Good afternoon, everybody, and thank you once again for joining us for the second day of the first annual iAI Summit at TD Cowen. I'm Yaron Werber from the Biotech team, and it's a great pleasure to have with us today Paul Hastings, CEO, and Nadir Mahmood, President of Nkarta. Gentlemen, thanks so much for joining us. We appreciate it. You bet. It's good to see you. Maybe there's a lot of updates from the ongoing studies that we want to cover and trust in one and two. Maybe just for the audience, kind of broadly, there's been a lot of, in general, new data with CAR T for iAI indications. There's been a little bit of data with NK cells too. Some of it's really coming out of China. Different dosing schemes, different doses, different protocols also with sort of steroids upfront. Maybe let's talk about the NK data so far that's out there. What have you learned from it? Let me tell you one thing that's consistent about it, about the data across all the NK data sets that are out there. Then Nadir can give you some other learnings that we've seen because he's done a lot of competitive intelligence in the space. We've looked at a bunch of stuff in China just because we think some of the technologies in China are very interesting, particularly on the in vivo side. They tend to move a lot faster than we can here, which is pathetic, but they can. The thing that's consistent across RuYi's data and Artiva's data from Fred and our data, and so there's a lot of patients there, by the way. Fred's got 30 some odd patients reported on. RuYi's got, I don't know, numbered near 60 or so. Almost 30. Almost 30. We didn't give the number, but all patients treated with fludarabine and cyclophosphamide plus cells have deep, what I would call complete B cell depletion. It's hovering at zero plus or minus immediately after, like a day after, hours after you inject the cell. It gets B cell depletion quickly. That's consistent across all the different data sets. If you look at the RuYi data set, which has much more follow-up than Fred's or ours right now, what you see are deep, durable responses. They went up as high as 4 billion cells times 5 or 5 and a half or 6 or forget the number. They gave a lot of cells. You can give a lot of cells. There has been little to no CRS, cytokine release syndrome, neurotoxicities associated with those cytokine release syndromes with any of the NK cells. What you're seeing with NK cells is so far, when you look, and we're trying to avoid, and that's why we didn't say how many patients we've treated so far that we've seen complete B cell depletion in 100% of them, but we'll give that update later. You're seeing if we can have the same response or even a little bit less, plus or minus, as the T cells, but have the profile of an NK cell with allogeneity, so it's allogeneic, off the shelf, on demand, engineered CD19 CAR NK cells. If you can have the same efficacy as CAR T, but you have accessibility in an outpatient setting where you would need not a cell therapist, but a rheumatologist, a chair, someone that can thaw cells. That's all you need. If you can do that, then you're going to have a home run. There's not enough data on the NK side yet to say it's the same, but it's starting to build. On the T side as well, the CAR T side with fluci plus T cells, autologous, allogeneic, you're seeing deep, durable responses. What you're also seeing on the CAR T side, and now I'm starting to dig into what I want to talk to you about, but I'll get them started, is that you see without fludarabine, and you could call bendamustine, whatever you want to call it, it's lymphodepletion. With any of these other lymphodepletion regimens, we led the way by saying, look, let's go sialone, let's see what we can do. You don't get as deep B cell depletion. And you're not seeing in the data that's being represented so far, small numbers from the CAR Ts, that when they're going sialone or no lymphodepletion or bendamustine plus something, you're also seeing inconsistent complete responses. It means that there's a place for modified lymphodepletion, probably less sick patients, probably diseases where they aren't as severe as others. If you take a lupus nephritis patient, for example, or a refractory lupus nephritis patient, that patient's going to need fludarabine, cyclophosphamide cells. The rheumatologist came to us and told us that. That's why we did it. Those things are consistent. Maybe Nadir, you can fill in the blanks that I left out here if I did. Yeah, I think just going back to the existing NK data in autoimmune disease. Paul touched on the data out of China from RuYi Therapeutics. I think what is compelling there is that looks most like our program, NKX019, in that it's a CD19-directed CAR NK. It's made from donor-derived NK cells, similar to ours. I think if you look at that at the time, it was really one of the largest single indication data sets with a cell therapy when they presented at EULAR earlier this summer in Barcelona. I believe they had about 28 patients that had been dosed up to that point in SLE. I think if you look at the response rates around nine months, 20 patients had gotten out to nine months. They were seeing over 70% alleled asset improvement and over 50% on the DORA side. From a disease activity perspective, they were seeing some really remarkable response rates there, really on par with what you've seen in the autologous CAR T space, but now starting to emerge from an allogeneic data set, from an NK cell data set, but with the safety profile that Paul alluded to that I think creates a completely new paradigm in terms of accessibility for the broad rheumatology population out there. I think that's really what gets us excited about the potential of our program, NKX019, as we think about sort of what the comps are that we should start expecting. Yeah, to your point, the RuYi study, though, has much higher doses. I believe they also are using steroids in those protocols, aren't they? I'm actually just opening the slides here. Can you talk to me? Yeah, so they continued, yeah. They got up to 4.5 billion cells dosed five times at the highest dose level. They were seeing responses even at the lower doses. I think they had some patients that got 1.5 billion, 3 billion cells. We have seen continuous responses even in the lower doses with them. We started at 1 billion. We are now enrolling at the next dose level, which is 2 billion cells per dose, given three times, at day zero, day three, and day seven. We have the ability to continue to dose escalate to even higher doses and even get in the range if we need to with what RuYi showed their activity. Yeah, we heard they got up to that high, but we heard they're also not going to use that high dose in their expansion. They're going to use the middle dose. We're thinking that's probably where the sweet spot is. The steroids are definitely maintained, I believe, post-treatment as a very low dose kind of taper just to modulate and try and keep the patients from flaring. During the Q&A, I think they talked about that as well as the investigators sort of felt this important piece of not shifting the treatment regimen of standard of care so dramatically. I think they will probably look to see if they can completely remove it. I think for anybody that's been treating patients with steroids for a long period of time, it's probably not a major contributor to the ongoing response here. Nor will they be dosing those at really high doses if they've been on chronic steroids. It's just not something they would do. Yeah. The steroids. It does speak to background therapy. Look, one of my pet peeves in this space is that we got to yank patients off of everything they're on in these refractory trials. If you're a patient that's on something that works and then you're being told you got to get off it to join a clinical trial, it makes things a lot harder. I think they haven't had that restriction as much over there. I think probably the standard of care, if you look going forward, if you look at everything else in oncology and other disease areas, maybe in combination with some of the standards of care, maybe not the more targeted agents, but maybe some of the agents that really do not work like steroids other than masking symptoms. We'll see how that plays out. Got it. Okay. So their steroids were on in the background, and then they just kept them at low doses to prevent a flare therapeutically or prevent a flare. What kind of a flare would they be preventing with the steroids? Disease flare or a flare related to the therapy itself and any CRS, which they're not seeing? Disease flare, just to try and maintain some low level of background therapy to manage ongoing disease biology. In any event, we're not doing that, so you'll be able to tell with our data whether it's. Yeah. I think in the U.S. trials that you look at, really the data suggests that you can probably remove most of it. I mean, I think we still have small data sets, but I think the bar that George Schett has set is drug-free remissions without any subsequent immunosuppressives or steroids. I think that's what the autologous CAR T data is showing us already. Yeah, but the autologous CAR T data is also slightly variable. Schett, obviously, is a very unique site. They have their own manufacturing on site, and they get remarkable activity. They also treated a bunch of young patients with very intact immune systems, which was great for them. By the way, we should all be able to treat those patients. They're not eligible for a trial because they're not refractory generally. Yeah, he's got an ideal patient population. I'm not sure that the on-site manufacturing makes a difference there, your own, but some people might think it does. I don't think it would. I think he's got an ideal patient set. He knows it. Everyone knows that no one's going to get the result he got in a multicenter clinical trial, more than likely. No one has so far. Yeah. So let's talk maybe, so you mentioned you're using 1 billion over three days, 0, 3, and 7. We're at 2 billion now, 0, 3, and 7. Okay, we're at the second dose level. You're in the second dose level now. Okay. So the data you've generated so far, the CRs were really in the first, in the 1 billion. And now you're enrolling the second billion. No, no. What we're saying is anyone that's been treated, they can be treated with one or two because we started this a little while ago. Remember now, we did this protocol amendment where we moved back to fludarabine instead of sialone. As I mentioned, we led the way there, and it was probably a mistake. Fludarabine, any patient that's been treated at any dose level with fludarabine plus our cells has seen complete or deep, what they're calling deep B cell depletion, which is kind of hovering in the zero kind of thing. All the patients we've treated with fludarabine and cyclophosphamide plus cells have had deep B cell depletion at any dose level that we've treated so far. Yeah. We have not talked about responses yet. We have just talked about the level of B cell depletion on fludarabine versus cyclophosphamide. Which is why we've moved the guidance out because when we present the data, and again, we don't want to play funny with what we've seen so far, but we're real happy with what we've seen, plus enrollment's up because of this as well. By sometime next year, we should have a robust and meaningful data set with fludarabine plus cyclophosphamide and 1 billion and 2 billion cells times 3 or maybe even higher than that. We will be able to have a robust number of patients, not just the B cell depletion data, but the reset data and the clinical outcomes data, which will have some varying degree of follow-up because as the patients get enrolled, there's fewer follow-up on the ones that have enrolled more recently. We will have something that isn't a handful of patients, we're hoping. I mean, one would imagine you probably want to do at least three patients per cohort before you go to the next cohort, or maybe you want to do even more. Yeah. Oh, yeah. Yeah. The other thing we didn't mention when we got this protocol amended, we got rid of that patient stagger. Originally, our patient stagger was every patient, 28-day follow-up for the next patient to go on. Now we've got the stagger that goes across interest one and interest two. After you've treated three patients, no matter what disease, at that dose level, you can move to the next dose level. You do have a 14-day stagger between the sentinel patient, patient one, and the other two patients in the protocol. You can dose more than three if you want to in that cohort, and you don't have to wait 28 days. That allows us to not have to say to a patient, let's just say there are two patients that are vying for that one sentinel patient dosing when that sentinel patient was every single patient and they missed, they have to wait 28 days or disease could relapse. We were sending them to other studies. Now we can say, hey, we can dose you all at the same time. That's a huge benefit, particularly since these patients have to come in from the outlying communities into these major academic centers, although we're starting to reach out to the more community-based settings as well. We think that's the place where patients get treated. The concept, by the way, that there aren't enough patients in the U.S. is just horse manure. There's tons of them in the U.S. They just don't have access to NYU and where you're sitting right there in that kind of an academic setting or here in San Francisco. They're living in the outlying areas, and they've got to travel. By the way, that's the other thing we've done. We've provided them travel services. We provide them childcare. We provide them fertility services, all kinds of things so that we can make their life a little bit easier when they get on a trial. Ultimately, we want to push all of the clinical trials out to the community-based centers where patients can be treated in a more convenient manner. Got it. Okay. And so interest one is lupus nephritis and primary membranous nephropathy. Interest two is systemic sclerosis, ANCA vasculitis, and inflammatory myopathy as well. Are you thinking you'll release data from both of them at the same time, or there might be not necessarily at the same time? The other thing is both studies, we're now working with the FDA with both studies together, which is nice. It is kind of one big basket study, even though they're still two separate studies. Our hope is that we'll be able to create and present data from a couple of those different disease areas. You mentioned myositis, vasculitis, and scleroderma, plus lupus nephritis. Then we have an SLE IST as well as a myasthenia gravis IST. We'll probably have some patients from a number of those different. As you said, you probably want to have three at least in each cohort to be able to present meaningful data, but we'd like to have even more than that. Yeah. What do you need to see to then expand the cohort or expand the indication? Some durable responses in the dose escalation. If you're seeing complete responses and durable complete responses, then you probably want to expand. What you don't want to do, and I've seen this happen in so many clinical trials, is you don't want to expand too early either. Say you get some good results at 1 billion, you still want to go to 2 billion to see if you're going to get better results. You might get more durable responses. We have an idea of what we need to dose escalate to. It could be two. It could be three. It could be four. We don't know. We're going to look at each one of those. We'll expand when we think that we've reached the dose level that we want to expand at. What RuYi did was they went all the way up to 4.5, and they kind of came back to the middle. That is what we have heard, but we do not know exactly. Okay. Makes sense? I think with that, the things you want to look at, of course, there's the response and the follow-up and durability of that response. I think tied with that, some of the earlier things that we can look at are some leading biomarkers, but also just the translational data around the B cell population and compartment and how that class switching occurs over time to really show that we're getting that immune reset. That might be, for some patients that have been dosed more recently, that could also help inform that you're headed in the right direction, and they could look like similar patients that maybe have more durable responses that have just been dosed earlier. How do you define? I mean, the CR is obviously defined, but durability, what is six months enough? Is a year enough at this point? Each disease is going to have a different, first of all, each disease is going to have a different time to response, and each disease is going to have a different durability that you want to see. It's nice to have six-month data. It's really nice to have that. Like I said, when you present your results, you're not going to have all patients with six months. You're going to have some with three, some with four, some with five, some with six, kind of thing. To see the 12-month results is also a good thing. Everybody wants data one patient at a time, which we're not going to do, by the way. We're going to give it in meaningful, robust clumps. Okay. Got it. Okay. And what has been the challenge to enrollment? I mean, I guess when it was sialone, that must have been a challenge. It's really interesting because we kept hearing that the rheumatologists wanted a safe lymphodepletion. They didn't like using fludarabine. But then all the rheumatologists came to us and said, "You know, it's great. You're using cyclophosphamide, but you might want to add fludarabine because you're going to get deeper B cell depletion. That's what we're seeing with the T cells." We went with their advice. We switched that over. The enrollment challenge before was everybody else was using fludarabine and cyclophosphamide. We were using cyclophosphamide with a new cell type. Patients had gotten used to seeing, "Hey, these CAR Ts work." I think now they know we've got the lymphodepletion regimen that's going to cause complete B cell depletion, and they know these cells are shorter-lived and have a better safety profile, and they're probably likely to go on it now. What we've seen with our investigators, and we just came back from ACR, we had a number of different events here. We had a reception. We've had investigator meetings. We had a booth right next to the poster session that was full of people, investigators. We have new investigators coming to us wanting to be part of our trial. We're seeing an incredible uptick in the number of investigators that have interest in the trial and an incredible uptick in those investigators in our trials being able to enroll patients. That's all good news that leads then to patients being enabled because what's going to take to get these patients enrolled is the rheumatologist. The other challenge to enrollment is rheumatologists do not want to give their patients up to a cell therapist. Imagine you've got arthritis, your own, and your rheumatologist says to you, "You've got to go see this oncologist to get your cells." I mean, it's just a little weird when you're a patient, being one myself with Crohn's, to say to my gastroenterologist, "Yeah, I'll go over to that oncologist and be treated by that person." They want to control that patient's follow-up. They've got that relationship for years with that rheumatologist. I've had Crohn's disease for 45 years. I've had a relationship with my gastroenterologist. I've had two so far. I mean, the one I have now, I've had him for 25 years. You don't want to go over to somebody else. I think that's another challenge here, which we won't be facing down the road because we probably won't need the cell therapists for NK cells, particularly in rheumatology in that outpatient setting down the road. Not that we don't like them. We like working with them, but they may not be necessary. They don't have to do apheresis. They don't have to do any of the heavy monitoring that goes along with the rapid expansion of cells because we don't have rapid expansion. Right. The rheumatologists now are getting more comfortable doing it themselves. Definitely. Yep, definitely. I've been tired of waiting for slots, by the way, from the cell therapists who have competing trials in oncology, which again, puts them both at odds with each other, which makes no sense at all. That has been an issue. Yeah. Got it. It's taken us a while to get here, my friend, but you know what? I think we finally found the sweet spot. Thank God we did what we did by raising the capital we did the last time we did that. We have cash into 2029, and we're able to get to proof of concept in these indications on that capital so that we'll have room on the other side to have if we need to finance again. We're in a position that very few companies are in, thank goodness. Just remind us, how many sites do you have open for interest one and two, which is the same protocol now or the same one big sort of master? Yeah, we haven't given guidance on that, but there's a number of sites that are open and a number of sites that continue to open in each particular disease state. We've got a phase one, two, three kind of setup. The other thing that's important, like everybody else, we've got agreement with the FDA. When we went in with that protocol amendment, they said, "Look, after your dose expansion, if you've got the kind of results you may have there, you can use your expansion." I'm sorry. "After your dose escalation, you can use your expansion as pivotal if you have the right kind of data." Everyone's got that agreement with the FDA, but the data have to be there to do that. You can decide how many patients you're going to expand. It depends on the indication, etc. I mean, in general, is there a sense yet as to what kind of durability FDA is going to want to see? I imagine at least a year. Still emerging, I think. Still emerging, and they have these follow-up studies they want us to do. The one thing about the FDA, and I say this to everybody because everyone loves complaining about the FDA, we've had nothing but good interactions with Dr. Makkary, Dr. Prasad. They like cell therapy. They want to enable cell therapy. They helped us get this protocol amendment done. They helped us combine the two studies together. They have been excited about cell and gene therapies, and they have been putting their money where their mouth is. That has been a good thing for cell and gene therapy because the investors have no interest in us right now. Hoping people will come back after they are done with these other shiny objects that they are looking at, like bispecifics, trispecifics, T cell engagers. Look at them all, but keep looking at us and stop sort of leaving us on the sidelines. That would be my plea. Yeah. Okay. So it sounds like we need to wait for next year. Any sense? Is this going to be sort of like an ACR, EULAR, or an ACR type event? Tell them Nadir what we did commit to, how we're going to do this. Yeah. So I mean, we've been working closely with our investigators, and we want to put this out in a medical meeting. We're going to aim for a venue where we can really put this out there along with our investigators to kind of talk about what we're seeing. Okay. None of the things in that landscape that we mentioned, by the way, have enough data to say they're the answer. The T cell engagers, the bispecifics, trispecifics, they do not have enough data. They have a lot of toxicity data they can talk about. They do not have a lot of long-term durable response data. Any of those agents without lymphodepletion, including the in vivo therapies so far, which are terrific, but there has been no lymphodepletion in healthy volunteers. Everyone is going to treat patients, and everyone is going to treat patients and see what the response is in those patients. That is why we feel like everybody is kind of on an even playing field right now. Make your bets on cell therapy, NK cell therapy. Yeah. Next year is going to be an important year. Yeah. Terrific, Paul and Nadir. Good to see you. Appreciate the time, and we'll continue to follow closely. All right. Thank you. Thanks for having us. Thanks, everybody.