Good morning. Trevor Davis, Healthcare Sector Specialist at Citi. We're going to kick off day two of our Global Healthcare Conference with Nuvation Bio, and with us from the company, we're happy to have David Hung, who's the Founder, President, and CEO, as well as Philippe Sauvage, who is the CFO, and I guess maybe the best way we can do this. I'll give you the floor for a few minutes if you want to sort of provide, you know, a bit of an overview of the company and the exciting things that you're working on, and we'll go into some Q&A. Thanks so much, Trevor. So, you know, I think we're entering a very exciting phase for our company. We are now a commercial stage company. We, as you know, acquired AnHeart Therapeutics a little over a year ago. And with that, we acquired two assets that we felt had great promise for us. The first one was Taltrectinib, which has now been approved as of June 11th this year, under the brand name Iptrozi. And in our first full quarter of our launch, we've had 204 new patient starts on this ROS1 drug for non-small cell lung cancer. And we're excited about that because that's about six times the number of new patient starts for Repotrectinib, which was the previous generation ROS1 inhibitor. So we think that that molecule is really shaping up the way we had hoped for. We had announced data recently showing now that in addition to the nearly 90% response rate, our duration of response has now moved out to 50 months, so more than 40 years, which is really unprecedented in the space, and we're very excited about that, not only for what it means for patient progression-free survival, but also that really sets up a very interesting dynamic on the commercial front for revenue stacking now going into the fifth year, and we believe that's going to make this a really substantial opportunity. We're also very excited about the second molecule we acquired through the acquisition called safusidenib, which is a mutant IDH1 inhibitor for glioma. As you know, the only other IDH1 inhibitor in the space is vorasidenib, which is marketed by Servier. In just low-grade glioma, that drug is poised to do about $1 billion in sales in its first 12 months. Vorasidenib was approved on an 11% response rate. The fact that at two years, only 41% of patients had progressed. We just announced a week ago and published today, in fact, our Safusidenib data in low-grade glioma showing a 44% response rate. At two years, instead of 41% progression, we have shown 12% progression, which we think is really striking and really fantastic news for patients. That drug has now entered a pivotal study in both high-grade and low-grade glioma. High-grade because there are actually no drugs approved in high-grade glioma. Vorasidenib is only approved in low-grade, non-enhancing, or low-risk glioma. Our pivotal study now has started off with high-grade glioma, including as well low-grade gliomas with high-risk features like contrast enhancement. So, we think that's a very exciting program and we're really, you know, delighted to be moving that forward. We also very well capitalized as of our last Q. We had $550 million in cash. So, you know, with these programs and our cash, you know, we believe that we have a lot of capability to not only develop these programs and get to profitability, but also to look at and potentially acquire other assets. And so we're very excited about the way the company is shaping up. Great. Thanks for that overview. Let me just zoom in on Iptrozi. You know, this is a product that, you know, as you mentioned, is approved a number of months ago, in ROS1 non-small cell lung cancer. I believe you've cited a pretty substantial market opportunity in this category and just that indication alone. So maybe you can sort of give us an overview on how, you know, the clinical profile of that drug compares to other drugs that are approved, in that space, and then sort of what your assumptions are for capturing that substantial market opportunity in terms of, you know, market penetration and how you stack up versus competitors. Sure. So there are three other approved drugs in the ROS1 non-small cell lung cancer space. Two first-generation agents are Crizotinib and Entrectinib. Their response rates are about 70%, and their progression-free survival is about a year and a half. Repotrectinib, the only second-generation TKI, has significantly better efficacy, about 79% response rate and double the PFS, so 36 months. But one of the main issues with Repotrectinib has been its tolerability. Because of its CNS toxicity, Repotrectinib has about a 50% discontinuation rate at five months. Taltrectinib or Iptrozi in the most recent data cut that we announced has almost a 90% response rate, but most importantly, the duration of response and PFS are now out to 50 months, so over four years. So that is, you know, that's really just not been seen in this space. In fact, in all of oncology, with any drug in any cancer, there's only one drug with a PFS longer than that, which is Lorlatinib in the ALK space. So, we think that this is a really, really robust profile. And if you look at the tolerability side, if you look at the six most common adverse events associated with Iptrozi, which are elevated AST, ALT, which are liver function tests, followed by nausea, vomiting, diarrhea, and dizziness, the total number of patients who discontinued Iptrozi due to any of those six events was one patient out of 337. So a very, very tolerable profile. If you look at all the clinical adverse events like diarrhea or dizziness or, you know, those. Diarrhea tends to occur within two days and resolve within one day. The dizziness, and it's primarily grade one. If you look at the dizziness, it's, you know, 90% grade one and resolves in about 72 hours. So very transient, clinical AEs. And then the non-clinical AEs like LFT elevation are clinically invisible because they're not symptomatic. So our discontinuation rate, we think, really says it all. And so we're really excited about the efficacy and the safety profile. The reason that profile sets us up well as a commercial company is that there are about 3,000 new ROS1 patients a year in the United States. That's by DNA testing. So we were just to multiply 3,000 times the current drug price, which is about $350,000 a year. That's about a billion dollars of potential revenue every year. And now, because the PFS goes out beyond four years, it means that, you know, that $1 billion of revenue should recur on average through year one, two, three, four into year five, and then starting in year two, you know, going to year six and then and so on and so forth. So that by year four, if we're just talking about DNA testing, we should still equilibrate well over $4 billion a year as the market opportunity. About a year, a little over a year ago, a new RNA test was approved, and that RNA test is about 30% more sensitive for ROS1 fusions than DNA testing. So that should increase the market from 3,000 new patients a year in the U.S. to about 4,000 new patients in the year, you know, a year in the United States. That should take the stacking opportunity to over 5 billion a year. The real question then is, what market share should we have of that market? We point out the example. If you look at Osimertinib, which is the best drug in EGFR and, you know, $6 billion a year drug, Osimertinib's benefit over its nearest competitor, which is Tarceva, is nine months of progression-free survival and eight points of response rate. If you look at Iptrozi's benefit over its nearest competitor, it's now, you know, 10 points of response rate, but more than a year of progression-free survival or duration of response. We think that if you look at Osimertinib's benefits over its competitor, just what they have is enough for them to take 100% market share. They literally own the entire market. In fact, they took a near 100% market share by the third year of launch. We believe that we're positioned to take the vast majority of this market, given the fact that our benefits over ours and the nearest competitor appear to be even greater than Osimertinib over Tarceva. We think that sets up a really good dynamic. There's also additional upside in trying to move testing to more sensitive methods. Not only will RNA detect more ROS1 mutations than DNA, but there's also a movement afoot now to also include liquid biopsies, which make it even more, you know, even easier and more convenient for physicians and patients to get further, you know, diagnoses of, you know, precision oncology mutations. I think that's a general movement in the field of oncology that will, you know, float all boats. So I think that, you know, we think that precision oncology is moving on to a golden age, and we're excited to be part of that. Yeah, no, that's a great point on the testing. You mentioned a more sensitive assay could, you know, result in, you know, more sort of available patients for your therapy. I was just wondering in terms of how many patients even get screened for ROS1 or other mutations. As these tests get better, I would imagine there would be, you know, broader awareness of this, and this could pertain to maybe thousands more patients. Is that how you sort of see it? So one side of it is, you know, a better assay, but the other side of it is just, you know, more patients being tested given there's a recognition of, you know, there's a therapy that could help you substantially. Yeah, I think that's exactly right. I think that if you look at precision oncology, it's still a relatively new field. So, only a few years ago, you know, we didn't even really recognize these mutations, much less have drugs that were so effective against them. But now with EGFR, ALK, RET, and now ROS, there are drugs against those targets that have transformed the practice of medicine for lung cancer patients. I mean, just two decades ago, lung cancer was almost, you know, invariably fatal, quick, you know, short survival diagnosis. And now with, you know, drugs against EGFR, ALK, RET, and now ROS1, lung cancer has suddenly become one of the most treatable cancers on the planet. So I think that that's a very exciting development for patients. Because of that, testing has increased dramatically, but still not where it needs to be. I mean, you know, the practice of medicine always evolves slowly. But I you know, what we can say is that in academic centers, we think NGS testing is virtually 100%. I think the community's behind that, and it's always a little bit slower, but I think that we are seeing changes in NGS testing among community centers. And some of that is assisted by the fact that many of these practices are now consolidated into large aggregated systems so that when you have now a standard of practice for a diagnosis in one practice, now it's spread over multiple practices. So I think that the consolidation of oncology is something that's going to be helpful in increasing NGS testing, but there's still, you know, significantly behind academic centers. So I think there's room for education there. I wanted to just zero in on the early days of the Iptrozi launch. You know, you mentioned the new patient start number. I believe you cited it for the third quarter of this year. So, you know, maybe you can sort of just walk us through what were the key drivers or continue to be the key drivers of this early success and how does it align with your internal expectations? Yeah, so I think that, you know, the problem with the ROS1 market, and I think the reason that it's been perceived as being small is because, you know, as good as Repotrectinib's numbers are with a 79% response rate and 36-month PFS, you just don't, until you get revenue stacked in the market, the opportunity is just not as impressive as you might hope for. And so I think if we look at repo sales for its first year, it was, you know, in the $30 million range or so. And it's because the patients just couldn't tolerate the drug and came off it after five months, and you just don't get any stacking. I think that, you know, if you look at patient starts in Bristol Myers' first quarter of repo sales, it was 34 patient starts. Our first full quarter was 204 patient starts. So that's six times the Repotrectinib sales in their first full quarter. So I think that already tells you something about the difference in, in the two drugs. And just from what we've seen so far, we believe, and with our numbers, we think that these patients will stay on drug for a very long time. First-line patients should stay on, on average for more than four years. We think that's, that sets up a really attractive commercial dynamic. And I, I think that, you know, we expect that to continue. And we, we just don't see, you know, justification at this point for using anything other than Iptrozi. If you look at a Crizotinib, this doesn't even get into the brain. ROS1 lung cancer is a cancer that starts 36% of the time in the brain and then another 50% progresses in the brain. We don't think there's any justification for using Crizotinib because it's just a, you know, you're rolling the dice and just a matter of time before you will get a brain met. Entrectinib, you know, with a 16-month PFS, pretty hard to justify why we picked that over a 50-month drug. And then Repotrectinib, you know, 36 months is good, is a good PFS, but tolerability has been an issue. We think that Iptrozi is sort of a no-brainer option for physicians and patients. And we would expect us to take, as I said, the vast majority market share. I think you've mentioned 80% payer coverage, you know, confirmed in the early months of the launch. So, I imagine that sort of speaks to the clinical superiority that you've been able to show with the drug. But sort of as we go from here in terms of reimbursement and payer, and you mentioned the $300,000, you know, price, how should investors be thinking about the reimbursement landscape as well as, you know, in terms of gross to net or pricing as it goes forward? So the one thing to remember is that patients with ROS1 are not the average lung cancer patient. They're about 20 years younger on average. So these are, you know, patients. The median age is 50. So it's very hard to deny coverage for a 50-year-old patient. I mean, some of our patients are in their 30s, and so it's very hard to deny coverage where, you know, the previous standard of care, which was IO chemo, would give you six to 12 months of progression-free survival. And now we're offering 50 months. I think that's going to be very hard to deny. So we think that we expect, you know, coverage to only increase. And because the market is still only, you know, a few thousand patients a year, you know, we're not talking about, you know, hundreds of thousands or millions of patients that they'll have to cover. But we think that it's important that patients have access to this drug because its response rate and duration of response are among the highest ever seen with any oncology drug in any oncology indication. So we think that it's easily justifiable. And to David's point and what you said, right, we said in our last quarter, we already had 80% coverage. But I think what's even more important is that it's coverage to label. So there, to David's point, there is really no doubt in our minds that this is the right drug for patients, that each patient should have access to this drug, and 80% coverage is to label. We had a pricing strategy when we launched that was to price slightly lower than Repotrectinib, the previous drug in the space, because repo is still at 30% of lives we set it at. And, of course, this is something you can fight when you have a better drug, but this is still red tape and it's not the right thing for patients. So we were a little bit, you know, lower than that, about 5%, a bit more than that. So not very meaningful, but 80% to label. And we think it's going to only increase after just a few weeks. We had like six weeks, seven weeks behind us. We were already at 56% at the end of the first full quarter. We were at 80% coverage. And we think it's going to increase. And that's the right thing to do. You know, the drug's been included, I believe now in the NCCN guidelines for next year as a preferred therapy. So I guess the question is, you know, what impact do you anticipate this will have on adoption and market positioning beyond already what's been, you know, as you've detailed, a pretty impressive first quarter of launch? So the NCCN guidelines were actually changed on January 7th of this year. So we are now considered a preferred agent. But, you know, there is actually currently no distinction between the different ROS1 agents. But the reason that the guideline changes are helpful is because, prior to this year, NCCN guidelines actually suggested two treatment options. One is, you know, finishing out IO chemo and/or selecting a ROS1 agent. And as of 2025, now that first option not only has been eliminated, but it's actually contraindicated. So now the guidelines say that IO is contraindicated in ROS1 disease. If you're on it, you need to stop it and you need to switch to a ROS1 agent. So that's clearly going to be helpful. I think the next step for us is that we believe that the guidelines need to be amended further because, as I mentioned, for a disease that starts 36% of the time in the brain, you just shouldn't have an option that's a brain, non-brain penetrant drug. We don't think Crizotinib should be an option. You know, these are things we're going to try to influence on NCCN to get them to change those guidelines. We think it's important that patients have a drug that covers the brain immediately because once you have a brain met, you know, even great drugs like Iptrozi are still going to have, if you look at our DOR after a brain met, it's not nearly as good as before a brain met. You always want to treat cancer as early as you can. I think that giving a non-brain penetrant drug for a disease that starts in the brain so often is just rolling the dice unnecessarily. We don't think that's the right thing for patients. You have an ongoing adjuvant study in early-stage ROS1 lung cancer. Maybe just walk us through the purpose of this study, and what are the timelines there and the market expansion opportunities that could be, you know, gleaned from a successful readout. Right. Right. So we've just started an adjuvant study. So this is, you know, very early, the earliest, you know, right after, you know, you have a post-surgery, lung mass resection. And we are the only company doing an adjuvant study. And I think that speaks to a couple of things. Number one, to be given that early in the disease, you need a drug that's very tolerable. And the fact that, you know, we had so much KOL support for our drug in the adjuvant setting, in this adjuvant setting, you know, it speaks to the tolerability profile of our drug. And so I think that's exciting. The second thing is that moving upstream also increases the market opportunity by probably about 30%. So if you look at what happened to Osimertinib sales when they got their adjuvant study done, and they, you know, they just, they became dominant. And as I said, they're a $6 billion a year drug today. They have, you know, they have coverage from adjuvant onward. So, you know, we're the only ROS1 drug in the adjuvant study right now, in the adjuvant study being studied. And we think that's going to position us really well for the future and expand our commercial opportunity beyond what's already substantial from what I outlined earlier. Maybe just switching gears to the pipeline. Safusidenib is a drug that you mentioned, IDH1 mutant glioma. Can you maybe just provide details a little bit on the clinical strategy here, including timelines and sort of what you're looking for and maybe, you know, you do have a product approved in this setting, with the same target. So, the commercial opportunity, as it stands. So yeah, the only IDH1 drug approved is called Vorasidenib. And they're only approved in part of low-grade glioma. So they're approved in low-grade gliomas without high-risk features. So these are called non-enhancing gliomas. And in spite of that only being a fraction of the glioma market, if you look at Royalty Pharma's royalties from which you can impute Servier sales, Vorasidenib is on track to do $1 billion of sales in its first 12 months, which has got to be one of the most robust launches ever for any biotech drug. As I mentioned earlier, Vorasidenib was approved based on an 11% response rate in low-grade glioma. And at two years had 41% patients progress. Our low-grade data that we just announced and published today, in fact, show a 44% response rate in low-grade glioma, the identical population as Vorasidenib, but at two years, only 12% progression instead of 41%. So we believe those are really extremely strong data. In high-grade glioma, Vorasidenib's response rate is zero. So that's why Vorasidenib was not approved in high-grade and they're not developing it there. Our response rate in high-grade glioma was not only 17%, but more notably, a third of those responses were complete responses, which in oncology means the tumor has disappeared. And note, particularly notably, of the tumors that have disappeared, one was really high-grade tumor called glioblastoma, which is the most aggressive of all brain tumors. And that tumor has been gone for about three and a half years so far. We have a second high-grade oligodendroglioma that's been gone for about two years. Again, data that just are not seen, especially with an oral oncolytic. So we are, our strategy now is to try to get approval in both high-grade glioma and at least a subset of low-grade glioma that Vorasidenib is not approved in. So our high-grade study is enrolling high-grade patients, because there is no coverage for high-grade in Vora's label. But in low-grade glioma, we're actually enrolling low-grade patients with high-risk features, which include contrast enhancement, so that is not covered by Vora's label. And we believe that if we show a you know robust response in high-grade as well as high-risk low-grade patients, we believe that will set us up for compendia listing. We believe that, you know, that will make us, you know, a very, very attractive treatment option for patients and physicians. You highlighted what you've seen so far in the clinic from an efficacy perspective versus, you know, the only other approved option in the low-grade setting. How about tolerability? I mean, you spoke of the tolerability benefit versus competitors for Iptrozi. How is it stacking up so far and what have you seen in early studies? So our tolerability profiles is even more interesting because if you look at all our adverse events, in fact, if you look at our top eight adverse events, almost all of them are grade one or grade two, extremely few grade three events. But of the top eight, five of them are immune type side effects. If you look at Vorasidenib's adverse events, their primary AEs are LFT elevation, but no immune side effects. And the reason that we find the immune side effects so interesting is that the way IDH1 works is that it's not only an oncogene that drives tumor growth, but mutant IDH1 actually plays a role in immune suppression. So that if you inhibit it sufficiently, you actually reverse immune suppression, you get immune augmentation. We're not only seeing, you know, tumor suppression with this drug, but the fact that we're seeing these adverse events that suggest immune activation. We've actually seen that in preclinical models with Safusidenib. We're seeing, unlike Vorasidenib, we're seeing far more activation of immunity in our xenograft models that result in reduced mortality of these animals than we are seeing with Vorasidenib. We actually believe that Vorasidenib, as good as our data are, you know, don't show the same mechanistic profile as we've seen with Safusidenib. We believe that may play a role in why we're seeing four times their response rate in low-grade glioma and why we've seen high-grade responses and they haven't. If you look at our responses, you know, we don't, they take about six to 12 months to kick in, which is just like an IO agent. That's what you see in immuno-oncology. And when you do get these responses, they're durable. As I said, we have a GBM that's been gone for three years, three and a half years. Again, that kind of long durability, that really long tail is something you see in IO. So we think that potentially Safusidenib could be a new generation of IO agent. And we think that our data right now are just hands down better than what we've seen with Vorasidenib. And therefore, we think our adverse events could potentially reflect part of the reason why we believe our efficacy is better. And we're actually excited about the tolerability profile from what we're seeing. You know, how can you size up for us the market opportunity here, within this indication? You mentioned Vorasidenib has been off to a very impressive start in low-grade. How should we be thinking about the size of this market from a patient count perspective and maybe low-grade versus also the high-grade opportunity that I know you guys are going after as well? Right. So the glioma market is divided into high-grade and low-grade, and they're split almost exactly 50/50. So low-grade glioma is half the market, high-grade is half the market. But within low-grade, probably the majority are still non-enhancing, but a significant number are enhancing. So Vorasidenib has the majority of half of the market, and they're still doing $1 billion a year in sales, and part of the reason that glioma market is so commercially attractive is that if you look at the survival of low-grade glioma, we're talking about 10 to 15 plus years on average. So you're talking about potential revenue stacking that could go on for a decade or more. If you look at a high-grade glioma, even those patients live for five to seven years. So you're still talking about, you know, very, very lengthy durations of therapy potentially. When we look at our low-grade glioma data that we just announced, we had 12% progression at two years. Now, if that were linear, we could expect about 50% progression at maybe eight plus years, well, that would be really long. That already would be twice the Iptrozi DOR, so again, that could set us up for revenue stacking that would even dwarf what we see with Iptrozi. So we think that given the fact that high-grade is half the market, we, if this trial is positive, we should get that. We're also going to capture part of the low-grade market, you know, there's still a significant number of patients who are high-risk features. We believe that if we can really demonstrate efficacy in high-grade and the more difficult to treat low-grades, we believe that there's, you know, that patients and doctors will probably pick what they believe to be the more efficacious compound. We think this is a really, really large market that will have very long durations of treatment. We think this commercial opportunity would be probably one of the largest commercial opportunities in oncology. I think Vorasidenib is already showing us that. And just maybe lastly on this program, in terms of the catalyst path here timelines, and when you could see yourself on the market and also, you know, as you approach the FDA, what the regulatory strategy is going to be versus, you know, with low-grade versus high-grade. I know the data would probably dictate, you know, that strategy as well, but how you're thinking about it today. Yeah, we started off. Vorasidenib was approved on a progression-free survival endpoint. The FDA did not accept overall response rate as an endpoint. They applied the same to us. You know, we actually had discussed with the FDA the possibility of an overall response rate endpoint, and they declined to accept that. They wanted a progression-free survival endpoint. Just like Vorasidenib, we are doing the same study, except in high-grade patients and high-risk low-grade gliomas. That will be a PFS study, and that will read out no later than 2029. Now, that said, the field of glioma is changing significantly in the assessment of glioma, which is by scans. You know, as you know, brain tumor imaging has really changed over the years, you know, from RECIST criteria to RANO criteria to now RANO 2.0 criteria, from 2D imaging now to 3D imaging. I think that part of the reluctance to accept the response rate endpoint has been the fact that depending on how you do your imaging, especially if it's 2D and you have you're not off on the same coordinates, you could interpret a misalignment of your you know your magnet focus as a change in tumor size when it really is an artifact. So I think as imaging becomes more standardized and more robust, response rate should be something that hopefully will reflect what's really happening in the tumor. Given the fact that there's absolutely nothing for high-grade patients, we would love to be able to revisit that with the FDA and see whether or not at some point with improved imaging and more standardization, whether or not they would reconsider response rate for high-grade gliomas, where there's nothing or even high-risk low-grade gliomas. We, you know, we haven't. We're not going to stop trying to do that. We're still going to run our PFS study, but we're still going to, once we get more data, re-examine with the FDA now with the new imaging techniques and whether or not we can convince them to that, response rate is still something now that should be, you know, a reasonable endpoint to consider for a disease where there is no treatment option and is otherwise invariably fatal. So we think that, you know, there's still this is still a changing field and we hope to continue to, you know, try to make inroads on that front. I just wanted to touch on outside of Iptrozi and Safusidenib, you are working on other things in the early stage pipeline, so maybe just give it a little bit of an overview of some of the other pipeline programs and technology work that you have going on. Yeah. So we have a drug-drug conjugate program. It's just kind of like an ADC without the A. So these are two small molecules and the data we've generated with that program, both preclinically and even clinically have been, you know, very interesting to us. So our first molecule NUV-1511, we took into the clinic in five indications where nothing works, you know, post-ADCs in breast cancer, platinum-resistant ovarian, Xtandi-resistant prostate, pancreatic cancer where nothing really works. We did see some very interesting clinical signals. But we also learned a lot while we were in the clinic. You know, no matter what you learn in animal studies, it's just not the same as being in humans. When we got into our clinical trial, we did learn things and we believe that there are ways to make that molecule even better. And before we, you know, take it into a pivotal study and spend $100 million or more on it, we wanted to make sure we took forward a molecule that we could address any potential liabilities before we made such a large investment. And I think we learned enough in the phase one study that we believe that there are improvements we can make to make the molecule with more consistent effects that we want to see. And so we remain completely committed to the DDC program. What we've seen with it, we think are really intriguing results that haven't been seen before with small molecules. And we believe that's still a really attractive program. We just have learned more and now we're going to be, you know, taking a little bit of a different tack within that same platform. Here's the last question. We have a few minutes left. In terms of the financial position of the company, strategic outlook, you know, you finished the third quarter with pretty robust, you know. Yeah, we finished it with $550 million roughly. So we've always guided that it will be enough to take us to profitability. As you might remember, we did a non-dilutive financing run back in March, with a $150 million synthetic royalty on taletrectinib in the U.S. for only 5%. So right there, $3 billion value for taletrectinib. And there was also a debt component on which we took only $50 million, so total $200 million. And we had said that even before that financing, we thought we had enough to get to profitability. So this additional firepower could be deployed for, you know, other programs, R and D and things of that nature. Yeah, very strong cash position. The other point, the other point we make is that with 204 new patient starts last quarter, even if we never had another patient growth and we just did that for the next three quarters, and if 100% of them were second line patients, so only treating them for a year, that's still $220 million a year. You know, with, with no growth and only second line, that's still 220. That should be the lower end if that's what we accomplished. We certainly hope to grow more than that. We certainly have, you know, we know we're, we're already getting some first line patients. I just think that if you look at, you know, what we are already, we think that, you know, we are well on our track to profitability. As Philippe said, we have a pretty reasonable buffer. Great. Well, thanks guys. Appreciate you joining us. Thank you so much. Thank you so much.