Good afternoon, everyone, and thank you for joining our H.C. Wainwright fourth annual virtual cell therapy conference. My name is Emily Bodnar, and I'm an equity research analyst at H.C. Wainwright. I'm pleased to introduce Nadir Mahmood, who is the president of Nkarta Therapeutics. For those who are newer to Nkarta, Nadir, if you can give us a bit of an intro to your allogeneic CAR-NK cell therapy platform and some of your ongoing programs with NKX019. Thanks so much for having me today. Apologies for a little bit of a late start here. Nkarta is an autoimmune disease company. We are developing a lead program, which is a CD19-directed CAR-NK cell, a natural killer cell that is engineered to express a CAR, chimeric antigen receptor, against CD19, and also engineered to express a membrane-bound IL-15 to enhance persistence in a variety of B-cell-mediated autoimmune diseases. We're particularly excited about this program and the profile of a CAR-NK, given the targeting, but also the unique safety profile that exists with NK cells that we believe really allows us to unlock the full potential of this type of approach in an autoimmune disease setting. We currently have two company-sponsored INDs. The first one, Ntrust-1, is in our nephrology indications, lupus nephritis, and primary membranous nephropathy. Ntrust-2 is a basket trial looking at systemic sclerosis, myositis, ANCA-associated vasculitis, recently we just added rheumatoid arthritis to that as well. We've got a couple of investigator-sponsored trials as well. One is in systemic lupus, the other one is in myasthenia gravis. Really, for us, the concept and idea here is building on the data that everybody's familiar with from Georg Schett at Erlangen and what we've now been seeing from a number of other companies using B-cell depletion strategies, is to really try and, what we believe, is find the sweet spot of where NK cells fit within this paradigm. Can we deliver potentially the transformative potential of cell therapy, like what we've seen from autologous CAR T with these incredible immune resets that lead to long-term drug-free remission with a safer and more convenient therapy that allows broader accessibility to the larger patient population that faces these diseases. Really trying to get out there in the community setting. That's where we believe NK cells, because we don't see cytokine release syndrome or any neurotoxicities, really have a safety profile that is unique that allows us to be able to do that. maybe going along with that, obviously, as you mentioned, majority of the data we've seen in the autoimmune disease space has been with autologous CAR T therapy. As an allogeneic CAR-NK therapy, how do you think that this may be a better suited type of therapy for autoimmune diseases where obviously patients have more chronic disease compared to the oncology settings? I think there's a really interesting feature that emerged from the very initial data published by Georg Schett and his colleagues, which was really demonstrating that the B-cell killing and that immune reset that occurs following that actually doesn't require this prolonged depletion and killing of B cells. That really that B-cell burden needs to be taken down and depleted early on in the first, say, three to four weeks. You don't need this continuous expansion of a population that then targets and kills this ongoing larger population of B cells like you have in a tumor setting, for example. We believe that observation really ties nicely with one of the key features of NK cells, which is they're not a very persistent cell type. When you put an NK cell in, it's going to last for a few weeks and do its job, and then it goes away. That's where we believe in an autoimmune disease setting where that risk-benefit ratio is really different than in an oncology setting. You're typically used to giving immunosuppressive therapies or glucocorticoids, for example, that this really presents an opportunity to have something that can come in, drive that deep B-cell depletion, trigger that immune reset, and give you these responses without having to deal with potential long-term toxicity or even near-term toxicity because the NK cells won't expand in vivo. When you have that biological, that fundamental difference in the biology of how NK cells work versus T cells, you're not going to see those side effects like CRS, ICANS that you typically see with T cells because the biology is just different. If we can drive that B-cell depletion the way that we believe we can, and you can trigger that immune reset, we believe you have a therapy that could lead to longer-term durable remissions. The other added benefit, and something that FDA has given us the green light to do now, is you can redose these therapies. If a patient is able to get into remission for a certain period of time, call it several months, a year, a couple of years, and then they relapse or they're starting to flare, there's an opportunity to go back and give them this therapy again because it's safe, because it can be administered in an outpatient setting. There's a lot of opportunity there where we believe as you tackle some of these chronic indications in autoimmune disease, the NK cell approach really does a nice job marrying the benefit of a cell therapy, but with the convenience of what looks like more of a traditional biologic, but with a really clean safety profile to date. Yeah, makes sense. Can you discuss some of the translational work that you've done and the results you're seeing in terms of B-cell depletion and how that kind of compares to what you would expect to see with some of the autologous CAR T trials? Yeah. The translational work that we're doing sort of is what you've seen from a lot of folks where we're going to look at peripheral B-cell kinetics. We are looking at BAFF elevation also as it's a surrogate for tissue depletion. Then, of course, we're going to look to see what the reconstitution of B cells is following depletion. Can we get a naive B-cell population indicative of a true immune reset? The other thing translationally that we're doing also is we're looking in tissues and lymph nodes. I think the peripheral B cells are a nice indicator that you're getting depletion, but ultimately the action is happening in the lymph and in the tissues, right? That is where we're seeing these pathogenic autoantibodies driving inflammation and damaging tissue. What we want to be able to see is, okay, we can get the peripheral B cells down, but what are we doing to actually get to the sites of action, and can our cells get there and deplete B cells? That's part of the data that we're generating. When we give our update this year, we will be sharing whatever data we have there. I think those are sort of how we're thinking about translational. One more point on that is when we started this trial, we were using only cyclophosphamide as the only conditioning agent. We've since moved over to a more robust conditioning with fludarabine and cyclophosphamide. The reason is because we see more deeper B-cell depletion when you have fludarabine and cyclophosphamide. We believe that is part of the regimen that can drive us to depleting enough of the peripheral B-cell sink so that the NK cells themselves can get to the tissues and the lymph nodes and do the activity there. That also is probably closest to what Dr. Schett has demonstrated in his autologous CAR T work using fludarabine and cyclophosphamide. Maybe moving to Ntrust-1, which is the lupus nephritis trial that you discussed. Maybe talk a bit more about the trial design there, where you kind of are in development in that trial, and what some of the key endpoints are for efficacy. Lupus nephritis, this is an important B-cell-driven kidney disease where standard of care is really chronic immunosuppression. There's an incredible need for a more durable intervention. What we're looking at are sort of your traditional renal responses as sort of the primary efficacy lens. There'll be complete renal response, partial renal response rates, proteinuria, complement, anti-double-stranded DNA. These are endpoints that the field recognizes and FDA has accepted in other programs. Now that we're fully outpatient, we can go with four billion cells per dose, given three times for a total of 12 billion cells, with only a two-hour observation window, I think it really gives us the opportunity to access a much broader population of lupus nephritis patients who are out there who can't always come into the large medical centers and the big cities to be seen and sort of put their lives on hold, especially when nephritis flares are being managed with immunosuppressives or corticosteroids. Those are sort of the primary efficacy endpoints we're looking at. Then we're also, as I mentioned earlier, on the translational side, we're going to be looking at B-cell kinetics, BAFF signaling, reconstitution of naive B cells. Yep. Are there any, I guess, numbers in terms of complete renal response that you're kind of looking to see to get comfortable with maybe moving that indication forward? Yeah, I think given this patient population really doesn't have much in terms of standard of care, you look at what some of the other companies in the cell therapy space have reported, which are really to date pretty small data sets. I think one study has about eight or nine, another's got about six. What the bar is exactly, probably trying to drive meaningful remission that is durable. I think it's a little early to say exactly what that bar is going to be, certainly something we're going to continue tracking as more data emerges, we can start to set expectations for ourselves as well for the street as to what that looks like. Really, I think we do want to see complete renal responses and see that there's durability there at least several months, potentially longer. With the ability to re-treat, we might have some examples where we could potentially put folks back into remission if we have that opportunity. Yeah. Maybe on that point, we did have a question come in about navigating reimbursement with potential redosing. I don't know if that's something you've thought about at all. Yeah. It's something still early in terms of how we're assessing things. I think the redosing provides an opportunity for flexibility in terms of how you can approach what the overall commercial approach and strategy looks like. I think we do believe, and we are confident that in the most cases, a single cycle of cells with the three doses given over the course of a week should be sufficient to drive, in our opinion, hopefully long-term durable remissions. We sort of see the redosing more as sort of an opportunity to create some additional flexibility for either patients that maybe got close and didn't quite get there, or that can have an opportunity to be retreated. We're not looking at it as a chronic, we're going to give this every couple of months sort of approach there. I think that's something we're going to look at. Right now, we're still focused on, okay, what does the original cycle look like in terms of what market access and reimbursement could be? Yep, makes sense. On the Ntrust-2 trial, you mentioned obviously it's a basket trial with several indications. I think RA is obviously an interesting one, and we've seen some NK cell competitor data this year in that setting. Maybe talk to us a bit more about why you're excited about RA and how you think NKX019 as an engineered cell therapy can maybe differentiate. Yeah. RA is an indication that we actually didn't originally have in the trial. It's something we added more recently, and that was really based on feedback from some of our investigators. As, I think, data has emerged from some of our competitors, Artiva had some really nice data at EULAR that they presented with a 71% ACR50 at six months in a refractory population. I think seeing a signal like that and the opportunity that's there, but still with a differentiated product relative to our competitors, I think that was something that our investigators were like, "You got to get this into patients. We want to support evaluating this in RA." I think scientifically as well, there's a lot of rationale around CD19 and targeting by that. I think the big difference sort of in our approach versus competitors' approach there is the fact that this isn't a combination that we're utilizing. There isn't a monoclonal antibody that we're co-administering to drive or help drive responses. For us, it's really an engineered cell targeting CD19, which we believe in these B-cell-mediated autoimmune diseases, including RA, is the primary antigen that represents the lineage of these autoantibody-producing B cells. We think with the engineering and a simpler trial design, simpler regimen, there's an incredible opportunity to potentially get some really strong responses, maybe in line with what our competitors saw. We think with that combined with the convenience, and also continuing to be outpatient in that setting, that there's incredible opportunity in this population. If you look historically, the response rates, even with rituximab alone, have been abysmal. I think there's a lot of room and a lot of opportunity to show that there's something truly meaningful for this patient population that can drive these durable responses. This is an indication that was just recently added. We're still kind of in the early days in terms of enrollment and treatment of patients relative to the other indications in Ntrust-2. Yeah. Maybe to talk more about the data update that you're planning for this year, what should we be expecting in terms of what you might share for Ntrust-1 and Ntrust-2? Obviously, you have different indications as we've discussed. How might that look? Yeah. I think given that this is going to be our first data update for the autoimmune program, I think that one of the fundamental things we want to do is basically provide an update across the board, what we're seeing in both Ntrust-1 and Ntrust-2 patients treated to date. I think it's going to be important to understand, and what we're going to try and communicate is there's a couple of things. One is we started early on with cyclophosphamide only as lymphodepletion, and now we have cyclophosphamide and fludarabine, which is the regimen that we are confident in terms of moving forward. We're going to share what we had from cyclophosphamide only, but really our focus is going to be on those patients treated who were pre-treated and conditioned with Flu/Cy. The next part is, unlike a T cell, you have to do a real dose escalation for an NK cell therapy. We started with 1 billion cells per dose times three, then we moved to 2 billion, and now we're at 4 billion. It was only earlier this year that we started the 4 billion. What we want to really focus our update around is what is that regimen and dose that we're going to take forward, and how do the responses at that dose with fludarabine cyclophosphamide inform what our next steps in clinical development are. We'll share all the efficacy response data, any translational data, because we understand and we believe, too, that demonstrating that you're getting a mechanistic effect here that's driving the responses. Especially for some of these patients who were dosed more recently, we're not going to have that much longitudinal data. The way you sort of bridge and get confidence in the durability is saying, we're seeing strong early responses, and with that, we're seeing translational data that suggests that we're driving an immune reset. Ideally, we want to be able to put data together in a way that we can convey all of that, but also very clearly articulate which particular indications and what doses we are moving forward. Yeah. Is that something that you're planning to do with this update, kind of disclosing go forward dosing and go forward indications, or would that be at a later time? Ideally, that is part of what we'd like to update, is really sort of not just here's the data, but here's the data and here are next steps in clinical development and sort of where we want to go forward with the program. To the extent that we will have any FDA or regulatory conversations and have guidance on sort of what the path forward looks like, we'd be happy and wanting to share that information in that update as well. Yeah. I think as we've seen some kind of pivotal trials in the space emerging, majority of companies have done single-arm, fairly small trials. Do you think that that's probably the same path that you'll be taking as well? Most likely. That's, I think, the really exciting opportunity here that FDA has demonstrated through now a few companies that unlike other modalities, and historically in these autoimmune diseases, we are now seeing multiple examples of single-arm trials and relatively manageable trials when it is a randomized control trial in the context of comparing cells plus rituximab to rituximab alone. Given that we've got the engineering, and if we can demonstrate strong efficacy with some early durability, then I think we do have an opportunity here to potentially accelerate development by moving into some single-arm trials. I think the FDA's told us, as they've told other companies, "When you're at that point and you're ready to have that conversation, we're ready to have that meeting with you." I think the door and the opportunity is there for us. Yeah, makes sense. I guess for durability, what would you like to see longer term, maybe next year, as you have more data to read out? And how do you think that might differ for an allogeneic approach relative to autologous therapies? Yeah. I think when you have something that has this really unique safety profile, like CAR-NK does, and the ability to redose, and we can manufacture this at scale, I think the logistical parts and accessibility really lend themselves to this idea of redosing. For us, like I mentioned before, it's not like this is going to be something we expect patients to be taking every couple of months. I think we want to see at least several months of durability before we get to redosing. Potentially 12+ months, something like that, I think would be an interesting target for us to look at. As the data emerges and we continue to have conversations with the rheumatology community around some of those aspects, I think there's definitely opportunity. We're already seeing opportunities to redose and potentially drive deeper responses with more durability with some of the patients that got our earlier doses. We'll be providing some interesting updates around that, too. Maybe to end, if you can go through a summary of what we should be looking out for the next 12 -1 8 months. Really the big catalyst for us is the data readout in 2026. Everything we're doing right now is 100% execution-focused and focused on trying to make sure we provide a robust and meaningful update where it's not a couple of patients here, a couple of patients there, but a meaningful number of patients with sufficient follow-up that we can actually say that we've, at least in the indications that we're focused on, that we can say we've got something here in terms of a program, and this is what the next steps look like. Really, any updates or anything else we do over the remainder of 2026 is going to be geared towards that. As we get into 2027, depending on what we talk about at that data readout, hopefully it provides opportunity to really take the next step in terms of clinical development and move this program forward. Really, I think that's where we're headed. I think that's what people really have their eyes right now on is our 2026 update. We're excited to provide that soon enough. Yeah, definitely. I think we're very excited for that as well. Thank you so much, Nadir. Thanks everyone who's been listening in. Have a great rest of your day. All right. Thanks, Emily.