Good afternoon, everyone, and thank you for joining me at the second day of the Needham Healthcare Conference. My name is Gil Bloom, and I am a senior biotech analyst here at Needham with a focus on immuno-oncology. Today we have with us Paul Hastings, CEO, and David Shook, CMO of Nkarta Therapeutics. Now, as a reminder for viewers who are watching through our conference portal, you are able to submit questions through the ask a question box. Now, maybe a good place to start a bit of introduction with you guys. For the audience who is not familiar with Nkarta, can you briefly walk us through the company's core technology?
Sure. So we're an off-the-shelf allogeneic CAR Natural Killer cell company. And when I say we're a natural killer cell company, I want to emphasize that. We don't look at ourselves as an indication-specific company versus another. We look at ourselves as where will NK cells make the most sense to be therapeutically applied for patients. And our most recent focus is in the area of autoimmune disease, which we've been studying now for a few years. And we have made a major focus in this area right now. So we're looking right now at a CD19-targeted CAR- NK cell, NKX019, initially first patient in for autoimmune disease, systemic lupus or lupus nephritis, which will be in the first half of this year. And then we're looking at a variety of indications to expand out in. What we've seen with an NK cell is that it's off the shelf.
It has a relatively short time in the patient. And in the case of B cell reset for autoimmune disease, the profile is perfect for an NK cell. CMAX day zero, knock down all the bad B cells, bring back all the good B cells. We've shown recently data outlining this. And based on that data, we've then recently done a pretty massive financing in order to give us a leg up on taking these CAR- NK cells that are targeted at CD19 and expanding them in many different areas in autoimmune disease. So very focused right now on autoimmune disease. We also have the same program, NKX019, which is CD19-targeted cell in a special protocol for NHL, patients with non-Hodgkin lymphoma, where we're looking at compressed dosing of the cells.
We've normally given these cells day zero, seven, and 14 with lymphodepletion pre-dose, and we're now giving them day zero, three, and seven. So we've compressed the dose. And the reason we've compressed the dose is because we've seen in NHL patients that were treated with our cells initially and were CRs and then became progressive disease that we were able to take four patients that progressed, retreat them, and have four CRs return. So we know we can retreat patients. This, by the way, is a very important aspect of an NK cell. You can retreat. It's a feature, not a detriment. And so we're able to do that. So we thought if we can compress the dose, we might be able to actually prevent having to retreat or get the durability longer.
So we're looking at that particular protocol in patients with NHL because we think if we're going to compete in NHL in a space that's really crowded, that we need to have a hook. And that hook would be in CAR- T and bispecific or refractory patients with this compressed dosing schedule. So we have that data coming out in midyear, and we have FPI for our lupus nephritis trial happening in midyear. And then we'll follow up after we get that first patient on board. Really feel strongly that unlike other cell therapies that are out there right now that are using fludarabine plus cyclophosphamide lymphodepletion, that are Cy-only lymphodepletion, cyclophosphamide being a drug that's used routinely in lupus patients.
So to be able to have a safe cell that could do the same thing the CAR- T therapy could do, but without the logistics of apheresis and manufacturing, without the safety profile of a CAR- T, even though they look pretty safe, but we're not going to know until we treat a lot of patients. But if we do the same kind of efficacy with a cell that's more convenient, more off the shelf, more friendly to the physician, more friendly to the patient, that we have an absolute home run here. So with that, I'll kind of stop with the intro because I know that was a long-winded intro, Gil.
I do actually have a bit of a follow-on there. We discussed a lot of the benefits. What are some of the challenges these NK cells derive from donors?
I don't mean to sound glib, but in autoimmune disease, I don't see one other than the fact that we have to get past the challenge that the 30 or so companies right now that are in the autoimmune space are autologous CAR- T companies, and people are looking at us as we initially started in this field as, okay, you're another cell therapy company. So I think the challenge is we need to differentiate ourselves as the NK cell company with the only engineered CAR- NK in the clinic in autoimmune disease. So we have a massive lead that we want to keep. And so I think that differentiation and what we owe people is to dose that first patient to see the results of that first patient.
And again, if we get the same result that they got with the CAR- T therapies with this profile of a cell, then that challenge will become much less of a challenge in terms of being lumped together with other companies because we're, again, as I mentioned before, cyclophosphamide-only preconditioning. So I think that's one of the challenges. Another challenge is the perception that an NK cell doesn't have the durability of a CAR- T cell in the area of oncology. And not to go off focus right now for just a few seconds, but I will. We are doing what I would call appropriate phase one development in oncology, which is single agent dose escalation followed up by tweaks along the way that make sense. So doing the compressed dosing, for example, and looking at retreatment in our protocol, doing it in an outpatient setting.
So all of those things are really positive for oncology and the potential to retreat. We'll find that out midyear with the NHL study if we have a hook there. I think that's a bit of a challenge is the perception that an NK cell doesn't have the durability. The fact of the matter is we don't know that because we haven't retreated a lot of patients, but the four we have have all gone back to CR. If we can do that and do that consistently, even in the area of oncology, maybe it's not our focus today. It is for NHL patients in this refractory population, but that would be an absolute home run if we're able to do that, replicate it, and do it in a consistent fashion with great durability.
Maybe defining it as a pivot to autoimmune disease is not that accurate, but if we are going to call it a pivot, what was the reasoning?
You're calling it a pivot. I'm calling it focus. Because I really believe, by the way, I love the fact that people are excited about autoimmune disease. I myself have Crohn's disease and have had it since I was 13 years old. And I think patients with autoimmune disease deserve cell therapy that works for them. And the CAR- Ts are working fantastically right now. We may have a better alternative, and we're going to find that out, and we owe people the data to do that. But the focus in autoimmune disease right now, the return on capital, so if you just want to be financial for a minute here, the return on capital in this area, the rapidity in which you could get a result in this area, because the relative and Dave has some fantastic data that he's talked about multiple times that you're very familiar with.
But the B cell reset data that we have, the switching data that we have, the PK that we have is perfect here for autoimmune disease. That focus right now, given the amount of capital we just raised, is a very strong focus so that we can create that value there. Then again, expand the NK cell into other indications. The first indications you'd be looking at are any autoimmune indications where CAR- T has shown some effect. If we can duplicate that with the safety profile and the convenience profile. Talking about these patients again, these patients are already losing now. I happen to have been in remission since 1979, so I've been healthy as an ox, haven't missed a meal since 1979. But a lot of autoimmune patients miss days, if not weeks of work every month.
If you take the traditional SLE patient or lupus nephritis patient that's out there, it tends to be a young female in their 20s or 30s. And they're missing work already. So if you're able to come up with a therapeutic approach for that patient, that's relatively easy and straightforward in the clinic to study, where you're looking at things like proteinuria versus a disease activity index, which means absolutely nothing to me as a person with Crohn's, by the way, or anybody else that has lupus or any other disease. When they look at those kind of endpoints, they make no sense, but clear endpoints make sense.
So if we can replicate that in any of those CAR- T experienced diseases that people like Dr. Schett has shown fantastic results in with an NK cell, then we have a quick and fast to proof of concept, proof of concept, and that's value creating. So that's where we're focused versus pivoted because, again, if we end up with 6 or so NHL patients that show compressed dosing, they help us prevent retreatment or that we have more retreatment data, then there's a niche there for us as well that we'll look at over time. But that'll all happen as we look at the data as they come out midyear.
I do want to spend some time on the specifics of the lymphodepletion strategy that Nkarta uses, which is differentiating for the company. First of all, maybe for David here, any speculation as to the role of lymphodepletion and autoimmune disease? I mean, I know we've talked about this before, but it seems that maybe Flu/Cy has, shall we call it, T cell specific benefits. What part of this is just B cell aplasia from the chemo?
Yeah, excellent point, Gil. As usual, I think teasing apart what's what is going to be critical here in understanding how these therapies will be rolled out. I think Flu/Cy, as you said, has some history. It's been around for a long time, has been developed for T cells. We've pioneered the idea of disease-tailored LD NK cells working more like a biologic off-the-shelf therapy rather than a more variable cell therapy, allows us to alter LD more appropriate for the patients. In the case of oncology, it's clear there's direct anti-tumor benefit and a concurrent benefit of providing a cytokine milieu in the case of autologous cells to really allow T cells to expand, particularly freeing up cytokines like IL-15 to promote T cell expansion and ultimately drive results.
Now, in the case of autoimmune disease, where there isn't that large tumor burden to eliminate, the burden really becomes on us to make it a safe, accessible therapy and really focus on really what has been viewed as collateral damage in the past of B cell aplasia. We, as cell therapists, have really seen B cells like, sure, we killed B cells and they move on. Now they're becoming front and center. I think what the field is realizing is that we need to tailor our approach, not in eliminating a massive tumor burden, but really turning the approach on its head and saying what we thought was collateral damage is actually our target. We've taken that really as a mandate to dial back lymphodepletion into saying what does lymphodepletion really do?
In the case of autologous CAR- T cells and even to some extent, the allogeneic T cells really drives this cytokine milieu to permit T cell expansion. We don't need expansion because we're not T cells. All that expansion happens ex vivo in our manufacturing platform. We don't need the cytokines. We don't need prolonged lymph immune suppression because the cells are immediately active on day zero. We don't need expansion delayed. Why don't we dial back the LD, make it massively safer for a patient population that needs less chemotherapy and not more? Because we look at it and say not whether or not Fludarabine is immunosuppressive. We know that it is. It does what Fludarabine adds make up for the risk that it imposes on the patients.
We don't think that it does, especially in the case of specifically a CD19 targeted cytokine independent allogeneic NK cell, which is what we are. That psi-only approach is not a one-size-fits-all, and we know that. We think that that's a feature of our engineering and our approach. We intend to leverage that on behalf of our patients.
The way that, correct me if I'm wrong here, the way I've kind of parsed.
It hasn't happened yet, Gil. So I don't expect it to start.
It's okay. The way I've parsed this to date is they play a slightly different role in each therapy. So if you're dealing with allogeneic cells, specifically the T cell variety, you're dealing with rejection because cells need to replicate. So you need immunosuppression in order to get there. If you're dealing with autologous, you need basically a cytokine milieu and immune homostasis, and that's why you're blowing up some of the cells. So they grow. Again, you need replication. And in your case, you don't need either. Your cells are expanded. All you really need is to reduce maybe the overall burden of B cells.
Yeah, yeah. And I won't call it correction. Let's say focus is that those is true for T cells, right? So in the allogeneic, you need immune suppression, at least suppress the immune system in time for your cells to expand. And I think you've seen some allogeneic T cell approaches that work well and focus on expansion and persistence, whether that be from modification, etc. But if you get rejected before you get that opportunity for expansion, then all of the editing isn't going to help you. And I think you've seen others pivot towards more of partial HLA matching or some other strategy, other agents to try and suppress immunity longer to allow for T cell expansion and delay. For us, it's not that we don't need allogeneic host immune suppression.
It just has shifted so much further to the left, and we do think that immune suppression is important here. Cyclophosphamide in the doses we're talking about is effective and has been used for immune suppression before. So for us, we get the benefit of that drug for the target therapy or for the disease in autoimmune disease. But it also provides that limited window for the cells to be active. And as you said, we don't really need that delayed immune suppression. And we don't need the cytokine support because of our engineering. So as I said, we think in fact, you asked in the panel earlier what was the most sort of surprising data that came out of it. It was the transience of it all, right? I mean, so far the field for a decade has been saying persistence, persistence, persistence.
That's the key to durability. And although there's never really been data to say that's ever been helpful for anything other than maybe ALL, has always been, oh, you're in an NK cell, how could you have a response if your cells aren't around? And the most surprising data for us, and we jumped on it right away, was the PK, right? In the B cell kinetics, they come up and they're gone. The B cells go down and they're back up. And all of a sudden, the same people who said persistence, persistence, persistence are saying, no, no, it's depth, it's depth, it's depth. And for us, we said, hey, that's what we've been saying all along. So I think the most surprising and helpful for us, and we think is validating, has been that this focus should be on depth and targeting of CD19.
I do want to play devil's advocate a little bit here. So assuming that a therapeutic is a one and done, right? You only need to give a T cell once and you're gone and everything's great. Doesn't that kind of reduce the benefit that you would get from having a milder lymphodepletion conditioning? I mean, there are rheumatoid arthritis patients, about 30% of them that get no benefit. It doesn't matter how long you wait.
Yeah, I'll have to push back on you on this one, Gil. I think saying that a little bit of chemotherapy is okay as somebody who has to routinely prescribe it to children, I disagree. I think the idea of a one and done is great. It remains to be seen whether or not treating somebody in their 20s is a one and done for life. But the toxicity associated with chemotherapy is real. And that long-term genotoxic stress and packs on everything from GI tract to fertility to hair loss, anything else that you want to add into chemotherapy, I think if you can avoid it, you do. And in oncology, we get free privilege to more is more until the cancer is gone.
Here, when we're trying to get targeted therapy, I think the burden on us is to make this as safe as possible and not toss away or discount the risk of chemotherapy.
Gil, I have to pile on there, if you don't mind, not on you, of course, but from a patient point of view, autoimmune patients today deal with a number of different therapeutic agents that are somewhat active to not active to more active. And in any particular instance of an autoimmune patient, no matter what the biologic is that they're being treated with, there are risks involved. And so if you can overcome those risks by not putting patients in harm's way so it just so happens and I work with Crohn's patients all the time. I'm on a camp for kids with Crohn's. The benefit outweighs the risk. But if you can take the risk away, why would you not do that?
So if you're giving autoimmune patients already cyclophosphamide, which is already in and of itself a pretty potent agent for a person with autoimmune disease that's got a chronic illness that wants to walk around. But if you add fludarabine to that and by the way, many of my colleagues don't like that we keep saying this, but we have to tell the truth, which is it's not something I want to get. It's not something that a person with rheumatoid arthritis wants to get, a person with lupus wants to get, ask the patients. By the way, that's the thing that I find people don't do enough of in our business is talk to patients because ultimately they are the consumers. And you want to know why enrollment hasn't gone as well as it should go.
There's a number of different reasons so far for some of the other therapies. But probably the most major reason is that patients have been through this before. They've been promised therapeutic breakthroughs. And they've got other things they have to deal with in their lives as well. So convenient, safe is what an autoimmune patient looks at and says, "That's what I want because I want to live a normal life, not an abnormal life that happens to be somewhat disease-free with risks of other things." So I think that's really, really important. And I think that's something that, again, we owe you the data. We're going to have it. And until we have it, we have to be careful. But once we have that data, I don't think there's why would you wait? Why would you want to wait for manufacturing of cells?
Why would you want to put a patient through that kind of situation when they don't need to go through that because it just happens to be while it works? Well, something works, but doesn't have to do that. Well, isn't that where you want to go? So that's kind of how we look at this.
Okay. I think the differentiation from autologous approaches is actually pretty clear. But maybe let's spend a minute on some of the allogeneic approaches. There's quite a few of them out there. We'll call them an alphabet salad. But I got iPSC-derived T cells. I've got gamma delta T cells. Other.
Yeah, I would say, look, as my friend Peter Maag said on his biotech interview TV, let the data show us what all these cells can do. Let's see who gets the data. By the way, let's wish everybody well because nobody wants these patients to suffer. We all want these patients to do well. So all the different cell types ought to be in the clinic and be thinking about how to be in the clinic and how to get patients enrolled. And we'll see the data. And to me, in this particular indication, there is so much room for innovation. It's just spectacular. So the more, the better as far as I'm concerned.
So today we haven't seen a lot of the specialized immune toxicities like CRS and ICANS in these indications. And kind of broadly, we haven't really seen them within NK cells in oncology either, not really. So I'm kind of trying to understand if there really is going to be a situation in which we're going to start seeing toxicities in autoimmunity given the lower antigen burden.
I think it's always a possibility, right? I think there is an association with antigen burden and toxicity. But there's also idiosyncratic reactions, right? I think there are some patients who you wouldn't expect to have toxicity and end up having it and vice versa. So I agree that I would expect generally less CRS and ICANS in this patient population. And thank goodness because it's no fun to get or to treat. And so I think that's great news for the patients. I think in terms of counting on that, if you could get a similar result without having to worry about it, I think that's what we're aiming for. Will we see toxicity? Yes. I think we're just now starting to hear more routinely about the overall toxicity. And the initial data was a clean safety profile. And it's clean for CAR-T.
I don't think that it's not going to be clean or as clean as it could be until we flesh out exactly how much concurrent therapy and LD you really need to get this benefit.
Okay. And we always complete each other's sentences. We work well together, Dave and I. So I will just say that we're in inning one right now, right? So just go back to the biologics in inflammation. And they've been spectacular, right? But remember what was going on in inning one and where we are now in inning 12, right? So we still have to respect that longer term. We have to watch for these things. And we want to be in a really good position inning one, two, three, four, five, through 12.
From a dosing perspective, you guys have gotten pretty high doses in oncology. Is there any thinking of it? I've seen your study protocol, but thinking of going even higher in AID?
In dosing?
Yeah.
Sure. I mean, I think one of the advantages here is we've not had a dose limiting toxicity yet. And I think there's probably going to be at some point where you can't continue to give trillions of cells without having some impact. That being said, I think we reserve the right to, and I think it's going to be important as you move into oncology and get into tougher indications where dose intensity and E:T ratio and things matter, actually don't expect there to be a need to push the dose very high. I think we've seen B cell depletion with relatively low doses in our patients, as low as 300 million. Data we've shown has been pretty low. And I expect that burden to be relatively low. But should it be necessary, we'll be ready.
Yeah. We've seen with a lot of times people talk about the Chinese data that's been out there that it really hasn't been published per se, but it's out there and people have seen it. They saw activity at every dose, and they started much lower than we did. So this is a good sign. Again, preliminary data. But if we can show data at every dose, even starting at by the way, the one benefit that Dave has done here was all that safety database and all that efficacy database in NHL is able to apply. So we're starting at a very high dose level in these lupus patients and in autoimmune patients because we know it's safe, right? So we can go higher. We could potentially look at lower doses if that's what's needed. But all that will be, as I said, after IND one.
Okay. Maybe a silly question. Have you guys ever thought of conducting a healthy volunteer study without any conditioning? Would that even be ethical?
I don't think it's necessary. I think we're as I said, I think we talked about the benefits and opportunities in LD and what we think it does. I wouldn't expect that the product itself adds any additional toxicity. I think we all have our own NK cells for a reason. I think maybe when you and I are retired, we can talk about way back when, and now we're getting prophylactic allogeneic NK cell infusions to prevent us from getting cancer in the first place. But I think we'll leave that for a future state.
Yeah. And as the two chief natural killer cell executives, the two of us probably wouldn't want to give something with the name killer to healthy volunteers. We're more gentle than that, Gil.
Okay. I don't want to completely forget about oncology. We said not a pivot, right?
Help us.
At your most recent earnings report, the prioritization of NKX101 and AML, can you discuss some of the emerging data and the reasoning behind the decision?
Yeah. I think first and foremost, what we say is we've learned a lot from oncology and a lot from AML. And again, we're a natural killer cell company, right? So we're going to be watching the space very carefully. Right now, I think the best thing to say about AML is the investment to get through a phase 1 study, even in AML, given the heterogeneity of that disease and the complexity of the cells and the NKG2D target, which is not like a typical CAR-NK CD19 target, is it's vastly different than what we could do in autoimmune disease and create the value here. So we're going to be watching. We're going to be continuing to look at NK biology in cancer as well as in autoimmune disease. And we're going to remain an NK company that will be opportunistic.
So right now, opportunistically, we're in the autoimmune space. The AML data right now is behind us. We didn't see what we wanted to see with the expansion of that cohort. But we believe there are ways to get that. But to get there, and the study designed to get there is infinitely more intense, more resources. And right now, with the precious resources we have, we want to make sure we focus on somewhere where we can create some value quickly so that we can continue to go back to those other areas. Because who knows from six months to a year from now, investors come back to us. And while today, they're only focused. You want to talk about pivot. They're pivoted on autoimmune disease.
But someone's going to say, "Hey, what happened to that cancer program of yours, right?" And so we want to be ready when that happens. And we want to be and by the way, if you look at our NHL protocol with 019, if in refractory CAR-T and bispecific patients, we can show something that no one else has shown so far with a safe, durable, off-the-shelf cell, then that's something that we will consider when we get those data in mid-year.
Yeah. That's literally my next question. Kind of thinking about this redosing paradigm, it's actually very interesting to me. I don't know of a lot of examples of providing patients with the same therapy post-progression and having activity. And I don't think it's even common for chemo, now that I think about it. So that suggests that maybe a CR is not fully a CR. David, maybe you have a comment there.
Yeah. I mean, it's hard, right? We're in early stages of development here. There's nobody doing. We don't have the decade of experience of dosing like CAR-T cells do. I think what we're finding and what we're understanding is that the mechanisms of resistance for NK cells is different than T cells, right? And I think often you'll see patients who have relapsed cancer and still have circulating T cells, and they've somehow just forgotten how to kill cancer cells. And it seems to be the agent that really is failing. Here, where we think we need to optimize, is how we deliver. We think we have an effective therapy that can drive a response. And it may be that we need to dial in how we do dosing to get more effective.
I think we were very encouraged by the retreatment data, not only because we allow patients to get back into complete remission, also told us that we're on the right track here. There isn't some cancers or some of these that some resistant cells were left behind. Simply, we just didn't eradicate them all at the same initially. Whereas the similar examples in CAR-T of trying to reinfuse and get those to go, it doesn't seem to be.
Doesn't do anything.
Doesn't really work.
Although, if we got to remember that some of that is rejection, right? Immune tolerance.
So think about compressed dosing here as well, Gil, besides retreatment, right? Because you could learn from compressed dosing in NHL, certainly for AML. Now, I want to keep the focus on autoimmune disease because that's what we want to keep you focused on. But there's a lot to be learned here from the work we've done. And I will tell you, from the moment I met David Shook, because our founder, Dario Campana, introduced him to me when he was still a practicing oncologist, hematologist, transplanter, we talked about the option with an NK cell of redosing, right? And so we've been thinking about this for as many years as we've been together working on these cells. So there's a lot of work to be done. We're going to do it. We're going to do it in time.
We're going to focus right now on where the greatest value is going to be created, which right now is in autoimmune disease.
Another question from investors that I got a couple of times regarding your manufacturing. And this is a bit of a pushback question. So there's still donor dependency, right? You have donors who give you cells. How much variability do you expect kind of batch to batch? And how do you account for that? Are you going to put some donors on the payroll, or how's that going to work?
Best way to answer that is work in progress. What we feel really good about, and particularly in light of all the issues that have just come up with BIO, that as you know, I'm the past chairman of BIO, and there's been a lot of issues here with CDMOs. We are very fortunate to be in a position where we have both a clinical GMP facility down the road here and a commercial GMP facility down the stairs here in this building where we're in control of our own manufacturing. It's expensive, right? And it's costly. Our facility downstairs, which is a 30,000 sq ft facility, is funded from multiple tens of millions of dollars of tenant improvements from our landlord. So we didn't use our precious capital that we're using to study these drugs to make that facility. We used tenant improvements to do it.
So we've got two facilities that are ready to make cells, and we are studying, scaling out, scaling up on a constant basis. And donors, absolutely. There are benefits to having multiple donors, by the way. And Dave can talk to you about that since we complete your sentences. So I'll let him tell you where that benefit could come from. But in terms of a single donor making trillions of cells, very possible. You could have a universal donor if you wanted to. Our position would be not to have one universal donor, but to have a few ultimately. But that's work in progress, right, Dave?
Yeah. I think you highlighted all the relevant points here. I think we want there's probably some advantages. Some NK cells probably kill more than others, etc. I think what we're learning is the vast majority of the activity is driven through the engineering, right? I don't want to say that simply that the NK cell is a vehicle for a CAR, I guess. I was just commenting on your point. Yeah. I was just going to say it as like vehicle for a CAR. It's not only a mechanism to deliver CAR-T therapy, right? That there are some intrinsic differences in terms of how well they expand, how well they persist, etc. And every time we get a product, we learn something, right? I think there's always going to be inherent variability.
But I think what we're learning is we can drive consistency through engineering when we follow our same manufacturing process. And anything we do to try and improve on that, we want to make sure that we understand how you don't want to pigeonhole yourself into you mentioned iPSC, etc. You choose sort of one way to do it. And if somebody has an antibody to that or that particular strain isn't we don't know, right? You have to decide a priori which one is better. And you committed to your entire product being that same one. And so I think as Paul mentioned in the very beginning, we're an NK cell company. I think there's collective NK cell expertise of several decades wandering around our hallways. And we're learning each day on how to find the how to make the best product.
Donor's probably going to be a part of that. But I think what we're most comfortable with is our engineering.
Yep. And should diversity matter, we'll be ready, right? So should resistance occur and again, inning one, right? We'll be ready.
All right, Paul. Maybe a last, last point, given your recent financing. Cash, cash runway, where does it get you guys?
You can't trap me into giving guidance before we give guidance. But I will tell you that we.
Maybe use very arbitrary terms. We have a few years.
I've just given you little troubles. Gil, so we ended the year with $250 million in cash, right? And we just raised $240 million, right? When we ended the year with $250 million in cash, we said we had cash into 2026, right? So with the infusion of capital and the functionality and optionality, which we like to have, of expanding in multiple indications and here where we're going to create the most value on autoimmune disease, we're in a really good place right now. It doesn't mean that cash is burning a hole in our pocket. So we've got, as I tell people in the company all the time, there are moats around this capital. There's fire in the moat. And there's Lisa to get through first, our CFO, and then there's me to get through if you want to use that capital.
Because we need to be careful with precious capital. So we're going to be careful with it. But we're going to invest it where we get the best return for our investors. And that'll allow us to remain an NK company for a long time.
All right. I think that's a nice positive note to end with. Thank you, guys.