Good morning, welcome to Curis' emavusertib update call. All participants will be in a 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 a question. 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' Chief Financial Officer. Diantha, please go ahead. Thank you. Welcome to Curis' emavusertib update call. Before we begin, I would like to encourage everyone to go to the investor section of our website at www.curis.com to find the Curis Announces Positive Emavusertib Update press release. I would also like to remind everyone that during our 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, actual results may differ materially. For additional details, please see our SEC filings. Joining me on today's call are James Dentzer, President and Chief Executive Officer, Dr. Ahmed Hamdy, Chief Medical Officer, and Dr. Jonathan Zung, Chief Development Officer. We will also be available for a question and answer period at the end of the call. I'd now like to turn the call over to Jim. Thank you, Diantha. Good morning, everyone, welcome to Curis' emavusertib update call. We're excited to report updated data from the TakeAim Lymphoma study in Primary CNS Lymphoma, one of the most rare and most difficult to treat of the NHL subtypes. As a reminder, the TakeAim Lymphoma study is a three-part study of emavusertib in combination with ibrutinib in patients with relapsed refractory PCNSL. Part A, the dose escalation part of the study, is complete. Part B is the single-arm study in BTKI-experienced patients, Part C is the randomized study in BTKI-naive patients. As you may recall, we reported data for patients treated in Parts A and B of the study last year with a May 1, 2025 data cutoff. At that time, we reported a 71% overall response rate in BTKI-naive patients, with five of seven patients achieving a response. We're pleased to report that as of the July 1, 2026 data cutoff, the ORR is now 86%, with six of seven BTKI-naive patients achieving a response. When we focus on evaluable patients, those patients who were able to complete at least one cycle of treatment, the response rate increases to 100% or five of five BTKI-naive patients. For context, it is important to note that published studies of BTK inhibitors in PCNSL have generally shown response rates of 40%-70%. Clearly, the combination of emavusertib plus a BTK inhibitor appears to be better than BTKI alone. For BTK-experienced patients, those patients whose disease has progressed while taking a BTK inhibitor, the results look arguably even more impressive. Last May, we reported a 27% response rate, with seven of 26 patients responding. A year later, we have increased the patient dataset by 50%. We now have 39 patients, and the response rate has remained consistent with a 26% ORR and 10 of 39 patients responding. When we focus on evaluable patients, again, those patients who were able to complete at least one cycle of treatment, the response rate increases to 33% or 10 of 30 BTKI-experienced patients. For context on this population, patients who have failed both frontline therapy and BTKI have a very poor prognosis, with many patients proceeding directly to hospice or best supportive care. That emavusertib is helping patients change that story and reverse their disease is very encouraging. In short, the updated data in both BTKI-naive and BTKI-experienced patients continue to show strong activity and continue to support the potential for accelerated approval submissions in both the U.S. and Europe. As the study continues to advance with strong support from clinical investigators and KOLs in the PCNSL community, we look forward to completing full enrollment in the registrational dataset on schedule in 2027. Now let's turn to CLL. As you recall, last year, we engaged with a number of KOLs who were excited about expanding our emavusertib studies into additional NHL subtypes. They were especially interested in exploring emavusertib's potential to fundamentally change the treatment paradigm for CLL patients, where the current standard of care is BTK inhibitors. Over the last decade, BTK inhibitors have become standard of care in CLL and NHL because of their ability to block the BCR pathway and help patients achieve objective responses. However, these responses are typically partial responses, not complete remission. The result is that patients treated with a BTK inhibitor end up having to stay on it in chronic treatment for the rest of their lives. Additionally, because they never achieve complete remission, many of these patients develop BTKI-resistant mutations, and ultimately, their disease progresses. We are looking to improve upon the current standard of care by adding emavusertib to a patient's BTKI regimen, applying a dual blockade to the two biologic pathways driving CLL. This dual blockade, with BTKI blocking the BCR pathway and emavusertib blocking the TLR pathway, can enable patients whose NHL subtype partially responds to a BTK inhibitor to achieve deeper responses with the combination, including the ability to achieve complete remission or undetectable disease and the potential for time-limited treatment. If we are successful, adding emavusertib to BTKI could change the treatment paradigm in CLL, reducing the risk of developing a treatment-resistant mutation and improving a patient's overall quality of life. The first step in testing this hypothesis in CLL is our proof of concept study in patients currently on BTKI monotherapy who have achieved partial remission but have been unable to achieve complete remission or undetectable MRD. Enrollment in the CLL study continues to gain momentum. Just a few weeks ago, we announced that we had 11 clinical sites activated and that we had consented our first six patients. Since then, we have consented four more patients, bringing the total to 10 patients consented. With that strong momentum, we are pleased to reiterate our guidance that we expect to dose the first five patients by the end of this month. We're raising our guidance for clinical data from five patients to five to 10 patients by year-end. It's been a terrific year so far, with updated PCNSL data reinforcing the regulatory strategy for our first NHL submission. Demand for CLL enrollment exceeding our expectations, reflecting both the clear unmet need in CLL and the support from the clinical community that emavusertib has the potential to address that need. We look forward to providing additional updates as the year progresses. With that, I'd like to open the call for questions. Operator? Thank you. Ladies and gentlemen, we will now begin the question and answer session. Should you have a question, please press star followed by the one on your telephone keypad. You will hear a prompt that your hand has been raised. Should you wish to cancel your request, please press star followed by the two. If you're using a speakerphone, please lift the handset before pressing any keys. One moment please for your first question. Your first question comes from the line of Srikripa Devarakonda from Truist. Please go ahead. Hey, guys. Thank you so much for taking my question. Congratulations on the progress. I was wondering if you can remind me what the specific number of BTKI-experienced patients required for the registrational data set is. Is there a floor ORR the FDA expects to see for this patient population? I know I don't think you mentioned it, but just was wondering if you have any sense of median duration of response for these responders that you talked about today. Yeah. Thank you, Kripa. Appreciate the questions, and thank you for joining. Just as a reminder, when we went back and had our discussions with FDA, one of the reasons we selected PCNSL in this salvage line setting is because the alternatives are so grim. Patients post-BTK, once they've failed, not just chemo and methotrexate in frontline, but then they've gone on a BTK inhibitor and their disease has progressed after that, they have no options. There's nothing approved. There is no consistent guideline. Many of those patients are, frankly, too frail to even take another round of chemo. Oftentimes, these patients end up going to best supportive care or hospice. The ORR in that population is really zero. Nobody publishes results for that population because nothing works. When we had the discussions with the regulatory authorities, what we said is, "Look, we all understand that the real-world response rate is zero. Let's just suggest a statistical lower bound of 10%. If we can get more than 10% responses, statistically, P value less than 0.05, would that be sufficient?" The answer from both the EMA and FDA says, "Yes. There's nothing for these patients. If you can show that you can exceed that lower bound, that would work." Now we had a discussion about the stats. If we see a response rate of 20% or higher, in order to achieve a P value of 0.05, we would need somewhere in the range of 45-60 patients. The question to EMA and FDA was, would that size of data set be sufficient, knowing that we need to address safety as well as efficacy? Our conversations were very successful. Both agencies thought that was reasonable, and so that's where we're headed, and that's why we expect to have that data set fully enrolled by next year. The follow-on question that you asked about duration was, well, what sort of duration do we expect to see? Well, in this population, as I said, nothing works, so any duration would be terrific. The largest study ever done in this population was the iLOC study by Carole Soussain in Paris. That study, as a reminder, showed that progression-free survival in BTKI patients is two months. We've shown so far that we can get to four to six months. In fact, some of our patients have been on drug now for over two years, approaching three years. I suspect we're going to have a very strong story to tell, assuming that the data hold between now and full enrollment. Our response rate and our duration are better than we were expecting. Thank you for those questions. Thank you so much. Thank you. Your next question comes from the line of Yale Jen from Laidlaw & Company. Please go ahead. Good morning, James, and congrats on the great data, and thanks for taking the questions. My first question is that given for the PCNSL, that both BTK naive and the BTK-experienced patients show very compelling data, would you also consider filing for the first line as well as for the second line? What might be the additional work needed for potentially achieve both sides? I have a follow-up. Thank you, Yale, first and foremost for the questions and also for dialing in today. We appreciate it. You raise a very exciting prospect. When you're looking at an oral-oral combination of patients that in the evaluable population has a response rate of 100%. Those are patients that are second line. They've already been through chemo and methotrexate, right? Chemo and methotrexate is frontline therapy. The published reports for chemo and methotrexate are that the response rate is 80. We're looking at a response rate in second line with an oral-oral, so a far easier regimen to tolerate than frontline with chemo and methotrexate. I'm not prepared to suggest that with our small data set, we only have five evaluable patients, seven ITT, right? It's a very small data set. I don't know that I want to take that next step and say that we think we can leapfrog into frontline therapy in these patients. I think that's premature. I would say we feel very confident that the drug is active, it's clearly adding efficacy to a BTKI regimen, and we think that the prospects for gaining our first label, first in the salvage line, and then with full approval, in combination with BTKI. Our overall thesis is there's a $12 billion market for patients with NHL who take a BTK inhibitor. Overview would be, we're going to go into all five of those indications, PCNSL first, but then CLL, Waldenstrom's, mantle cell, marginal zone. Wherever a patient takes a BTKI inhibitor today, those patients tomorrow, if these data hold, suggest they should be taking BTKI plus EMA. That's a really exciting place for us to be. Thank you for that question. Okay, great. Maybe just a follow-up. With this data at this moment, would you thinking of schedule a meeting with the FDA or you will wait until, for example, end of the year to have a meeting with FDA, maybe even accelerate the process further, instead of waiting for the completion of the enrollment in next year for the salvage line? At the time also in terms of the BTK naive, if you have more data there, again, the same question, whether you will have a conversation with the agency to discuss all the possibilities. Thanks. Thank you again. A great question. On the regulatory strategy, I'd say we've got a really good dialogue going with FDA. They greatly appreciate it. We should remind everyone, when we went to the FDA, we brought with us two key opinion leaders, right? The head of primary CNS lymphoma for Sloan Kettering and the deputy chair of lymphoma for Mayo Clinic in Rochester. The support from the community and then the support that we gained from FDA and EMA was really encouraging. At this point, the dialogue is terrific. They're glad that companies like Curis are pioneering novel molecules in areas of clear unmet need, where patients really do need access to a therapy that can extend the quality of their life. So far, the data seem to support that enthusiasm. I'd say right now, we plan as the data come in to reach out to the FDA, EMA where appropriate, to take advantage of any opportunity we can for accelerated treatment or favorable regulatory action that could be beneficial to getting this drug to patients as fast as possible. As I said, right now we are continuing to look at a drug that is performing really well in its first indication and the second one, CLL, the much larger indication, the enthusiasm from the community is really exciting for us and I look forward to both better data as we move forward, in CLL as well as PCNSL, but also an ongoing discussion with regulatory authorities. I'd say stay tuned. Okay, great. Thanks a lot. Again, congrats. Thank you very much. I appreciate it. Thank you. Your next question comes from the line of Sara Nik from H.C. Wainwright. Please go ahead. Good morning, thanks for taking the question. Congrats on the progress. Happy to hear it. Just had one question regarding the PCNSL. If I heard correctly, the BTKI naive cohort, enrollment has been, I think, still at seven patients since the May 25 cut. I just wanted to understand if Part C is still actively enrolling, and if it's not, maybe if you can provide some color on any potential impediment. Is it just the competing frontline options, site prioritization, or something else? Thank you. Thank you, Sara. Again, just as a reminder, we started enrolling in the early days, in Part A, which was dose escalation. We enrolled patients as low as 50 mg all the way up to 400 mg, and we did it in multiple indications, and we did monotherapy, we did combo, we did naive patients, we did experienced patients. In those early days, we dosed several naive patients in PCNSL, and it's those patients that we continue to follow. In fact, one of those patients who wasn't a responder last year in May, has now become a responder. In fact, we have another CR in that population, which is very encouraging. The next step strategically for us is to gain our approval. Once we had our dose and we were following those patients, we moved into relapsed refractory patients in the experienced setting because those are the patients that are going to support what we hope is an accelerated approval. We know that, once you get accelerated approval, you have to follow on with full approval, and that has to be a randomized study. It will be a BTK in one arm, BTK plus ema in another arm, and we're going to need to be able to show as part of our submission that we've got a contribution of components, that in fact, what appears to be true now, it continues to hold that emavusertib plus BTKI is better than BTKI alone. We've made really good progress on our approval data set. I expect the full approval data set is one that's, typically with most companies, that comes several years later. Yes, we are getting started in that study, and we're beginning to enroll patients. We need to have that study ongoing by the time we file for our BTKI-experienced label. We will. As those data mature, we look forward to obviously reporting out on those as well. The lead and clearly the emphasis is on the registrational data set, which is the BTKI-experienced patients. I hope that's helpful. No, that's helpful. Thank you. Thank you. Your next question comes from the line of Boris Peaker from JonesTrading. Please go ahead. Great. Thanks for taking my questions. I'd like to add my congratulations on the progress. Maybe my first question on PCNSL, if we look at BTKI resistance, at least from what I could find on PCNSL, it's either typically with BTK C481S mutation or just a bypass of activation of MyD88 TLR pathway altogether, which obviously what IRAK4 targets. I'm just curious if you've sequenced the baseline tissue or liquid biopsy of these BTKI-experienced patients to get a better understanding what their actual mutation was and how your drug kind of fits in within that mechanistic pathway. Sure. Thank you, Boris. I appreciate the question, and thanks for joining. I'm actually going to ask Ahmed Hamdy to chime in on that. Ahmed, if you wouldn't mind. Hi, good morning. Cys481 mutation will happen in a subpopulation of patients who are currently on a BTK, yet some part of the population is responding. On the other hand, our emavusertib works on the TLR IRAK4 pathway. Adding ema to BTK in that population, although may help in some of the patients or the population that has the Cys481, but it should augment the BTK inhibition. The dual inhibition of the TLR and the BCR should inhibit NF-κB, which is the driver of the disease, regardless of the presence of a subpopulation that is mutated. Yeah. Let me answer that as well, Boris. Again, I'm going to take you back to the mechanism of the drug. On our website, in our corporate deck, I think we elucidate this, I hope fairly clearly. The problem of disease for patients with non-Hodgkin lymphoma, for B-cell lymphoma, is NF-κB is in overdrive. What's driving NF-κB is the BCR pathway and the TLR pathway separately. BTK inhibitors are blocking the BCR pathway. We block the TLR. Blocking both pathways ought to allow better downregulation of NF-κB and better control of this dysregulated process that governs survival and proliferation of the malignant cells. Cys481 is going to prevent covalent BTK inhibitors from binding at the binding pocket, and that's clearly going to impact the ability to knock down the BCR pathway. By blocking the TLR pathway, again, we're in a completely independent pathway, we should be able to help those patients. For patients with MYD88 mutation, typically, as you know, the Myddosome complex, where MYD88 lives, is in the toll-like receptor pathway. When patients have a MYD88 mutation, and the majority of PCNSL patients do, for example, that's going to cause constitutive activation of the toll-like receptor signaling, which all things being equal, will cause extra overactivity, if that's the right way to think about it, of NF-κB. Whether it's a Cys481 mutation or a MYD88 mutation, knocking down toll-like receptor activity ought to be helpful, and that's exactly what emavusertib does. I think you're right. Those are two key mutations that we would look for. As you know, there are a lot, there are probably 15 - 20 different mutations, depending upon the patient and the type of B-cell lymphoma, that matter. We expect to gain more information on that, especially as we add different NHL subtypes into our studies. At this point in time, I think it's very clear. Based on the PCNSL data that we've seen to date, based on the mechanism, preclinical data, and enthusiasm in CLL, emavusertib and knocking down TLR signaling seems to be making a difference. That's a really long explanation. I hope that's helpful. No, absolutely. That was very helpful. I guess I just had a quick follow-up question. Just in the PR definition of PCNSL, I know you look at brain MRI, eye examination, CSF cytology. Is there any way to kind of report how close these patients were to the threshold of PR, or were they far away from the threshold if the FDA reanalyzes to be confident that they'll come back with a PR as well, versus a patient may be right on the threshold could be reclassified potentially as progressive disease? Yeah. This is one of the reasons why we went for primary CNS lymphoma, because it is such an aggressive lymphoma. It's part of the DLBCL disease space. It's DLBCL that's in the brain. In these patients, 80% of them are going to come under control with chemo and methotrexate. Once they fail, they're going to go on a BTK inhibitor. Some lower percentage, 40%, 70%, depending upon the study you look at, can gain a response. Once they fail BTK inhibitors, they unfortunately progress very quickly. Those are the patients that are coming into our study. It's not that they're close to PR and they're stable. They're in fact progressing. Their brain tumors are physically growing, and if they do nothing, which is unfortunately what happens to many of these patients, their prognosis is very grim. There isn't an expectation that some sort of magic will happen, and had they stayed on a BTK inhibitor while their tumors are growing, that it would magically start not just stabilizing, but reduce. That's why it was so powerful. It's why the FDA and EMA were so supportive of us, that we've got a data set that shows clearly when patients who are on a BTK inhibitor have started to progress and their brain tumors are no longer impacted by that BTK and their brain tumors are physically growing, we can do more than stabilize them. We reverse them. That is really unusual. There are no other published data sets I'm aware of in PCNSL where that's ever happened. I think that's why FDA and EMA were excited. It's certainly why we're excited, and I'm hopeful that with our full registrational data set next year, we have the ability to see this have an impact in patients much more broadly as we commercialize. I hope that's helpful. Great. Thank you for taking my questions. It was very helpful. Sure. Thank you. This concludes our question and answer session. I would now like to turn the conference back over to the company's President and CEO, James Dentzer, for any closing remarks. Thank you, operator, and thank you everyone for joining today's call. 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 investigators and academic community for their ongoing collaboration and support. We look forward to updating you again soon. Operator? The conference has now concluded. Thank you again for your participation. You may now disconnect.