Good morning, everyone, and thank you for joining us for our H.C. Wainwright at Home event with Nkarta Therapeutics. My name is Emily Bodner, and I'm an Equity Research Analyst at H.C. Wainwright. I'm pleased to introduce Nadir Mahmood, who's President, and Shawn Rose, the new Chief Medical Officer of Nkarta. Maybe to start, for those who are a bit newer to your story and given all the recent changes in the cell therapy landscape, can you give us an introduction to your CAR NK allogeneic cell therapy platform and some of your ongoing programs?
Absolutely, and thanks for having us, Emily. It's a pleasure to participate in this discussion today. As a background, Nkarta is an autoimmune disease company developing natural killer or NK cell therapy for people living with B-cell-mediated immune diseases. We originally started, like many companies in this space, in oncology, but we've pivoted very recently into the autoimmune disease space, given just the enormous potential that cell therapy has in these indications. I think most people are probably aware of the data out of Dr. George Schmidt's lab at the University of Erlangen in Germany, where they really demonstrated that CAR T-cell therapy has got this incredible ability to drive disease-free remission in people suffering with autoimmune disease. Not only do these patients achieve incredible clinical outcomes, but many of them have now gone on multiple years without any other medication.
This is a transformative opportunity to treat, completely changed patient care in this field. The other kind of really interesting things in the data were that it appeared you don't really need a prolonged persistence of the cells, and that the depletion of these autoreactive B cells that drive the disease actually happens pretty quickly, and then that causes the emergence of this new naive B cell subset, and what we call this sort of the immune reset. Some of these features, I think, make NK cells really uniquely ideal for these specific indications. NK cells are allogeneic. These are off the shelf, which means they're readily available when patients need them. They're scalable. They have a favorable safety profile compared with CAR T cells.
Ourselves, from our oncology trials and many other companies, have now shown that we've got this incredible safety profile that doesn't have high-grade CRS, and we don't see ICANS. I think this is going to be especially important in the context of autoimmune disease versus oncology, where that risk-benefit ratio is quite different. The other point about them not persisting forever, you know, we know that NK cells come in, they do their thing, and they leave. From a kinetics perspective, this makes a lot of sense based on what we've been seeing from the emerging CAR T data. Ultimately, I think what this means for CAR NK cells is there's an opportunity for much greater accessibility compared with the CAR T. We want to get these cells in the hands of rheumatologists and nephrologists who see the vast majority of these patients. We have a LEAP program, NKX019.
That's what we're going to spend probably a lot of our time talking about. This is a chimeric antigen receptor CAR NK engineered cell that expresses a CAR against CD19 for targeting and a membrane-bound form of IL-15 for enhanced activation and persistence. We have two IND studies going on right now. One is for lupus nephritis and primary membranous nephropathy, and the second one is in systemic sclerosis, myositis, and ANCA-associated vasculitis. We also have two investigator-sponsored trials, one in systemic lupus and one in myasthenia gravis.
Great. You mentioned, obviously, the Dr. Schmidt study, which kind of spurred this interest in evaluating CAR T and CAR NK therapies for autoimmune diseases. Maybe taking a bit of a step back, what does the role of CD19 play in autoimmune diseases like lupus and systemic sclerosis, and how has the landscape kind of developed to showcase that in the clinic?
Yeah, I'll take that one. Thanks, Emily. Pleasure to be here. CD19, when I think about this as a target, what comes to mind are things like well-validated and importantly across multiple modalities. This is, of course, initially established by Dr. Schmidt, as you heard from Nadir, where we've seen really robust, deep, durable responses when targeting using CAR T cells. We think importantly for CD19, it's not just limited to the current indications under study in autoimmunity, potentially more broadly as well, to the landscape of other B-cell-mediated disorders. We think the potential goes beyond what we're currently investigating as well.
Right. Obviously, the majority of the clinical data so far has been using autologous CAR T therapy. What are some of the key differences of CAR NK versus CAR T therapies, and why might an allogeneic CAR NK cell therapy be better suited for autoimmune disease?
Yeah, we think that CAR NK has a number of advantages over CAR T therapies. In addition to the potential for a more favorable safety profile, as discussed, importantly, the potential to not have these high-grade, potentially life-threatening ICANNs and cytokine release syndrome. There are also a lot of practical measures for our CAR NK cells that are really a benefit for their delivery. The first being, as an example, CAR NK cells are really short-lived. They come in the body, they do their job, which is killing the effector cell, the target cell as an effector cell, and then importantly, they disappear quite quickly, and we really have a good understanding of this. Within a month, they're completely gone. This is different than a CAR T cell, where they're necessary for them to expand, and actually, they persist quite long in the body.
The CAR NK cell instead is really primed and ready to go and to kill the target effector cell. The second major difference is very practical. As you heard, this is a scalable modality. It's off the shelf, and it's given in an allogeneic manner. Why this is a big advantage is it means a lot to patients. When you have this platform, they don't have to undergo leukapheresis, for example, which is a time-intensive and very uncomfortable procedure. Given the safety profile, we think it'll allow for broader access and delivery, potentially in an outpatient setting, where CAR T, given the safety profile, that may never get there. These are some of the advantages that really give us a lot of excitement about the potential of the CAR NK.
Awesome. Can you discuss some of the translational work you've done, particularly with patients from your B-cell malignancies trial, and how that's kind of compared to the autologous CAR T data that we've seen?
Yeah, there's a number of central factors that we can measure across the CAR NK cell platform. Importantly, B-cell depletion is a common unifying factor, given that we're targeting CD19. This is a pharmacodynamic effect where what we've learned is that you really need a deep B-cell depletion to enable those deep responses that we're seeking. The second, in the setting of both oncology and autoimmunity, are things like cytokines, right? We see a lower cytokine release with the CAR NK platform and CAR T. The third are chemokines and other circulating factors that can drive inflammation. Importantly, as it pertains to autoimmunity as well as oncology, we're looking for immune reset. This is a shift from a pathogenic type of cell that then gets eliminated, and as the immune system repopulates, we see a more naive phenotype. We look closely at this.
In addition, in the autoimmune space, we have a number of disease-specific markers that we'll be looking at that are particular to each indication under study.
With CAR T, we tend to see peak expansion typically occur around 10 days, whereas we've seen with CAR NK, that tends to occur earlier, usually around day one after administration. How do you think this kind of translates to potential for clinical efficacy or differences versus CAR T?
As I alluded to earlier, CAR NK is ready to go, off the shelf, and ready to eliminate target cells. We don't require that expansion. In fact, that expansion is associated with potentially life-threatening events, such as high-grade cytokine release syndrome and ICANS. We actually see that having the ability to deliver our CAR NK cell platform in a short fixed period of time over the course of a week provides an advantage and a convenience, as well as a benefit from a safety profile, and will likely require less monitoring than a CAR T platform.
Obviously, there's been some challenges on the allogeneic side since we don't actually have any allogeneic cell therapies approved yet. How do you think that Nkarta is kind of working to overcome some of these challenges, and particularly for autoimmune diseases?
Yeah, happy to take a shot at this one. I think generally, when you think about oncology, the allogeneic cell therapies just haven't quite lived up to the expectations. You can look at durability and best responses not translating to durable responses six, 12 months later. When you combine that with the continued strength of a lot of the autologous data moving into earlier lines of therapy, competition from the bispecific antibodies, there's just a lot of headwinds in the allospace in oncology. I think when you look at this in the context of autoimmune disease, Dr. Schmidt's inspired the world with his pioneering work in this space. Like us, many folks have moved from oncology to autoimmune, and I think that's really where these allogeneic approaches make a lot of sense. I mean, you need to have a medicine in this patient population that is really accessible, right?
These are the nephrologists, the rheumatologists. These aren't oncologists that are out there who are used to giving toxic substances to their patients because what else are they going to do? They're looking to save them from potential, you know, terrible outcomes within a matter of weeks to months. That equation is just very different. That accessibility feature becomes critical. Like Shawn said, the accessibility is enabled through the scalability, the allogeneic approach, and then the safety is critical. That's where NK cells really, I think, have this unique advantage, is that safety profile. We've had over 40 patients' worth of data in oncology without any high-grade CRS, no neurotoxicity. I think there's an opportunity here.
I think the other part, when you look at the B-cell burden in an autoimmune patient versus a tumor, probably not, you're not asking the cell therapy necessarily to maybe do as much in that context. Maybe from an efficacy standpoint, that's where we can get sufficient B-cell depletion to drive an immune reset. Ultimately, I think the concept is being able to get this powerful therapy into the hands of the clinicians, where they see those patients, and those are more in the communities outside of the large cities. I think that's really where the allotherapies are going to have that potential to be transformative here.
Yeah, definitely makes sense. Maybe diving deeper into your clinical programs now. You obviously have your phase I trial for NKX019 that's ongoing in lupus nephritis. Can you touch a bit about the study design there and what endpoints are kind of the most relevant for efficacy?
We're currently conducting a phase I trial, as you mentioned, Emily, and it's a dose escalation trial. We're looking at different doses in the lupus nephritis population, as well as other indications, for example, primary membranous nephropathy in that trial. We continue to enroll participants in that trial. Our goals there are really to establish the early safety and pharmacology of NKX019 in this autoimmune disease population. Of course, we'll be looking at clinical effects as well. Importantly, there are a number of early readouts that are very relevant here when it comes to clinical efficacy. For example, we look at markers such as creatinine in the circulation, as well as the urine. We also look at protein in the urine, as well as a concept called glomerular filtration rate, which tells you how well the kidney is filtering in the body, or GFR for short.
Those markers have direct translation to real outcomes that are significant for patients with autoimmune renal disease, such as lupus nephritis. For example, end-stage renal disease, outcomes like the need for dialysis, the need for renal transplantation, and importantly, ultimately, mortality and death are directly linked to these markers. If we see favorable movement in those markers, this could mean direct translation to real outcomes that matter to patients and the healthcare system.
Okay, makes sense. On your lymphodepletion regimen, you recently updated the protocol to include fludarabine, which previously you weren't using. Curious if you could touch a bit more on what kind of drove this change, and do you believe that this has any impact on the trial, if at all?
Yeah, I think, you know, we, as you said, we initially started off with the cyclophosphamide-only approach in our conditioning therapy and just recently revised this to now include fludarabine. The decision is really based on the fact that fludarabine and cyclophosphamide together is really the standard lymphodepletion regimen in cell therapy. I think when you look not just at Dr. Schmidt's data, but pretty much all the other data that continues to emerge in the field, the standard lymphodepletion regimen of fludarabine and cyclophosphamide is there. There's probably an impact on being able to bring the B cells sufficiently down to drive an immune reset. We made this decision and made the change because we felt we wanted to give NKX019 the best chance to do its job. We want to get that immune reset, address symptoms, deliver better health.
We still have an option in the trial for patients to receive cyclophosphamide only if they are cytopenic. We haven't completely moved away from that cyclophosphamide only, but we found that over the past year or so, compared with when we started the trial, more and more rheumatologists are getting comfortable with having fludarabine as part of that conditioning regimen. I think it was pretty new at the time, and there were some concerns about that, but now it's pretty much standard, and they're seeing all these responses happening in the presence of fludarabine and cyclophosphamide. To be consistent and try and give that maximum opportunity for success, we made that shift. I think we'll still be agile here and adaptable. I don't think cell therapy is necessarily sort of a one-size-fits-all. NK cells give us the flexibility.
Ultimately, I think we'll give the regimen that's appropriate for a patient that gets them the best chance of getting that deep, durable response.
Okay, got it. Along those lines, you also were previously evaluating a dosing regimen of three doses over one week versus three doses over two weeks. You've now moved forward with one week for all three doses. What was the reasoning for choosing the three doses over seven days? Are you seeing, or were you seeing, better results with that dosing regimen?
Yeah, I'll take this one, Emily. We made this shift, and it was really a data-driven shift. We think that this regimen gives us the best opportunity to really maximize our PK of our NKX019 CAR NK therapy, but also importantly translating to PD outcomes and namely looking at B-cell depletion. By giving this compressed regimen on three days given over the course of a week, not only are we maximizing the potential of the platform, but it's also convenient compared to some of the other regimens that we were exploring. We think it'll give us a real advantage there.
Got it. Makes sense. How do you think about the bar for success for the NTRUST-1 trial in lupus nephritis patients, given what we've seen so far with some of the autologous CAR T therapies in that setting?
Yeah, I can start, and Shawn, feel free to jump in. I think one of the key things here is, you know, the Schmidt data obviously was a single study, a single-center study. We saw clinical remission in all those patients. Now that we've started seeing more of these company-sponsored trials reporting data, we're not seeing that 100% response rate, which, by the way, is normal. It should be expected. These are multi-center studies. There are more heterogeneous patient populations. Also, pretty small patient numbers to date. I think we've probably seen more in systemic lupus maybe than in lupus nephritis just yet. Not surprisingly, the response rates have been lower. We've also seen some relapses and side effects like cytokine release syndrome and ICANS. Those are really happening in the autologous CAR T studies, right?
In the allogeneic CAR NK-1 study that's been updated at ACR and EULAR, we haven't seen any of those side effects. With that said, I think when you think about what that bar is, what we know is the standard of care for these patients is woefully inadequate. A transformative therapy that's safe and broadly accessible probably doesn't need to meet that same bar that may be something that has a more serious toxicity profile. Now, exactly what that bar is, you know, maybe hard to say right now as data continues to emerge. Shawn, feel free to share any thoughts that you may have there.
Yeah, thank you, Nadir. The only thing that I'd add is the fact that we're actually talking about durable response and remission and immune reset in these treatment-refractory serious autoimmune conditions is just a mindset, a massive shift for the field. We could have only dreamed about talking about this for the last several decades, frankly. This is the potential of CAR cell therapy in general, and particularly we believe for our CAR NK cell platform. When you look at remission rates in natural populations or even in clinical trials with other modalities, it's pretty much nonexistent for some of these conditions, and for some of them, it's very low. The fact that we're even talking about this, this is truly transformational data that's coming out now for these patients. I think we acknowledge and appreciate that Dr.
Schmidt is a world leader, and they're the most experienced center in the entire world with CAR therapy. It is a single center, and now that we're branching out into more broad populations with heterogeneous disease manifestations, this is totally to be expected. In fact, we know this, right? We've known this for years that when you do this, it's a general drug development principle that you start seeing as you introduce more heterogeneity, your response rates become more heterogeneous. That said, bringing it back, the transformative potential of CAR NK cell therapy is truly remarkable here.
Right. How do you think about durability for an allogeneic CAR NK therapy? I guess, what would be kind of considered positive and what would a physician kind of consider to be practice-changing in your view? How do you think about the potential for retreatment here? Obviously, with autologous CAR T, you can't really do retreatment. I think that potentially is one of the benefits of an allogeneic CAR NK therapy. Curious on your thoughts on that.
What I would say is that we've already seen that with the available data that even out to one and two years has really caught the attention of clinicians, the scientific community, the investor community, and more broadly, of course, in patients and their families. We think this is a fantastic early read, and we look forward to seeing how long and how durable these therapies are. We do anticipate for many patients they actually will be durable and hopefully continue in that durable remission state. I'm really, really intrigued and inspired by the data that's been coming out, and we think it really, really is quite remarkable. I think within that timeframe is, you know, reasonable for now, but obviously, we want to see it further out in the future.
I think the fact that we're seeing this across multiple different disease states, although the majority of the data is in lupus and lupus nephritis right now, is also truly remarkable.
Great. The potential for retreatment, I guess, how do you think about that relative to?
Yeah, so from a retreatment standpoint, this is one of the real potential advantages of CAR NK cell therapy, where yes, we do have and others have experience with retreating. In fact, we, in our own experience in oncology, had a handful of patients where we did retreat them, and we found we were able to achieve durable responses and remissions where a single treatment was unable to do that. I think this is another competitive advantage potentially for CAR NK cell therapy and something that we're very interested in understanding further in the autoimmune disease population moving forward.
Okay. You mentioned earlier you have an investigator-sponsored trial in SLE going on right now as well. How do you kind of think about potential efficacy in the broader SLE population relative to LN, which obviously comes with different baggage and a bit more complicated?
Sure. SLE is a systemic autoimmune disorder that can impact any organ system in the body. It's really broad in terms of the manifestations that can occur with that disorder. Lupus nephritis is more specific to the kidney; it is a manifestation of SLE. We believe that based on what we've seen emerging in the field with CAR T and CAR NK cell therapies, we will be able to impact a broad swath of the disease manifestations that are seen in SLE in addition to lupus nephritis.
You also have the NTRUST-2 trial that's ongoing in other immune diseases, like you mentioned myositis and systemic sclerosis, which are also indications we've seen some data from the Dr. Schmidt study. I'm curious to get your thoughts on some of these other autoimmune diseases and if you think potential for these to make more sense than lupus, where obviously a lot more companies are focusing.
Sure. Yeah, I couldn't agree more, Emily. We're seeing data emerging now on these other diseases, and the data has been quite compelling. There's a shared pathogenesis across these disorders, and that's really the pathophysiology of the B cell. We think that's important and potentially ties together these different disorders. We're really, really excited about enrolling and understanding these populations as well in our trials and look forward to sharing data when available. We think the potential there is really, really remarkable as well, and not just limited to those disorders that we're studying. By the way, ANCA-associated vasculitis is another one that's in our NTRUST-2 trial. There are a whole host of other indications we're currently looking at as potential opportunities that would be differentiated from those which are currently being studied by ourselves as well as competitors in the field.
Right. On the topic of data, when are you kind of guiding to having initial data from some of these trials, and what might that look like given all these different indications that you're evaluating?
Yeah, so we have guided to giving the initial update on NKX019 in the second half of the year. That is what the plan is right now. We are still currently enrolling in the dose escalation phase of the study. We'll look forward to sharing any data that's available at that time. It's probably going to be a combination of patients across the two INDs and the various different indications. That's five different indications. We will share what we have by the end of the year.
Got it. Is there anything you can share about how large of a data set to expect, or, I guess, how long a follow-up some of these patients might have at this point?
Yeah, probably not too much granularity that you're hoping for, but I would say that the initial update is going to be from the total number of patients that we would have had enrolled up to that point. Again, it's going to be across the five indications from those two INDs. We'll endeavor to share whatever data we have, but there's going to be some patients naturally that will have a longer follow-up time because they were treated much earlier, and then others who are more recent who won't have as much follow-up. The other thing to note is we did just modify the lymphodepletion regimen, like we talked about before, to be fludarabine and cyclophosphamide. That's a more recent change. In terms of patients that would have had that exposure versus previously, you know, will also come much later, follow-up more recent.
Ultimately, I think the data, as we see it, should really start to give us an initial sense, one, of confirming the safety profile and then also start giving us an initial idea of how the drug is working in these patients and what kind of B-cell effects we're seeing.
Yeah. I guess on the topic of safety, obviously, we talked quite a bit about the differentiation versus autologous CAR T. Are there any safety events that might be more expected that we should be looking out for? If you don't see the typical events of CRS and neurotoxicity, would you consider that a win?
Yeah, I think that you've hit the nail on the head. You know, cytokine release syndrome and neurotoxicity are the two big ones that we look out for. That said, there are other potential signals that could be occurring in the setting of autologous CAR T therapies that we may not see with allogeneic CAR NK cell therapy. For example, the cellular therapies can have impacts on bone marrow and production of blood cells due to that. Sometimes they can be quite durable impacts over the long term with autologous CAR T therapies. Thus far, we haven't seen prolonged effects on the bone marrow with allogeneic CAR NK cell therapy, but that's something we'll be paying close attention to. I think another example is, obviously, with any sort of therapy and that they're getting a lymphodepletion regimen, we want to pay close attention to serious infections.
We've got a good safety profile in that regard thus far with NKX019, and we'll continue to monitor. That's always going to be on the minds of clinicians, right, and understanding the broader safety profile. There could be an advantage there as well, given sort of the compressor regimens that we're talking about to delivering our therapy and then following. Time will tell on that.
Got it. I know you discussed some of the biomarkers you're looking at in the lupus nephritis trial, but are there any other kind of key biomarkers or translational data that investors should pay attention to in the upcoming readout?
Yeah, I think in addition to the pharmacogenetic markers that we spoke about regarding B-cell depletion and the accompanying immune reset that we're paying close attention.
Did it freeze? I think where Shawn was going with that, it appears to be frozen there. It's just making sure we can see sufficient B-cell depletion and then the immune reset, which means a reconstitution of a naive immune system over time, sort of being some of the key things there.
What are some, I guess, considerations you're looking into in order to kind of figure out maybe one or two indications to move into more advanced trials? Is that driven more by efficacy versus competitors or just kind of like where there's less competition?
Yeah, I think it'll be sort of weighing safety with efficacy and potential for commercial differentiation. I think we have to kind of look at all of this. We've seen other companies dosing rare disease populations like with the idiopathic inflammatory myopathy, like the beacon example there where a 15-patient cohort is potentially sufficient to move towards registration. We're starting to get a bit more picture of this. We'll continue to monitor the landscape, look at our own data, make the decision really based on the most recent data and analysis we have. Obviously, we'll be taking a very close look at our own efficacy data and trying to understand across the indications we're currently studying what that looks like. At the same time, we need to understand this is a competitive area. We have to continuously look for ways that we can differentiate.
That's not only are diseases currently understudied, but are there other opportunities as well where we can differentiate by maybe looking beyond the current indications as well?
Makes sense. What could next steps look like? In terms of larger phase II, phase III trials, is there any sort of benchmark to go off of?
I think the main thing that we have right now is we have a bit of an example, and I think the Cabaletta update earlier this year, which was the first real FDA-based information that we got around what could a registrational trial look like, what do you need to show, how many patients, etc. I think that's like the beacon and example that most people are looking at. It suggests that FDA is engaged and thinking thoughtfully about this in a way that we maybe saw more in the oncology space.
Whether that's a 15-ish patient registrational trial with a 100 or so patients' worth of safety data across different indications, I think a lot of folks are kind of looking at that and saying, okay, maybe this is the potential pathway that we need to be considering in this space, assuming we can hit these, continue to see these transformative efficacy and durable remissions over time.
Okay, makes sense. Have you had any recent regulatory interactions with the FDA regarding any of your ongoing programs, and what's been the general feedback or tone of conversations?
We haven't really talked publicly too much about interactions with the FDA, but I think the real sort of the stuff that we can say is we've had good communications ongoing with any of our studies as we've reached out to them for various bits of information. We haven't seen any noticeable change in the interaction or in the communication yet. I think as things continue to evolve there, as they have in the last 24 hours, we just need to keep a close eye on things. Thus far, we're still in the pretty early stages of our trial, but we hope that we can engage them in the near future.
Right, makes sense. Based on conversations with KOLs and clinicians, where do you kind of see the most enthusiasm for cell therapies in autoimmune indications? What might some of the market opportunities look like in these larger, I guess, lupus nephritis or SLE indications?
Yeah, I think if you go to any of the conferences in the field over the last couple of years and you see who's presenting, the cell therapy leaders are sort of up there, right? With these scientists, the opinion leaders, physicians, these are packed rooms. Your practicing clinicians and your key opinion leaders are all there. I think, obviously, as today's discussion, like investors, innovators, patients are there, patient advocacy groups are attending. I think, as Shawn mentioned earlier, just the fact that we're talking about the potential for a durable response and remission in diseases where we've really only been able to dream about a kind of breakthrough like this for such a long time, like it really moves the field forward. When you think about the market opportunity, there won't be opportunities for everybody right out of the gate, right?
I think we're going to start with probably the most severe patients who are multi-treatment refractory. That said, I think one of the upsides for an allogeneic NK cell approach is really that safety profile and then convenience of delivery, right? It's back to this point of accessibility. How do you make these therapies more accessible, particularly in this context versus the oncology context? We believe our product can be, you know, walked back and administered to patients earlier in their disease course. That's our goal, that's our ambition. We want to address the disease before it progresses and the symptoms get out of hand. I think that can really shape what is the competitive advantage for us going forward.
You touched a bit earlier about potential for outpatient use. I know that term gets thrown around a bit, but I guess what does the reality of that potentially look like? Do you think that that would be a big differentiator in this space?
Absolutely. You know, when we were in oncology, we were already outpatient sort of towards the end of those trials in non-Hodgkin's lymphoma. We know that we can administer outpatient. We know what that safety profile looks like. We know that this is something that we have achieved before and we will strive to achieve again. I really believe it can be a major differentiator in this space because if you are forced in looking at this from solely sort of that inpatient setting of having a rheumatologist partnered with a cell therapist who's probably a hem-onc transplanter, right? You're going to be limited to the centers that have the beds, that have the infrastructure to support and monitor life-threatening cytokine release syndrome, to manage and monitor the ICANS. ICANS is new for the autoimmune space, right?
Like a confused patient who is unable to coherently communicate and understand what's going on around them. Oncologists may be used to this, but for rheumatologists, it's still a pretty new and often very scary space. To move away from that, to move from that inpatient setting and really get into that, hey Shawn, outpatient setting is going to be critical to get this into the much broader population of rheumatologists, nephrologists outside of the big cities, in the more community-based hospitals, in the settings where the vast majority of people who live with these diseases every day go to visit their specialist.
Great. I know you've had some efforts to restructure the organization a bit recently. Can you touch on your current cash position and ability to fund some of these ongoing programs into larger trials?
Yeah. As you mentioned, we just did a major restructuring in March of this year. It was very difficult. We had to part with about a third of our team. The idea there really, and what it has enabled for us now, is focused and total focus and effort on executing an autoimmune disease, extending the runway into 2029, really giving us that flexibility. We ended the first quarter of this year, I believe, with about $350 million in cash. That capital, we're careful, thoughtful, want to be good stewards of our precious capital there. It's really focused on executing on these trials and having the runway to 2029. This gives us flexibility in terms of being able to read out data that can truly create value without having been forced to raise capital in the near term because we're going to run out of cash.
In this continuingly evolving market where it seems like the bar for good data for positive results continues to get higher and higher, we want to make sure we have as much flexibility as we can so that whether it's the next readout or the readout after that or the one after that, we aren't beholden to being forced to go and raise capital, and we can just focus on execution, and we'll be opportunistic when we need to be. Having flexibility in a challenging market is a place where we feel very fortunate to be.
Yeah, that's great. Okay, maybe just as a last final question, just kind of end on a summary of upcoming catalysts and milestones. Obviously, we talked about the ones for this year, but maybe how you're also thinking about next year.
Yeah, we haven't talked much about 2026 yet, but clearly, you know, 2025, the big thing is, you know, that'll be our initial update for NKX019 in the autoimmune space. Still planned for the second half of the year, which I realize we're already in, so stay tuned. 2026, look, I think as data continue to emerge, I think we will be, you know, thoughtful about when is the appropriate time, and obviously, there'll be additional follow-up on some of those patients, additional patients. Potential for, you know, additional updates there. Shawn, I know unfortunately you got dropped off there, but any other thoughts sort of in terms of key things sort of looking forward to on the clinical side over the next six months?
Yeah, thanks. The only thing I would add is, yes, I mean, these leading indicators, right, that Nadir and I have been talking about, some of the biomarkers, some of the early readouts and clinical data, they'll give us confidence, obviously, in the current indications under study. They will also, you know, potentially trigger activities as we think about other indications and what else can we do, right? I can't emphasize the importance of that. You know, what we're doing now is meaningful in these highly refractory patient populations. We also need to, you know, think broader and think about opportunities for reaching broader swaths of patient populations with serious autoimmune conditions.
Great. Awesome. Thank you very much, Nadir and Shawn, for your time this morning. Thank you everyone who's been listening in. We'll conclude the call here. Have a good rest of your day.
Thank you.
Thanks, Emily.