up local regional distribution and manufacturing sites across the U.S. We're very pleased that we have a site in Iowa where we've been supplying products for our clinical trials. This time last year at the JP Morgan Conference, we announced a transaction with Lantheus, where we acquired their site in Somerset, New Jersey, and I have to say I'm really proud of our team. We actually got that site operational within six months, and we've been starting to produce product there that's Lead-212 labeled for delivery to patients.
We've also announced in our quarterly filings we've acquired buildings in Illinois, in Texas, and in California, where we also are building out our Lead-212 infrastructure to supply radiolabeled product and drug that can actually go out to all the sites. As we look at the sort of challenges and opportunities in distribution, we're not trying to get our drug to every local pharmacy. We're trying to get this drug to sites that are licensed for radioactives and cancer care centers. The patients will travel to a cancer care center. We don't need to actually get it to every home pharmacy. And so, that actually really simplifies logistics. We have a fabulous team of people that we've recruited over from General Electric that used to run their two-hour and six-hour half-life drug programs.
So, actually giving them 10-hour half-life on this drug and almost a 24-hour shelf life has really made this a really interesting opportunity for them. We're thrilled about the kind of people we're attracting and how quickly we can scale up these facilities. So, touching briefly on the clinical side, we do target neuroendocrine tumors with our lead program, VMT-α-NET. Neuroendocrine tumors are quite interesting. They can show up anywhere in the body. They're highly secretory in nature, which means that the patient journey initially starts with symptomatic control. So, the patients are on somatostatin analogs for a period of time, and eventually, they'll start to break out. When they break out, they need some sort of alternate therapy. And so, the unmet medical need is pretty clear. You do have these patients.
There is a drug out there which can actually help address this with Lutathera, but we feel with some of the smart biochemistry and designing the right kind of molecules, we hope to do better. So, I want to show you an example of a head-to-head in an animal study of the drug. So, if we look at DOTATOC and look at the distribution of tumor and kidney in the animal versus our drug with tumor and kidney, we have a higher tumor-to-kidney ratio. So, for any quantum of radioactivity going into this animal, you get more on tumor than you do on kidney. That really should help skew your safety profile. If we look at actually what this did in the animal model, this is we're looking at neuroendocrine tumor volume and what happens over time. So, neuroendocrine tumor volume grows unchecked.
You can see how that tracks through. If you actually give these mice Lutathera, you can see the right shift on that curve of about 24- 25 days, which corresponds to about a two-year PFS in humans, and you can see why the FDA approves something like this, a clear impact on these animals. However, if you look at our drug with either a single dose or four fractions, you actually end up with this kind of curve. And so, this is the difference between betas versus alphas. With a beta particle, you can sort of damage the cells, suppress them. You can induce single-stranded breaks, but you need about 1,500 or 1,600 cumulative betas to actually kill the cancer cell, whereas with an alpha, that single-cell hitting it has such potency.
We took this data to the FDA and asked them for a fast-track designation in the post-lutetium environment similar to what RayzeBio had done, and they said, "No. We're giving you fast-track designation pre-Lutathera," and so, it's been really exciting to work with them in the sort of PRRT-naive setting to actually see what can happen in patients. When we actually get to the patient journey, we can scan the patients in advance, so we can scan them with an off-the-shelf SSTR2 imaging agent, or we can use the Lead-203 variant and see exactly where the drug goes, so what's extraordinary about these images is that one hour post-injection, you see an awful lot of activity on tumor. You don't see it in other places, so you're not seeing it in the brain. You're not seeing it in the heart. You're not seeing it in the liver.
You have kidney clearance, but not necessarily retention. Then, 21 hours later, you've actually seen that the drug that doesn't roll off of tumor, that dumps to the bladder, stays on tumor, right? You've either still got tumor or bladder at one day later. Two half-lives, which means about 75%-80% of all possible alphas will show up in that first day. That means that if you can see exactly where the drug is going, you can predict the side effects and the safety. The one thing we can't predict from these scans is bone marrow toxicity. We actually do separate the doses a bit. We do fractionated dosing to allow any issues in the bloodstream to recover. This really gives us a great validation as to a way to move forward with this therapeutic modality.
We're currently actually in a phase 1-2A dose escalation study. As part of that discussion with the FDA, we had agreed to pause after the first patients in the first two cohorts and actually look at safety and efficacy before we get clearance to move forward, so we did submit some data to them at the end of last year, looking to get the go-ahead to actually increase doses. We enrolled two patients at the lowest level of activity. We enrolled seven patients at the five millicurie level, and as we were preparing the data for the FDA to let them understand the safety profile of the drug, we also presented some data at the NANETS conference, the North American Neuroendocrine Tumor Society conference in Chicago last year, and this was the data that we showed.
It was pretty remarkable from in a dose escalation study, so not at the highest tolerated dose, we had eight out of nine patients with durable disease control, so these are patients that were stable on somatostatin. If they started to progress, we were then able to administer our drug and actually get eight out of nine patients with disease control, and we also had a pretty compelling partial response. This patient had a 57% reduction in their tumor volume. This is quite early in the study. Other programs that have been reviewed in the space will tend to look out at this sort of four-month, six-month, eight-month, ten-month, one-year points to look to see for all possible responses, and so we're early in these patients' journeys and really looking at the data.
We press released this week that at ASCO GI next week, there will be an update in terms of having a little more incremental time to see what's happening with these patients as well. From a safety side, it feels very, very clean. We did not have any dose-limiting toxicities that we're aware of. The grade 3 AE profile was very, very clean. Drugs are very, very well tolerated. We do keep an eye out for any kind of bone marrow toxicities and also any potential kidney effects, and so what we also disclosed was that if we actually plotted eGFR pre and post-therapy, there was no meaningful change in these patients.
For everything that we can look at for acute biomarkers as for safety, we did not see anything that gave us cause for concern, and the data safety monitoring committee recommended we increase the dose to a higher level. They also recommended that we include up to an additional 40 patients in that second dose cohort at five millicuries. Post the NANETS conference and between August and December, huge physician interest, where they've come and enrolled in the study. We have 11 more patients that we've announced have been on drug at some point between August and December last year and more physician interest after there. With physicians from around the world coming up to us really trying to see if this could be an option for their patients, this program is moving forward without any DLTs.
We asked the FDA if we can actually go up to a higher dosing cohort. When we get clarification from them with what our sites will be doing, we'll let the street know that as well. It's always nice with an imaging program to show images, and so it's really great to see that we could actually look at specific tumors, for example, in this patient's liver, and we can see these tumors ahead of time and see them disappear. It's very gratifying to help the patients symptomatically and also with their tumor volume. Touching on our next program, the Melanoma program, VMT01. I don't need to go too much into what melanoma is, but what's interesting about melanoma is that 50% of patients will actually express something called MC1R on some of their tumors, not necessarily all.
And if we look on the left side of the screen here, we see an image of a patient with metastatic melanoma, and we're seeing all the sites that actually pick up and express MC1R. And so, those that have had to deal with these patients will realize that it's always tricky to figure out what to do in the brain. Can you identify brain metastatic sites? And you'll see, if you look at this image, that you do see activity in these lesions that are in the brain. We think that the blood-brain barrier breaks down just enough to let a small peptide kind of squeak through and give it the image. But since we use the same molecule to image and treat, this also means we should be able to carry in, again, the small molecule with the metal to actually then treat those tumors as well.
We know melanoma is a clear unmet medical need. We've seen dose response in a monotherapy environment. We've seen the combination setting as well, that combining with checkpoint inhibitors, you actually get the ability to do a lot more to the patient. For the sake of time, I just want to focus on one set of data in particular in the center here. This is an immunocompetent mouse model showing melanoma. The black line is untreated and what happens with those mice. The light blue is Ipi/Nivo. Using that combination, you actually do help these mice a bit. The dash below the line is monotherapy of an alpha particle. Using alpha particles as a target, you actually get some boost. But this pink line is the combination of an alpha particle and a checkpoint inhibitor.
It's absolutely extraordinary that, actually, it's not a synergy of one plus one is two. What's even more compelling is that 70% of those mice cannot regrow tumor on rechallenge. So, if you try and rechallenge with new tumors, they cannot regrow. And there's something happening in the immune system that's really, really compelling. So, as we look at the ability to screen, we do screen with our VMT01 product, so either a Ga-68 version or a Lead-203 version. Compared to an FDG scan, we can identify tumors that only have the surface marker. We're not trying to diagnose disease with these markers. We're not trying to stage the disease. We know they have metastatic melanoma. We're trying to characterize if they're suitable for enrollment or not into a trial such as this one.
So, the patient screens positive, and we've had about a 50% positivity rate for patients that screen into the study. We see that we can actually. We've been dosing in a dose cohort. We've got a three millicurie dose cohort and a five millicurie that were treated. We presented data at the Society for Melanoma Research last year. And what was really striking there was that we actually showed some really interesting efficacy at a lower dose versus a higher dose. We feel it may be a bell-shaped curve. And so, this makes sense given how active the immune system plays a role in suppressing the disease in patients with metastatic melanoma. Those three millicurie patients were expected to have a PFS of approximately sort of three months or so with best possible standard of care.
Looking at nine, 11, 13 months out, those patients were almost as if their disease was frozen in time, and one of those converted into a partial response. When we actually look at the five millicurie dose cohort, those patients did not do as well. And so, we've actually found an upper limit, we think, to what dose we want to give these patients. So, this tells us clearly there's such a difference between the kind of pink cohort and the blue cohort here that we want to go ahead with this three millicurie. And for good discipline and a combination, we have a partnership with Bristol Myers Squibb with Opdivo. We actually can lower the dose down a bit and be able to start dosing these patients. We did not see any major treatment emergent adverse events show up.
And so, without any major grade 3 toxicities, we felt it was appropriate to move forward and actually start dosing in the combination, as well as opening up the monotherapy at a lower dose still. So, we know we got a nice initial signal at three millicuries. Going up to five didn't give us a benefit, and then we want to test to see what happens if we drop it down as well. We're now open for enrollment in these cohorts. I want to talk about our third program, which is coming to clinic this year. We're really excited about FAP Alpha, and this is a pan-cancer target. It shows up in a lot of different tumor types. It tends to be expressed as the tumors get large enough. So, if a tumor starts growing, it then forms its own infrastructure, right?
It recruits various tissue to form blood vessels, to form its own scaffolding, and what's interesting about how this expresses is that FAP Alpha will show up on either some tumor cells or on some stroma, and the nice thing about the nuclear medicine community is we've done an awful lot of work to really look at all the kinds of tumor types where this can be expressed. These are massive TAMs. We're looking at things like breast cancer, colorectal, lung, prostate, ovarian. A lot of interesting tumor types where, if the tumors get large enough, they will start to express FAP. And if they express FAP, we can image it, and we can also target with an alpha therapy, so showing how we actually develop these programs, right, if we can hit something like sarcoma, we have seen some other candidates try in this space to target FAP Alpha.
We focused relentlessly on trying to get the best possible biodistribution. If we give a targeting agent to a patient and not all the drug goes to the tumor, those alphas are going somewhere else. So, we want to make sure we can really get it into the tumor and nowhere else, and on the scan, you can see in this mouse model, we're hitting sarcoma. We don't have kidney retention. That's great. We've seen some great animal efficacy studies in mice with various xenografts. Jumping into humans, we've then seen some other things as well, so we try and show always human images. We saw a metastatic colorectal cancer patient with a really phenomenal scan. We've previously presented a neuroendocrine patient with tumors. We've shown a lung adenocarcinoma patient. This is an osteosarcoma patient.
We encourage anyone in the radiopharmaceutical space or radiopharmaceutical careers to look at these images over time. Look at an early and a late image to see what's the area of the curve going to look like. If it goes somewhere else, goes to tumor, and then washes out, it may be a great diagnostic. It may not be as good a therapeutic as if you can get it to the tumor right away and have it stay there over its entire life. So, we always like to show early and late images and see how things roll forward. Our preclinical data imaging looks terrific. We've actually gone and we announced that we submit an IND in 2024. So, we'd expect to start dosing humans by mid-2025 this year. We're really excited.
The sites are very keen to actually start moving with this compound and moving it forward. And lastly, in general corporate information, we love sort of the team of people we've grown around with. We've got 133 patients, excuse me, employees in the company. We've recruited people from all across the industry. We recently announced a new CFO who's joined us as well. We've got a terrific group of MDs, PhDs, about 40-some patients in Iowa, excuse me, 40-some employees in Iowa, 40-some employees in New Jersey, and spread across all of our other sites across the country. Everything we do, we file composition of matter on. We've got a very strong IP portfolio. Our patents start to expire in the late 2030s. We focus on a chelator as well as novel compositions on the peptide.
As we roll things forward, every program that we roll forward will have new composition of matter on it as well. Lastly, we're in a very strong financial position. As of December 31st, 2024, we pre-announced that we have just under $228 million on the balance sheet, giving us a cash runway into late 2026. This allows us to support our clinical programs. This also allows us to use our various programs in the dose escalation phases across all three clinical areas: neuroendocrine tumors, melanoma, as well as FAP. With that, I'd like to pause for questions. I know we've gone through a lot here. Appreciate your patience. I know there are questions from the audience.
Yep, we'll open to questions from the audience. I can start us off. This is your second JP Morgan conference as the CEO. How do you think things have changed over the last year, and what are you looking forward to most in 2025?
Sure, thank you. So, this is actually my 18th JP Morgan conference as a person in the healthcare ecosystem, but a second presenting, which is great. What's been really interesting to see is the extraordinary interest in radiopharmaceuticals that have come about. This time a year ago, there was a lot of interest in radiopharms, but we've seen some great data across various isotopes that are all showing that if you actually keep exploring further, you get better and better results in these patients. And we've seen some data come out, for example, at ESMO last year that showed with some compounds, if you go into first-line prostate cancer, you get better results. So, across the board, the field is waking up to the idea that you can treat patients earlier, and the targeted therapies can make a huge difference. We've got huge interest now in supply chain.
People understand the half-life now. They can sort of talk to me about isotope selectivity, but the interest has been extraordinary at the CDMO level, the innovator level, and it's just great to see all the enthusiasm.
And sort of there's a lot of debate, and you also touched upon it, between alpha and beta particles. Sort of, where do you, and how does Perspective look at the debate?
So, ultimately, we're trying to focus on the patient first. So, how do you actually get the best possible dose to a tumor and not to healthy tissue? The nice thing about the alpha is they have that incredibly powerful punch that travels two cell diameters. So, if you can actually get the product to go onto the tumor nowhere else, you then minimize collateral damage. And we can see in advance how that happens. Betas are really interesting as well. Betas are lower energy. They travel further, so there's a broader zone of damage versus destruction. And if you can chelate them properly and bring them to the tumor nowhere else, they all have a role.
Radiation and radioactive particles, the alphas and the betas, have a clear advantage if you can actually hit the tumors directly from the inside out versus necessarily trying to cause a lot of extra sort of tissue damage.
Could you also touch upon your relationship with Lantheus and how you're looking forward to the partnership?
Thank you. We actually have a very good relationship with Lantheus. We announced at this conference last year that we did a deal with them. They are an equity holder of the company. They're a fairly large position. They have an option to negotiate on our lead program and one of our pipeline programs. They're one of the world's largest medical isotope companies, and they do a really good job at sort of developing technologies in that field. They've been a great partner to have. They have a board observer, and we actually have had a great collaboration.
You know all the data that you've walked us through today for VMT-α-NET and VMT01 is very exciting. Talking about VMT-α-NET a little more, you said there's potential for expansion into other SSTR2 indications. Is there anything you can tell us about that right now?
Sure. Actually, I'll let Dr. Puhlmann, our Chief Medical Officer, talk about what other tumor types excite him as an oncologist in drug development.
Thank you very much for this question. Obviously, SSTR2 is expressed in a wide variety of tumor indications, not just in the neuroendocrine tumors. It is expressed in, obviously, lung cancer to a certain degree. It is expressed in other malignancies, such as meningiomas and a variety of other potential targets or target indications. I think developing, obviously, a drug in this space may eventually require, as we, for example, go into a small cell lung cancer, an indication that is SSTR2 expressing, also combination approaches, and that's obviously something we contemplate a little bit further down the line.
You presented data from VMT-α-NET back in November. Can you tell us a little bit more about what the investigator and patient reaction has been to that?
Sure. So, we got actually a lot of really positive feedback. Investigators did understand that we're still in the dose escalation phase of our program. They liked the safety profile, which is very benign at the moment at this current dose level. And the fact that we already see efficacy was very well received. We received actually a lot of interest also from abroad to participate in our studies. And obviously, that's something we're going to follow up.
Switching gears to talk about VMT-01 for a little bit, you presented the dose-finding data in October. Sort of, can you explain a little bit more about the impact in the clinical context, especially for second-line or later metastatic melanoma?
Sure. Thank you for this question. I think we have to understand malignant melanoma is an extremely aggressive malignancy. If you look, despite the recent emergence, of course, of the immuno-oncology field, if you are nowadays still diagnosed with stage four metastatic melanoma, your OS, your median OS, is still about, according to the SEER database, about 12 months. It is an extremely aggressive disease. As we are looking currently with our VMT-01 program in the second-line plus indication, what we are currently estimating is that these patients have an estimated two to four months of PFS, meaning progression-free survival, and we are very encouraged by the early signal that we saw in our lower dose cohort.
And if you look at this graph that you see here on the screen, it's actually a very rare sight that you see a delineation of an immunostimulatory effect versus an immunosuppressive. I personally, since I worked a lot of time in this field, I'm very excited about this. And we're currently dose-escalating, a step that is a little bit novel and not quite intuitive. But we are following our preclinical data. And our next cohort, actually, we have not just a monotherapy cohort at the moment open, but we also have now a cohort open in combination with nivolumab. And we're looking forward to enrolling patients to our study.
So, we'd like to thank everyone for coming. We're at time here. We have lots of information on our website as well. But thank you for your time looking at Perspective Therapeutics.