Thank you for staying with us. This is the last session of the day, and, my name is Kelly Shi, one of the biotech analysts here. In this session, please join me in a welcome Dr. Arthur Sands, CEO of Nurix Therapeutics, for this presentation. Arthur, welcome. Thank you, Kelly, and I'd like to thank your research team and also the Jefferies banking team for inviting us to the conference today. It's my pleasure to walk through our pipeline with you. I will be making certain forward-looking statements and direct you to our Securities and Exchange filings regarding the risk factors that face our business. So today, I'd like to walk through our BTK-targeted protein degrader programs, NX-5948 and NX-2127, in that order, and some of the latest data associated specifically with NX-5948. But while I'm on the pipeline slide, I'll just mention some of the other programs. We also are in phase I with our CBL-B inhibitor program for immuno-oncology. That's in a basket trial, phase I basket trial. We have multiple programs with collaborators in the area of targeted protein degradation, Gilead being a major collaborator for Nurix for some years now. We're based in the San Francisco Bay Area, so we've worked very closely with Gilead in that neck of the woods. Recently, they in-licensed one of our targeted protein degrader programs in our internal portfolio, which is at the bottom of this slide, the IRAK4 degrader, and they are progressing that through IND-enabling studies targeting rheumatoid arthritis with that compound. Then also, most recently with Sanofi, we disclose our STAT6 degrader program. Both of these programs, IRAK4 and STAT6, are actually several years in the making as we've coming from when we first started those alliances, so it's nice to see them progressing toward entry into the clinic. STAT6, of course, a very exciting anti-inflammatory target, which is basically on the Dupixent pathway. These are all oral molecules. Our target product profile are once-a-day oral molecules for I&I. And then, also as part of the INI portfolio, we're listing our own NX-5948, the BTK degrader, which I'll spend most of my time on. Just before I leave this slide, I do want to mention our DAC programs, which are highlighted in a separate color there with Pfizer. That alliance was formed formerly with Seagen. DAC stands for Degrader Antibody Conjugates, a very exciting new class of ADCs in which the degrader is a payload, and I'll talk a little bit about that at the end of my talk. So, turning to the BTK programs, this, of course, is a very well-established target, BTK, and well-established multi-billion dollar market, focused largely in B-cell malignancies, CLL, chronic lymphocytic leukemia, being the driver there. You can see the lion's share of sales are in the covalent BTK inhibitor category, initiated and dominated by Ibrutinib for many years, but now acalabrutinib and zanubrutinib are taking market share, largely due to some of their demonstrated improved safety profiles, as well as excellent efficacy. But there's a very important need for targeted protein degraders in this. So why are we pursuing BTK with targeted protein degraders? I'll show you data related to the first point there, which is overcoming treatment-emergent resistance mutations, which are a growing problem in this category of disease, CLL, specifically. Secondly, by degrading or removing BTK from the protein, we can address a newfound function of BTK, which had been hypothesized, and it's known as the scaffolding function, which is a structural signaling function for growth. The kinase inhibitors really cannot address this. They are enzymatic inhibitors, but by hitting the scaffolding function, taking that out, degrading that protein, we get an extra boost of efficacy, we believe, with the BTK degrader. And so then clinically, it has broad use and application in B-cell malignancies, as already mentioned, but furthermore, in autoimmune disease, and we're headed in to examine that direction as well. So overall, we think our BTK degrader program can displace, has the potential to displace inhibitors and really be the next-generation favored BTK targeting agent. So on this slide, I'm just showing you a bit of data regarding the molecular basis for that statement, that we could displace, degraders. What you're looking at in that colorful heat map is, across the top, the extreme potency in green, the highest potency of 5948 across the several different mutations, C481S, V416, and so forth and so on. And we maintain our nanomolar level of cell killing. These are these mutations, we've engineered by CRISPR into a cell line and then done an apples-to-apples comparison of, with our degrader against all the inhibitors. So the first generation, of course, was Ibrutinib, then you see the other two covalents, and then on into the non-covalents, down the list. By looking at the color of this, so blue means loss of potency at about a 1,000-fold loss in potency, and those are known resistance mutations to Ibrutinib, C481 being the most predominant. But then red is, of course, a severe loss, down to a 5,000-fold and loss of function in cell killing. And what you can see clearly by this analysis of emerging resistance mutations is that all of the inhibitors have their liabilities and their defects, and that's why we believe we have this great opportunity to help patients in these categories of mutations. So a little bit now on our NX-5948 trial, and some of—I'll just review a little bit of our ASH data, mention some of our recent AACR data, and then bring you up to the current with the EHA or European Hematology Association data. So it's a dual-track dose escalation trial in both CLL and NHL. I'm gonna focus primarily on CLL, and as we move through the dose escalation, you can see the doses are from 50-600 milligrams. So this is going back to the ASH data set at the time, which is December 2023. At that point, we had enrolled a total of 26 patients between CLL and NHL, only 7 in CLL, and you can see the treatment profile there. Median prior lines of therapy were three at this point, and we started monitoring the BTK mutations at the bottom of this. So as we present, just to fast-forward to EHA, we now will plan on seeing over 20 CLL patients. We'll have a much more mature BTK mutation data set, and we're advancing the lines of therapy in our patients as well. Again, back to ASH, the treatment was very well tolerated, and NX-5948 had an excellent safety profile. You can see the predominant events were cytopenias associated with the disease. Primarily, we believe, patients can be admitted into this with grade 4 cytopenias, with significant bone marrow and lymph node involvement. But most notably, at the bottom there, we saw no atrial fibrillation, which had been considered a problem in the BTK inhibitor class, and that was very gratifying to see, as well as no hypertension, and really patients remaining on therapy quite well. This was the swim lane plot at the time of ASH in December. You can see in CLL only seven patients, but at that point, we were already starting to see responses in the lowest dose group of 50 milligrams. Again, that was very gratifying to see, and we're eager to mature the data set and see more patients, longer duration of therapy. With longer duration of therapy in this indolent leukemia, we tend to see improvements in response rates. And so now to fast-forward to the EHA abstract publication, which just took place April sixteenth, you can see we have enrolled quite a few more patients. We see our response rate going up to 70%. It had been 43% at ASH, so a very solid progression there of response rates. We see with the green arrows, you can see all of the patients who remain on therapy, very high rate of patients staying on therapy and obtaining benefit, the responses being the green triangles and stable disease being the open circles. You can see several of the open circle patients progress as they stay on therapy, achieving a partial response then, the green triangle. So that's also a very nice progression of increased response rate. To the left, on the slide, you can see check marks indicating those patients with BTK mutations, as well as the next column, p53 mutations, which also are associated with very poor prognosis. So as we go forward to the EHA presentation, we do have an oral presentation on June 16. We will be detailing these mutations, i.e., their DNA sequence, which category they're in, whether they are kinase proficient mutations or kinase-dead mutations. And that's a very important point that I didn't really bring up on the slide with all the mutations. But several of the mutations that are emerging have no kinase activity, which is actually a somewhat surprising finding for a kinase, that without kinase activity, it can, through mutation, still signal growth of the cell and is a source of resistance. Clearly, kinase inhibitors will not have an ability to affect that mutation, and again, degradation, we think, is the superior modality to address all of these. So this—we'll be elaborating on this swim lane plot with more patients and longer evaluation and greater detail around the kinase mutation status for BTK. I do want to share one case study that we did report. Now, I'm turning to our more recent AACR presentation revolving around CNS involvement with leukemia and lymphomas. We do enroll patients, allow enrollment of patients with primary and secondary CNS lymphoma, as well as CLL with CNS involvement. This is somewhat unusual for a phase I study, but preclinically, we had seen very good evidence that NX-5948 crossed the blood-brain barrier and had activity in animal models of tumor growth in the brain, as well as in multiple sclerosis animal models. So we knew we had brain activity preclinically and could rationalize going into patients. So this is a case study on a 58-year-old male with CLL, who developed the disease back in 2015, and was on three prior lines of therapy, a PI3 kinase inhibitor. You can see his first, and then venetoclax, rituximab in 2018, 2022, and then was on acalabrutinib when he developed CNS involvement and progression of the disease. It was actually a significant progression of disease. This is the patient journey, looking at his absolute lymphocyte count on the Y-axis, as well as the total white blood cell count, so the two colored lines. And at time 0, initiation of therapy, when a BTK-targeted therapy is working, paradoxically, one sees an elevation of white blood cell counts. So you see that big spike, and this lymphocytosis is associated with actually a good result. As patients remain on therapy, you can see the study day along the X-axis, we start to see that resolve. By the first assessment, the patient had achieved a stable disease status, which was at eight weeks, is our first assessment. By 16 weeks, had already achieved a partial response, and you can see the individual parameters, too, actually becoming quite normalized. In fact, the platelets and hemoglobin, it's not shown on this slide, but at baseline were very low and abnormal. We see elevation of platelets, hemoglobin, anemia going away, coming up, really excellent resolution of these primary symptoms, and then the 24-week response being even better. If you look at the CSF involvement, which is the last line in this slide, the patient during screening in week 8, 16, had malignant cells in the CSF, but by week 24, that had resolved. So we're very pleased to see this rather dramatic and sustained response in a patient with CNS involvement. We've seen other responses like this in primary CNS lymphoma and others. So very encouraged by this and look forward to further reports on the CNS activity of the drug. So I wanted to share some quantitative data about drug levels and how degraders can achieve this compared to inhibitors that have not been able to do so. And so what I'm showing you on the graph on the left side, in green, you see the drug blood levels from our trial of over 24 hours. In red, you see as the drug is administered at time zero, really rather immediately, within four hours, BTK goes down to basically baseline levels of detection, and by western blot, we actually cannot detect the protein anymore. And you can see that that lasts all 24 hours. If you look off to the right at the blood levels that achieve this, I think this is where it gets really interesting with a degrader like 5948. Our Cmax, or our max blood levels, are 0.09 nanomolar, which is very, very low. And pirtobrutinib, a non-covalent inhibitor, by contrast, achieves its therapeutic doses at 6,000-fold higher drug levels than our degrader. So these are very, very small levels of degrader drug in the blood, and you can see zanubrutinib is about 40, ibrutinib about 8, is their therapeutic dose level at Cmax. At min, it's even less. And so even at very, very low blood levels, we're achieving this, these kinds of responses in the clinic that we've been reporting on. So this tells you that this is a fundamentally different PK/PD dynamic than a small molecule, and we think speaks to the efficacy level and also the emerging favorable safety profile. I'd like to shift gears to the second BTK degrader. This will be more brief, but this is a dual degrader of not only BTK, but also IKZF1 and 3, which gives it immunomodulatory activity, so as in Revlimid and the IMiD drugs. So a dual-acting degrader, this is the trial design. We had dose escalated up to 300 milligrams. This product now is reentering its dose escalation phase with a chirally controlled drug substance now. That was a good achievement and in terms of our manufacturing process improvements, and it actually allowed us to get off partial hold, which was associated with this manufacturing chirality of this drug. So now we have a chirally pure compound that is going to be reentering in NHL. Here, we have data both on CLL and NHL, but I really want to focus on the aggressive lymphomas for this combination. It's essentially a combination molecule, a dual-acting molecule in one, both the BTK degrader and the IMiD-like activity. The patient populations here at the time of this study presented at ASH in December, where overall was 54. We had seen and reported about a +4% response rate in advanced CLL. These were in fifth-line patients, and we were very encouraged by that in CLL. But we also witnessed in NHL some very interesting results, and here I'm showing the NHL results in terms of lymph node decrease in lymph node size. We have some pretty dramatic responses as monotherapy in very advanced NHL patients. A couple case studies here, just really briefly, that were most impressive, and I think direct this agent to diffuse large B-cell lymphoma, number one. This is an 84-year-old woman with very extensive disease, had been on multiple prior lines of therapy, including R-CHOP, R-ICE, other triple immunotherapies. And you can see the bulky lymph node disease on the initial baseline scan. By week 16, basically all of those nodes were gone, and this is a really dramatic response... which has been sustained over 18 months. Again, with monotherapy, impressive, I think, once-a-day drug result. This is another impressive finding in a complete response in mantle cell, advanced mantle cell lymphoma. Similar story, off to the left, significant lymph node involvement at baseline, and by week eight, in this case, all the nodes had been completely responded, and it was a complete response at the first assessment at week eight. So these are two very encouraging stories about NX-2127 in advanced aggressive lymphomas, and that's how we see NX-2127 fitting into this treatment landscape. NX-5948 will be more on the indolent lymphomas, CLL, Waldenstrom's, mantle, potentially mantle cell and marginal zone, and then in DLBCL and the aggressive forms of MCL, the dual degrader, we think, would do well. And this is sort of pictorial of how we see the market landscape. The size of the circles indicates the numbers of patients involved in each, and you can see the very largest area of need, CLL, with resistance mutation and DLBCL, even more patients. And we think that we've got a degrader portfolio that can really be quite powerful across this landscape of B-cell malignancies. So with that, just a couple comments on our degrader antibody conjugates. Exciting new class of ADCs, cleverly called DACs, which is a name that both Seagen and Pfizer have completely endorsed. How do these compounds work? So this deal we signed in September of last year, while Seagen was in the midst of its negotiations or its closure process with Pfizer. And we received a significant financial term, $60 million upfront, a multibillion-dollar milestone package, also, accompanied by appropriate single- to low double-digit royalties. And very importantly, we maintained cost profit share opt-ins post human proof of concept on two projects out of the total number of products coming from this. So these are molecules where the payload, in the lower right there, is a targeted protein degrader molecules, these bifunctional molecules I've been telling you about, as in 5948 and 2127. These do not. This deal does not involve 5948 and 2127. These are novel targets, selected with Pfizer to-- and customized to their antibody delivery platform. So the payload there is now a degrader instead of the more typical toxins that have been associated with successful ADCs of the past. But we think these will even more greatly improve the therapeutic window of ADCs. And how does this work? The antibody is decorated with degrader molecules, as pictured in the upper left, as with, as is done with ADCs. Antibody enters the cell, goes into the endosome, the degrader molecule is detached and is then delivered into the cytoplasm, capturing the E3 ligase system, as well as the desired protein target, which triggers it for proteasomal degradation. So this is a really elegant approach to creating what we believe will be a highly specific, next-generation ADC type of molecule that will bring targeted therapy to the world of ADCs in a very effective way using degraders. So one of the reasons, just my last point, that this actually can even work is because degrader molecules are so potent. As I showed you with that previous blood level slide depicting the really trace levels of drug that are required to get efficacy. And because with the DAC platform or an ADC platform, the amount of payload molecules delivered to cells is actually very low, and so those molecules have to be extremely potent. So we're very happy to be teaming up now with the Pfizer team. This is off to a great start. They bring to bear the real leadership in ADC technologies, linkerology, and we think we're bringing to bear a leadership position in targeted protein degradation. So a really exciting class of drugs to watch. This, just to close, we have several milestones we anticipate over the remainder of 2024, including the upcoming disclosure at EHA, which I think is going to be what has been most watched to date by investors. But NX-2127, we see that resuming in its clinical trial path in aggressive lymphoma, we'll provide clinical updates on NX-1607, and we anticipate identifying new development candidates from our very productive research platform. We're in a very strong cash position. We'd like to thank all the investors who participated in our last follow-on round, which was after April eleventh. This brought in additional cash, which brings us pro forma with that raise to $442 million in cash in the bank. This gives us a very strong foundation to move all of our pipeline forward and to get into later-stage trials as rapidly as possible with NX-5948. With that, I'll close.