Good morning, and welcome to Curis's Q4 2023 business update call. All participants will be in listen-only mode. Should you need assistance, please signal a conference specialist by pressing the star key followed by zero. After the company's prepared remarks, call participants will have an opportunity to ask questions. To ask a question, you may press star then one on your touchtone phone. To withdraw your question, please press star then two. Please note, this event is being recorded. I would now like to turn the conference over to Diantha Duvall, Curis's Chief Financial Officer. Diantha, please go ahead. Thank you, and welcome to Curis's Q4 2023 business update call. Before we begin, I would like to encourage everyone to go to our investor section of our website at www.curis.com to find our Q4 2023 business update release and related financial tables. I would also like to remind everyone that during the call, we will be making forward-looking statements, which are based on our current expectations and beliefs. These statements are subject to certain risks and uncertainties, and actual results may differ materially. For additional details, please see our SEC filings. Joining me on today's call are Jim Dentzer, President and Chief Executive Officer, and Jonathan Zung, Chief Development Officer. We will also be available for a question and answer period at the end of our call. I'd now like to turn the call over to Jim. Jim? Thank you. Thank you, Diantha. Good morning, everyone, and welcome to Curis's Q4 business update call. I'd like to start today's call with a look back over the past 12 months. Entering 2023, the whole biotech industry was struggling in the headwinds of a grim financial market. Curis faced all of that and the daunting challenge of seeing our leukemia study stalled on partial clinical hold with the FDA. In the face of that adversity, the Curis team rose to the challenge. We worked tirelessly in answering questions posed by the FDA. This included enrolling additional patients at 200 milligrams BID and performing additional analyses. As a result, we were able to confirm the safety profile of emavusertib, gain alignment on the optimal dosing regimen for monotherapy, and secure the removal of the partial clinical hold a full quarter earlier than expected. We then redirected our energy to reopening clinical sites and enrolling new patients. In our monotherapy study, we are targeting a genetically defined population of relapsed refractory AML patients with a FLT3 or spliceosome mutation. Enrollment is going quite well, and we expect to have a data update by midyear. While that study advances, we have initiated a frontline study of emavusertib in combination with azacitidine and venetoclax for all AML patients, regardless of their mutation status. This study is being conducted at sites in Spain, Germany, and Italy, and we expect preliminary data from this study in the second half of this year. All in all, a terrific year of progress in leukemia. Now let's turn to our lymphoma program, which is generating an equally high level of interest. After reviewing initial data collected across multiple NHL subtypes, we focused our efforts on the ultra-orphan indication of primary CNS lymphoma, or PCNSL, where we are evaluating emavusertib in combination with ibrutinib. We identified key sites, initiated enrollment, and in December, we released new clinical data in relapsed refractory PCNSL at the ASH conference in San Diego. The meetings we had with physicians at ASH were terrific, and we were especially pleased to have Dr. Grzegorz Nowakowski and Dr. Han Tun from the Mayo Clinic present the data. As a reminder, frontline treatment in PCNSL is high-dose methotrexate and chemo. When that no longer works, there is no approved second-line treatment. In our study, three of five patients were able to achieve complete remission of their disease. It is admittedly a small number of patients. However, the response and interest from the clinical community was very encouraging. In the 8 weeks since ASH, our team has been fielding calls from clinical sites across the U.S. and Europe wanting to participate in our trials. In fact, by the end of Q1, we expect to have doubled the number of clinical sites versus where we were a year ago. Obviously, this is a reflection of the excitement about emavusertib, but it is also a reflection of the indefatigable efforts of the Curis team. I couldn't be more proud of them. Finally, in December, we announced that we entered into an agreement for an investigator-initiated trial to study the combination of emavusertib and pembrolizumab in patients with metastatic melanoma. We're excited that this study presents an opportunity to expand upon the research done at academic centers and the NCI to explore the potential of emavusertib in solid tumors. In short, we had an incredibly productive 2023, and we look forward to continuing that momentum in 2024.... With that, I'll turn the call back over to Diantha to review our financial results for the quarter. Diantha? Thank you, Jim. For the Q4 of 2023, Curis reported a net loss of $11.7 million, or $2.03 per share, as compared to a net loss of $11.3 million, or $2.35 per share, for the same period in 2022. Curis reported a net loss of $47.4 million, or $8.96 per share, for the twelve months ended December 31, 2023, as compared to a net loss of $56.7 million, or $12.14 per share, for the same period in 2022. Revenues net for the Q4 of 2023 were $2.7 million, compared to $2.9 million for the same period in 2022. Net revenues for the 12 months ended December 31, 2023, were $10 million, compared to $10.2 million in 2022. Research and development expenses were $10 million for the Q4 of 2023, compared to $8.7 million in 2022. The increase in R&D was driven by higher clinical development costs. R&D was $39.5 million for the 12 months ended December 31, 2023, compared to $43 million in 2022. General and administrative expenses were $4.9 million for the Q4 of 2023, compared to $4.3 million in 2022. The increase in G&A was driven primarily by higher professional, legal, and consulting services. G&A was $18.6 million for the 12 months ended December 31, 2023, compared to $19.6 million in 2022. Other income net was $0.5 million for the Q4 of 2023, compared to other expense net of $1.1 million in 2022. Other income net was $0.9 million for the 12 months ended December 31, 2023, compared to other expense net of $3.7 million in 2022. Other income expense net consists of interest income and non-cash expense related to the sale of future royalties. As of December 31, 2023, Curis's cash, cash equivalents and investments totaled $56.3 million, and there were approximately 5.9 million shares of common stock outstanding. We continue to be in a solid cash position and expect that our existing cash, cash equivalents, and investments will enable our planned operations into 2025. With that, I'd like to open the call for questions. Operator? We will now begin the question and answer session. To ask a question, you may press Star, then one on your telephone keypad. If you are using a speakerphone, please pick up your handset before pressing the keys. To withdraw your question, please press Star then two. At this time, we will pause momentarily to assemble the roster. Our first question will come from Ed White of H.C. Wainwright. Please go ahead. Good morning. Thanks for taking my questions. Jim, you mentioned that, in the primary CNS lymphoma trial, you have double the clinical sites open versus this time last year. I'm just wondering if you can let us know how many sites that is and how many sites you plan to open. Yeah, we try to get out of the details of the number of sites that we have in any given time, because, of course, we're always increasing them. But I think the reason why we mentioned that this call is because it's a reflection of the kind of conference we had. Obviously, we were very encouraged by the data ourselves. And if you were at ASH, you saw that our booth was incredibly busy. But that's been followed up by being able to get these new sites up and running and online, and we've got, as I said, not the expectation to double by the end of Q1, but enthusiasm more broadly across the world, not just in the US. So it's really exciting from our perspective, and I'm hopeful that we can keep that momentum going forward. Hey, can you give us your thoughts on the size of that primary CNS lymphoma market? Sure. It's an ultra-orphan market. It's one of the reasons why we selected it. So if you think across the landscape of non-Hodgkin's lymphoma, and everywhere where BTK gets used, of course, we have been targeting broadly. Anytime you use BTK, you're downregulating NF-κB from one pathway. There are a lot of BTK inhibitors targeting that path. We're the only one that targets the other path. When we look across the landscape of non-Hodgkin's lymphoma, we focused in on primary CNS first because it's so small, incidence of 5 per million. That yields a lot of very attractive benefits from a development perspective, especially in conversations with regulatory authorities. But also, within primary CNS lymphoma, it's a fairly aggressive lymphoma where we can, we believe, we can address the disease quickly. As you saw in the data, the 3 of 5 complete responses, we got a view of that in the first 3 months on treatment. So that's very helpful. And of course, there are no effective treatments. There are no approved drugs for relapsed refractory PCNSL. So if we can go after a disease that is ultra-orphan, where there are no approved treatments and we can see this kind of response from the drug, it's really encouraging. Okay, thanks, Jim. Sure. Now, if I could just ask a big picture question. I wanted to get your thoughts on the potential in solid tumors. You had mentioned the IST beginning with in combination with Keytruda in metastatic melanoma. I just wanted to get your thoughts on that market and large in solid tumors overall. Yeah. So solid tumors is really exciting. We have been, of course, from the very beginning, in identifying this target. One of the things that was so exciting was that the role of IRAK4 in oncology, more broadly, was something that Curis had discovered and no one else knew about. So when we were designing the molecule originally, we had the Pharmacyclics template in mind of how do you go after a blockbuster indication, or an indication with multibillion-dollar revenue potential when no one else knows about it yet? And we designed that molecule so that it would be effective in lymphoma, but also would confer some competitive advantage in leukemia and in solid tumors. As you know, our first studies started in lymphoma, and that's of course, where our most recent data are as well, and that's really compelling. The data in lymphoma in the targeted populations that we would expect to hit in the IRAK4 or spliceosome population and the FLT3 population, those data look really compelling. We've just started the frontline study, and then to your point in melanoma, this is the first time we've gone into solid tumors. Now, there's been a lot of work done by the NCI and by academic centers studying emavusertib in various types of solid tumors. So, we know there's a lot of interesting work going on, for example, in bladder cancer, in gastroesophageal cancer, in ovarian, in lung, in pancreatic. There are a number of different solid tumors where it looks like IRAK4 plays a significant role in where our drug might be able to confer benefit. This is the first time we're going into that. I think it's a little premature to talk about how large all of those markets are, but the idea that we have a drug that looks as though it could provide incremental benefit that no other drug does in these very targeted markets, individually, and of course, at the high level across the world of human solid tumors, is, is really quite exciting. Thanks, Jim. And a last question- Sure. If I could. Just wanted to get your thoughts on partnering the product in solid tumors. Is that something that you'd be looking at, or is this something, as you expand into solid tumors, that you think you could fund on your own going down the road? Sure. So, yeah, I mean, take the melanoma study as a case in point. Obviously, that's a study we would rather not pay for. There are a lot of trials, gosh, maybe 1,000? There are a lot of clinical trials going on right now of a company's drug in combination with Pembro, Merck's PD-1, which is most people consider it the leading PD-1. But the way most of those work is they beg Merck to give them free drug, and then they run the study. We have the opposite. We're gonna get data from this study, and we're the one providing free drug. Merck's the one picking up the tab for the study. So, obviously, what you know, what most companies would hope for is just getting free drug. Ideally, if we're gonna expand the number of clinical studies that we can run, whether it's in lymphoma or in leukemia or now in solid tumors, at the minimum, we'd like to get a 50/50 study. I think it's overly optimistic that we're gonna be able to find all of our future studies are 100% funded by the partner without giving up any rights. But at this point in time, obviously, we're really excited that we're gonna have the opportunity to get data across lymphoma, leukemia, and now solid tumors, and we can afford to do it. So as long as we can afford to keep our rights and generate the data that show that this drug has such significant potential, I think that's our plan. Okay, great. Thanks for taking my questions. You bet. The next question comes from Soumit Roy of Jones Trading. Please go ahead. Good morning, everyone, and congratulations on all the progress on multiple fronts. One question on the frontline, the triple combo with emavusertib, HMA, and venetoclax. You're starting... You mentioned three different countries in Europe. Are you planning on initiating some U.S. trial sites also? The second is- Go ahead. PCNSL trials. Is that in combination with ibrutinib, or still you are planning to do monotherapy emavusertib patients? Okay, so the first one first. So the initial study for the triplet, we're really targeting some sites where we think we can get data relatively quickly. Because we want it in these early stages, the most important thing is to generate the data as quickly as we can and prove that the triplet works. We've got a lot of preclinical data that suggests that IRAK4 is the primary driver of disease in half of all AML patients. There's a published article, as you know, the Smith- Choudhary article that was published in Nature in 2019, pointed that out. Half of all patients, this is the number one driver of disease. In the other half of patients, it's not the number one driver of disease, but it's a secondary or tertiary driver. So really, this, this should provide incremental benefit from a new mechanism that no other drug does. So the long term, to capture as many patients as we can, is to, of course, go front line in combination with standard of care. That's azacitidine and venetoclax. So our hope would be, that we can recapitulate in humans what we found in the lab, and that is whether you add emavusertib to AZA or to VEN or the AZA/VEN combo, this significantly increases the efficacy of that standard of care treatment. So that's what we found in the lab, and again, that's what we want to try and identify very quickly, if possible in the clinic. And of course, we always want to, check for safety. AZA and VEN, as you know, are a pretty tough regimen to tolerate. They're effective, but they're, they're pretty tough to tolerate. Anecdotally, half of all patients that go on that AZA/VEN doublet have to discontinue treatment. So what we're going to be doing in the early days is putting patients on and confirming that there is no safety overlap, as we expect. And then second, of course, we're going to be looking for that, that efficacy signal. And if you want to do that kind of exploration quickly, it, it really helps to identify the sites that you can focus on in a very concentrated way, and those are the sites we've chosen to, to initiate that study. Your second question, could you remind me? So, yeah, that's totally understandable. So on the PCNSL trial, so are you expecting to get frontline patients? Yes. Or not to get to that, you want to combine with or ibrutinib? Yeah. What's the plan? No, thank you. Thank you for that. So, right now, the combination is emavusertib and ibrutinib, and it's in relapsed refractory patients. And that's the initial starting point. And again, the rationale for first, the combination of ema and ibrutinib, that one's clear. In the case of lymphoma, the problem driving disease for patients with NHL is NF-κB overactivity. So when NF-κB is overactive, what happens is it disrupts the apoptotic process of the malignant cells. So if you're on a BTK inhibitor today, the reason you're on that BTK inhibitor is that it blocks the BCR pathway, which is one of two pathways driving NF-κB overactivity. We now know that that's effective. You get a pretty high response rate on BTK inhibitors, and in fact, as you know, it's a $10-$15 billion market today. Ibrutinib itself is $10 billion of that, the AbbVie, J&J drug. What we're looking to do in lymphoma is hit NF-κB as hard as we can. There are now 5 big pharma companies that are chasing after BTK inhibitors of various flavors, covalent or non-covalent, all of them working effectively the same way, all of them blocking that BCR pathway, driving NF-κB. The second pathway, the toll-like receptor pathway, is currently unaddressed. Curis is the only company that has a drug that blocks that path. That's emavusertib. It binds to MYD88 myddosome, and without that binding, in the absence of IRAK4, the myddosome and the toll-like receptor path more broadly shut down. So it stands to reason when you step back, if you have lymphoma that's effectively treated by BTK, you'll always want to block the NF-κB or downregulate NF-κB as strongly as you can. So hit the BCR path with BTK, hit the toll-like receptor path with IRAK4. The combination, not monotherapy, the combination should always be better than either one alone. And that's what we found in the lab, and of course, that's what we're finding so far in the clinic. So that's the logic for the combination with emavusertib. In terms of going to frontline, eventually, of course, you know, we would like to suggest that the long-term possibility that we're going to explore is this an opportunity to have a companion frontline standard of care with BTK across non-Hodgkin's lymphoma. Now, it's a little premature for that. We've chosen primary CNS lymphoma as our proof of concept, indication to prove it out, and, and we've been able to show that we can generate data pretty quickly. But long term, I think, of course, we're going to want to go frontline in combination with BTK inhibitors. For now, having an ultra-orphan indication where we can go into the relapsed refractory setting where there are no drugs approved, that should offer a pretty compelling regulatory opportunity. So that's why we're going down that path. Great. That was a pretty long answer. I hope it was helpful. No, you got it. Okay. Speaking of companion, since you're moving into the solid tumor, I'm curious if you're going to push forward the companion diagnostic for IRAK4 mutation assay, and if that would be helpful in kind of a carving the market both for inside the solid tumor space and also eventually in the leukemia setting. Yeah. So the short answer is yes. The long answer is it's a little more complicated. So in the short answer, are we pursuing the identification and the regulatory path for a companion diagnostic for IRAK4 expression? The answer is yes, absolutely. In the more complicated answer is we don't want that to slow down our path to development in making this drug available for patients. So the way we're ensuring that fastest path is in monotherapy, in the leukemia side, where we're looking to go into patients that have either a FLT3 mutation or an IRAK4 overexpression. We're gonna focus the IRAK4 population using spliceosome mutations. Now, spliceosome mutations are a subset of patients that overexpress IRAK4. The reason why you'd go after spliceosome mutations is those mutations are already identified in existing gene panels. So a companion diagnostic is much easier. We don't need to have a new assay identifying IRAK4. We can just lean into the existing panels, the Illumina panel, the FoundationOne panel, places like MD Anderson that have a proprietary gene panel. These panels are already run on their existing patients, and we can lean into that and say, "If you have one of these specific mutations, by definition, you have IRAK4 expression," and use that as our mechanism, but longer term, of course, we're gonna want a diagnostic. Separately- Thank you again. It's the logic for going frontline in combination. We're gonna go all comers, where we won't need a companion diagnostic. Thank you again for taking all the questions, and congrats- Sure. Sure. Thank you. The next question comes from Li Watsek of Cantor Fitzgerald. Please go ahead. Hey, good morning. Thanks for taking our questions. Jim, I guess for the data that you're going to present from the leukemia study around midyear, maybe just, you know, set the expectations for us a little bit, what data set that we are going to see, what the bar is for FLT3, as well as for spliceosome mutations. And then for the combo data that's gonna come second half of this year, maybe tell us a little bit about the bar here, because, you know, AZA-VEN, as we know, the bar is fairly high. It's pretty effective. And also, as you alluded to earlier, about, you know, toxicities, I mean, do you expect any overlapping tox with this regimen? Yeah. Thank you, Lee. Appreciate you dialing in. So on those questions, first, in terms of the number of patients, you know, we've consistently said what we'd like to have is a data set of 10-20 patients, where, you know, we now have a data set of 3 patients in spliceosome, 3 patients in FLT3 at our target dose, and 5 patients, of course, in primary CNS. We'd like to increase that data set to an n equals 20-50, somewhere in that range. I hope that we're gonna be in a position where we've got data collected. Of course, you enroll the patients, treat them, follow them for a period of time, and then assess the responses. My hope is that we'll be in a position to have that level of n, that level of data, in leukemia, spliceosome, and FLT3 by midyear, and in lymphoma, by year-end. In terms of the benchmark, what we think we need to do to be, effective in the monotherapy side is we're targeting a CR/CRh of 20%, lower bound in the, in the low teens, a 12, 13% kind of lower bound. But a, a 20% CR/CRh rate in, salvage line therapy for either FLT3 or spliceosome in leukemia, we think is, is very compelling. Of course, our first 3 patients look better than that, but, you know, let's not get ahead of ourselves. It's only 3 patients. As we get to 10-20 patients, what we'd really hope is that we can clear that CR/CRh rate of 20% and be compelling. On the lymphoma side, because there are no existing treatments, that bar is probably lower. What we do know is that the largest data set available for BTK as a monotherapy in primary CNS lymphoma was a study of 52 patients. The CR rate was 19. So you'd expect, you know, 1 out of 5 patients or again, roughly a 20% CR rate in that population, and that's in BTK-naive patients. Once they've failed BTK, you'd expect that rechallenging them with BTK yet again probably wouldn't work at all. You might expect 0 out of 5. That we're getting 3 out of 5 so far is obviously highly encouraging. I don't think we need to maintain quite that rate, but if we can maintain in BTK-experienced patients a 20% or higher CR rate in lymphoma, I think that we've got a very compelling data set to have a discussion with FDA. So 10 to 15, I'm sorry, 10-20 patients in all indications is what we're hoping for. We look to be in a position to have data in that range for leukemia by midyear and for lymphoma by year-end. Is that helpful? Overlapping toxicities with AZA-ven? Oh, yes. Yeah, yeah. So that's the number one thing to look for in the triplet. Of course, it makes sense that if you looked at our preclinical data, and we've got a really nice outline of the preclinical data in our corporate deck, it's very clear that from an efficacy perspective, in the lab, we were able to add efficacy to AZA to AZA-VEN. And it looks like if the consistency that we saw from mechanism to lab to clinic works the same way in the leukemia triplet that it's worked everywhere else we've tested, we would expect to see that. The part that I’d say really merits some exploration is making sure, knowing that the tox is high in AZA-VEN, that we don't add to it. We don't have any reason to believe that it would be that adding emavusertib would make it less tolerable. Based on what we know, there is no overlapping safety profile. However, as we said, half of all patients that go on to AZA/VEN have difficulty tolerating it. First thing we're gonna look for as we add our drugs to AZA/VEN is to make sure we're not exacerbating those toxicities. Okay, got it. Of course, efficacy, you always look for. But, you know, first things first. Let's make sure that we've got a drug that's tolerable in combination. What are your thoughts on the maintenance setting in AML? Are you collecting any data points that could potentially maybe support off-label use? Well, obviously off-label we use is something that happens, but companies don't target that. What we do look for is, do we have a drug that first and foremost is safe? Second, has a compelling and unique efficacy profile so that we can provide a measure of efficacy that you can't get from other drugs. And then third, to your point, you wanna make sure you've got a drug that can be taken chronically for long periods of time. You know, some of the indications we're going after, like AML, are fairly aggressive, but others, like Waldenström's, are quite indolent. We have a patient that's been on drug for, I believe, over four years now. So we've got a great track record. These are still early days of drug development for emavusertib, but I think so far we've been able to check all three boxes. The drug looks in almost 200 patients tested to have a really good safety profile. It looks as though it does provide in humans the same kind of clinical efficacy that we were seeing in the lab. And it looks as though you can take this drug over a long period of time in a maintenance setting. And that's, of course, the trifecta that you hope for as a drug developer. Thank you. Yep. Next question comes from Yale Jen of Laidlaw & Company. Please go ahead. Good morning, and thanks for taking the question. Jim, you have talked about that, you will be interested to move to MDS, a high-risk MDS as second line, but you're waiting for the VORONAH study readout. Just to your best knowledge, when you think that might happen, and what, and if that, if that takes place, sometime in the future, and what is... what's your plan at this point? Yeah. Thank you, Yale. Appreciate the question. So you're exactly right, and the opportunity in MDS looks terrific. The clinical data that we've put out so far looks as though in MDS, just as it did in AML and just as it has in lymphoma, it appears as though this drug, as a single agent, is active. It provides unique and compelling anticancer activity. We would really like to do in MDS what we're doing in leukemia, which is go front line in combination with standard of care and see whether or not we can provide benefit. Can this really add to the effectiveness of standard of care? Well, in AML, we know what the standard of care is. It's AZA/VEN. I think MDS development has just gone a little slower with AZA/VEN. A lot of people were expecting it might have read out this past ASH. Now people are looking for ASCO. To be frank, we don't know any more than you do of when those are gonna read out, but we, but we do expect it's imminent. And the answer is: standard of care in MDS is going to be, either AZA or the AZA/VEN doublet. If VORONAH reads out positively, it's AZA/VEN. If it reads out negatively, it's AZA. And what we wanna know is which of those two wins, if you like, so that we can then initiate a combo, whether it's a doublet or a triplet, to see whether we can add benefit to that population in the front-line setting. So we're eagerly anticipating it as you are, and as soon as we have those results, we'll be looking to initiate a frontline study in combination in MDS as well. Okay, great. That's very helpful. Sure. My, my second question here is that earlier, we thought we were sort of expecting that you guys may conduct a meeting with FDA to talk about the next stage of development after the AML data. Do you anticipate this meeting could happen later, much later this year, or you anticipate this potentially be a 2025 event? So, I really can't speak on behalf of the FDA, how quickly we're gonna have that meeting. We're of course very interested in having it as soon as possible. You know, I think we have the kind of drug that the FDA should likely be as interested in as all of our investigators are, and that is, we've got a drug that has a great safety profile, that really seems to add efficacy wherever we're testing it, and may be able to provide benefit in areas like, you know, second-line PCNSL, where there are no drugs approved. The FDA ought to be receptive to that. So as soon as we can get a sufficient number of patients together, and it's probably in that 10-20 range... Depending upon what kind of results we're getting, if the results are consistent moving forward to what we've seen in the past, we'd be looking to have a meeting with FDA as soon as we can. And then, of course, as you know, the FDA's got a lot of guidelines about when you apply and how quickly they have those meetings, but we'd be somewhat subject to the FDA's scheduling on their end. But we look really forward to being able to tell you when we've got that call on the docket, so that we can push forward these drugs as quickly as possible. Okay, great. Maybe just tackle one last housekeeping question. Sure. I know you guys do not typically give guidance in terms of the operating expenses, but could you give more directional sort of suggestion in terms of the operating expenses this year, 2024 comparing to 2023? And thanks. Yeah. Why don't I ask Diantha to chime in on that? Thanks, Jim. So, yeah, I mean, we believe that our operating expenses are gonna remain relatively consistent. As we've guided the $56 million of cash gets us into 2025, so that gives us a burn rate in the kind of $10 million-$12 million, may peak up to $13 million, depending on timing of, you know, some manufacturing and other things that tend to be a little bit more chunky. But I think it... You should expect it to be fairly consistent year over year. Okay, great. Thanks a lot, and congrats on the development. Look forward to the data readout. Thank you. The next question comes from Bill Giangiri of Truist Securities. Please go ahead. Hi, congratulations. Thanks for taking my questions. We were wondering if there were any. Could you tell us anything about strategic or partnership interest at JPM from your end? And then also for the triplet study in AML, for the patients you're enrolling, could you just remind us what the bars would be for that one? Thank you. Sure. Thanks, Bill. So as you can imagine, the interest that we've seen on the partnering side kind of mirrors the interest that we've got on the investigator side in participating in our trials. And we, of course, are always having conversations with potential partners. And at some point, you know, I think many people would like to imagine that if we can go broadly with this drug everywhere where we think it could work, so that's across lymphoma in areas wherever BTK gets used, in leukemia, AML and MDS in a frontline setting, and now in solid tumors. We've just started in melanoma, but as I mentioned, there are a number of other solid tumor indications that have been studied with our drug by NCI and academic centers. And Curis just can't afford, you know, we're too small. We can't afford to run studies in all those areas. At some point, it's gonna make sense to turbocharge those clinical efforts, with the help of a partner, both with bankbook and manpower. You know, going forward, I think it's unlikely that we're gonna strike a deal as we did, in melanoma, where, we don't have to give up any rights, and we get, just providing drug, we get data. But I think at some point, that will make sense, and I would say we're, we're not giving guidance on timing for that, but I'd say stay tuned. You know, this, this looks to be a really compelling drug, and Curis is not the only company that's recognized that. And could you remind me, Bill, the second part of your question? Yeah, sure. Yep. Yeah, the triplet. So I'm not really sure what the patients look like and the eligibility criteria. So I was wondering if you could just tell us, like, what the bar would be for success there and just overall- Yeah, I think the- benchmarks. Right. Thank you. Yeah, I think as I mentioned to Li Watsek at Cantor, I think the bar really is a, it's a safety bar in the early days. You know, we are cognizant that the doublet of azacitidine is difficult for patients to tolerate. You know, when we look at the drugs we're combining with, whether it's azacitidine or ibrutinib for that matter, these are all drugs that they're effective, but their safety profiles are tough. And so the first order of business, if we're gonna combine with those, we want to make sure that we don't take a difficult regimen to tolerate and make it worse. So first things first, there's no reason to believe we have an overlap of safety profile, but we need to test that out in patients and make sure that's so. It's easily the thing we're looking for first. Now, of course, whenever you're looking for safety, once you pass that hurdle, you're gonna be looking for signs of efficacy, and we're gonna want to be able to see that we can replicate in the clinic, with the triplet, what we've been able to do in all of our other studies to date, and that is recapitulate the preclinical experience and show that adding emavusertib, that addressing this novel driver of cancer in IRAK4, that addressing that target does yield incremental efficacy above and beyond current standard of care. And if we can do that, I think that's the home run. First things first, safety, but of course, we're gonna look for efficacy as well. Hopefully, that's helpful. Wonderful. Yep. Yeah, and I guess one last one. Just... I just want to verify, make sure I'm not thinking about this incorrectly. It seems like you're already hitting the duration bar in CNS lymphoma, right? We just need that data set to grow. Yeah, I think it's exactly right. I think the dataset looks fantastic, in fact- Yeah. It looks quite a bit better than we would need. But- Yeah ... it's early days, 3 of 5. So as we go to 10 and then to 20 patients, you know, as I said, I think what we need to be able to show, if you had 20 patients with primary CNS lymphoma that you were treating, that had failed high-dose methotrexate and chemo, today, they're gonna go on BTK, they're gonna go on ibrutinib. You'd expect 4 of those 20 patients to get a response based on the largest study that's been done on ibrutinib monotherapy, CR rate of 19. So let's round up a little bit, call it 20. You'd need 4 CRs out of 20 patients. In our case, we're 3 of 5. We need to add 15 more patients and get one more CR just to match the earlier line. Because remember, all of our patients have failed ibrutinib. You'd expect 0 out of 20 if you rechallenge them with ibrutinib. So in our case, if we can match that prior line of get 4 out of 20 or 1 more CR out of the next 15 patients, I think we've got a really compelling discussion to have with FDA, and I think, frankly, our odds are pretty good at that. Great. Thank you. You bet. Thank you. This concludes our question and answer session. I would like to turn the conference back over to the company's President and Chief Executive Officer, Jim Dentzer, for any closing remarks. Thank you, Andrea, and thank you everyone for joining today's call. And as always, thank you to the patients and families participating in our clinical trials, to our team at Curis for their hard work and commitment, and to our partners at Aurigene and the NCI for their ongoing help and support. We look forward to updating you again soon. Operator? The conference has now concluded. Thank you for attending today's presentation, and you may now disconnect.