Paula O’Connor, our Chief Medical Officer, and Hans van Houte, our Chief Financial Officer. These are our disclaimers. At Nurix, we're advancing a pipeline of innovative targeted protein degrader drugs in oncology and inflammation and immunology, or INI, each with best-in-class potential. The majority of today's call will be focused on an important update on our lead program in CLL, Bexobrutideg, or NX-5948, or Bexdeg for short. This will include our pivotal clinical development plans and some important new data supporting differentiation and Bexdeg dose selection for registrational trials. Next, with respect to our partnered INI pipeline, we are able to share with you today some new preclinical data from both STAT-6 and the IRAK4 programs. Our STAT-6 program is partnered with Sanofi, and this is the first public disclosure of preclinical data profiling some key characteristics of NX-3911, the exciting clinical candidate that is now in IND-enabling studies. We will also describe, for the first time, some key differentiation data from our IRAK4 program with Gilead Sciences, GS-6791 that is currently in phase I healthy volunteer study. Importantly, Nurix maintains the potential to opt into these two partnered programs in a 50/50 co-development, co-commercialization structure in the U.S. This is an option that will be available after our partners have obtained human clinical data. Although we won't be discussing the exciting potential for Bexdeg in INI indications today, I would like to mention that we continue to move a new tablet formulation through multiple ascending dose studies in healthy volunteers. This is a formulation that is ultimately intended for use in an autoimmune setting as a distinct product. Overall, we believe the emerging best-in-class drug profiles of our BTK, STAT-6, and IRAK4 degraders are no coincidence, but rather the consequence of Nurix's rigorous science focused on the discovery and development of targeted protein degradation drugs. At the end of the call, we'll take questions on any topic, including our recent ESMO poster presentation on NX-1607, our first-in-class cIAP inhibitor, a novel immuno-oncology agent that has demonstrated some very encouraging single-agent activity in solid tumors. The poster is available in the resource library on our website. Now, before we go through our very thorough update, I do think it's important to take a moment to step back and place Nurix in the context of a much larger evolution of drug discovery that is taking place literally before our eyes. We believe targeted protein degradation is poised to take the stage as the next major modality in medicine, probably on the scale of antibodies and potentially even larger since we can address a much larger target class. It is indeed inspiring to recognize the potential for such drugs, with Nurix pipeline truly on the cutting edge of this evolution. The headline for today's call is that we have announced the achievement of a significant milestone in the development of our lead program, the initiation of our pivotal trials in CLL. This advancement has been enabled by obtaining regulatory alignment on dose selection for registrational purposes with the FDA under Project Optimus. Importantly, we also have alignment with global regulatory authorities, including the MHRA in the U.K. and the EMA in Europe, to begin our global registrational program. As a reminder, Bexdeg also has fast-track status in the U.S. and PRIME designation in the EU. The dose of Bexdeg we are taking forward into registrational trials is 600 mg once per day. This is the highest dose we tested in our phase I studies to date, in which we encountered no dose-limiting toxicities. This dose selection was based primarily on data from the phase I-B portion of our study that included randomized cohorts of 200 mg once daily and 600 mg once daily, according to the guidelines of Project Optimus. We are very pleased that the 600 mg dose group showed a favorable safety profile that was comparable to that of the 200 mg dose group. By selecting 600 mg, therefore, we are able to maximize for efficacy while maintaining safety. We believe this represents a strategic advantage over competing molecules, both BTK degraders and inhibitors. The selection of the 600 mg dose has enabled the initiation of our first pivotal trial, which has been named the Daybreak study, a single-arm, phase II study in approximately 100 patients with relapsed refractory CLL for potential accelerated approval, addressing a population of high unmet medical need. Today, we are also announcing that this global clinical trial has initiated. In addition to Daybreak CLL 201, we are actively planning the implementation of the phase III randomized confirmatory trial in CLL in the second-line setting, moving Bexdeg up in the CLL treatment paradigm. Paula O’Connor will be describing our core CLL clinical development plan in this call. Turning to the fifth and sixth checkmarked items on this slide, a key question we will endeavor to answer this morning is, what are some of the clinical and preclinical data that support differentiation of Bexdeg and the selection of the 600 mg dose? Elements to this answer to this question can be found in some of our latest data that we will share today, which will be presented by Gwenn Hansen, data that distinguishes Bexdeg from both BTK inhibitors and also the competing BTK degraders from B1 and ADV. We believe these data clearly support a best-in-class profile for Bexdeg. As we turn to details on the Bexdeg update, I would first like to briefly highlight the overarching advantages of the degradation mechanism of action and of Bexdeg in particular. First, Bexdeg is active against not only wild-type BTK, but also the entire range of clinically relevant BTK mutations that render current BTK inhibitors ineffective. Second, Bexdeg addresses the scaffolding function of BTK, a function that promotes tumor cell growth and B-cell receptor signaling, and a function that is neglected by inhibitors. Third, Bexdeg, like all bifunctional degraders, acts catalytically, which means very low drug levels can deliver incredible potency. What do we mean by that? Remarkably, we have measured in cells that one Bexdeg drug molecule can degrade between 10,000- 20,000 BTK proteins per hour. This fundamental difference in PK/PD from inhibitors is what allowed us to justify recognition from the USAN drug naming authority that Bexobrutideg deserved the new suffix deg, which indicates an entirely new category of drugs, the degraders. Bexdeg is indeed the first deg in this category. It's a real landmark. Fourth, Bexdeg crosses the blood-brain barrier and has demonstrated significant clinical activity in the CNS of patients with advanced brain involvement. Fifth, we have demonstrated robust clinical activity in multiple difficult-to-treat B-cell malignancies across the board in CLL and NHL. Last but certainly not least, we believe that Bexdeg and our degraders for IRAK4 and STAT6 will bring their mechanistic advantages to autoimmune disease by addressing the scaffolding function of these targets and by delivering the powerful catalytic activity of targeted protein degradation. In sum, we believe the best-in-class drug profiles of Bexdeg, NX-3911, and GS-6791 are no coincidence. They are a consequence, once again, of Nurix's rigorous science focused on the discovery and development of targeted protein degradation drugs. Now I would like to turn the call over to Paula O’Connor, our Chief Medical Officer, to provide a brief review of our previously presented Bexdeg data that was featured at EHA earlier this year, and then an overview of our pivotal clinical development plan in CLL. I will be changing the slides for you, Paula, and if you could prompt me by saying next slide, I would appreciate that. I certainly will. Thank you, Arthur. Next slide. Good morning. I'm Paula O’Connor, the Chief Medical Officer here at Nurix. I'm thrilled to be working here at Nurix as we advance the next wave of innovation on the BTK pathway with our best-in-class molecule, Bexobrutideg, as Arthur has already said. We have confirmed our 600 mg dose with the FDA, MHRA, and the EMA, and are moving forward at full speed on our pivotal programs. I'll review these in more detail in just a moment, but just to summarize, as you can see here, our phase II trial DAYBreak, with the potential for accelerated approval, is now underway, with our first site activated earlier this month. Our key startup initiatives are also underway for our confirmatory phase III study. This study will begin in the first half of 2026. The entire company is laser-focused on the initiation and conduct of these two critical programs. As Arthur has already noted, we have also had many positive interactions with the major health authorities regarding Bexobrutideg, and as previously disclosed, we have received fast-track designation with the FDA and PRIME designation with the EMA. These will be critical for us as we review our evolving data in our path toward registration. Our interactions have not only set the stage for our development of these agents and have clearly informed our pivotal trial designs and our registration plans. Next slide. Reporting in progress. In the next few slides, I will summarize the efficacy and safety data shared for Bexobrutideg most recently at EHA and Lugano. Every time we share this data, it reinforces the potential of this asset and the power of protein degradation. As you look at the slide, I'm going to direct your eye to the left, where you see the objective response rate in patients in the fourth-line setting of CLL. As you can see here, the ORR of 80.9% has occurred in patients in whom 75% are double exposed and more than half have TP53 and/or BTK mutations, representing a group of patients with the highest unmet medical need. On the right, you see the waterfall plot and the genetic profile of our enrolled patients, showing meaningful reduction in their lymph nodes over the course of therapy, irrespective of high-risk clinical and genetic features, including CNS involvement and the mutations I previously mentioned. Next slide. The swim lane plot provided on this slide shows the speed, durability, and depth of the responses we've seen with Bexdeg across dose levels. The median time to response is fast, less than two months. The treatment effect is durable, with 17 of the 18 patients reaching a year on therapy continuing treatment. You can also see the pattern of deepening responses over time, evidenced by our first complete response being documented after 18 months of treatment on the first patient that is represented on this swim lane. Next slide. The safety profile for Bexdeg depicted here remains consistent with our earlier reports, even in the setting of longer follow-up and increased numbers. There are no new signals, cardiac, infectious, or otherwise. In the next couple of minutes, I will turn to our clinical development programs that we have for Bexdeg. I'm pleased to share with you our three pillars for the development strategy for Bexdeg. They are, first, Speed to market; second, Addressing the needs of relapsed and refractory CLL patients as early as the second line; and third, Utilizing combination therapy to further improve patient outcomes in the relapse setting and potentially to move us to the front line. Before delving into these pillars and how they address the needs of our patients, I'll take a moment to give an overview of the CLL market. Pardon me. Across the major markets in the U.S., EU, China, and Japan, there are approximately 120,000 patients initiating new treatment each year. 50% of these are in the second line plus setting. In the U.S. specifically, there are 38,000 new patient treatment starts each year, 19,000 of which are in the relapse setting. Our clinical development plan is competitive and is designed to address the needs of CLL patients across the global marketplace. Next slide. This is the schema for our DAYBreak study. This, as we've already noted, has the potential for accelerated approval and started earlier this month. The study addresses the first pillar of our development strategy, namely speed to market. Utilizing this study, we hope to bring Bexdeg to physicians and their patients as quickly as possible. This single-arm, phase II study is designed with registration intent and has the potential for an accelerated approval. We plan to enroll approximately 100 patients with Bexdeg at our 600 mg dose. The enrolled patient population will consist of triple-exposed CLL patients who've been previously treated with a covalent BTKI, a non-covalent BTKI, and a BCL2 inhibitor. These patients have a clear and unmet medical need. The primary endpoint for this study is objective response rate, as assessed by an independent review committee, and will be further supported by duration of response data. We are thrilled that this important study has started, and the team is working diligently to enroll it. Next slide, please. The second pillar of our development strategy is to address the needs of patients with relapsed and refractory CLL as early as the second line, thereby helping a broader set of patients. This is the schema for our confirmatory phase III study. We plan to enroll approximately 400 patients. They will be randomized to either 600 mg of Bexdeg given once daily by mouth or one of the three treatment options in the physician's choice control arm. These options include the globally relevant regimens of Pirtobrutinib, Idela, and Rituxan, or Bendamustine and Rituxan. The primary endpoint of this study is progression-free survival, and we plan to initiate this study in the first half of 2026. Next slide, please. The third pillar of our development strategy in CLL is utilizing Bexdeg in combination with other active agents in CLL to improve patient outcomes. The schema on this slide is for our combination basket study. The combination data generated in this study may support future registration studies in the second line or even the first line. The study is designed to establish the go-forward dose for Bexdeg in combination with venetoclax, venetoclax and Rituxan, venetoclax and obinutuzumab in both the second and first-line patients. We will enroll approximately 20 patients in each cohort. The dose that we identify in these cohorts may be used in our subsequent studies. This study, like the confirmatory phase III we discussed earlier, is slated to begin in the first half of 2026. The datasets generated in this study will inform future potential pivotal studies in CLL and may inform future development more broadly. Next slide. Having reviewed our immediate plans in CLL with you, I will close this section out of our presentation by saying that we are mobilized as a company to enroll the studies I've just reviewed to support the rapid registration of Bexdeg in CLL in patients with relapsed disease, triple-exposed disease in particular as it relates to the phase II, and to address the medical needs of relapsed and refractory CLL patients as monotherapy or in combination. We look forward to sharing our emerging data with more patients and longer follow-up with you at the ASH meeting in December. With this, I'm going to close this section and turn things over to Gwenn Hansen, who will give you more information on how we are differentiating Bexdeg from the other BTK-directed therapies, as well as speak to our other pipeline agents. Gwenn? Thank you, Paula. Good morning, everyone. My name is Gwenn Hansen. I am the Chief Scientific Officer at Nurix, and today I'm pleased to be able to share with you some new preclinical and translational data that we think underpin Bexobrutideg's potential best-in-class profile. Next slide. I will describe in the next few slides several key points of differentiation for Bexobrutideg, including potency, mutational coverage, and selectivity, particularly in comparison to key competitors in this space. This data, along with Bexobrutideg's ability to cross the blood-brain barrier and show activity in patients with CNS disease, as well as today's disclosure of having reached alignment with regulatory authorities to use the highest dose tested of 600 mg as our go-forward dose for our pivotal and confirmatory studies, give us confidence that Bexobrutideg represents a potentially best-in-class BTK degrader for the treatment of B-cell malignancies. Next slide. First, in terms of potency, Bexobrutideg demonstrates peak molar potency in primary human B cells, showing 20-fold more potency and five-fold more potency than B1 and ADV degraders, respectively. Next slide. Next, in terms of mutation coverage, Bexobrutideg exhibits a pan-mutant profile, wholly distinct from all known inhibitors of BTK, each of which show two or more liabilities across this growing list of clinically impactful resistance mutations that arise in the active site of the BTK protein, and then in some cases actually render the kinase inactive while still allowing it to drive cell growth and disease. This illustrates a scaffolding function that was otherwise unappreciated for BTK and ultimately is not addressed by the numerous small molecule inhibitors that have been developed to date. Next slide. Degraders, in contrast, are ideally suited to address scaffolding function, but also inhibitor-driven resistance. Comparing Bexdeg's ability to kill the same DLBCL cells engineered to express, again, the same set of BTK inhibitor resistance mutations, Bexdeg shows consistent levels of cell killing across wild type and all mutant forms of BTK, where both B1 and ADV compounds show liabilities against T474I and maybe slightly more severely V416L. While these observed potency differentials between wild type and mutant forms of BTK, ranging from as little as five-fold to as much as 50-fold, might not prevent a degrader from obtaining clinical response in patients harboring these mutations, the ability for a drug to provide a long duration of benefit to patients harboring cells with these mutations will require dosing that drug at exposure levels that far exceed that which would be otherwise needed to fully degrade wild type BTK, and safely achieving such levels requires exquisite degrader selectivity. Next slide. Looking closely at the dose and corresponding exposure levels observed in patients during phase I-A or B of our trials, you see that our optimized dose of 600 mg shows steady-state clinical PK exposures that easily cover not only wild type BTK, that is shown here on the bottom of the PK plot with that dotted line, but also all of the previously mentioned oncogenic forms of BTK marked according to the free drug exposures necessary to completely degrade more than 95% of each protein form. The ability to effectively degrade all or nearly all of the BTK protein found in circulating lymphocytes is something that we've been observing consistently in our translational data and is shown on the right-hand side of this slide, where we directly measure BTK protein levels following once-a-day oral dosing with Bexobrutideg. This data shows that regardless of the dose that we have been using, we consistently eliminate BTK signal in the disease setting across baseline mutation profiles. However, with approval to proceed using a 600 mg dose, we are assured that we can address the totality of relapsed or refractory disease that has otherwise amplified through the use of inhibitors that fail to fully control BTK function. Next slide. Speaking directly to not only our motivation for exploring the 600 mg dose during Project Optimus, but maybe more importantly to why we obtained approval to move forward with our highest dose tested, this slide addresses our selectivity profile. Using a very high sensitivity mass spectrometry-based global proteomics approach, we have attempted to directly compare Bexobrutideg to our competitor degraders and show here that we have an exquisitely selective profile that identifies BTK as the only target degraded at doses exceeding that required for near-complete coverage of wild type BTK. This superior selectivity profile allows us to safely dose Bexobrutideg in our patients at exposures that meet or exceed what is necessary to completely eliminate malignant cells. Next slide. Based on these data, we explored in more detail dose response experiments to show selectivity over critical kinase targets, starting with targets that are well known to be off-targets for BTK targeted agents. This slide shows those experiments using K562 cells, confirming that Bexobrutideg displays a superior selectivity profile with respect to the TEC protein kinase, which has been associated with bleeding and cardiac safety effects across the spectrum of BTK targeted drugs. Next slide. Further, profiling additional targets such as LCK, CSK, and ADK in more detailed dose response studies in their respective cell types of relevance, we confirmed the data that I just showed you from the global proteomics study, namely that Bexdeg has a superior selectivity profile. In sum, we hope this data helps you appreciate our enthusiasm for what we think is a potentially best-in-class BTK Degrader, Bexobrutideg. Next slide. Moving on from oncology to discuss our growing INI pipeline. Next slide. I would like to highlight two programs that we have developed in partnership with Sanofi and Gilead and that are advancing through IND-enabling studies or through early phase I clinical trials in INI. Next slide. First, through a longstanding collaboration with Sanofi that culminated in a licensing event earlier this year, we discovered and are now developing a highly potent and selective degrader of STAT6 that was derived from our Degrader Discovery platform. STAT6 is a transcription factor that plays a central role in mediating type 2 immune responses, which are implicated in a wide range of inflammatory and allergic diseases. Eliminating STAT6 using targeted protein degradation offers the promise of controlling allergic and inflammatory diseases with high efficacy and fewer side effects than broader immunosuppressive therapies, while providing the convenience of a once-a-day oral dose afforded with small molecule therapies like degraders. Next slide. Our compound, NX-3911, shows peak molar potency of degradation in human primary B cells in both the resting and stimulated states, suggesting that NX-3911 has a high catalytic activity and competence to control the inflamed disease state in a cellular setting. Next slide. Similar to the profile shown for Bexdeg, NX-3911 displays exquisite selectivity, here assessed using global proteomics and measured across multiple human donors, where we were able to quantitatively measure the protein levels of over 9,500 unique proteins. In this study, you see that STAT6 is the only protein that is modulated by this drug. Next slide. This highly potent and selective compound also shows profound efficacy in preclinical models of both atopic dermatitis and asthma, using either prophylactic or therapeutic dosing regimens and assessed by measurements of serum IgE levels following 20 or 24 days of dosing, respectively. Importantly, in these studies, NX-3911 restored inflamed levels of IgE triggered by disease induction back down to levels found in naive animals, and that can be seen in the pink bar and the pink dotted line. In our experience, this level of disease prevention or control has only been possible in the context of genetic knockouts, emphasizing to us the promise of this new class of induced proximity drugs. Next slide. Our second INI program highlight comes from the first licensed development candidate emerging from our collaboration with Gilead. NX-0479, or now known as GS-6791, is a highly potent degrader of the scaffolding protein IRAK4 that is an essential component of the myddosome that mediates toll-like receptor signaling pathway control. Next slide. Several updates from this program have been communicated at recent conferences, including ACR and more recently at EADV in Paris. Here we are showing just one vignette that speaks to the differentiation of our IRAK4 degrader in comparison to a competitor degrader from Chimera Therapeutics. In this slide, we are showing degradation and control of cytokine signaling in human basal keratinocytes following treatment with either GS-6791 or KT-474. This data reveals our superior cellular potency, target coverage, and control of inflammation in both basal keratinocytes in isolation, as well as a model of reconstructed human epidermis. These data highlight the importance of the detailed cellular and in vivo disease cell profiling for this emerging class of induced proximity drugs. GS-6791 has now entered the clinic, and we look forward to seeing how this agent performs in the clinical setting and ultimately having an opportunity to opt in in the development of this potentially first-in-class INI drug. Thank you for your attention, and now I will pass the presentation back to Dr. Arthur Sands. Thank you, Gwenn, and thanks, Paula. That was terrific. I'm going to just make a few summary statements here, and then we'll go to Q&A. I think you'll appreciate that Bexdeg has indeed the potential to produce incredible value for our pipeline over the course of its lifecycle. We're looking at CLL. We're also interested in Waldenstrom's and NHL, and of course, potentially INI indications. You've seen and heard today that we have advanced Bexobrutideg one step closer to registration and commercialization. The 600 mg dose is selected as per Project Optimus. We have regulatory alignment, global regulatory alignment, and our pivotal phase II is initiated, and the confirmatory phase III planning is underway, and we anticipate launching that in the first half of 2026. Indeed, there is definitely best-in-class potential emerging for Bexobrutideg, as well as our other pipeline programs as Gwenn outlined. These partnered programs, STAT6 and IRAK4, have the potential for significant milestones in the future, as well as data events anticipated in 2026 and 2027. Regarding our cash balance and economic position, we're in a very strong position, having completed our registered direct offering. Our pro forma cash is anticipated to be $678 million, which can provide us expected runway into 2028. During the Q&A, we'll also be joined by Hans van Houte, our Chief Financial Officer. As 2025 here in Q4, we've really accomplished quite a bit, as indicated by the check marks along the left-hand side of this slide and we've discussed today. What we have remaining we are presenting at ASH coming up in December. We have accepted abstracts at ASH, and we look forward to being there. As usual, we'll plan an investor event as well. In 2026, there's a number of very exciting milestones that we believe will be important. We'll have our phase I- A and B results in NHL. We've yet to disclose significant NHL results. Those cohorts have proceeded quite well and have some impressive results, as with our CLL cohorts. We have multiple cohorts in CLL in the phase I- B portion of the study in very important patient populations, and we look forward to sharing those results with you as well. As I mentioned, we do intend to initiate a confirmatory phase III in the first half of 2026, as well as the combination study in CLL that Paula has outlined. With regard to INI, I think it'll be a very exciting year in 2026. We will have our potential GS-6791 opt-in potential in 2026 based on Gilead's phase I results, which are currently ongoing. Bexobrutideg, its own SAD-MAD study, is currently ongoing. We anticipate data for that in 2026, and this is intended to enable an IND indication. The potential for the NX-3911 STAT6 degrader is really quite substantial, and we can anticipate an IND filed by Sanofi in 2026 as well. With that, we'll turn to the Q&A section, and I'm going to stop sharing as I continue to run these slides. We've got, I think, all members of our team on for the Q&A. Let me see if I can see all the participants. If you'd like to ask a question, you need to raise your hand, and I'm going to call on you, which is going to be interesting. You'll be unmuted, ask your question, we'll respond, and then we'll go on. I'd like to start, I think, with Roger Song. Roger? Great. Can you hear me? Are you there, Roger? Can you hear me? Yeah, go ahead. I can hear you. Awesome. Thank you for calling me. Congrats for the start of the pivotal and then sharing with us a lot of the new data today. Thank you. My question is really related to the detail of the pivotal study design. Given your phase II, it's a single arm, what is the STAT assumption for the 100 patient for this post-covalent and non-covalent BCL2? A similar question for the second line, second plus line randomized confirmatory study. You have a dealer's choice, multiple comparator arms. How should we think about the statistical assumption on the primary endpoint? Maybe more specific, any caps for all of those comparator arms you will be enrolling in order to power the study? Thank you. Okay. Thanks, Roger. Paula, I hope you got all that. Do you want to answer that question, please? Roger, thank you so much for your question. Addressing your first question, what are the statistical assumptions underpinning both of our studies? Certainly, you know that each of our programs has been discussed with the agency. While we're not going to go into all of the details that you would like, what I can certainly say is that we have alignment with the agency on the plans specifically for the single arm phase II and for the phase III. We've touched upon the primary endpoint for the single arm phase II being the objective response rate with duration of response data as part of the supporting information. Typically, as you know, the agency looks at the agents that are available and assesses to those patients and then looks at your results in comparison. I think that's all I'm going to say there. As it relates to our confirmatory phase III, once again, we have reviewed our program with the agency and are aligned on its design and the primary endpoint moving forward. We feel really good about this. As you will see with our emerging data at ASH, the data that we're generating really supports our ability to establish benchmarks in each of these studies that should support registration. Great. Thank you. Thanks, Roger. Next, we'll turn to Derek Archila. Derek, if you can get unmuted. All right, I think I'm unmuted now. Hey, Arthur, and congrats on the update here. Just two questions from us. First, on the combo trial that you guys are talking about, maybe more discussion around the 450 mg dose and what you think could be the differences between 450 and 600. Also, given the additional cash with the financing today, is there any plan to kind of expedite Bexdeg's opportunities in IND? Thanks. Great. Let Paula take the first part and I'll take the second. Sure. As you know, Derek, it's very common to initiate a dose finding study at one dose level minus or one dose level below your monotherapy dose. We're utilizing this approach as we start therapy. It is our hope and our plan that we will be able to advance that dose to 600 mg once we've demonstrated the safety and tolerability of the combination at 450. Arthur? Yes, and Derek, regarding the second part of your question, the answer is yes. With the really successful, extremely successful completion of this offering, we now are in a position to accelerate Bexobrutideg's entry into IND. I think that is really going to be a strategic value creation occurrence for us. We're really interested in doing that. Thank you for your question, Derek. Next, we'll turn to Brian Skorney. Brian, if you can find your way to unmute. Okay, hopefully you can hear me. Yes. All right. Congrats on all the updates today. I guess maybe my question's on the confirmatory trial design. Just wanted to get, you know, sort of early thoughts on the control arm. You're not sure based on the proposed enrollment criteria if there's any studies you would specifically point to to reference for what you might expect the control PFS to be. Just looking at like the benda, Ritux, Idela, Ritux, second line studies, I think they're about 20-month PFS. Do you think is that a reasonable assumption to go on, or are there, you know, since these studies were done kind of prior to BTK and BCL2 usage, you know, are there reasons to think that the control arm would come in at less than 20 months or more than 20 months? Just any thoughts you had on those considerations. Thanks. Thanks, Brian. Paula, go ahead. Thank you, Brian, for your question. I think that your best analogs right now for BR and IR in the second-line plus setting are going to be based upon the Bruin data, Bruin 321. While it is true that that population is mixed with both BTK inhibitor and BCL2 inhibitor-exposed patients, 50% of the patients did not have BCL2 inhibitor exposure and 50% did. Your estimates there for the control arm in the 321 study with BR and IR is about nine months, and the estimates for pirtobrutinib in that setting are 14 months. We anticipate truth being someplace between that in our ongoing study. Right. That's awesome. Thank you. Thank you. Next, turn to Gil Blum. Gil? There he is. Okay. Can you hear me now? Yeah, we can hear you. That's a little tricky. Okay, a couple of quick ones. I'm not sure I saw this, but how's the trial protocol in the pivotal study addressing the patients with potential CNS involvement? I have a follow-up. Right. Paula? Neither of our pivotal trials, the phase II or the phase III, will enroll patients with CNS disease. However, we continue to enroll those patients in our ongoing 301 trial. We have a cohort designed specifically for patients with CNS involvement, and we'll have the opportunity to share that information at a future update. Go ahead, Gil. Is there a difference as it relates to the intellectual property in regards to your competitors? We haven't seen any too much going on there, but are there similarities, or is there anything you can comment on there? Actually, no. I don't think we're going to comment on IP of our competitors at this point. We're in good shape with our intellectual property around Bexobrutideg. I think that's all we can say on that. As the last one, as it relates to competition, it looked like your drug had higher potency in molecular assays. The overall doses that you guys are using, like the total dose, is actually a little higher than what they're using. Maybe you can help us understand the differences in pharmacokinetics there. Thank you. Sure. Gwenn, would you like to take that question? I will. A dose ultimately really relates to bioavailability. There are differences between the degraders and bioavailability. Ultimately, our drug and our free drug levels in vivo are actually required to be lower in accordance with the potency to cover target protein. I think in the end, it's better to compare the free drug levels when you're thinking about total drug needed. That improvement in potency allows us to stay closer in line to the wild type protein level target coverage than maybe other drugs that have differential potency to BTK. All right. Thank you. All right. Thanks, Gail. We'll go to Matt Bigler. Matt? Okay, can you guys hear me? Yeah. Great. Thanks so much for this update, guys. Exciting news. Arthur, can you tell me about the motivation for going after triplet exposed? Ostensibly, you guys see PIRTO and the other non-covalence as kind of their own entity in the continuum of care. I'm interested to know what went into that decision. I guess more importantly, what do you think the bar is for success in a PIRTO-exposed population? I don't think we really have a lot of data on that. I'm interested to hear your thoughts. Thanks. Yes, thank you. When we look at the emerging landscape in treatment of CLL, we believe that the non-covalents will gain approval, full approval, pertubutinib in particular. Looking at also the definition of unmet medical need, it is according to accelerated approval guidelines, we need to address a population that does not have any treatment alternatives. That would be this post-triple-exposed patient population. Our goal there is to be eligible ultimately for accelerated approval in the timeframe of completion of the trial. We think that's going to be the best positioning. With regard to where's the bar and what kind of response rate we might see in this population, I think I'll hand that to Paula because we're talking about patient populations in the fourth or fifth line. Paula? Yeah. Matthew, thanks again for your question. As you've accurately denoted, there are no great studies that speak to the activity of agents in this specific patient population. That having been said, if you look at monotherapy data for chemo or immunotherapies, Rituxan-based regimens or bendamustine or even chlorambucil, et cetera, in this fourth line setting, you can see rates in the 30 up to, if we think about pertubutinib, up to as much as 65%. Ultimately, those are not specifically in this patient population. We know the truth is going to be someplace between this 30 and 60% range. That assessment will occur at the time that the agency is reviewing the data. That gives you a sense of what exists. There are no perfect analogs. That makes a lot of sense. Thank you. Yep. Thanks, Matt. Next, turn to Joe Cansaro. Joe? Okay, I think I'm here. Can you hear me okay? Yes. Great. Perfect. Great. Thanks, guys. Thanks for taking the question. Maybe actually somewhat related to the last question. When you look at your dataset and consider these triple refractory patients, what kind of efficacy are you, can you say you're observing there relative to the broader relapsed refractory CLL population that you've enrolled? Have you seen a notable difference, or is it sort of similar behavior? Paula, do you want to take that? Thank you for the question. As you know, in our phase I-A, we've enrolled patients at dose levels from 50 mg- 600 mg. In the 48 patients that we certainly discussed today, you might imagine that while we've treated patients who are triple exposed, they have not all been treated at the 600 mg dose level. What I can say definitively is that we've clearly seen responses, deep responses, including PRs. It is hard for me to give you an exact number on what to expect at the 600 mg dose level just because we don't have a lot of patients at that dose level. That having been said, what we have seen is still consistent with our overarching data, which shows that our response rate is in the high 70%- 80%. Thanks. That's something if we could, yeah, I thought I could squeeze a follow-up in. Maybe this 200 versus 600, I think the phase I-A was complicated a little bit for dose response because of intrapatient dose escalation, at least from the outside looking in. In the dose optimization, 200 versus 600, was there an obvious dose response as it relates to efficacy? Did it come in response rate? Is it trending more towards durability? Is it a little bit of both? Thanks. I'll drop off after that. Thanks, Joe. Paula, any comments? You see me smiling, or maybe you don't see me smiling, but know that I am smiling. First and foremost, when the agency is looking at your data as it relates to this dose optimization, they are looking not only at safety, which is their primary objective, an improved and a tolerable safety profile, but they're also looking at efficacy. Suffice it to say that the balance of data, both safety as well as efficacy, supported the use of or the choice of 600 mg, not only by us, but obviously by the agency. We're really thrilled with that. I look forward to seeing what we will show in our pivotal trials. Perfect. Thanks so much, everybody. Thank you. Great. Thanks, Joe. We'll turn next to Brian Abrahams. Brian? Hi there. Can you hear me okay? Yes. Great. Thanks for taking the question and congrats on all the progress. Thank you. Maybe just on sort of how the overall landscape in CLL might play out. You spoke a lot about some of the preclinical advantages versus other degraders. I guess I'm curious how you see those playing out in the clinic, if you're seeing any hints so far as you kind of look at other data. I guess I'm also wondering how you would expect the initial commercial market and use to look here, having potentially two degraders available that might have different labels based on different accelerated approval trial designs, but having the potential for Bexdeg to have greater efficacy across more mutations, which may be relevant in a refractory population? Thanks. Thanks. Okay. A two-part question. Gwenn, we'll give you the first part, which was about the differentiation, I think. I think speaking to the differentiation, we see several key points that really speak to the ability of Bexobrutideg to outperform the competitor agent. First, it is the selectivity. We have observed such a safe profile across all of our doses. I think that really speaks to that distinction that I was showing you in all the preclinical data, particularly the proteomics, that really just allows us to press on this target pathway. That high dose is really there because we have safety, which means we can control more of that signaling pathway than would otherwise be possible. I think that really is the important point. The potency is supportive as well, of course, and the mutation coverage is obviously an advantage. I'll pass it back to you, Arthur, or Paula, for the clinical interpretation of that. Okay. Paula, any comments on the clinical interpretation of what we've seen? Yeah. I will begin by saying that without doing some sort of randomized study, our ability to say anything definitive in terms of the difference between the degraders that are being developed is somewhat limited. I will say, based upon just an overall comparison, that the similarities in terms of the activity of our agents in the I-A setting are remarkable, at least as it relates to B1 and our agent. Where we've started to see some potential early differences are in the safety profile. That having been said, they may or may not reflect the proteomic differentiation that Gwenn has already mentioned. We continue to follow that data. Obviously, your whole profile will not be known until you treat hundreds and hundreds of patients. What I can say right now is that our drug appears to be incredibly active and incredibly well tolerated. That has been supported further by the selection of the 600 mg dose, according to Project Optimus, to be utilized in our pivotal trial. That speaks to the safety relative and the activity relative to our competitors. I'll stop there. I think the second part of your question with regard to the market and potentially two degraders and the profiles, what we can say at this point is that in the CLL market, really the best-in-class drug does tend to take the predominant market share. I think we've seen that with the covalence as the first generation Ibrutinib being displaced by more selective agents that came onto the scene even years later, Zanubrutinib, Acalabrutinib, and their selectivity profile at that time, as with all kinase inhibitors, was first measured with those kinome scans where you see the various spectrum of the kinases that are hit by a drug. The cleaner that kinome scan profile in general, the better, the safer the drug, the more selective the drug. We did see that play out, as I said, with the covalence, and that also then played out into market, translated into market share. That is why we're very excited about Bexobrutideg. We believe we do have this best-in-class profile. We've shown for the first time now the molecular and cellular underpinnings of that. We believe that'll manifest in the clinic and ultimately in the marketplace. The last point I make about the marketplace for degraders in general is that it's large. It's going to be a large opportunity for more than one drug. We think that this is a substantial opportunity in general and that ultimately, over time, degraders will possibly displace all the inhibitors because they basically have a better efficacy and a better safety profile. Anyway, great question. Thanks, Brian. We'll go on to Sudan. I'm not going to try your last name because I won't do a good job on it. Hi, Arthur. Yeah, this is Sudan Loganathan. Hi, Brian. No problem. Thanks for having me on and congrats on achieving this milestone and taking my questions. My first question, what will be the number of prior lines of therapy you plan to include in the Daybreak trial? Will it be similar to the phase I-B that had around four prior lines? Would patients that have failed or passed through B1's BGB-16673 be included in any of your trials? Secondly, in regards to the NX-3911 STAT6 degrader, I know the models of AD and asthma were tested, but are there any other indications you could go after to differentiate yourself from either Chimera or others that you can share with us today? Lastly, maybe to get Hans in the mix here, can you divulge what the cost breakdown is for these trials and any changes to your cash runway with the new capital raise? Okay. I hope everyone got their section of the question. Paula, your section? Okay. Your question was specifically about the number of lines of therapy for patients enrolling in our triple exposed trial and also our phase III. Being triple exposed in this era of combination therapy does not mean that you need to have had three or four lines of therapy, as patients can receive combinations where they're getting two of those agents, i.e., a BCL2 inhibitor and a BTKI concurrently. We would anticipate that you will see some patients as early as the third line, but I think you're probably right that we will see many patients who are in the fourth line and potentially later lines in our single arm phase II. In our other study, post-BTKI, that means that you will have patients as early as the second line, irrespective of whether they've received a BTKI alone or whether they've received that in combination with other agents. I'll turn it back to you. I think there was one part of that question, Paula, too, was if we would enroll patients that are post degrader, and I don't think that. Yes, those patients are not eligible. Thank you. Okay. Great. Gwenn, on the STAT6 question. Right. The question was whether atopic dermatitis and asthma are really the two primary indications and whether there could be other indications to differentiate from the competitive agents in the space. I would say there are a number of indications that are relevant for the use of STAT6, and you can think first about the extent of that market by thinking about all of the indications that are being pursued or have been approved for dupilumab. Beyond that, there may be additional indications that are far more relevant for oral once-a-day pill rather than an injectable. I think we think the market is very broad. We think even within the disease areas that are the primary to STAT6, I think the extent of the population that. Treated by a very safe oral once-a-day drug could be much broader than are currently captured by the antibodies in the space. We are very excited, and obviously the field is very excited about this as a target. I think the market potential is very big. Great. Hans, the last part on the... Yeah, Sudan, we haven't given a cost breakdown between all of the trials, but obviously all the trials that we enumerated in this presentation are included in our runway. The additional cash gets us into 2028. Okay, thank you. I think we'll turn next to Alexander. Hello? Can you guys hear me? Yes. Great. It's Alex on for Peter. Thanks for taking our question. I have two. First, how should we think about the time to enroll the single-arm study? The single-arm study, Paula, do you want to address that? Yeah, I mean, I think having established a clear unmet medical need, it is our goal to enroll this as rapidly as possible. We have certainly suggested that it's potential based upon the enrollment rate to get data as early as 2027. Obviously, this will be dependent upon how quickly we enroll and know that we are looking at sites globally with previous participation in Nurix studies to enhance our ability to get these patients in quickly. Thank you. Great, thank you. Just piggybacking on your earlier comments, Arthur, to accelerate entry into INI, what does that imply for your investment in oncology? As we look to 2026, should we expect more updates around the autoimmune side of the business relative to oncology? Thank you. Yes, in 2026, you should expect more updates on the INI side. I think that that'll include Bexobrutideg, but also, as we mentioned, IRAK4 is anticipated, phase I data. Next would be the STAT6 program. That timing is, of course, under the control of Gilead and then Sanofi. With regard to Bexobrutideg, we control that and we're in the midst of our multiple ascending dose study with our new formulation in healthy volunteers. That'll inform us as to dose and also aid us in selecting the indication, ultimately. I think that's all to look forward to in 2026. With regard to INI versus oncology, I don't think it's a zero-sum game. These are both really incredibly important indications where we can bring forward great therapy with great benefit potentially for patients. I don't see it, I don't think we see it as a zero-sum game there. We are eager to accelerate the INI, that's certainly true. Thank you for your question, Alexander. We'll next turn to Faisal Khursid. Great, go ahead. Hey, guys, can you hear me? Yes, but speak up a little bit. You're a little bit quiet. Got it. Thank you for creating the question. This one is for Gwenn. Really fascinating preclinical data on the STAT6 degrader. Could you maybe speak to the extent to which you guys see differentiation or how you should advise us to think about comparing your degrader versus the competitor STAT6 degrader from Chimera? Sure, thank you for the question. I think at this point, we are limited with what we can disclose for NX-3911. We do intend to work with Sanofi S.A. to be able to release more of that data as we go forward. I think, you know, comparing the data that we did release with the publicly disclosed data from Chimera Therapeutics, you can see that, you know, we are both achieving peak and molar potency. We both are showing selectivity and we are showing efficacy in animal models. I think the one other point that I can give you is not direct in terms of answering your question, but know that we have run all of the comparisons that we were able to run, at least the agents that were available to us before licensing. We tried to illustrate that point a bit by that data that we disclosed from our other collaboration, Gilead Sciences, to show you the credentialing that we do as we try to get enthusiastic about a particular molecule and make sure that it has a competitive position in the space. Sorry that I can't give you all the answers, but please stay tuned for the advancement of the information that will come out of this program as it completes IND-enabling and then gets into the clinic. Got it. Appreciate the perspective. Thank you for taking the question. All right, thank you. Next, we'll turn to Josh Nickerson. Josh. Hey, team. Good morning. Can you hear me? Yes. Awesome. Congrats on the progress. Thanks for taking our question. I just had a quick question on the duration of follow-up you would need in the single-arm phase II trial and how that coincides with projected timelines for meeting this threshold for obtaining sufficient enrollment into the confirmatory phase III trial? Sure. Paula, you want to address that? Sure. Josh, typically in a single-arm trial that you're using for potential accelerated approval, the agency does like to have follow-up. Typically, that's in the 9- 12-month range. As it relates to the second part of your question regarding the amount of enrollment that's necessary for the confirmatory trial at the time of assessment or evaluation by the agency, there is no specific number. They do ask that it be clear that it be significantly enrolled. That is not, there is no distinct number. Does that answer? Okay, great. Thank you. I just had a follow-up on this mutational coverage breakdown. Thank you for showing some of that proteomics data. I was curious, in terms of mutational coverage, is there a level of importance between wild type and BTK mutation coverage? Is degrading wild type BTK considered more significant? Is it more important to be more selective for wild type versus these other BTK-resistant mutations or any kind of color you can provide there? Great. Gwenn, go ahead. Thank you. Thank you. Thank you for the question. No, I don't think there's any criteria that would say that you should favor wild type over a mutant. Your real goal is to be able to cover all forms as close in proximity to potency as you can. What that means is that you have an easier way to ensure that your dose is going to cover all the forms. The PK graph that we showed you really distributed all of the coverage across those mutations for our drug. It was drawn using this criteria of DC95, which is 95% protein removal. What's interesting, if you compare that back to the cell killing graph that I showed you, where the killing seemed to occur at very similar potencies, you don't need to always degrade all of the protein to actually achieve cell killing. Each of those mutant forms has a different ability to maintain signaling. What is really ideal is to have a profile that is selective enough that you can push on the dose all the way to the greatest extent of protein removal of all forms that you can. That's what we were trying to speak to, that freedom to use dose to get biodistribution of your drug and get target coverage in all of the cells that really are relating to disease. That's our objective with all of our programs. I think our proof really is satisfying, I think, in that regard for Bexobrutideg. Awesome. Thank you. Thank you. Next, we'll turn to Jeet Mukherjee. Jeet? Hey, good morning. Can you folks hear me? Yes. Great. Thanks for taking the question. I was hoping you could dig into a bit more detail and compare and contrast your pivotal study strategy versus B1's, where they have a couple of randomized studies, including one head-to-head versus PERTO, and maybe some control arm differences in investigator choice therapy. I was just hoping you could elaborate on those differences. As a follow-up question, as a part of the ASH update, would we get a look at potentially median duration of response and/or median progression-free survival as a part of the phase one study? Thanks. Thank you. Paula, go ahead. What I'll begin with is by saying that both we and B1 have clearly shown that our goal is to get to the second-line setting in patients and to get to the market as quickly as possible. We are going to be getting to the second-line setting in two trials where they are ultimately going to be utilizing probably three trials. The way in which we are proceeding to utilize two trials to get to the market, specifically when we look at the confirmatory trial, what we are doing is utilizing one trial that looks at all of the globally relevant comparators that are used in the second-line plus setting. You will get information specifically about how our agent does relative to the total control arm, but also each of the individual components of the control arm, namely PERTO, BR, and IR. That, for me, speaks to our efficiency and our commitment to moving quickly to address the largest patient population or an unmet medical need possible. I'm so sorry. I lost your second question. Would you mind repeating that? It was just regarding the ASH update, and if we could get a look at duration of response in PFS. Right. We will certainly be updating our I-A data set and providing some insight into how we got to our 600 mg dose level. Yes, we will have more follow-up there on our long-term outcomes. Okay, we're coming to the end here, almost out of time. Just time for one more question. Kripa, if you're still on. Hey, guys, can you hear me? Yes. Great. Thank you so much. Congrats on all the progress. Appreciate you guys taking my question. A lot of the questions were answered already. I just have a couple more logistical questions. One for Hans. Given the capital raise today and the 1607 data that you guys recently reported, where does that program fit in in terms of priorities with CLL and the INI programs that you're expanding? From a phase III initiation, you said that you plan to initiate it in the first half of 2026. What are the gating factors for initiation of the phase III trial? Thank you. Okay, Hans, you and I will take that question. Take the part you'd like to take. Yeah, sure. For NX-1607, we are continuing to enroll and monitor patients in the phase I-A. We do have a phase I-B expansion planned, but I'll turn that over to Arthur. Yeah, this data is very new, as you know, recently published at ESMO. We are eager to fully interpret it and complete that I-A study. We still have patients being treated. It does look like we're seeing single-agent activity, most intriguing in colorectal cancer and prostate cancer. I hope everyone gets a chance to look closely at that poster. It really does appear to be exciting. The phase I-B plans can be formulated now, and we'd keep you updated on how we progress that program. I think, anyway, it's a great new immuno-oncology agent, and we look forward to progressing it. Paula, the last part of that was any gating factors to start the phase III? No. Excellent. Great way to end, and we're out of time. Really appreciate everyone participating today. We look forward to giving you future updates. Nurix Therapeutics is entering a new era in late-stage development and also a new era, I think, in IND-enabling studies with our programs as they're progressing. Thanks a lot, and we'll see you next time.