Nurix Therapeutics, Inc. (NRIX) Earnings Call Transcript & Summary

Welcome, everyone, to the 44th Annual JPMorgan Healthcare Conference. My name is Tessa Romero, and I'm one of the senior biotech analysts here at JPMorgan. Our next presenting company is Nurix Therapeutics, and presenting on behalf of the company, we have President and CEO, Arthur Sands. Arthur, over to you.

Well, thank you, Tessa, and I'd like to thank the entire JPMorgan banking team for inviting us to this great conference. Another great year starting off here in 2026 jam-packed schedule. I will be making certain forward-looking statements. I refer you to our filings with the SEC. So at Nurix, we're dedicated to our mission to establish degrader-based mechanisms at the forefront of patient care. And this is an important emerging class that we see in the context here as shown on this slide, as a major new class of agents. And as agents have evolved over time, we've seen many new categories of therapeutics. Of course, if you go way back, small molecule inhibitors on the left, the original drugs, really very little innovation has taken place in the area of small molecules, I'd say, in terms of modality until targeted protein degraders all the way on the right. And these are unique small molecule drugs. I'll describe some of the attributes that distinguish them and make them what we believe will be a category medicine at least as large as antibodies, share certain things in common with nucleic acid-based therapies in terms of knocking down targets or trying to knock out targets, which really have been reserved for the use of nucleic acid-based therapies where you could delete a gene with CRISPR or knock down a transcript. But although these are very exciting and effective, but they do not have the breadth, or the expansive market opportunity that targeted protein degrader drugs have to knock down, or essentially knock out protein levels via small molecule agents that can be orally delivered. So, they hold this promise to fulfill this idea of being able to hit any target actually and do so in a very effective and pharmacologically relevant manner. So, we see the big picture is a new category of drugs emerging. So, before I dive into describing that, just a great nod to our terrific 2025. We think we really had a terrific year achieving several key milestones, starting with entering pivotal trials with our DAYBreak-201 study. And this is in CLL. It's designed to be a study for accelerated approval for bexobrutideg, our lead BTK degrader. We recently -- very recently presented very robust results at ASH in Orlando, with an 83% objective Overall Response Rate in patients that had received a mean of 4 prior lines of therapy. So very heavily pretreated patients. And for the first time, we revealed, we're able to calculate our initial calculation of progression-free survival or PFS at 22.1 months. And that's across all doses tested in the Phase 1a dose escalation arm of the study. In addition, we secured the 600-milligram dose, which is our highest dose tested. We did not see any DLTs along the way under Project Optimus. And this really puts us in a very strong position to push on efficacy, with a safety profile equivalent to lower -- all the lower doses, basically, I'll show you some of the data there. But this 600-milligram dose, we've now taken into pivotal studies. And again, that initiated in October 2025. With regard to our pipeline and our partnership momentum, tremendous progress made -- we're in collaboration with Gilead for our IRAK4 degrader, which is in an ongoing Phase 1 SAD/MAD study in autoimmune disease. And for STAT6, we are in IND-enabling studies, a STAT6 degrader NX-3911 with our partner, Sanofi. And we initiated our healthy volunteer study for bexobrutideg with our new formulation, which is specifically designed and intended for autoimmune disease. So really, you see our emerging partnership pipeline and our wholly-owned pipeline really enabling autoimmune disease as the next major indication for Nurix. And we secured a very strong financial position. We strengthened our balance sheet with a very successful follow-on offering of $250 million that was led by JPMorgan. Thank you. And we earned significant milestones along the way, $47 million through our partnerships with Sanofi and Gilead and Pfizer. So, we're very well capitalized with cash and investments of approximately $650 million, greater than that. So that was all 2025. Let's turn to 2026, where I'll spend most of the time giving you the most recent data from ASH reviewing that for our bexobrutideg, our lead program, our BTK degrader there at the top. I'll hit on some of the other programs and also at the end, be able to highlight our progression of bexobrutideg and our other programs into autoimmune disease. So let me start off with, again, looking at the bigger picture here in terms of why degrading BTK and degraders in general are such an important new class of medicines. And this will be illustrated by bexobrutideg's latest results. So first off, we are the first deg, which means we earned the Suffix deg, bexobrutideg deg, unlike IBS or MABS, because it defines a whole new category of drugs. And this was endorsed by USAN and international naming authorities, which really took quite a bit of work and really recognizes the fundamentally different pharmacology of these agents as compared to regular inhibitors or antibodies or anything else actually. So, we are the first agent that has this new suffix. And why is that? Okay. So first, Degradation unlike inhibition removes all the functions of BTK or any target you degrade, unlike inhibitors. So, this includes the structural functions of proteins, which are known as the scaffolding functions of proteins as pictured here on the left of the protein falling apart or being -- it's actually being actively degraded by the ubiquitin proteasome system. Number two, it acts -- these molecules act catalytically. So, a single drug molecule, as pictured on the very left here, cycles from capturing the E3 ligase, tagging the BTK protein with a ubiquitin ligase, a ubiquitin protein tag via creating this bridge between BTK, or the target protein and the ligase. And then once tagged, the target protein is degraded by the proteasome of the cell in a highly specific manner. The drug molecule is then released to remain in the cytoplasm and go do it again and again. So, what does that mean? Well, we've calculated and actually measured that one drug molecule in a cell of bexobrutideg can degrade up to 10,000 BTK proteins per hour. So, one drug molecule can remove 10,000 target proteins. Compare that to the one-to-one stoichiometry of traditional inhibitors, extremely different, exquisitely potent is what that translates to. In addition, what's pictured here is exquisite selectivity as measured by global proteomics. So, the upper left protein -- the upper left quadrant of this plot, all you see is one dot, which is the BTK protein as measured under proteomics. And all the other gray dots at the bottom are all the other proteins that don't move at all or are nonsignificant changes. So very significant degradation of BTK. In addition, we are active against all known resistance mutations that have evolved in the presence of BTK inhibitors, the current class of drugs. And so it's pictured below bexobrutideg, you see bexobrutideg across the top. All green means nanomolar-based degradation potency in cell lines. And these cell lines across the bottom have been engineered specifically to contain BTK inhibitor resistance mutations that we are encountering in the clinic currently. So, each of these confers resistance to different inhibitors. And then you see the list of inhibitors. And then the color is indicated in red means the inhibitor lost 5,000-fold potency and ability to kill these tumor cells. And blue is loss of 1,000-fold potency. Basically, they're inactive. So, you can see the inhibitors have vulnerabilities across a wide spectrum of BTK inhibitor resistance mutations. But our degrader is mutation agnostic. It can degrade all of them. And so, this is very different again compared to having to design a new inhibitor for every mutation that occurs. That these degraders and our degrader has this terrific ability to address the resistance mutations. This is really quite a phenomenal additional attribute and quite distinguishing for bexobrutideg. We cross the blood-brain barrier, and we can hit tumors. In this case, you're looking at a primary CNS lymphoma tumor in the pretreatment scans across the top, you can see in the red circles where the lesion was. By 8 weeks, complete response of lesion has disappeared. We've seen this not only in primary CNS lymphoma, but also CLL with CNS involvement, quite extensive CNS involvement. So, these molecules have the ability to enter the brain and continue their catalytic activity to treat disease. very encouraging. And this all adds up to across the board, very robust objective clinical response rate of 83%. This is our Phase 1a data in its totality. And again, the progression-free survival, now measurable at 22 months, although not the final measure, we see this extending even beyond this, especially at our higher doses. What does this look like for patients? This is their lymph node reduction. So, every bar on this graph is a patient, and we're measuring their -- the size of their lymph nodes as they've been reduced when on therapy. And right off the bat, you see the overwhelming number of patients, overwhelming proportion respond to this drug with significant lymph node reduction. Across the bottom, you're looking at with these colored dots, the different mutations that each of these patients are harboring. So, in the top series of boxes are the -- what's called high molecular risk features. This is p53 and other tumor suppressor gene mutations, a whole spectrum of those. And then the bottom 2 rectangular areas are the BTK mutations, all the different types. So, when you add this all up, you see this is a heavily burdened -- heavily genetically burdened patient population. And regardless, the degrader shows this terrific activity across the board. So very, very impressive. The gray boxes, by the way are wildtype -- wildtype mutation or they're not mutations, the wildtype status of each of these genes. And so, the degrader works in wildtype as well. So, it's not just mutation specific, although I've been dwelling on that, but it also covers wildtype proteins as well. So, a very broad patient population overall. Here, we're looking at this 22.1-month progression-free survival curve as generated in our Phase 1a data set. These are patients that, again, are heavily pretreated, median of 4 prior lines of therapy, 83% response rate and this PFS curve, which is really showing great duration of response in this patient population. So, we're very encouraged by this. And again, to emphasize, this is including all doses tested from our lowest dose of 50-milligram, those patients as well, 100 milligrams, 200 milligrams all the way up to 600 milligrams. So, we don't think this is even optimized yet. So, turning to dose optimization. We were very pleased to have aligned on the 600-milligram dose under Project Optimus with the FDA as the go-forward pivotal dose. And what's so important under Project Optimus and in dose selection is drug safety. That's number one. And what we're looking at here on the right is the drug safety profile of the 600-milligram dose as compared to all other doses, so 70 patients compared to 126 patients, really good patient numbers. And the bar graphs going each way show you rough equivalence between the 600-milligram dose size of the bars and the other doses. So really, there's no difference in safety profile between the high dose and all lower doses. This enables us to really push on efficacy with the 600-milligram dose while not sacrificing safety. And we see no dose-limiting toxicities, no systemic fungal infections, which we think is important. And I think that speaks to the selectivity of bexobrutideg and not hitting other targets associated with T-cell function. So, infection is a known risk factor for patients with CLL, but it is also known to be an issue if there are off-target effects that can hit T-cells, and we think we're very clean against T-cells. In addition, from a cardiovascular standpoint, we're very clean. We only had one new event of atrial fibrillation in the trial. And this compares to the background rate of Afib in this elderly patient population. So, we're seeing only background rates there or essentially or below that, but at least at background. And so, we're very encouraged by the safety profile. Again, this allowed us to move forward with the 600-milligram dose as the go-forward dose. So why is this important for efficacy? So, what we're showing you here is in that randomized Phase 1b cohort of 200-milligram versus 600-milligram under Project Optimus, the PFS, the early PFS curves in maroon there for the 600-milligram compared to blue for the 200-milligram dose. And you can see right off the bat that we're trending towards even a higher PFS than that 22 months that I cited earlier with the 600-milligram dose. So, we think this is very encouraging from a safety and efficacy standpoint. It puts the drug really in a best-in-class profile for degraders and I think also for inhibitors. And so with respect to that statement, here, we're just lining up a comparison between bexobrutideg data from the Phase 1a and pirtobrutinib, the latest data that they published in BRUIN-321, the non-covalent inhibitor from Eli Lilly, which has shown some excellent results. Now granted, this is a cross-trial comparison, so take it with the appropriate grain of salt. But doing our best to look at some of these parameters, our overall response rate of 83% compares very favorably to the 65% with pirto. Median duration response, 20.1 versus 13.8. Median PFS, 22.1 versus 14. And overall, we think this compares extremely favorably to the most recently approved agent, new agent in the field, which was just approved December 3, just before ASH kicked off. In addition, if you look at the bottom of the slide, we're achieving these results in a patient population that is quite arguably a more difficult-to-treat patient population than what pirto encountered in their 321 trial. So median lines of therapy, 4 versus 3 and greater than 4 lines of therapy, we've gone up to 11 lines of therapy in our trial. The prior non-covalent exposure, of course, now we're seeing pirto failures in our trial. About 1/3 of our patients have failed pirto, and yet we're seeing responses in those patients. And then I think this is very important, the bottom bullet there prior BCL-2 inhibitor exposure, which is approved second-line therapy, venetoclax largely. In that population, we're seeing an 83% response rate versus 50% that pirto reported. So, we think along many lines of analysis, this puts bexobrutideg in an extremely competitive position to the non-covalent inhibitors and the leader in that space, pirto. So that has led us to -- we've already launched this pivotal trial, I'm showing you here, but it's led us to also modify our Phase 3 design for our randomized controlled trial, which I'll tell you about in the next slide. But first, just a moment on DAYBREAK-201, CLL-201. This is up and running. It started enrollment in late October. We're targeting approximately 100 patients to enroll in this trial. We proactively altered the enrollment criteria to include patients that have failed pirtobrutinib as well as the prior BTK covalent inhibitor and a prior BCL-2 inhibitor, most likely venetoclax. So the so-called triple-exposed population, an area of high unmet medical need. There are no approved agents. We were anticipating here pirto's approval, full approval. So that's why we altered this group to be in this triple-exposed population. And so, this is enrolling as we speak. And again, we're at the 600-milligram dose level. Our primary efficacy endpoint will be ORR, and this is designed for potential accelerated approval. So, with the latest results that I described, this today, we announced we've modified our Phase 3 plan, our Phase 3 design, the confirmatory trial, randomized controlled trial will be between bexobrutideg at 600 milligrams once a day against pirtobrutinib head-to-head with standard dosing for pirtobrutinib of 200 milligrams once a day. So, this is a modification from what we had formally announced, which was an investigator's choice arm in the control arm, which included traditional chemoimmunotherapy as an option. But given our results, as I just -- as I went over, highly competitive results and given that now pirto has full approval, this becomes a new standard of care, and this becomes a very clinically relevant and timely trial to implement with the latest approved agent in CLL going head-to-head. We think this will really put us in a great position to harvest these results as they come and ultimately take up, we believe, an ability to prove that degraders are superior to inhibitors because of all the attributes, unique attributes to how we hit the target, how we remove the target so thoroughly and how we can address resistance. So, this is a major study, not just for CLL, but I think it will have implications for oncology more broadly with respect to degraders being the way to hit an oncology target as opposed to inhibition. In addition to those main 2 trials, we are also launching a Phase 1b/2 to start to look at combination agents. Combination trials with bexobrutideg. Bexobrutideg plus venetoclax is going to be a key study ultimately, that's on our list here. Then a triplet, Bexobrutideg plus venetoclax and rituximab, and these are in the second line. And then obinutuzumab also, so anti-CD20s starting in the second line, but also enabling on the bottom there across the bottom, a frontline trial. So moving bexobrutideg to the frontline in combination. And there are many other combinations possible given our excellent safety profile. And of course, given the efficacy we can deliver, we think we can drive very deep responses here in combination, and we're looking forward to initiating this trial in 2026 as well. So just from a standpoint of what kind of patient populations we're looking at, in the second line and third line. Starting -- looking globally, there are about 60,000 patients that are treated initiating treatment per year. So, a very large patient population, just in the U.S., 19,000 in just the second line and third line. If we can penetrate the first line, that will grow. Current BTK inhibitor sales are annualizing at $12.5 billion per year, about $9.5 billion just in CLL. So, we're addressing very large markets. And I think the big picture here again is can the degrader displace the non-covalent inhibitors first? And then can we challenge the covalent inhibitors to show, again, degradation being the superior way to treat cancer. So, we -- this is graphically showing you how we can unleash waves of clinical benefit and value creation. Starting in the dark blue, the accelerated approval trial, relapsed/refractory CLL, second line plus, that confirmatory trial now head-to-head with pirto and then moving into combinations of potential in the front line. But then also another wave of value creation in Non-Hodgkin's Lymphoma, where we've seen some great results in Waldenstrom's, 83% ORR, 83% to 85%, really corroborating our CLL results. And then we have designs to go into immunology and inflammation indications, including those based in neuro, derm and heme, where BTK inhibitors have made some inroads. And I'll just wind up here, so we'll have some Q&A time. This is Nurix's industry-leading wholly-owned and partnered degrader portfolio in autoimmune disease. Bexobrutideg, we have a new formulation that we've made designed for autoimmune indications. It's a tablet formulation. It has certain PK/PD attributes that we think will be really appropriate for that. We're going to look at much lower doses for autoimmune disease than what we're seeing in cancer. This is a huge market opportunity. And then our STAT6 degrader with Sanofi. So again, addressing a very large market opportunity and IRAK4 degrader with Gilead. So, I mentioned the SAD/MAD studies ongoing for bexobrutideg, we'll have data this year. For STAT6, we anticipate Sanofi filing an IND for the STAT6 degrader NX-3911. Those IND-enabling studies are ongoing under Sanofi's guidance. And with this program, we maintain an opt-in right post human proof of concept for 50-50 cost profit share in the United States. It is a very important part of our portfolio with this very important option. Again, this is after we see data from Sanofi in patients with type 2 inflammatory disorders. We have a very similar option with our IRAK4 degrader with Gilead, picture on the right. This compound now called GS-6791 is in the SAD/MAD study currently, so about a year ahead of the Sanofi program. We expect to see data from this study this year. So, a lot to look forward to in 2026, which is summarized on this slide. So -- in terms of our pivotal development pathway, enroll, enroll, enroll for our Phase 2 DAYBreak study, launch our Phase 3 confirmatory study with the new control arm, pirtobrutinib head-to-head and then initiate our combination protocols for bexobrutideg. In terms of the I&I program, I think I already mentioned, we anticipate data from the Phase 1 with Gilead. We look forward to an IND filing for NX-3911, STAT6 degrader and then as well as many clinical updates anticipated for bexobrutideg with our additional CLL cohorts, including BTK-naive patients, BTK mutation patients with resistance mutations exclusively, CNS patients. So, a number of CLL cohorts that are still ongoing as yet to report on. We look forward to reporting on them this year. And then also our NHL cohorts where we have not given any really substantive NHL data to date. And we have some exciting data. We've seen complete responses in basically in every category of NHL malignancies. And then our NX-2127 zelebrudomide, we anticipate to report on the Phase 1a cohorts in dose escalation. So, I think I've taken up a fair amount of time, but left some for Q&A test, so we can go to that. Thank you.

Great. Thanks, Arthur. So, I thought I might start our conversation with a little bit of a bigger picture question here. How do you see your portfolio evolving over the next several years? And how do you think about relative risk and where you could see the highest reward?

So clearly, as I indicated, I think we'll have an I&I portfolio that will be substantial over the next couple of years. And the targets are already on the board that will be clinically reading out. So BTK, number one, IRAK4 and STAT6, probably data from IRAK4 before BTK and then STAT6 would come. So, I think those are 3 major target categories that basically cover many, many indications. So, we'll have that. We'll see that. And that will be -- with our options, that's part of our portfolio. In terms of oncology, I think we've -- in terms of risk, I think, too, I think there's probably still risk in oncology, but we've significantly derisked. I think we've moved CLL from derisking to now best-in-class profile. So, it's not a matter of risk so much as how good can it be. So, I think that's a great position to be in. I think with some of our earlier compounds in oncology NX-1607, we're going to be able to derisk that in solid tumors. That's a novel IO agent where we've seen some encouraging results in 1a in prostate cancer and colorectal cancer. So, I think that could be derisked over this same time horizon. And then I think with regard to new indications, we'll have to see. But I think that the risk profile has been really materially changed here for Nurix in terms of the degradation modality being effective, again, moving from risky to how effective is it.

And we're kind of -- well, not that fresh off, but relatively fresh off of ASH. Maybe you could talk a little bit about that conference for Nurix and -- but specifically, what the feedback you're really hearing from physicians and institutions around the asset and the BTK class overall?

So what we clearly heard at this most recent ASH was that bexobrutideg is really adopting this potential best-in-class profile. When you look at safety, dose at the 600-milligram dose level and you look at efficacy. I think it is dawning on people that this is really a best-in-class -- potential best-in-class agent, number one. Number two, that degradation mechanism itself is going to be a player and probably a big player in CLL and B-cell malignancies. And I hit on all the points of why. And I think that we had tremendous uptake and enthusiasm from our investigators as we're launching these studies. So, I think that -- those were some of the main sort of take-homes for me in terms of what's next and majorly innovative in CLL, I believe the consensus that I sense was it's going to be the degraders.

Okay. And can you talk in a little bit more detail around how you think about the time lines for your pivotal Phase 2 DAYBreak trial? And how quickly do you believe you can enroll 100 patients? And what type of activity profile do you think could allow for registration in the U.S.?

So our goal is to fully enroll DAYBreak-201 by the end of this year and to have data in 2027. So, we're at the front end of enrollment going well, but we're still at the front end. So, we can't put a finer point on that yet. But as soon as we can, we will. And I think in terms of the data in terms of efficacy, we're in a patient population with no approved agents. So typically, the bar is rather low. And the accelerated approval opportunity should be significant. So I can't quantify that either. But in this patient population already in the data we have so far, we've been seeing a response rate of about 65% or so. And this is, again, a heavily pretreated patient population. And what was the second part of your question?

I think you actually nailed it.

Okay. Great.

I think you nailed it. So -- and you talked a little bit today, Arthur too, just around the change to your Phase 3 trial. Anything else you would like to say on what drove that decision to not use a physician's choice arm? And like what were the key levers that you really thought about in making that decision and deciding that was the right decision for Nurix?

Well, driven by the data that I reviewed, so I won't repeat it here, but that was a key piece of decision-making information. But I think also that the goal here is to design a trial that can be practice changing that can really advance medicine. I mean, that's really what we're here for. And what we're really looking at here is taking bexobrutideg a degrader and looking at the best next class inhibitor made. And if we can beat that, that is practice changing. And as I said, I think it has implications for all of oncology more broadly. So those -- that was a major strategic consideration for the change. There are logistical advantages and considerations, too. It's an easier trial to enroll. It's a simple head-to-head. Even the control arm is attractive to patients. This is the latest approved agent. So very attractive trial to be involved with. Either way, it's a win-win for patients to be involved. So that was another -- so those are the 3 main areas of consideration.

Okay. And at the current time, how do physicians tend to compare and contrast the evolving clinical profiles of bex deg and BeOne's competing BTK degrader. What are the lingering questions that physicians have as they are trying to understand these relative profiles?

So, there are classic questions that people grapple with in the early stages of trials. And so we have some physicians who say, well, these agents look more similar than different. That doesn't really say much. If you really read between the lines, we think they look very different. So, we think that we have exquisite selectivity, number one, as measured by global proteomics, and we've done some comparisons there that we think substantiate that. So, selectivity is key as it relates to ultimate clinical safety. So, we think we win there. We have measured relative potency. We're 20x more potent on the cell-based assays for degradation than the BeOne compound, 20x is a large number. So that kind of potency, combined with safety usually translates to better efficacy. So, I think people are going to start to connect these dots and see us as a distinguished best-in-class profile, but that's sort of the forward-looking way. The current view is perhaps they're more like than they are different. And what this does, though, is it substantiates the field that it's not just one company showing these kinds of results and their response rate is very high, 80-plus percent. But now it's 2 companies, with different molecules corroborating similar results. So this is a real thing, a real opportunity.

This might be a hard question to answer in the time that we have allotted here, but where do you think the most compelling opportunities are for Bex deg beyond CLL?

So, we're very intrigued with our brain activity that we've seen in CLL. So, we're talking about seeing really dramatic responses in patients with advanced brain disease and tumor burden in the brain. And so that obviously opens up non-malignant CNS disease. The most large opportunity and significant would be multiple sclerosis, so MS is an area, I think, that we are highly interested in. Now that would be a major next step for us. We're not declaring our indications yet, but we also are very intrigued by dermatologic applications, which could be faster, to proof of concept, may take much lower doses actually and really could offer another major more mass market opportunity. So, I think those 2 areas are very intriguing. And then you have nonmalignant heme. So, things like ITP and wAIHA, where inhibitors have shown results as well that are positive. And a number of these areas, inhibitors have given us some proof of concept. But we have evidence that the degrader mechanism can be superior to inhibitors in autoimmune disease, just like it is in oncology. And again, because we're hitting that scaffolding function, which is a major signaling function that is completely unaddressed by inhibitors.

And maybe I'll just jump here and do like 1 or 2 more questions.

Sure.

So, what are the recent key learnings from the broader landscape targeting STAT6 degradation that you believe has -- may have read-throughs to NX-3911? And how does 3911 compare with other STAT6 degraders in development?

So clearly, the only other STAT6 degrader in development is Kymera. So that must be what you're asking about. I think they showed great data in Phase 1. I think they have established STAT6 mechanism proof of concept with their early data. So, it's highly encouraging for the field. We believe that they will go forward successfully. It is -- it will expand the market dramatically, as they've said in their presentations beyond the injectables. So, there's room for many, many compounds here. It doesn't -- it's not an all or nothing game here, a winner-take-all game. I think there's going to be several winners here. We've designed our compound to be a winner with Sanofi. We've been working with Sanofi for 6 years on this compound from target inception to where we are now in IND-enabling. And we've met every milestone along the way in terms of optimizing these compounds to big pharma standards, if you will. So, I think this is another league in terms of 3911 is in another league in terms of preclinical development and polishing and rigor. So, our goal -- our design goal is to be best-in-class. I mean, that's our design goal across the board. It's sort of -- that's a corporate policy. Now we have to see that play out with data, but that is -- that's our policy. We're down to a minute.

Yes, I might have to leave it there.

Okay. Well, that's good.

Arthur, thank you so much and to the entire Nurix team for being here. We really appreciate it. And thanks to all the investors for joining. Thank you.

Yes. Thanks.