Thank you for standing by. Welcome to the Nkarta Business Update Call. At this time, all participants are in a listen-only mode. Please be advised that this call is being recorded at the company's request. I would now like to turn the call over to the company. Thank you, operator, and good morning, everyone. I'm Greg Mann, Senior Vice President of Public Affairs and Investor Relations at Nkarta. Thank you for joining our call this morning. Earlier today, Nkarta issued a press release announcing a new pipeline program in autoimmune disease and the extension of cash runway into 2026. This press release and today's webcast are available on our website. We're looking forward to discussing these recent developments. On the call today from Nkarta are Paul Hastings, President and Chief Executive Officer, Dr. David Shook, Chief Medical Officer, and Elise Levin, Chief Financial and Business Officer. Before we begin our prepared remarks, we'd like to remind everyone that comments made by Nkarta management and responses to questions on this call may include forward-looking statements, including, among other things, statements concerning Nkarta's expectations regarding Nkarta's estimated cash position and expected cash runway. Plans, strategies, and timelines for the continued and future clinical development and commercial potential of our programs. The therapeutic potential, accessibility, tolerability, and safety profile of NK cell therapies. And plans and timelines for the future availability and presentation of NKX101 and NKX019 clinical data. These forward-looking statements are based on current information, assumptions, and expectations that are subject to change and involve a number of risks and uncertainties that may cause actual results to differ materially from those contained in the forward-looking statements. These and other risks and uncertainties are described in our periodic filings made with the SEC, such as our most recent 10-Q and subsequent filings. You're cautioned not to place undue reliance on our forward-looking statements, and the company disclaims any obligation to update such statements. With that, I'd now like to turn the call over to Paul Hastings. Good morning. We're pleased that you can join us. In today's press release, we reported the expansion of our cell therapy pipeline into the autoimmune disease setting with our first autoimmune IND cleared in lupus nephritis, and in parallel, we announced an organizational realignment that extends our cash runway by one year into 2026. We've enabled multiple shots on goal while focusing resources on our key lead programs, including those in acute myeloid leukemia and non-Hodgkin lymphoma, both of which we expect clinical readouts from in 2024. Now, I'll start by covering our runway, and then I'll ask Dave to discuss our clinical pipeline. Nkarta has more than $275 million in cash as of September 30, 2023, multiple high-potential programs, and several planned upcoming data readouts. We've been disciplined, I'd say even austere, in our budgeting and spending over a long period of time. The urgency of this responsibility becomes even more important in the current market. We understand that we must adapt accordingly and take further measures to conserve our cash and prioritize expenditures. Nkarta's strategy must be based on stringent capital allocation and careful business prioritization to weather these challenging times, continue building value in our assets, and advance important treatments to patients. Now, the extension of cash runway into 2026 increases Nkarta's optionality and opportunities for success. We maintain our commitment to developing novel therapies for patients with cancer and now have three promising clinical-stage programs in our pipeline. These programs are largely uncorrelated and distributed across different diseases of high unmet medical need. With our current resources, we expect to advance each of these programs to a meaningful data readout in the next 12-15 months. Until we evaluate the activity and safety from these next updates, we will minimize or gate further spending in each program and allocate dollars to those areas that demonstrate the greatest potential for value creation. Now, our extension of runway has required us to make some difficult and painful decisions. As part of our cost containment measures, we have reduced our current workforce by approximately 10% and reallocated talented researchers in discovery to development, thereby avoiding the addition of approximately 60 new headcount that would have been needed to accelerate our clinical programs further and achieve near-term milestones. We took the unhappy step of informing the affected employees yesterday, and I extend our heartfelt gratitude to each of them for their valuable contributions to Nkarta, as well as their loved ones and families. I also appeal to members of the local and national biotech community in search of valuable talent to contact us for a list of resumes of people who will be transitioning out of Nkarta. So in 2023, we elected to keep headcount flat versus the significant growth anticipated in our original forecast. As I mentioned earlier, we plan to continue the zero-growth policy and forgo the previously planned hiring of about 60 new FTEs over this two-year period. Now, this year-over-year discipline in managing headcount contributed significantly to the expected extension of our cash runway. As well, we plan to centralize operations into a single location and have optimized manufacturing scale-up in a way that enabled us to forego an intermediate process change, thereby generating a savings benefit on the order of tens of millions of dollars. Before Dave reviews our NKX019 IND for lupus nephritis and other clinical updates, there are a couple of points that we'd like you to keep in mind. For anyone following the cell therapy space over the last 12 months or so, the excitement around the potential of cell therapies for autoimmune disease is unmistakable. Academic investigators, including the team at Erlangen, led by Dr. Georg Schett, have reported profound and durable responses to cell therapy in patients suffering from severe refractory autoimmune disease. Early evidence suggests that the targeting of autoantibodies via depletion of B cells causes a reset of the immune system that is disease modifying. While these data are early, they have captured the attention and hopes of many. We have deep conviction that NK cell therapy is particularly well suited to succeed in the autoimmune setting. In addition, we believe strongly that NKX019, our CD19-directed CAR-NK cell, could demonstrate clinical advantages that distinguish it from the crowd of CAR T cell therapy programs that are beginning their own evaluation in autoimmune disease, some as first-in-human products. NK cells and T cells operate differently, and as leaders in NK cell therapy, we believe that the safety profile, off-the-shelf accessibility, engineering enhancements, and cytotoxicity of NKX019 against B cells could differentiate it from the other approaches. Admittedly, we're not the first cell therapy program in autoimmune disease. However, when it comes to dosing patients, what separates us from the lead may only be a matter of a few months. We have bold plans for accelerating and expanding our autoimmune program that we will be sharing at a future date. For now, we look forward to dosing the first patients with lupus nephritis in the coming months and believe that NKX019 could rapidly become a best-in-class therapy in autoimmune disease. Now, I'll hand it over to Dave. Thank you, Paul. Systemic lupus erythematosus, commonly called SLE or simply lupus, is a systemic, chronic autoimmune disease with potentially life-threatening complications. The burden of disease is profound, with several hundred thousand people living with the disease in the U.S. alone, predominantly women and people of color. While the mechanisms of inflammation are complex, the immunologic hallmark is the presence of autoantibodies, particularly against nuclear antigens, including double-stranded DNA. These autoantibodies, driven by autoreactive B cells, trigger immune complex-induced damage throughout the body, including in the kidneys, in up to half of people with SLE. Lupus nephritis can lead to renal failure, requiring dialysis or kidney transplant, and has considerable risk of mortality. Unfortunately, there's no cure for lupus, and patients usually require lifelong treatment. Given the role of pathogenic autoantibodies, several agents that target B cells or their pathways have been developed for lupus, including the anti-CD20 antibody rituximab and the anti-BAFF antibody belimumab. Unfortunately, their benefit is limited by ineffective targeting or poor tissue penetration, especially in the kidneys, leading to persistence of autoreactive B cells and ongoing disease. CD19 has emerged as a potentially attractive target in lupus nephritis, given its expression on plasma cells, which may be responsible for producing autoantibodies. Notably, plasma cells do not express CD20, making therapies like rituximab inherently ineffective. Targeting CD19-positive B cells has been proposed as a mechanism by which long-term remission might be possible in lupus. As Paul mentioned, this idea was recently and impressively demonstrated using CD19-directed CAR T cells by a group led by Dr. Georg Schett. In the initial description, five young patients with severe treatment-refractory SLE with lupus nephritis were treated with autologous CD19 CAR T cells after lymphodepletion with fludarabine and cyclophosphamide. The CAR T cells expanded in all patients, with peak levels occurring around day nine, followed by rapid decline. While three of the five patients developed low-grade cytokine release syndrome, or CRS, there was no high-grade CRS, no neurotoxicity, and no substantial elevation of serum IL-6 levels. Further, while depletion of circulating B cells began within two days, it was transient, with B cell numbers returning to normal within two to four months. Taken together, these data suggest that the kinetics of CAR T cells in the context of lupus nephritis is different than what is commonly seen in B cell malignancies, likely due to lower target cell numbers. Despite the somewhat transient persistence of CAR T cells, all patients had seroconversion of anti-double-stranded DNA antibodies and decreases in levels of other SLE-associated antibodies. More remarkably, all patients showed significant improvement of clinical symptoms, including drug-free remissions after about three months. Again, this improvement occurred despite reappearance of normal B cells and without need for immunoglobulin replacement or impact on vaccination responses. A subsequent update, presented at EULAR in 2023, expanded this initial data set to seven patients, all of whom had seroconversion and disease remission. Median follow-up in that group was 13 months, with some patients having up to 22 months of remission. The observation that CD19-directed cell therapy could provide durable responses in patients with severe lupus was transformative. Even more striking was the fact that this activity could be achieved with only modest persistence and proliferation of the CAR T cells. Indeed, one of the advantages of NK cells is their pharmacokinetics. Unlike T cells, NK cells are active immediately, allowing clinical impact without the need for proliferation or long-term persistence. This allows patients to avoid prolonged B-cell aplasia or other cytopenias. This difference also impacts the lymphodepletion or preparative conditioning regimen prior to cell infusion. This regimen, commonly comprised of the chemotherapies fludarabine and cyclophosphamide, serves two main purposes: prevention of rejection by the patient's immune system and the creation of an optimal cytokine environment for cell persistence and expansion. While cyclophosphamide alone can facilitate engraftment of both NK cells and T cells, fludarabine is added to increase cell expansion by increasing serum cytokines, particularly IL-15. The engineering of NKX019 with a membrane-bound form of IL-15 may allow patients to avoid the potential toxicity of fludarabine while still realizing the benefit of cytokine support. With its off-the-shelf availability, NKX019 eliminates the need for costly hospital infrastructure necessary for the preparation of autologous CAR T cells. Further, patients need not be subjected to apheresis or the delays associated with product manufacturing. These potential advantages of CAR NK cells, including our clinical experience with NKX019, led us to develop our newest protocol and culminated in the acceptance of our IND submission within 30 days. In this phase I dose-finding protocol, we will enroll patients with refractory lupus nephritis. Patients will receive three doses of NKX019 derived from allogeneic healthy donors on days zero, seven, and 14, following lymphodepletion with cyclophosphamide alone. Patients will be followed for clinical and laboratory evidence of improvement, including the elimination of pathogenic autoantibodies. We plan to dose the first patient by first half of 2024. We are excited about the potential for NKX019 as a treatment for lupus nephritis and are continuing to evaluate other autoimmune diseases. I'll now provide updates on our other clinical programs. Earlier this year, we presented data from our ongoing phase I trial evaluating NKX101, our NKG2D CAR-NK, in relapsed refractory AML. This included a cohort of six patients who received NKX101 following lymphodepletion with fludarabine and ara-C. Four of the six patients achieved complete response, and three of six had negative MRD. We were encouraged by this response rate in a patient population with few options, and we'll be providing an update on these patients at a medical meeting later this year. We believe that this approach could lead to a potentially registrational phase II study following the enrollment by the first half of 2024 of 12-20 additional patients, and we still plan to give a more comprehensive update at that time. To that end, we worked hard to create an optimized manufacturing process to increase yield ahead of an anticipated increase in demand. While this effort culminated in a scaled-up process that is now online with a cleared FDA amendment, it resulted in a delay in enrollment while we built sufficient inventory. Today, enrollment is ongoing, with patients receiving material from our most advanced manufacturing process. Our other clinical program is evaluating NKX019 in relapsed refractory non-Hodgkin lymphoma, a program about which we last gave an update in December 2022. At that time, we announced the opening of three expansion cohorts evaluating NKX019 in relapsed refractory large B-cell lymphoma, both alone and in combination with rituximab. This is a disease area where autologous CAR T-cell therapies and now bispecific T-cell engagers are being increasingly used, and as a result, enrollment has been challenging. In addition, among those treated with NKX019 thus far, responses have not met our expectations as compared to our early results. Therefore, we have amended the study in efforts to improve antitumor activity and accessibility. First, we have moved to completely outpatient treatment. Despite off-the-shelf availability and a very tolerable safety profile, even 24 hours of mandatory hospitalization created a barrier to enrollment. Second, we added a six-patient cohort evaluating a new compressed dosing schedule, giving NKX019 on days zero, three, and seven, compared to days zero, seven, and 14 previously. This is based on our clinical experience, as well as pharmacokinetic studies that demonstrate maximal NKX019 exposure in the first week following lymphodepletion, and we feel that this approach has potential to significantly improve activity against refractory tumors. We plan to report outcomes from this cohort in mid-2024, and while we await those results, we have decided to no longer enroll into the three previously announced expansion cohorts. I'll now hand the call back to Paul for closing remarks. Thanks, Dave. We're very excited about the opportunities for Nkarta in 2024 and beyond. We continue to be disciplined about conserving our cash and allocating dollars to the programs with the greatest potential for value creation. Through some very careful belt-tightening, including not hiring 60 new positions in our forecast, a reduction in headcount, and a reallocation of resources, we expect our cash runway to now carry Nkarta well beyond a series of important 2024 milestones and into 2026. In parallel, we've expanded our pipeline with our first clinical program in autoimmune disease. We are very excited about the prospects of disease-modifying therapies for patients with lupus, as well as early proof of concept in multiple autoimmune indications of high unmet medical need. Now, we're well-positioned with multiple near-term shots on goal across our AML, NHL, and autoimmune programs, and we'll continue to execute towards important data readouts next year. Now, we will stop and look forward to hearing your questions. Operator, if you would please review the instructions for the Q&A section. For today's call, we will be utilizing the Raise Hand feature for Q&A. To ask a question, please click the Raise Hand button on your screen. Once you are called upon, please unmute and ask your question. If you are dialed in via phone, use star nine to raise your hand and star six to mute and unmute. Our first question comes from Salim Syed from Mizuho. Please unmute and ask your question. Great. Good morning, guys. Thanks for all the color this morning. I guess a few for me, if I can. One, on NKX019 in SLE, is there an expectation here to also treat CNS involvement? I think according to literature, about 40% of SLE patients have CNS involvement. Number two, just curious why you aren't using the new dosing schedule in the lupus study, if you do indeed think that it is better, could be [went out in NHL? And then lastly, what other autoimmune diseases, y ou mentioned you're looking at maybe several others. What others are you potentially considering for this CD19-based therapy? Thank you. William, Dave will take the three questions you just asked. Good morning, Salim. I missed the-- you kind of broke up on the first one. Was it about CNS? Oh ... lupus? Yeah, will this NKX019 treat CNS involvement as well for lupus or? Not that, that won't be the focus of this, of this study. The focus here will be on lupus nephritis. Okay. It's 40% that had kidney. Yeah, you're talking about CNS lupus specifically. But yeah, so this study will specifically be evaluating- [Surprise] SLE with lupus nephritis. And then- Okay, thank you. Yeah, the follow-up question in terms of the compressed dosing. Mm-hmm. So compressed dosing is one that we feel like has an opportunity in refractory disease in malignancy. It has a pretty... NKX019 has a pretty well-established safety profile in the zero, seven, and 14 dosing, and it's not ineffective there. We don't think that exposure early is quite as critical. We wanted to make sure that we maintained our well-established safety profile until we established what that safety profile looks like in compressed dosing. In terms of the last question in autoimmune disease, obviously we'll be looking at a lot of different autoimmune diseases there. I'm not gonna go into any specifics other than to say, there's several autoantibody-driven diseases where targeting autoreactive B cells would be attractive, and we'll be looking at those specifically. Yeah. More on that later, Salim. Thanks, and just if I can follow up just quickly, on the first question, does NKX019 cross the blood-brain barrier or no? So we haven't evaluated NKX019 specifically in terms of CNS sampling, but NK cells do cross the blood-brain barrier. Okay, all right. Thank you so much. Of course. Thank you. Our next question is from Jon Miller from Evercore. Please unmute and ask your question. Hi, thank you for taking the question. I would love to ask about your expectations for enrollment in SLE, given I think you had mentioned in NHL, it was challenging given the competition in the field. Yeah. And as you say, there are a bunch of CD19 cell therapies getting started in autoimmune. How do you expect enrollment timelines to be? Interrupted. Am I on? Yeah, Jon, it's Paul Hastings. We, we can't hear you. So, either you're in a, you have a bad connection, but we're only getting, like, every other word. Sorry, can you hear me now? That's better. Yeah. Okay. Well, I was asking about enrollment in SLE, given the, as you said, the large number of programs getting started there. What's your expectation of competition for patients, given Novartis and other large players are in the space? So the differentiation of NK cell- Yeah, thanks for the question. So I think NK cells have several advantages in this space, where we don't feel like it'll be a direct sort of head-to-head competition, though we recognize this is a busy space. So we think that the off-the-shelf allogeneic approach is gonna be a considerable less burden to patients, to providers, to healthcare facilities about building infrastructure for autologous CAR T cell therapy. In addition, the reduced lymphodepletion approach of not the requirement for fludarabine, particularly in CAR T cells. We think allowing these patients to get away from a medicine that's not standard of care will be particularly compelling. As we've talked to KOLs and others in the network, both of those things speak as real advantages and has generated a lot of excitement in the community. Do you have sites already selected to begin this trial? Sorry, did you hear that? Yeah. Yeah. So, we're working with sites right now in terms of site selection, and more to come on that one later. Okay. Our next question is from Sami Corwin from William Blair. Please unmute yourself and ask your question. Good morning, and thanks for taking my question. I was curious what dose of Cy you plan on using, and how it compares with the dose of Cy that most lupus nephritis patients receive as standard of care? How you expect the use of only Cy to affect the area under the curve for NK cell expansion, relative to the use of Cy in combination? Yeah, so in terms of cell dosing, we're not covering details of study design today, Sammy, but I'll tell you that it's within the range of what we think will be tolerable and effective for NKX cell exposure. In terms of its ability to allow engraftment, we're pretty comfortable there. You know, cyclophosphamide alone has been demonstrated historically now for quite some time to be able to allow temporary engraftment of NK cells. And we feel a combination of cyclophosphamide and tissue engineering with membrane-bound IL-15 is gonna give us good exposure. Gotcha. And then, do you think you'll be able to dose all patients in an outpatient setting immediately in the lupus nephritis trial? I think right now we're gonna err on the side of caution here, and have a temporary. Similar to what we did initially, we're having a short-term observation after a cell infusion. But the majority of the therapy will be outpatient. Great, thank you. Our next question is from Jeff La Rosa. Please press star six to unmute yourself and ask your question. Hi, thanks for taking the question. I'm on for Dana. If I could, you know, follow up on a couple prior questions, like, how do you plan on, how much do you plan on further dose optimizing, when you start the trial, for instance? You know, whether you do the quicker dosing at a lower dose, like you want to do with the, you know, the new cohort for DL BCL, or, you know, would you plan on adding fludarabine, changing the cyclophosphamide dose? Sort of, what sort of, you know, preclinical work and modeling have you done, that you feel comfortable with the way you're starting, and how aggressively might you change that or quickly early on? Does this autoimmune disease in general, is the second question, is this something you're looking to partner, or given your core focus on oncology, or are these capabilities you intend on building out in the future, at Nkarta? Thank you. Why don't you take the first question? Yeah. So I'll cover the first question. I'll let Paul start on the second question, and then fill in from there. So we've always been agile when it comes to following data, and we'll continue to do that. So we'll follow clinical response, PK, and tolerability in terms of adjustment. We do feel good about going in with a dose that we feel will be therapeutic right away. And if, you know, some clinical data or other data come in that suggests that we need to make a change to conditioning regimen, dose, schedule, et cetera, we'll certainly be flexible in doing that. We've done that so far with our programs, and we'll continue to do it. Yeah, in terms of where we are from a strategic point of view, just to be clear, we're an NK cell therapy company. We happen to have some great assets, both in oncology and autoimmune disease, and as we develop these assets, we'll decide exactly, you know, how to continue to develop them, once we see some interesting proof of concept and some value creation from each of them. Our next question is from Dane Leone, from Raymond James. Please unmute yourself and ask your question. Hi, thanks for taking the questions, and yeah, thanks for all the information about the updates and the change in strategy here. Two from me. One, could you maybe expand a little bit around NKX019, and what you've seen from the lymphoma studies around duration of B-cell aplasia and how you think about what you've achieved with the drug product, with B-cell depletion in the lymphoma studies, and how that would relate to expectations of what would need to be achieved for lupus? You know, I take the point that you're looking at a potentially different B-cell population or plasma cell population that you're targeting with CD19. But, I would still be curious around your, thoughts of depth and, time course, of B-cell depletion needed to effect, an immune system reset. And then secondly, on the AML program, it sounds like you do, have some optimism for this program with the ara-C component. Could you maybe give us a sense of what you have pegged as the duration or durability of response hurdle for those patients, that you generally need to see within the context of a CR, rate, to, you know, trigger a really going into that pivotal cohort you described next year? Thank you. Okay. Thanks for the question. So first, the 019 question regarding B-cell aplasia. This is something that we find particularly compelling. So, short answer is we feel like we're going to get adequate B-cell aplasia to make an impact. The data and CAR T have shown that absolute B-cell aplasia is unnecessary. There's been no impact, really fairly rapid recovery of B-cells, very little impact on immunoglobulins and vaccination responses. And in the CAR T space with persistence, you simply don't see that. So, we feel pretty confident those CAR T cells aren't lasting very long. And the B-cell aplasia, you know, is relatively short-lived as well. That's what's been described. And I would say is in range with our data on what we're able to derive for peripheral blood B-cell aplasia. And I think even judging from the rituximab experience in lupus nephritis and SLE more broadly, sometimes the peripheral blood B-cell aplasia really, you know, isn't the complete story. It's really tissue-level B-cell aplasia, and that we've heard that sort of over and over again from our investigators in our network. And we think one of the potential advantages, really, of cell therapy in general and certainly in NK cells, is the ability to get tissue penetrance and local B-cell aplasia. But I would say we feel comfortable with what our experience has been with B-cell depletion, that it's well within range of what should be able to drive a meaningful benefit in an immune reset. And the 101 question regarding AML. As you know, this is a space that has very few options. The recent approvals have been on sort of marginal improvements on standard of care chemotherapy in the range of sort of 20-25% CR rate, with durations in the sort of three to six month frame. And we obviously so far surpassed that in our early data, and we're optimistic that we'll continue to surpass that. So in terms of a bar, you know, I think the space would welcome, you know, even a 30+ CR rate at, you know, three to six months. Those, we're optimistic we'll be able to surpass that, but the bar with AML is, as you know, far lower than in other diseases. Our next question is from Steve Willey from Stifel. Please unmute yourself and ask your question. Yeah, good morning. Thanks for taking the questions and for providing the update here. I think you maybe just kind of spoke to it a little bit, but can you just kind of speak to some of the preclinical data that you have that suggests that the trafficking capacity of NK cells to some of these tissue-resident compartments, where a lot of these autoantibodies exist, might be better than T cells? And then I just have a follow-up. Sure. I think the CAR T experience thus far has, you know, is something that we feel like we need to surpass. So far that's been, you know, pretty definitive. I think what we would like to surpass when it comes to CAR T cells is accessibility, tolerability, and the avoidance of exposure to chemotherapy. In terms of our preclinical data for sort of resident B-cell depletion, you know, we've shown that NKX019 is very potent when it comes to eliminating CD19 positive cells of any kind. And I think that's, that's been demonstrated clinically for us with the elimination of resident malignancies, you know, tumors, you know, so hematologic tumors that exist outside of the, you know, bloodstream, extranodal disease, et cetera, including in the kidneys. NK cells are, are known to, to traffic through organs pretty consistently, so, including, including the target organs in, in SLE. So preclinically and clinically, we feel confident in the trafficking of 019. Okay, and I guess just with respect to the data that we should maybe expect to see from a preliminary perspective out of a lupus trial, presumably, you'd be looking at reductions in autoantibodies. But we would just be curious as to whether or not you would maybe also be looking at renal biomarkers to suggest that you're having an improvement at the clinical level in the kidney? Yeah, absolutely. The both of those will be important outcomes here. I think we're certainly interested in the scientific outcomes of the decreases in autoantibodies, but, you know, we're in this to help patients, and so we would expect biomarkers to be improved when it comes to renal response as well as clinically. Okay, and then maybe just one more quick question. I know that you're now talking about a compressed dosing schedule for NKX019 in B-cell malignancies, but just curious as to how you're thinking about the prospects of maybe trying to compress dose within the context of AML. Yeah, yeah. I think every disease is going to need a slightly different exposure. And again, we're always looking to optimize our programs, whether that be LD, whether that be dose or conditioning regimen, as you've seen. The compressed dosing schedule in NKX019 was designed to specifically address you know, some challenges that we had, but also some sort of positive responses that we've seen. And in terms of whether or not it goes to AML, I think we'll continue to look at pharmacokinetic exposure as well as patient responses. So far, we're very encouraged by what we've seen with AML. And so, we'll obviously look to improve any program we can. Right now, we feel like we're in a pretty good place with AML. Yeah. Think of the compressed dosing regimen in NKX019 as a platform program, Steve. So that's something we'll be looking at in the future for all of our programs and for all of our dosing, but individualizing it by disease. Okay. Thanks for taking my questions. Our next question is from Emily Bodnar, from HCW. Please unmute yourself and ask your question. Hi, good morning. Thanks for taking the questions. On LN, it sounds like you're looking at a single-cycle treatment. I'm curious if you think there could be any benefit of using multiple cycles, which I know you've used in some of your other studies. And then, how do you get confident that the new dose compression cohort in NHL could be replicated in dose expansion based on what you might expect to see in the dose-finding portion? Thanks. So, with the multiple cycles in LN, I think that's not something we're looking at right now. We feel good that we'll be able to see responses and get the level of B-cell depletion with single cycles. Though in, you know, our ability to go back, one of the advantages of a cyclophosphamide based conditioning is something like that isn't quite as burdensome in terms of going back and going. I think, you know, that includes not only deepening of response, but also retreatment. So I think one of the many advantages of NK cells here, an allogeneic product versus one that has to be manufactured per doses, is things like additional cycles, retreatment, et cetera remain advantages. So, more to come, but I think that it's sort of, again, a differentiating advantage on NK. So, help me understand your second question. Yeah, I guess because, you know, the dose escalation data you had in NHL looked quite positive, but then it wasn't replicated in the dose expansion. So curious how, if you see the same type of positive data with the dose compressed cohort, how you feel confident that that could be replicated in dose expansion? Yeah. Yeah, so great question. I think two things. So one, we think dose compression, as Paul mentioned, is a platform program. And I think this will help us understand the role of compressed dosing, particularly in refractory malignancies. But as we've seen, you know, and we have some clinical data and some PK data showing that we could dramatically increase exposure here. In terms of how we would use this to further develop the program, I think some of the things that we'll be looking at in particular would be the most aggressive malignancies, large B-cell lymphoma, and especially those who've been exposed to CAR-T, where the bar is somewhat lower. So, you know, we'll look at the totality of the data. You know, I think we want to make sure that we're mindful about that. So, no really strict go-forward data here. But we'll make sure we look at those data closely, as you know, and as we make a decision. Yeah, I mean, I'll only add to that, Emily, that what we've seen or haven't seen has been based on very small numbers. What we're doing here is reprioritizing where we wanna put our capital in terms of looking at indications. And so, the compressed dosing is something we're really excited about at NHL, but also across the platform, and obviously, to move into autoimmune disease, given the current environment that we're in, the crowded space in NHL made more sense to us, to go in that direction and not some of those expansion cohorts. When we find out what compressed dosing does, we'll take another look at that. All right. Thank you. Our next question is from Gil Blum at Needham & Company. Please unmute yourself and ask your question. Good morning. This is Ethan Markowski on for Gil Blum. Thank you for the time and for the update. I think most of my questions have already been addressed, but just wondering if you could provide maybe a little more color on why now is the best time to make these financial budgeting decisions? I mean, I know you, you mentioned the marketing conditions or the market conditions, but it seemed like you guys did have a relatively strong cash position going into this and runway into at least 2025, past several of the key updates. So I know you mentioned it gives you a little more optionality, but any additional color you could add would be helpful. Thanks. No, I mean, Ethan, that's, that's exactly what it is. It's, in this environment, giving ourselves as much optionality as possible, and as we move forward and hit milestones, decide where we want to go next, where we want to spend money next. So we just think it's financially prudent to make sure that the cash we have takes us to a point in which we think things will return to somewhat normal. We'll be able to create some milestones and be able to do what we need to do to keep the company thriving. So it's nothing more than that. Thank you. Thank you. Our final question is from Bill Maughan at Canaccord. Please unmute yourself and ask your question. Hi, good morning, and thanks. So in, for 019 in NHL, I just wanted to ask if you could kind of help set the bar on, on what you need to see out of the, the new cohort to justify further investment after, after the next data update? Maybe, maybe in the context of, of the recent cohorts that did not live up to expectations. And then, I also wanted to ask about, comparing and contrasting, maybe see if there were any, any features to call out for your construct versus the competitive, NK construct from Fate that's also going into autoimmune diseases. That'd be helpful. Thank you. Yeah. So, the first question regarding NHL. Yeah, I think we'll—we want to see what the data look like before we make any decisions, so there's not a strict decision on those. But I think the totality of the data, both the responses and laboratory data, will help drive that. We will. And as Paul mentioned, we'll be sort of somewhat gated as we see those responses. In particular, with the advent of, you know, the expansion of particular CAR T into earlier lines, the more widespread use of bispecific T-cell engagers, we want to see activity after those therapies, and know that there's a path forward here. Recognizing that the bar there is somewhat lower. So I think first and foremost, what we wanna see is activity beyond those therapies. I think those are therapies that are here and established and will need to drive responses there. I think the bar is much lower there. I think, you know, while CAR T and upfront gives sort of 30%-40%, six months CR is probably closer to 20%-30% in the relapsed or post-CAR T setting. But that's where our focus will lie. Yeah, in terms of the construct, we're quite confident in our construct and moving our construct into autoimmune disease. Where Fate is with their construct, you'll have to ask them about that. But where we are with ours is we're very, very comfortable that this is a great program to go into autoimmune disease. Great. Thank you. I'd like to turn the call back over to Nkarta for closing remarks. Thank you all for joining us today and taking the time with us to ask questions and get our answers, and we appreciate your time and effort. Thank you very much.