Hello everyone, and thank you all for joining us during the Lytham Partners Fall 2025 Investor Conference. My name is Robert Blum, Managing Partner at Lytham Partners, and today, Raphi Levy, Chief Financial Officer at Alpha Tau , will be taking us through the slide presentation. Alpha Tau trades on the NASDAQ under the ticker DRTS. All right, Raphi, let's get started. I'll turn the floor over to you for your presentation.
Excellent. Thank you, Robert, and good afternoon. Thank you, everybody, for joining us for this presentation. It's a pleasure to be back here at the Lytham Conference to share the story for those who haven't heard it before and give quite a number of updates for those who have. Just to give you a quick reminder as to who we are, we are the only ones who have figured out how to use alpha radiation directly applied locally into cancerous tumors. Now, alpha radiation has been known for years to be significantly more efficient and more effective, and I'll talk about that. We're able to harness it in a way that others haven't, using an injection made directly into the tumor that is then designed to release this alpha radiation from the inside out, the goal being to destroy the tumor and spare the surrounding healthy tissue.
We've seen some fantastic evidence to date, and I'll go through that. We think this is a broadly applicable treatment. We've done this in around 20 tumor types in animals and have yet to see any type of tumor that doesn't respond. It is really a broad, broadly applicable treatment using a very simple and straightforward physics methodology. We've seen evidence that the treatment not only destroys the tumor, but actually seems to catalyze the immune system to recognize these tumors and fight them elsewhere in the body. We are exploring this right now, both on its own, as its own standalone cancer treatment, as well as in combination with other treatments such as immunotherapy. I'll talk about what we're doing. We're a very busy company. We've got a number of milestones coming up.
We've got excellent dialogue with the FDA, and we're going after massive markets using our continually growing global manufacturing network. Obviously, given how many things we're working on, there's a lot of news flow. We are generating a tremendous amount of a number of milestones over the next few months. Just a couple of highlights, and we'll talk about them in more detail during the course of this presentation. First of all, in the recurrent cutaneous SCC, our lead indication in recurrent skin cancer, we expect to finish our pivotal trial, our last U.S. trial, hopefully for approval, finish recruiting those patients later this year, and then get that data by the middle of next year for submission to the FDA. Actually, pancreatic cancer is a very exciting program for us. Earlier, a couple of weeks ago, we announced we had our first treatment in the U.S.
that was done in that program, coming on the back of some other treatments we've done elsewhere in the world. A very exciting program for us, looking as well for our first brain cancer patient, glioblastoma, to come later this year, hopefully in the U.S., and also targeting a response from the PMDA in Japan on our request for approval for treating head and neck cancer. We will talk about a number of these programs, but a very, very robust and meaningful pipeline of news is expected over the next couple of months. Just stepping back for a second and looking at what it is that we're doing, we are the only one using local alpha radiation. Today, more than half of cancer patients get local radiation. All of them are doing it using gamma and beta radiation. These are more historically commonly used forms of radiation.
They've been around for many years. Gamma rays, like X-rays, can penetrate tissue. They've got a very long range, and we're able to cover the whole tumor. The issue, of course, is that since we are using a radiation that has that long range, it's also going to spread to the area around it. That form of radiation, which requires chance encounters with oxygen, is inherently a very inefficient form of cell death, but it is also, first of all, damaging the healthy tissue around the tumor, and secondly, also requires higher doses, not only because of the inefficiency of the radiation, but also because it is being diluted into the areas around it because of its long range. The alpha particles that we're using, these are also emissions from certain isotopes. These are heavy alpha particles. They have size. They have mass to them.
They transfer a tremendous amount of energy very quickly. The issue is actually the opposite. Here we've got no range whatsoever. When we place alpha particle emitters into a tumor, we find we get about 40 to 90 microns of range around that injection, which means you've got three or four cells that are very, very dead. You can't do anything killing three or four cells at a time. Actually, here, the short range, it's a very efficient form of radiation. It's very powerful, but the short range is actually holding us back because now we really can't do anything clinically useful with this kind of radiation. The way in which Alpha Tau has overcome this is actually not by trying to shoot the alpha particles any harder, but rather by releasing alpha-emitting radioisotopes into the tumor in a very controlled fashion.
The way we do that is by taking a small piece of metal we call a source coated with radium-224. The radium is useful because it will naturally break down one, two, three, four, five, six times before it stabilizes. It will release a bunch of these alpha particles along the way. What's really unique here, though, is that we've put the radium onto the surface of that piece of metal where it's trapped there and can't escape. It's right next to the surface. When it breaks down, its daughter atoms are designed to recoil off of the surface of that source, of that piece of metal, into the tumor.
Now you have these free-floating isotopes, the rest of this chain, which has a total of about 12 hours of half-life between them, which will continue to move and decay again and again and release a number of these alpha particles as they go. What happens is, as you can see here, we're going to inject and leave this source, multiple sources, inside of the tumor. Each one of them, again, is coated with myriad radium-224 atoms. While they can leave, once they break down, their daughter atoms will recoil and move into the tissue, and they will then proceed to move deeper and deeper as they diffuse into the tumor over the 12-hour total half-life. They will release those alpha particles deeper and deeper as they go. We're not actually getting the particles to move any farther.
We're just having them be released deeper into the tissue because of the fact that the isotopes are actually moving into the tumor. Now, instead of that 40 to 90 microns of range, which is really useless, we get about four to five millimeters of a very well-defined range of radiation around that injection, which is very useful. We know how to use four to five millimeters. That's a reasonable range that we can use to sculpt the area of the radiation of the tumor. We will place a number of these injections into the tumor in order to get the tumor coverage that we want. We also see we get a very, very well-defined range that doesn't see meaningful amounts of radiation outside of that tumor. We can get exactly the coverage that we want with a very powerful, very efficient form of radiation.
When I say efficient, we are dosing hundreds or thousands of times less than other forms of radiation that are used locally today, so much so that, in fact, we can ship this in the mail. We can do this in most cases in a standard procedure room with no protections, no lead in the wall, lead in the floors, and a lead vest. It is a very light touch, just given how little radiation is needed. Number one, because the alpha particles are so much more efficient in the way they kill cells. Number two, again, because we're not having our dose being diluted to the areas around it through that long range and the spreading to the healthy tissue where you don't want it.
For us, we've had to figure out where we want to spend our time, given, as we said earlier, we think this is a very broadly applicable treatment. We've chosen three core focus areas to look at. In previous conferences, we've mostly focused on the first one, which is the localized and unresectable. These are tumors that have other available options, like skin cancers, like prostate cancers, will come in for those who have failed other surgical and radiation options, and hopefully show we can be a very relevant later line therapy. We started in superficial tumors, tumors of the skin or the head and neck. This was a natural place to start, given it's easy to inject locally. It's easy to see and control where you're placing it to monitor for side effects.
As we started here with very good preclinical data in cutaneous squamous cell carcinoma, SCC, of the skin or the head and neck, we moved into humans. We treated hundreds of tumors. We've seen, thankfully, a very mild side effect profile. We generally don't see the systemic side effects of radiation therapy, the nausea and the fatigue and the vomiting. What we see are local side effects for the most part, generally grade 1 or grade 2, mild or moderate, in the area of the treatment, some swelling, some redness, things that we can manage pretty easily. We've already gotten approval in Israel to market this for SCC of the skin or the oral cavity. We've also submitted for approval in Japan, where we hope to hear back later this year on treating recurrent head and neck cancer. Our focus really is in the U.S.
Our last trial that we ran out in the U.S. was a pilot study in skin cancer led by Memorial Sloan Kettering Cancer Center in New York. You can see an example here. This gentleman has a recurring basal cell carcinoma tumor on the nose. He's already had surgery. The next surgery will be even more deformative. Instead, in order to avoid that kind of a treatment, we've injected some of these sources. You can see here three months later, the nose looks great and the tumor is gone. This patient had a complete response. Actually, all the patients had a complete response. We had a 100% complete response rate. Every tumor we treated disappeared completely and stayed disappeared over the life of the study. We also saw no treatment-related serious adverse events, only those mild and moderate local side effects, things that we can manage very, very conservatively.
This study was actually published in the Journal of the American Medical Association. Right now, we're in the middle of our pivotal trial for approval in the U.S. This is an 86-patient study running across 25 or so different centers in the U.S. We expect to finish treating patients later this year and then looking for the data from that trial sometime around Q2 or around mid of next year, 2026. It's a very big patient population, even though we're only going after those more difficult tumors. Those who have simple skin cancers that can get lopped off in a dermatologist's office should do that. We're going to focus on the ones that are recurring and coming back again and again. Actually, even though we're focused on those patients, it's such a massive skin cancer incidence that it's actually still a pretty large patient population that needs our help.
The Skin Cancer Foundation estimates about 1.8 million new cutaneous SCC cases a year. Literature shows that about 3.5% of cases will ultimately recur after surgery or recur in the area or spread into the nodes around it. Those are those more difficult patients we're going after. That's about 3.5% of those cases, which we would then estimate at about 64,000 cases a year in the U.S. Beyond that, we're focused on two other core areas for us. The first one is really actually looking at ways we can be part of a metastatic solution. While this is at its core a local treatment, we've seen quite a bit of evidence that treating a tumor not only helps that tumor respond but helps the body find tumors elsewhere in the body, ostensibly by spotlighting the tumor and generating an immune response to that treatment.
We have seen this in quite a number of ways in preclinical work in animals. We have shown that we can effectively make mice immune to the cancer that we treat them for, as it were. We will challenge them again, and they will be immune to that cancer after treatment, but susceptible to other cancers. We can show that mice will respond to checkpoint inhibitors when they previously were not. We can also show actual immune proliferation. We can actually see immune cells more prominent in the tumors that we treat versus what would be without the Alpha DaRT treatment. We are seeing quite a bit of evidence of an immune response to the treatment. Most importantly, we have seen a number of patients like this one over here. This woman who came into Italy with multiple tumors on her legs.
When the doctors treated one tumor, you can see here a 3 cm lesion. A month later, that tumor is gone. What you see is just a suture from a biopsy looking for cancer and not finding it. She was a complete responder on that tumor. They went to treat the other tumors, and they wanted to measure how large they had gotten before treatment. They found that they had actually spontaneously disappeared. While we know the alpha particles have no range and we never touched this leg, ostensibly, those tumors disappeared of their own right. We think that may be related to that immune effect. What we wanted to examine was, can we actually show this more systematically? We have seen a number of these cases where treating one tumor will then make other tumors disappear.
Can we show that when we treat a tumor, if we combine it with immunotherapy, we improve the response rates potentially to that immunotherapy? What we did was we designed a study for metastatic or recurrent unresectable head and neck patients. Very much built around the design of KEYNOTE-0 48, which was the trial that was a phase three that got Keytruda its approval in these patients, in the recurrent unresectable or metastatic head and neck SCC patients. We basically replicated that design as much as we could, but added in an Alpha DaRT treatment. What we asked ourselves was, if we treat a tumor in these metastatic patients, we know we have good conviction that that tumor should respond.
The question is not, does that tumor respond, but do the other tumors in the body respond to the Keytruda, to the pembrolizumab, where they might not have otherwise done so? When we look at that study at KEYNOTE-0 48, we see that about 20% of the patients in this population had an objective response, meaning their tumors shrank across the body in response to the treatment with the Keytruda. About 5% had a systemic complete response where the tumors disappeared around the body. About 1 in 5 are responding with some shrinkage, and about 1 in 20 are being cured, as it were.
Our question was, when we add in the Alpha DaRT into a tumor, can we show that these response rates go higher, that Keytruda is more successful when we've added in a kick, as it were, into a tumor and spotlighted that tumor for the immune system to hopefully pick up on them elsewhere and really work in tandem with the Keytruda? We read out some data earlier this year. This is what we had recruited eight patients into the study by then. Two of them, unfortunately, passed away even before we got to check how they were doing. That's how it is when you recruit these very difficult patients. Of the other six, when we were actually able to recruit, treat, and measure how they did, every single one of them responded to the Keytruda, and half of them had a complete response.
If you include those two of the denominator, those who died before we evaluated them, which is the way these studies are built, 75% had an objective response versus 19% of what we saw historically from KEYNOTE-0 48. Thirty-seven and a half percent, or three out of eight, had a complete response where the tumors disappeared across the body versus the about 5% that was seen historically in KEYNOTE-0 48. Again, a massive difference, albeit with small numbers and early data, but a massive difference in the response rates. Now, just to give you a sense for why we're so excited about this, I want to show you a quick study. This was one of the patients we had treated in that study. Originally, she was 94 when she came to us. She had this horrific squamous cell carcinoma tumor in the lip.
You can see it's in the lip over here and in the jawbone. This would be a very, very difficult surgery and probably not one they would have done for someone who's 94 years old, suffering from cardiac issues and dementia, as well as obviously the age as well, making it very, very difficult to do such a horrific surgery like this. We also noticed that she had some metastases on the neck, on the skin. We didn't even touch the lip. We used the skin as a platform, as it were, to treat her while she was getting Keytruda. You can see here we did a couple of these Alpha DaRT injections, took them out two weeks later. You can see here after three months, those tumors are gone. That's, again, very classic for us. That's our bread and butter. We're not surprised by this.
We've always seen great data in treating these superficial tumors using the Alpha DaRT. What's amazing, though, is that we haven't touched the lip. She's getting the Keytruda, and now, nine weeks after treatment, this horrific tumor has disappeared. Her tumors all across the body disappeared. She took Keytruda for a year and then stopped. Last time we looked, over two years after treatment, she was still alive with no evidence of disease. This is the dream. We're helping these patients ostensibly respond to Keytruda. This is what Keytruda wants to achieve, to take this 94-year-old woman with a horrific cancer and show she can be durably free of cancer years after treatment. We'd like to believe we played a role there as well in really kickstarting the response of the immune system and helping the Keytruda do its job.
We've seen a number of patients like this, a very exciting area that we're continuing to explore and in discussions with the FDA around ways we can run studies like this in the U.S. in larger and larger sites. The last area we're focused on, the last pillar of our strategy, is the high unmet need. If we really do have a treatment which is indifferent to the nature of the tumor, we should be going after those tumors that don't have good available options. Options that come to mind include pancreatic cancer. We have a stoma of the brain. These are obviously horrific cancers with poor available treatments. If we find that we can be relevant there, then unlike in the skin, here we don't need to go after the most difficult patients who have failed other options.
Here we can say, if I have a treatment that's relevant to these patients, I could potentially be a first-line treatment too for them. We are exploring a number of different organs right now. We already have trials underway in the pancreas and liver metastases and the lung and the prostate and are targeting a few other ones as well. Now, in the pancreas, we released some data earlier this year, and we saw from the first number of patients we had treated, 33 had reached the response. We saw over 90% disease control rate in a very, very difficult cancer. Very, very exciting results. What we wanted to know, though, is can we show a survival benefit for these patients? These trials that we're looking at, which were run in Montreal and in Jerusalem, were all comer studies. It was all sorts of different patients there.
When we looked back at the patients who were treated, we found they fell into three distinct groups. One of them were patients who came to us without having gotten chemotherapy, ostensibly too old, too sick, too infirm, or just refusing to get chemotherapy. Literature showed that these patients who are not being treated should live around three to three and a half months. When we did the Kaplan-Meier survival analysis, we found that these patients in this group were living to a median of seven and a half months. We are giving them a treatment which doesn't have the same horrific side effect profile as some of the other therapies available to them. It seems to be offering them a better outcome from this initial look so far. We had 10 patients who came in who were metastatic patients who failed first-line FOLFIRINOX chemotherapy.
Here, because that's the gold standard, there's quite a bit of literature. It's fairly consistent. Ten to 11 months is the expected median overall survival. When we were 15 months in with the median follow-up, we still had not seen what the median survival was because the patients weren't dying. We had 8- 10 patients still alive, we don't actually know what the median survival is. We know it's more than 15 months. Whether it'll be 15 or 16 or 20 or 30, we'll have to wait and see how long these patients live. So far, looking very, very good in comparison to first-line FOLFIRINOX on its own. Finally, we also had a group of patients who were coming to us after second-line gemcitabine Abraxane chemotherapy.
This is a very interesting group because when you start these trials for the first time, the first time treating humans in a cancer, you get the worst patients, the ones who are really most desperate at the very beginning. These are actually our oldest vintage of patients because in many cases, they came to us very early on in the study. You can see here, second-line gemcitabine Abraxane, the patients should live, according to the literature, about 7.5 to 10 months since the initiation of chemo. Yet we were seeing a whopping 23 months median overall survival since the beginning of that chemo. There are a lot of difficulties in comparing cross-studies, but very, very exciting signs here of looking at how these patients are doing versus how long they should have lived.
When we showed this data to the FDA, and particularly this slide over here, which is looking at the survival of patients who are metastatic coming after first-line FOLFIRINOX, on the basis of this and other data, we were able to get an FDA sign-off to start a U.S. pilot study. In fact, as I mentioned, just a couple of weeks ago, we announced the first patient was treated in Texas in this trial. This is a very exciting trial for us, looking at 30 patients with newly diagnosed pancreatic cancer, 15 of them locally advanced cancer, 15 of them already metastatic. They're going to get gold standard FOLFIRINOX chemotherapy. We're going to come in in the earlier cycles of that chemotherapy and add Alpha DaRT from the beginning and show and look for, can we show not only good safety, but also survival, improvement of pain?
For these patients who aren't yet metastatic, is there a way we can actually shift them towards being surgically resectable in a very, very meaningful definitive treatment as well? This is a very exciting study that we'll continue to talk about over the coming months. Obviously, there's a massive unmet need. Pancreatic cancer, we see about 66,000- 67,000 new cases a year in the U.S. 87% of them are known to be unresectable when they're diagnosed. 87% is about 59,000 patients a year who don't have a definitive surgical therapy, a definitive local therapy available. We would like to try and find a way to be helpful to those patients. In our unmet need pillar, the last frontier, or really the big frontier for us that's next is glioblastoma, which is a deadly, deadly brain cancer.
We've also announced that we have an IDE approval from the FDA to start a U.S. study in GBM as well, look for the first patient in that study, hopefully coming in later this year in 2025. As we started off, a lot of our historical data was in the tumors that are localized and unresectable, like the skin and the head and neck. We've now shown some initial data in combination with Keytruda and potentially having a benefit for metastatic patients beyond just the tumor or tumors that we're treating. Again, a very exciting area we continue to explore and very actively going after the tumors with the high unmet need, like the GBM and the pancreas. Now we can look briefly at the milestones, and they should make a bit more sense.
Again, the pivotal study in the skin is expected to complete recruitment later this year and get data by the middle of 2026. The pancreatic cancer, which we've now started treating a couple of weeks ago, is looking to finish recruiting patients early next year and then get data hopefully as early as the second half of next year. Looking to treat patients in the brain in the U.S., hopefully later this year, as well as in pancreas in France, and also looking for that PMDA approval in Japan, hoping that we'll get, fingers crossed, we'll get approved in head and neck cancer later this year. We are continuing to build out our manufacturing facilities. We are currently manufacturing out of a small facility in Lawrence, Massachusetts, as well as a small facility at our headquarters in Jerusalem.
Together, they're really only clinical trial scale facilities, probably 1,000 to maybe 1,500 patients a year at most. We are building our first commercial scale facility right now underway in Hudson, New Hampshire. It's a much larger facility. We're building it out in three phases in order to manage the cash flow investment. This one is really our first commercial scale facility, up to about maybe 15,000 or so patients a year capacity when it's fully built out. That construction is underway. We will look to do the validation and equipment over the course of the year and aiming to get it up and running early next year in the U.S. and New Hampshire. The company has been public now for about three, a little more than three years. We had $83 million in cash and deposits at Q2 balance sheet. We were pretty well financed, thankfully.
We're burning pretty consistently about $5 million a quarter. That's been true since we went public about three years ago. There's some one-off CapEx associated with our New Hampshire facility. We've already invested most of it, but again, a few million dollars left there. Other than that, though, our run rate remains about a little over $5 million a quarter, which we think is very admirable for a company with about 130 employees and 15 or so different clinical programs. We're very careful with how we manage our cash balance. Thankfully, I'm in the enviable position of a biotech CFO who doesn't have to worry too much at night about how to finance the company in the near immediate term. We're confident that we can keep executing on milestones and continue to deliver news flow over the coming months with the resources that we have available.
We are focused on execution. With that, I will stop. I will thank you very much for your time. I'd love to continue the conversation. If there are questions, please reach out to the Lytham representative if you want to set meetings. I will turn it back to you, Robert.
All right. Fantastic. Thank you, Raphi, so much. Thank you, everyone, watching the presentation here. As Raphi just said, if you have any questions or would like to schedule a meeting with management, shoot me an email. That's blum@lythampartners.com. If you'd like to learn more about Lytham Partners, you can visit our website as well or follow us on LinkedIn to stay connected on future events. We hope you all enjoy the rest of the conference and have a great day. Raphi, again, thank you so much.
My pleasure. Be well, everybody, and thank you very much.