I'm Alex Hantman, and I serve as an Equity Research Associate here at Sidoti & Company. Today, I'm pleased to be in conversation with CFO Raphi Levy of Alpha Tau Medical, ticker DRTS. During the presentation, please feel welcome to submit questions using the Zoom Q&A interface at the bottom of your screen. After the presentation, we'll open to your questions. With that, Raphi, I'll turn it over to you.
Excellent. Thank you, and thanks very much to everybody who's joining. Good morning and afternoon. Good to be back here. It's been, I think about nine months since we presented at the Sidoti conference. We have quite a bit to share. We'll go through the story for those who don't know it, and there'll be some updates there as well for those who are familiar. So again, thanks very much for the time, and of course, as Alex said, welcome the questions through the Q&A as well. So just to give you guys who aren't familiar, sort of a quick overview as to who we are, and we'll go through this, of course, in more detail. We are the inventors of the Alpha DaRT technology, and this is our proprietary method for using alpha radiation in treating solid tumors locally.
So just to explain what that means, alpha particles are a form of radiation, which are known to be incredibly more potent and efficient than other forms of radiation. So we can use orders of magnitude less radiation than the other forms being used today, and we are using it for local treatment, where what I mean is we are injecting it directly into the tumor. We are competing in the world of where a clinician looks at an image and says, "I see a tumor over there. I want to cut it out or irradiate it." We are the only ones who have figured out how to do it using alpha particles, and I'll explain that in just a minute. And so we are providing a treatment to hospital to be used, a personalized kit that matches the particular cancer or tumors that the patient has.
And we are trying it now in multiple cancer types with some exciting data that we've recently read out, as well as some more that's forthcoming, and looking for our first approval at the end of next year in the U.S. or early 2026. So just to quickly review what it is that we're doing, we are focused in the world of alpha radiation. When you look at how cancer therapy is done today for local radiation oncology, it is all being done using the conventional gamma and beta radiation. These are the forms of radiation where a clinician will flood the area with radiation. Hopefully, some will encounter oxygen and/or and generate free radicals. With any luck, those free radicals will encounter tumor cell DNA and will generally cause repairable single-strand breaks.
And so while this is the radiation we know how to use today because it penetrates the walls and the body, et cetera, and gets stopped by metal or by concrete, it is inherently a very inefficient form of radiation and requires a very high dose to be effective. The alpha radiation, which is the emission of these heavy alpha particles, is known to be much more efficient. These particles are very high energy and very heavy. They can break through both strands of the DNA, and in doing so, they generate these irreparable double-strand breaks with significantly less use of radiation. Whereas here, one might need a few dozen hits to a cell to kill it, here, just one or two hits can be sufficient.
Now, the reason nobody is doing local alpha radiation is really this point about the range, because when it comes to the traditional beta and gamma radiation, we know that they can penetrate tissue. We're going to put a very large dose into the center of the tumor, and it will cover the whole tumor, but it will continue to spread beyond that. It's got that very long tail, and so we will inevitably see damage to the surrounding healthy tissue. In the case of the alpha particles, it's exactly the opposite. We find that the alpha particles can travel 40-90 microns of range in tissue, which is 40-90 millionths of a meter, which is great for killing three or four cells of depth, and they're very, very dead, but we can't do anything clinically useful with 40 microns of range.
And so this inability to get these potent alpha particles to travel into the tissue is the reason nobody does local alpha radiation, because they simply can't get the particles to move deep enough into the tissue to be of any use. Now, the way in which we've overcome this is actually by releasing alpha emitting radioisotopes into the tumor in a very controlled fashion. What we'll do is we'll take a little piece of metal, call it a source. It's coated with Radium-224. The radium is useful for us because it will naturally break down one, two, three, four, five, six times and then stabilize. It's no longer radioactive. Along the way, it will release a number of these alpha particles, each of which won't get very far, each of which will smack into something and kill it and stop very quickly.
But what's really unique here is that where the radium is fixated into the source in a way in which it's unable to leave, we put it right up against the surface so that when it breaks down and the alpha particle flies off in one direction, what's left flies off in the other direction. That's Newton's third law of equal and opposite reaction. And so what we end up with is, while the radium is trapped, its daughter atoms, as we call them, these steps in the chain, which are themselves alpha emitting radioisotopes, they will move into the tissue, and they will diffuse deeper and deeper into the tissue over their 12-hour half-life and release these alpha particles deeper and deeper into the tissue.
And so, for lack of a better analogy, what we get is basically a cluster bomb, because a cluster bomb moves and explodes and moves and explode multiple times. So the same thing here, we're going to inject this radioactive source into the tumor and leave it there. The radium is trapped onto the source in a way in which it can't escape, but right near the surface, and when it breaks down and its daughter atoms release into the tumor, so they will then continue to diffuse into the tumor, and they will decay and release alpha particles deeper and deeper into the tumor. And so now, instead of those forty microns of range, which is totally useless, we're getting about five millimeters of range, which is quite a bit more useful.
And again, we're doing so not by shooting the particles any harder but rather, as it were, by throwing the gun on auto fire into the tumor and letting it move around until it runs out of bullets. And that's as such we're getting significantly more useful range inside the tumor. Now, we believe that this treatment is relevant to any solid tumor. And the reason I say that is because, number one, it is fundamentally physics at heart. It is really just about delivering a wallop of radiation, less so about anything specific to the type of the tumor. Number two, we've done this in over twenty different tumor types pre-clinically, and we have never found a tumor type that doesn't respond. And so we believe this could ultimately be a wonderful local tumor control option for nearly any solid tumor.
When we need to figure out where to focus our time, so we've chosen three core focus areas. The first one we call the localized and unresectable, and these are tumors that have other available options, like squamous cell carcinoma of the skin or the head and neck, like prostate cancer. There are treatments available to offer these patients, but the patients who have failed the local surgery and radiation options, they run out of these local options very quickly, and we have found in some of our earlier studies that we'll talk about, that we can potentially be a very good option for these patients, a way to give them a new alternative for local control. The second group that we're focused on is those with a high unmet need.
Again, to the extent that, as we've always posited, we believe it can be relevant to any solid tumor, so we may as well go after those which have the fewest available options and the worst outlook. And so ones that come to mind include glioblastoma of the brain or pancreatic cancer, where again, it would be tremendously impactful if we could deliver a new treatment alternative for these patients. The third one, which is a theme that we'll go through a couple of times during this presentation, it'll arise in a few different locations, is the fact that we're seeing that the treatment is not only destroying the tumor that we're inserting it into, but also seems to be catalyzing a systemic immune system recognition of the tumor.
This is a really nice, sort of unexpected side effect of the treatment, which may help us treat metastatic patients. I'll go through examples of where we see this playing a role, but it could be that if we can use this in combination with immunotherapies like checkpoint inhibitors, that we can potentially apply this not only as a local therapy, but as part of a systemic solution, and that'll come up in a few different places. I wanted to show you a little bit of the data that we've put out. We've done a wealth of experiments so far, but here's just a taste of some of the stuff that we've done. First, I'm gonna start with a trial that we published last year in the JAMA Dermatology, the Journal of the American Medical Association.
This was a small skin cancer study run in the U.S. and led by Memorial Sloan Kettering Cancer Center in New York, as well as a number of other centers across the U.S. Just to give you an example of a patient being treated, this gentleman has a recurrent basal cell carcinoma tumor on the nose. He's already had surgery before. A repeat surgery will potentially be deformative, would have to cut out a chunk of his nose, et cetera. We're trying to avoid that. And so instead, what we're gonna do is we're going to inject a number of these radioactive sources. You don't see them here. They're inside of the nose.
They are strung onto a suture inside of the needle, and then the doctor will come in on one side, come out the other side, and leave those sources inside for two weeks and just tie off the suture with a button, like a washer on a screw, so it can't move around. And then two weeks later, the treatment is done, the patient comes back, we cut those sources, string, and pull out those sources. This is a single treatment regimen. It's not done for five or six days a week for eight or twelve weeks. It's done one time, and that's it. It's also a relatively straightforward procedure. Because we are using a fraction, and I mean hundreds or thousands of times less than other radiation forms generally used, we have tremendous flexibility in how we do this.
This can be done in any room in the hospital. We don't need particular shielding or protection. This can go in the mail on UPS or FedEx, because again, we're using such low levels of radiation, it doesn't really necessarily require any special protections, so we'll inject the patient. We'll take it out two weeks later. You can see a bit of redness. That's a classic side effect for us, some radiation dermatitis there, but again, relatively mild and will go away pretty quickly, and in fact, you see at three months, the nose looks great and the tumor is gone, and the patient avoided a very drastic potential surgery there, so we did this in this first study across a number of patients in the States.
In terms of the side effect profile, generally consistent with what we've seen elsewhere, which is that we don't really see serious side effects, and we don't see the systemic side effects, the nausea, the fatigue, et cetera, that one tends to see from radiation oncology, and the reason is because of how tightly controlled the radiation is. It's not really escaping the tumor very much, and therefore, we're not seeing those distant, side effects. We're seeing local side effects in the area of the treatment, what's called grade one or grade two, mild or moderate, nothing serious or life-threatening, things like that irritation and the swelling, things that we can treat with Tylenol or with cream, and they'll go away pretty quickly.
And just as importantly, we saw a 100% complete response rate, meaning every single tumor we treated disappeared and stayed disappeared over the life of the study. So obviously, that was an outstanding result, better... You know, best thing we could have possibly hoped for, and we're very excited to have been able to publish that in a prominent journal. And on the basis of that study, we're now in the middle of our pivotal study in the U.S. This is our trial for getting our first FDA approval, to looking for approval in the same indication, in recurrent squamous cell carcinoma of the skin. And so this trial is running right now, across 20+ centers in the U.S., and up to 86 patients that we're looking to treat.
Interestingly, it's anybody from, you know, the big names, UCLA and Emory and Mayo Clinic, et cetera, all the way down to, you know, a community dermatologist. You can walk into a community clinic and get an injection and go home because, again, we don't need the sort of CapEx and infrastructure that we generally needs for radiation oncology because of the relatively low doses of radiation. We expect to complete the recruitment of these patients around the end of this year or early next year, and then submit it for FDA approval, assuming the data looks good, and we have breakthrough designation from the FDA in this indication, which means that we have the potential to offer a new alternative for patients with poor options or, you know, high mortality.
And then the FDA should be giving us a faster review of the application because of that breakthrough designation. I want to spend a few minutes on data that we released, I think since we last spoke, on the pancreas. It's some very exciting initial data from us. So this is our first foray into the pancreas. It's a trial we're running in Montreal, looking at both safety and feasibility, as well as efficacy of treating pancreatic cancer patients using the Alpha DaRT, and we are taking anybody who is non-resectable. So if they qualify for surgery, which is only about 10%-15% of patients at diagnosis, they should do that. That's standard of care. But the other 85% or 90% can come to us at whatever stage they are, and we will treat them.
In this trial, the treatment is only Alpha DaRT. They can be coming to us after chemotherapy or immunotherapy, but during the treatment itself, they're only getting Alpha DaRT because we want to be able to observe the specific responses and potential side effects from the Alpha DaRT. Now, what we're doing is we are injecting these sources while the patients are awake, but sedated, using the same procedure that's being done for biopsy. Normally, for biopsy, a clinician would take an endoscope, a camera, come down through the mouth into the stomach, and then perforate with a small needle into the pancreas to take samples. What we've done is, we've preloaded these standard needles with the Alpha DaRT for injection into the pancreas. Instead of taking out samples, we're pushing in these darts.
Going into this study, our biggest concern was really about safety, because we were gonna be doing a number of injections through the stomach or colon into the pancreas. We didn't want to see that if somebody had, you know, bleeding, for example, we'd have 50 holes bleeding out of the pancreas or some massive pancreatitis. What we agreed with the regulator, with Health Canada, was that we would limit ourselves artificially to one patient per month for the first five months, and then check the safety very carefully, and if there are no safety issues, we would remove that restriction of the recruitment.
We also decided to give minimal amounts of radiation, suboptimal doses, well below what we would normally want to give, just to test for the safety issues, so that if there are some safety issues, they're minor at first and not full-blown. What we did is, we put out data from these first five patients, from the interim look. As you can see, we got a good mix of patients across stage two to four, types of cancers, across various parts of the pancreas, some metastatic, some just unresectable, almost all of them coming to us after chemotherapy or even two rounds of chemotherapy of various sorts. As promised, we gave minimal amounts of radiation. The first patient got only three sources, which was totally not a therapeutic dose. It was just to test safety.
The second patient got 11 sources in a cluster on one side of the tumor to look for safety issues from the clustering or response from the treated side versus the untreated side. The next patient got 21 sources. Now, it happens to be because it was a smaller tumor, 21 sources was a relatively high coverage level. It was about half of a therapeutic dose. We ended up getting about 44% coverage. Again, even though we were giving very low amounts of radiation, just because that patient had a very small tumor. And then finally, again, we had two more patients with more radiation, but again, they were larger tumors and therefore lower coverage. We would have wanted to give even more radiation to these patients.
The safety and feasibility is really all we were looking for at this stage, and it was really an A+ . Everybody was delivered successfully with the treatment, and we got great feedback from the clinicians on the ease of use. Everyone went home the same day. The longest procedure was about an hour. And really, the side effect profile was fantastic. Not only did we not see any associated serious side effects, we didn't even see moderate side effects. All we saw from the product were grade one mild side effects, like GI discomfort, loss of appetite. Again, very, very mild side effect profile, certainly for such a deadly cancer treatment. Now, this is supposed to be the last slide in the section. This is all we were looking for at this point.
What was really cool, though, is when we actually looked at those patients, we saw a hint of efficacy, even though we were giving non-therapeutic doses. We're giving suboptimal doses. So the first patient only received three sources. That was completely not a relevant therapeutic dose. That patient, unfortunately, continued to progress and died three months later because they had late-stage pancreatic cancer and really were not being given any material dose of therapy. The second patient, also coming to us post two rounds of chemo, had 11 sources in a cluster, but they continued to progress out of the other untreated side of the tumor, and they also died three months after treatment. And you get a sense for, right, what is the life expectancy of these patients, unfortunately, by the time they're getting to us after failing chemo?
The third patient had a smaller tumor, so 21 sources covered 44% of the tumor, and in fact, we saw stable disease at one month, meaning that the tumor was not progressing, and then at two and a half months, we saw a partial response. The tumor had shrunk by more than 30%, which is a fantastic outcome, and then finally, the last two patients who had higher doses, but lower coverage because they had larger tumors, so they demonstrated a stable disease as well, so I mean, again, you have to take this in context. It's only five patients, and it's suboptimal doses, but this gets us so excited because, number one, we're seeing a 60% disease control rate, right? 60% of the patients are seeing the tumor kept in check with a suboptimal dose.
20% of them are responding, we're actually seeing the tumor shrink. You see correlation. The least radiation, they've got a very low life expectancy. A little more radiation, the disease stays in check, stays stable. A little more, the patient actually responds. So now, following this data, we no longer have that restriction on recruitment. We are now treating multiple patients per month, and we've said that we opened multiple sites, another site in Canada, another site in Jerusalem. We expect that in Q1 of 2025, we will share some data from these additional patients as to how they are doing as we increase the recruitment rates and as we increase the coverage levels from the lower levels we had started with. I want to spend just a minute on preclinical data.
I gave a hint of this earlier, the fact that we're seeing an immune response from the treatment. Just to give you some examples of this, where we're getting it. So this is looking at mice who are growing tumors. We're tracking the growth of the tumor. Now, the black line is the group that have not received any treatment. That is the control group. The red line is the group that received a PD-1 inhibitor. This is a checkpoint inhibitor immunotherapy drug. You can see that those lines are overlapping... right? This is the almost 90% of patients who don't respond to checkpoint inhibitors, right? We're seeing no incremental slowdown of the growth of the tumor from adding in the drug.
The blue line is a single DaRT in the middle of a large tumor, so I'm deliberately underdosing so that I can leave some residual tumor behind and look for this synergy in it. That's on purpose. You see an effect there. The tumor is much smaller. That's not surprising. What's really cool, though, is the combination of the two, whereas before, in the absence of the alpha dart, we see no incremental benefit from adding in the drug. When we have the alpha dart there, adding in the drug actually has significant benefit. It's as though we've somehow activated the immune system's ability to use this drug to unleash the immune system on the tumors. Again, it's as though the treatment is not only destroying the tumor at hand, but actually contributing to the immune recognition of the tumor.
You can see why that is. This particular slide is looking for CD3 positive tumor-infiltrating lymphocytes, a form of T cells, in response to the tumor. Those are the little brown dots here. You can see there is a population of T cells in the group with the PD-1 inhibitor, but it is meaningfully higher with the group with the Alpha DaRT and the PD-1 inhibitor. Here you see visually observable proof of a local radiation oncology treatment deriving that systemic response in from the immune system. More recently, earlier this year, we published data and presented data at a conference with a very similar direction, in particular focused on pancreatic cancer tumors, which are known to be very cold. They're not immunogenic. They're not really trigger immune system response, unfortunately.
What we did was very straightforward. We gave mice two separate pancreatic cancer tumors. We treated only one of them, and we measured only the untreated tumor, and you can see that that untreated tumor grows significantly more slowly. By significantly, I mean with a 0.002 p value when compared to the mice that aren't receiving the Alpha DaRT, right? Somehow the Alpha DaRT in the is having an impact not only on the tumor that it's treating, but actually the unrelated distant tumor is also being affected by the Alpha DaRT being in the first one again. Where this comes into play, for example, this is a patient who came in in Italy with multiple tumors in the legs. The doctors treated one tumor. You can see it's a three-centimeter tumor, which a month later is gone.
This is just a suture from a biopsy looking for cancer and not finding it. She had a complete response on this tumor. They said, "Let's go check the other leg and measure the other tumors for treatment," and they found that, in fact, the other tumors had spontaneously disappeared, right? We never touched this leg. We also know the alpha particles have no range to go from one leg to the other. So we suspect, again, the immune system recognized the treatment and picked up on the tumors elsewhere in the body. And again, we've seen this now in a number of patients where we will treat one tumor and see other tumors start to disappear. So we've got a lot going on in our clinical pipeline. I'll just hit on very quickly on some highlights. First of all, our lead program is the skin and oral cavity program.
We are already approved in Israel. We can market this for oral cavity and skin squamous cell carcinoma. We've submitted a request for approval in Japan in head and neck cancer after we finished our pivotal study there, and we're hoping to hear back by the end of the year, ideally from the PMDA. But really, our focus is on the U.S., where we want to launch commercially first. And so as I said, we finished that feasibility study last year. It was published last year with a 100% complete response. We are now in a pivotal study, which we expect to submit hopefully next year for approval.
Now, alongside that, we have a number of other great trials going on, really dipping our toes into a few different cancers to show hopefully that we can be effective there, like we've seen in other situations. And so I mentioned that pancreatic cancer trial in Canada. We have a liver metastases trial running in Canada as well. We're treating vulvar cancers in the Cambridge in the U.K. We've got prostate cancer trial running in Israel, as well as about to start treating in breast cancer and lung cancer as well. And so with so many things going on, we have a number of shots here on goal and continue to generate good data and important milestones.
There are some ones that aren't here on the page, but just to hit on a few highlights, we're hoping to finish recruitment on our U.S. pivotal study end of this year or maybe even early next year, and then submit next year for approval. We're hoping to publish some data in the pancreas in the beginning of next year, as I mentioned. Look to start treating patients in brain cancers and lung cancers very soon, and also we're looking for that response from the PMDA on our request for approval in Japan. We've been a public company now for about two and a half years. We raised $104 million when we went public two and a half years ago. We still have $74 million in the bank at our last quarterly readout.
We are very careful with how we spend our money, so we, if you look at our financials, we've spent pretty consistently about $5 million a quarter, which I'd argue is incredibly lean for a company with 130 or so employees and 15 different clinical programs. We are very careful how we spend our money, even though we're very active, and we continue to, you know, expand our growth, our burn rate, but very, very slowly and carefully. And so we, you know, we've said we easily have at least 2 years of runway, if not more. And we are really out there just telling our story because we think it's a fantastic story. It's underappreciated, underappreciated by the markets, and so we'd love to find new people who want to join us for the ride.
So with that, I'm going to pause. I'm going to say thank you very much for your time, and Alex, happy to take any questions if there are any.
Great. Thank you very much, Raphi. Let's start with, you know, the most recent release, the June publication. Can you talk to us about, you know, the commercial implications of a near 100% response rate in treated lesions, particularly that these are cancers that are hard to conventionally treat?
Sure. So if you're asking specifically about the skin opportunity, I'd say a couple, you know, two key highlights. Number one is that these patients don't have great options, as you mentioned. In fact, in many cases, these may be patients with a single tumor, but they're gonna go onto a drug, to a systemic therapy, once they fail the local therapy. So, you know, they will often go either to a checkpoint inhibitor, like Keytruda or Libtayo , and those are, you know, $100,000+ for a regimen of treatment, or $300,000-$400,000 if you survive the full, you know, two years. And or they may go to chemo, which is crazy because chemo is poison unfortunately, and we have, you know, it is what it is, right?
But we use that even if there's a single tumor right there, you can see it on the person's body, but you can't cut it out because the margins are poor or there's too many blood vessels in the area or whatever it is, right? And so we are offering, you know, an alternative there that's much simpler than a lot of these drastic therapies. Now, in fact, if you look at our design of our pivotal study for approval, it is focused on those therapies. The FDA is comparing us to the response rates in, for example, checkpoint inhibitors, Keytruda and Libtayo and others, where, you know, the response rates tend to be 25%, in some cases, 45%, right? They're certainly way below the near 100% response rates we generally see.
We also think it's a very attractive market. There is quite a large population of patients who are in need of therapy in this particular situation. The Skin Cancer Foundation estimates that there are about 1.8 million new skin squamous cell carcinoma cases a year. We're obviously not gonna go after all, though. That's a pretty large number. Most of them will have relatively simple cases that will get lopped off to a dermatologist. However, the data shows that about 20% some-odd tend to be high-risk cases, and that about 8% tend to see some sort of local recurrence or nodal metastases, local advancement in the area of the cancer, and those are really the patients that we're targeting.
We're targeting those patients with those high-risk cases, which I think in many cases, which, you know, the simple math would say should be about, you know, a hundred and fifty thousand new cases a year that will get to that situation. And our goal there is to go to clinicians and say: "Look, I know you can give, you know, Keytruda, or you can cut the guy's nose off. You've got these options, but we have a better option. We have one which seems to have better efficacy and a much better safety profile and is much more straightforward." And I think that's a very compelling argument for us to be made.
I will say that we've seen increasingly over the past few months, given some of the data that we published and other data that we've seen on the pancreas, that it's clear that the excitement there is even more, you know, more, more palpable. You can feel the excitement from the clinicians who really have nothing to offer these patients. And there, I think it's, you know, to the extent we can demonstrate efficacy in those tumors, it's a much more straightforward commercial approach, a much more straightforward discussion with the clinicians, right? You have patients who are unfortunately going to die of pancreatic cancer. You've got nothing to offer them, and here's a new alternative, and it's just a much, much easier discussion.
Great context. Thank you. And so I guess given some of the lack of alternatives in treatment and some of the powerful synergies that you're able to get, you know, with some of these checkpoint inhibitors, what do you think is the pricing power? Like, how might the cost of your treatment compare to some of the other alternatives?
Yeah, it's a good question, and probably one we can't answer fully in the minute we have. But I'd say, you know, it's a tricky question because if you just focus on skin, so which is our lead indication, of course, so the comps show that simple radiation can cost about $30,000 for a regimen. More advanced and targeted forms of radiation cost anywhere from $60,000-$90,000, and in some cases, even $150,000 for some really specialized treatments. You know, I look to the comparators. I look to the fact, as I mentioned earlier, that we are ultimately avoiding the need to go to a checkpoint inhibitor in many of these cases, those regimens that would have cost $100,000 or more.
I think, you know, to the extent we are just the best skin cancer treatment for these patients, then certainly we could look for something in the fifty, sixty, seventy range. And again, we haven't set a price yet, so I'm not going to give formal guidance. But I think to the extent that we end up seeing good data in the pancreas and the brain and elsewhere, then we'll have to consider that as well in the pricing discussion, and those have interplay, right? We can't necessarily charge one price for the same technology in the skin and three times that for the same technology in the pancreas. And so we have to be mindful of that in looking at a relatively uniform set of prices.
But thankfully, you know, we are continuing to generate data in those indications, in the pancreas and the liver and elsewhere, and we'll use that to guide our views on pricing as we get ready for a commercial approach, which we are. We are currently, you know, in the plan. We are working on preparation for reimbursement, for working with insurers and Medicare as well. And so while we wait for patients to come out of that trial, right, once we finish recruitment, let's say, you know, early next year, we'll have to wait about six months for that durability data to mature. And so that means we could probably submit, you know, second half of next year at some point.
During that time, as we work on our commercial prep to build our own sales force, we would be able to reflect on data from other indications in our commercial assumptions in the skin.
Great! Well, it sounds like, you know, there's a lot of exciting updates, and it's been a pleasure having you back, so Raphi, I'd like to thank you for sharing the story with us, and also thank everybody listening for spending time with us today.
Thank you. I appreciate it. It's a pleasure to be here. Thanks to everybody who joined, and look forward to staying in touch and having more updates to share.
Perfect. Take care.
Take care, guys. Have a great day.