Good morning, everyone, and thank you for joining me at the first day of the annual Needham Healthcare Conference. My name is Gil Blum, and I am a Senior Biotech Analyst here at Needham & Company, covering the immuno-oncology and gene therapy sub-sectors. It is my pleasure to have with me today Dr. Arthur Sands, the President and CEO of Nurix. As a reminder, any viewers who are watching through our conference portal are able to submit questions via the Ask a Question box below the video feed window. With that, Arthur, maybe a bit of overview on the company. So 2023 was maybe a bit of a reset for Nurix. Could you briefly walk us through some of the changes that happened last year? Sure, thanks, Gil, for having us. Let me just use a few slides to illustrate some of our advancements in the past year. So actually, even before 2023, I think at Nurix, we've established ourselves as the leader in targeted protein modulation. We were the first company to introduce the concept of degradation of BTK with targeted protein degrader into the clinic, and we demonstrated efficacy now with two programs, which I'll talk about both of those BTK degrader programs. And established really a foothold in how degraders can be potentially superior to BTK inhibitors, which is, of course, a very large therapeutic and medical marketplace. We also licensed to Gilead a new IRAK4 degrader. So in 2023, we really unveiled the fact that we have an autoimmune component to our pipeline, which is rapidly growing. IRAK4 is, of course, a very exciting target for inflammation. This was the product of a big collaboration with Gilead that spanned now approximately four years, and this is the first program. There are multiple programs in the Gilead alliance, and we just recently announced an expansion of that alliance. But this IRAK4 degrader entering as a clinical candidate with Gilead was a very important advance in 2023. And then also, I think, probably the most transformative alliance that we recently signed in 2023 was with Seagen, now Pfizer, of course, and that is to introduce degraders as a new class of antibody drug conjugates that is using degraders as the payload on antibodies. So this brings us now forward with, in addition to the targeted protein degrader pipeline pictured here on this slide, also an antibody or degrader antibody conjugate pipeline known as DAC. So that's my sort of brief overview for the company, and we can go to any question areas you'd like, Gil. Absolutely. I think, the way I'm gonna parse this conversation, I'm gonna start with NX-5948 in oncology, and then we may talk a little bit about the potential in autoimmunity for the same asset. So first of all, there appears to be increasing evidence for the role of resistant mutations in relapsed refractory CLL, even with the advent of reversible BTK inhibitors. Can you discuss some of the progress the company has made with its internal assets, NX-2127 and NX-5948, in that regard? Certainly. So, NX-5948 is a pure BTK degrader. It's highly selective, and it is in the clinic now in B-cell malignancies. NX-2127 is a dual degrader of both BTK and IKZF1 and IKZF3, which are the targets of Revlimid or lenalidomide. Many people are familiar with that whole pathway, so it's a dual degrader. But in terms of addressing mutations that are arising specifically, and in a most troublesome way in CLL, let me illustrate that by turning to a very interesting slide here. Can you see that, Gil? Colorful slide here with the... Yeah. So, we're looking at NX-5948 across the top here, and in green indicates its highly, highly potent cell-killing ability, which is really basically nanomolar level, and not only in wild-type cells, but also C481S and these other designated mutations. These are mutations in BTK that arise most commonly in the clinic, and we have these patients harboring these resistance mutations in our trials now, both 2127 and 5948. But I'm focusing on 5948 here. What you're looking at below that are all the inhibitors, starting, excuse me, with the first-generation inhibitor, ibrutinib, which is a covalent. The next-generation covalent inhibitor is acalabrutinib, zanubrutinib. And if you look at their activity level across these mutations, you see by virtue of the different colors, their loss in potency. So ibrutinib falls off by about a thousandfold for both the C481S mutation and the L528W mutation. Now, when acalabrutinib and zanubrutinib were created, they did so in order to attempting to be more selective, but there really was not a lot of awareness of these resistance mutations, so they also have these liabilities. You can see actually falling off thousandsfold with regard to C481S. And then you get into the non-covalent, and the development of the non-covalent was with the understanding in the time frame that they were developed of the C481S mutation. And so pirtobrutinib, for example, was developed specifically to address that mutation, and you can see certainly it is green. It does address that mutation. However, it has introduced essentially or selected for new mutations and does not address some of the newer mutations that, that have been identified in the clinic. So what you see here is a whole class of inhibitors really all have their own liabilities. And so after breaking through one of the inhibitors, we think the next step for a logical step for patients would be to go onto a degrader, where we can address all of these mutations. So we're very excited by these findings. This was recently published in Science, and, we have, really established ourselves as, I think, being the leader in this concept that, degraders can be potentially superior to, to, inhibitors, and we, we, we think really represents the next generation of BTK, agents. I can talk more about how these work, if you like, getting into the scaffolding effects and all that, but I'll pause there. So maybe as a follow-on to that logic, I mean, if a degrader does not care what mutation arises, doesn't it make more sense to move it earlier and earlier in therapy? Yes. In fact, we do see it that way. On this slide, we're sort of listing it in the stage at which they were developed, but we think that our degraders could actually go all the way to the front line. You really wanna put your best foot forward when you start therapy, because it's been demonstrated for patients that the faster you get a response, the deeper the response, and the longer the duration of the response really bodes well for how the patient will do overall. Progression-free survival and overall survival all relate to how well they do up front in therapy. And so we think that these degraders can move forward in lines of therapy. We actually have quite a development plan that we're going to be outlining that covers both third-line, second line, and even first-line therapy trial, in order to establish these agents as really the therapy of choice. Okay. I mean, there, there's a good analogy here with venetoclax for that, you know, putting your best foot forward story, which is kind of what happened in CLL. Absolutely. And, venetoclax, in combination with a degrader, we think could be quite a potent therapy. We're very interested in getting going on our combination trials as well, with the degraders. However, also single-agent therapy still continues to be very important, in CLL, especially. We are dealing with an elderly population. Many, many really cannot tolerate necessarily dual agents or hospitalization or complicated therapies. However, we do think combination therapy is what could ultimately lead to the limited duration therapy. Of course, with the inhibitors, as with the degrader, you'd have to stay on for years. Limited duration therapy in combination could be quite exciting. Okay. So maybe to remind our audience, what is the initial response data we've seen for NX-5948 in CLL? This was most recently reported in ASH. Yes. Let me jump to that. So this was the trial that we recently reported on in ASH, and we're in the midst of dose escalation. As you can see, CLL, at the time, we reported only up to the 200-milligram dose. NHL at the time was at the 450-milligram dose. They're on two separate dose escalation tracks. But let me just also take a quick look at the patients that we are enrolling in the study. You can see that in CLL, we have 100%, of course, that have failed on a prior BTKI. So far, we have one pirtobrutinib failure. I should mention in the NX-2127 trial, which has a larger number of patients, we've had slightly over 30% pirtobrutinib failures already in that indication. Then you can see in NHL, where we have quite a heavily pretreated population, including patients. A significant fraction have had CAR T or bispecific, almost 50% have failed there, too. The drug was well-tolerated, and most importantly, if you look here at the bottom, we really saw no atrial fibrillation or hypertension at the time of this reporting. So off to a really good safety start in terms of this NX-5948. This is looking at all patients across CLL and NHL, so 26 patients at the time. And nothing really stands out in terms of safety by dose. And let's see if we can get to the results here that you asked about. Starting here on the right, you're looking at a very potent, BTK degradation at every dose level, and, this is characteristic of NX-5948. Very rapid, degradation of BTK. By day two, it's basically down to the limits of detection of this flow cytometry assay. This is a blood draw in patients taking it multiple days, so we're looking directly at the target disappearing, from, the bloodstream. And on the right, you're looking at our PK data that we have to date so far, so a limited number of patients. But in this group of patients, we're seeing, lymph node reductions pretty much across the board. We, at the very early stage of this trial, already we had a 42 or almost 43% partial response rate, same for stable disease. So, over 80% of patients showing some detectable benefit. We expect this to improve as we go forward in therapy. These responses take time to mount within each patient, and so at an early stage in the trial, this is quite encouraging... and you can see in the CLL patients, that we have a number of them, of course, still on therapy. And so we're accumulating a increasing response rate, and we're very encouraged by this. Okay. I'll pause there and just on the summary of that trial there, Gil. Well, that, that makes a lot of sense. So maybe focusing on this update- Mm-hmm that is currently guided for mid-2024, what, what can we expect to come up here? We're talking about longer follow-up, additional patients. How many additional patients? Yes, we expect this to be a very meaningful follow-up on the trial. I would say we would probably be looking at perhaps almost double the number of patients that we have. We'll have to see, of course, as we proceed in our data cut, as we approach our mid-year target for the disclosure. But enrollment has gone extremely well. It's actually accelerating, and I think that's a very good sign as investigators are seeing their patients respond to NX-5948. A lot of enthusiasm. We're open now, well, in the U.K. and the United States. We've been open in the U.K. and the United States, and now also we're expanding into Europe, the Netherlands. Those sites are open, and we're expanding into countries in Europe. This will be a meaningful mid-year update, and we expect also at the end of the year to once again provide a clinical update. Okay. And kind of to set expectations, what would you consider a win in CLL? Well, if you look at these advanced lines of patients, so these patients have multiple prior lines of therapies. And we'd estimate that if you saw between 50% and 70% response rate, that would be a big win. That's really, by the way, also in a dose-escalation trial. These are patients at different doses. Once we optimize the dose, pick a dose or two doses to go forward in phase I-B, then we think we're gonna be trending towards that 70% response range in this group of patients. The earlier lines you go, the earlier lines of patients, you could probably see even higher response rates. Makes a lot of sense. So we've also received quite a few inquiries on ongoing work at BeiGene, which seemed to show an ORR for their degrader of about 70%. And how, from what you know, how would you be able to compare and contrast NX-5948 with the BeiGene asset, or for that matter, with AbbVie's asset, what you know here? Well, I would say that they have entered the degradation space, and we're very happy that we now have some company. We are first in class, and we believe we're going to be best in class, but it's gonna take time to see enough patient data to really see these agents, if they can, if they distinguish themselves from each other. But you know, a year ago, we were the only degrader out there. And now we have both BeiGene and AbbVie, who I think are very much understanding of this resistance mutation story. But at any rate, I do think that we will be very competitive, if not best in class, based on everything we've seen so far. But it's a big market. If you look at this market, there's plenty of room for more than one degrader. These are the current inhibitor sales, and as you can see, ibrutinib, which is... It's a little bit hard to see, but it's in the darker green here, is losing out slowly to venetoclax and Calquence. So, I think the folks in the inhibitor space need to do something in order to maintain their market space. And I think, again, just to remind you, I think, you know, this kind of mutation data is not lost on BeiGene nor AbbVie, and so this is why I think they're addressing it. But we think we're going to have, really with both of our degraders, NX-5948 and NX-2127, which is the dual degrader again, we think we're gonna be offering, the kind of degrader, you know, spectrum that'll really cover, the unmet medical needs in both, CLL and some of the other indolent, NHL, Waldenstrom's, marginal zone, and mantle cell. And then with NX-2127, a dual degrader with dual activity, we think we can address the more aggressive lymphomas. So we've got, we've got quite a, a span here in terms of market potential, that, we think could be, ultimately superior to either BeiGene or AbbVie's, positioning. Also, we're motivated to sort of displace the inhibitors. You know, the- these two companies do have their entrenched. Different, yeah. Yeah. Yeah. Different generations. So we have a different strategy, too. So maybe again, to the analogy I made with venetoclax earlier, is there a potential for NX-5948 to be part of a fixed-dose regimen? Yes, limited duration therapy. And I'm showing you this mechanistic slide here. Here's one of the reasons why we think we could drive the therapeutic effect to a deeper level. It's on the left here is the whole complex that BTK forms, and it's really quite a, it's not just a kinase activity, it's a whole signaling or scaffolding function leading to the oncogenic growth signal. The inhibitors block one aspect of that right here, that is the phosphorylation or the kinase activity. But what we've shown through our degraders and our mutation studies in patients is that there's a whole scaffolding function that takes place, and by degrading it, we can actually wipe out the whole pathway. So we think we're able to drive a deeper and a stronger response. I think in combination with other agents, we certainly could look forward to limited duration therapy as being perhaps the future here. Kind of a last point in oncology before we shift to autoimmune disease. So NX-5948 can cross the blood-brain barrier. Would you consider conducting a small registrational study in CNS-involved patients? Usually, most studies exclude those patients. Well, so we are including those patients currently in our trials. And we are very excited by the preclinical data we've seen in terms of crossing the blood-brain barrier and showing activity in terms of degrading BTK in the resident microglial cells of the brain. So actually, we're at AACR here this week in San Diego, and our Chief Scientific Officer will be giving a talk on this very topic of the blood-brain barrier and how degraders can be engineered to cross the blood-brain barrier. And we'll be addressing then our aspirations, I think, around primary CNS lymphoma and secondary CNS lymphomas, which are very serious subsets of both CLL and NHL. But one of the real tricks here is to be able to get your compound across the blood-brain barrier and see activity. And so that's really what we'll be looking for and reporting on at AACR. There have been some pretty significant disappointments recently for using BTK inhibitors in autoimmune disease. There's a study from RKGA, Sanofi discontinuation, and myasthenia gravis. How would you say NX-5948 is differentiated from these other assets? Yes. Well, so one of the things that does differentiate us is you're looking at it, which is, again, we're destroying the scaffolding function of signaling. So it may be that some of the efficacy that people can expect to see with with BTK as a target, it's not enough to just block the kinase function. So that's one hypothesis. The other would be our ability to get into the brain. And what I'm showing you here, we've talked about a little bit, our preclinical models. This is a multiple sclerosis model. I'm sorry. No, this one is the arthritis model. Let me flip to the... Here we go. This is the EAE, or multiple sclerosis model, and you can see we're comparing 5948 here in dark blue to FTY-720, which is Gilenya, a very potent agent in MS, and we're seeing excellent abrogation of this autoimmune model in mice. So we do think we have the preclinical evidence that would support it. If we see now in the clinic, if we see activity in the brain, any activity in the CNS lymphoma patients, we think would provide us evidence that that we really have a real opportunity for CNS-based disease. Basically, as a proof of concept before moving into autoimmunity. Yes, and I think it's a very important proof of concept. Because, you know, these degraders, it had been theorized that it would be very difficult to engineer them to cross the blood-brain barrier, but we think we've overcome those difficulties, so it puts us in a very unique position. You know, the other thing I should mention that distinguishes us from inhibitors is it takes very few degrader molecules to actually get these therapeutic effects. If you look at the absolute drug levels of inhibitors that's required to cover BTK versus our degraders, we're talking about thousands of fold lower drug for degrader required to get a therapeutic effect, and we're seeing that in the clinic right now in oncology. So I think part of the issue with inhibitors is they can't-- they simply. It's simply very difficult to get enough drug on board and keep that target covered. With a degrader, one degrader molecule can destroy thousands of targets within the cell, and it's catalytic. So I think there's a lot of reasons to believe the scaffolding function, the catalytic nature of our degraders, that we're gonna be in a different class, and that we could bring success to autoimmune indications. Yes. I also think that's very notable in your dose response. When you show your preclinical data, all levels of BTK go to zero. Yes. Yeah, that's a proof of concept for catalytic activity. So just generally, when it comes to your discussions with investors, have you gotten pushback because of recent failures in the autoimmune space, or is that like a reason to believe? It's been more of a reason to believe. When they look at the total body of evidence that we already have built in oncology and the absolute potency of our degrader agents, people are very encouraging. Our investors are very encouraging in terms of going into autoimmune disease. Now, we're going quite methodically over this year to evaluate the opportunity to file an autoimmune IND for NX-5948, and we'll be updating that in the second half, updating everyone in the second half. But people are very enthusiastic for being the first BTK degrader to enter autoimmune disease. Currently, you have not guided to a specific indication. Should we expect focus to be CNS involvement indications because of the brain penetrance, or this is an open question? I t's still an open question. Certainly, if we see any kind of clinical activity in, again, the CNS lymphoma patients, that would, MS would definitely rise very high on our list. Let's put it that way. Now, when we approach these multiple indication opportunities, which there are many for BTK as a target in autoimmune disease, we like to evaluate both the large market opportunities, which could be, you know, very significant, but may take longer, and like to balance that with, is there a small, rapid opportunity we could also look at? So it may not be just one indication. We'd likely look to balance our portfolio of indications to allow for rapidity to potential approval as well. I'm not forgetting about NX-2127 here. So could the recent CMC improvements potentially make it more tolerable? The company has not seen additional cases of the earlier AFib signal. It's in that context. Yeah. So this was the safety profile of NX-2127 that we disclosed at ASH. Yeah, we have not seen new cases of atrial fibrillation. So the rates here have come down to, I'd say, BTK inhibitor-like rates. We reported on, you know, very significant BTK degradation in the center here. And what you're looking at here is also IKZF1 degradation at various dose levels. Now, so by the way, you don't wanna have complete degradation on this. This is really kind of pegging a lenalidomide-like degradation activity. This has translated to lymph node reduction in our CLL patients, quite significant, so we are seeing good activity in CLL, but also NHL. If I skip forward, we think the real opportunity for 2127 is in NHL, especially with these, a couple of these complete responses we've seen in very significantly advanced patients. This is one patient that we continue to follow. Here, if I can get the slide to advance for me. Well, let's see. Here we go. So I think you're looking at the scan, are you, Gil? Mm-hmm. Okay, so this is an advanced DLBCL patient. You can see the bulky disease. By eight weeks, we had a complete response, then, this is actually the 16-week scan, but this was maintained. This patient has been on study at this report for over a year and a half. We also have had a complete response in mantle cell patients. You can see this patient has all the lymph nodes have basically disappeared. These are heavily pretreated patients. This patient actually had had a stem cell transplant, as well as multiple rounds of chemo, immunotherapy, and ibrutinib most recently, and failed all of those. So we're very enthusiastic about these advanced, aggressive B-cell malignancies for 2127, where it really is gonna take. It does require a combination agent, and NX-2127 is, as a single therapy, essentially a combination agent of BTK degradation, plus, the immunomodulatory activity. Given the fact that you've seen some of the longer-term responses, one question that we've gotten a couple of times was: Is there any way to predict or find a biomarker that would tell you which of these patients are more likely to respond? It's an excellent question. And in DLBCL, and MCL, people have been looking. I just attended a conference on this entire on this topic of aggressive lymphomas, and the genetics are very diverse. So I don't think there's going to be an easy biomarker selection strategy. And we've seen responses in both the non-GCB subtype of DLBCL, as well as the GCB subtype. And then if you really drill into those subtypes, you see that there are actually many different genetics operating there. So I think in terms of DLBCL, it would basically be all comers. And we think that our dual agent could offer, you know, potential for all comers to be treated. So from a practical perspective, are you gonna need additional dose escalation for bridging your new, quote, unquote, "formulation" here? Yeah. So that's correct. So we've we're already in the process of distributing the protocols to sites. We have cleared the partial hold based on our new manufacturing process, which creates a chirally controlled product, which we think can be the commercial form and process for production of the product. So that's very important. But yes, we'll be starting out a 3+3 study design to bridge to where we were with the original mixture form. We think that this is going to behave very similarly, if not the same as the mixture, but it is a chirally controlled form, which is superior for manufacturing and for commercial development. Makes sense. Kind of a last one here: Is there still a potential role for NX-2127 at CLL? T here is. It could be fourth line plus. You know, there are patients, you know, or in combination or prior to CAR T, CAR T now being approved for these very advanced patients. So patients really still need options at the, you know, third and fourth line plus area. But I think that in terms of our primary development path, it would be NX-5948 for CLL, and NX-2127 for DLBCL and the more aggressive lymphomas. That's really the way we see the landscape for these two degraders. As for the next data disclosures in MCL and DLBCL, what guidance can you provide for investors, and what kind of activity would support a move forward? I'm sorry, could you repeat that? You cut out for just a second. So I was saying, there's an additional data disclosures for MCL and DLBCL, and what should investors expect, and what kind of activity would support moving forward? Oh, you're talking about NX-2127? Yeah. Yeah. So we have to, again, do the bridging study. So we have not guided specifically for data for 2127 this year. I think it'll be getting the study underway and looking for the biomarker data. All of that comes first, and then looking for response data. But we haven't guided in terms of timing. What I've got on the screen now is, is our guidance in terms of each of the programs we'll expect to be able to achieve this year and provide information on. Okay. I'd like to spend some time on NX-1607, a very interesting molecule. So you guys have basically the most advanced stage, CBL-B program in development. Can you elaborate a little bit on CBL-B as a IO target? What does it mean to be able to block it? Well, yeah. So, what I'm showing you here is where CBL-B works and lives. The T- cell, of course, but also the dendritic cell, and the NK cell. And CBL-B is an E3 ligase that basically down-regulates the immune response in all of these cell types. So it is essentially an intracellular type of checkpoint, if you will, but it's broader than a typical checkpoint. And so by inhibiting it, we believe we can elevate this immune response and increase anti-tumor activity. Now, we do have the first inhibitor in the space. It is NX-1607, acts as an intramolecular glue. So it glues the conformation of CBL-B in a closed conformation, turning it off, which then increases the immune response. So this is the effects—here are some effects we see in preclinical models, anti-tumor effects, which are quite potent across the spectrum of tumor models, colorectal, triple-negative breast. This is an increased survival curve here, and also B-cell lymphoma models. And we can also see activity in combination with anti-PD-1 antibodies here in red, our CBL-B inhibitor in blue alone, but the combination in this grayish color is superior. So we are in the midst of this trial, where we're continuing our monotherapy dose escalation and exploration, and we also have a combination arm with paclitaxel. So we have guided to reporting on this trial in the second half of the year, and that I think will be an important disclosure. This has been a program that we've kept pretty close to our chest in terms of our disclosures, and it is, we believe, a increasingly competitive field. We are the first in class, and we look forward to sharing news on this this year. Okay. And will we know ahead of that, disclosure, kind of patient number, type of cancer, or is this, you know, wait and see? It's a basket trial, so it's across indications, which, as you can see here, covers quite a lot of significant solid tumor indications. So it—what we'll be looking for is any signs of a partial response to stable disease, tumor shrinkage. It'll be difficult to compare since this is not apples to apples. These are very different indications. So it's primarily a dose identification and safety trial, with a traditional phase I trial. Now, you know, contrast that to the B-cell malignancies we were talking about. There, you get very rapid responses in these liquid tumors, a lot easier to assess what's going on very early. This is a more challenging space. As a follow-on to that, you had seen single-agent activity in preclinical models, but should that be our expectation here as well? I mean, as you said, solid tumors are more challenging. I would—no, I think it should be a much lower expectation for a dose-escalation trial. Yeah In solid tumors. Now, if we select a dose, and we're able to conduct a single-agent optimized dose trial in a single indication, then, yes, I would hope to see single-agent activity. But ultimately, this field of solid tumor treatment is a combination therapy field. But yeah, we need to optimize our dose before we can hope to see really kind of meaningful response rates. So maybe drilling down a little bit on the combination here. You're using a chemo combination. How informative is ORR in that setting, right? You can drive responses with chemo alone. It's usually durability that really kind of shows you that IO effect. Yeah. So I think you'd have to, obviously, you'd have to do a controlled trial in order to really illustrate this. What we're doing, looking at with the paclitaxel arm is establishing safety. Can we dose these together safely, and can we get meaningful biomarker activity on the CBL-B immune axis of the treatment? And that really needs to be established early, and that's why we started this combination early. Okay. I don't wanna forget about the very broad level of partnerships you guys have. Maybe it's worth kind of reminding people what key milestones should investors be looking for from Nurix's partners in the near term? Yeah. So, with Gilead, we just hit one, which was expansion of the alliance that we announced for three programs they're advancing, and of course, the IRAK4 degrader compound that they're developing in rheumatoid arthritis. So those were major milestones there. Sanofi is a program that started after Gilead, but it's on a similar, I think, pace for development of new development candidates. So, I'd say stay tuned for updates on that as we have done with Gilead. We've hit a number of preclinical milestones. They amount to a significant amount of cash addition, as you can see here in the green portion, and the upfront portion is in blue. And then Seagen is a very new alliance, so that was $60 million up front in September. A little early for updates on that program, but a very exciting program to create the degrader antibody conjugates, and we expect that to be advancing, as well. Altogether, we have, you know, quite a robust pipeline. Most of the time, we've spent talking about our own internal programs, but we have over a dozen programs with collaborators. We have also a 50/50 opt-in rights for six programs out of the total. So that's co-development, co-profit sharing options for each program. They're each slightly different between the collaborations, but that does give us significant product rights potential as well. Yeah, and maybe as a last point, because obviously you have a very productive partnership pipeline, why do you think there's a bit of a disconnect regarding the way that investors view the company? I mean, you may have the most, most productive pipeline with partners. Well, I think we do. You know, I think that we have not disclosed a lot about our targets with our partners, so I think that does create, you know, a little bit of mystery and hard to describe value if you don't disclose a target. What I can tell you is that we have highly valuable programs within each of these, and as they are disclosed, I think that our value will sort of correct to where it should be. Also, I think that people have been waiting to see data and competitive data from the degrader versus inhibitors. I think we're now just really entering that realm because we would often get questions like, "Well, it's so crowded with all these BTK inhibitors," but we're proving that, in fact, no, they all sort of look alike after a while, the inhibitors, and the degrader is really what you need, and we're, we're gonna inherit that very large market. Yeah, I think. Yeah, go ahead. I think the venetoclax story is very telling there, right? Yeah. What ends up happening is you pick the best agent first. Yes, exactly. So I think that this is gonna be a really important year for us in terms of investors seeing the sort of hidden value that is within Nurix pipeline. It won't be so hidden anymore. Maybe as a last technical point, just remind us of cash position and runway. Sure. So I think let me flip to that last slide that I had up there previously. Here we go. Yeah. Yeah. So, approximately almost $300 million in cash as of November thirtieth, which is the end of our fiscal year. And again, we've continued to accumulate milestones. We brought in, approximately $100 million in non-dilutive cash through our deals, last year as well. So, we do have a very productive, partnership base that helps our cash position consistently. All right. Arthur, thank you very much for your time. Thank you, Gil. Excellent.