Sana Biotechnology, Inc. (SANA) Earnings Call Transcript & Summary

Well, hello, everyone. I'm Maxwell Skor, biotech analyst with Morgan Stanley. I'm happy to host Sana and Steve Harr, CEO. Before we get started, I just want to read a brief disclosure. For important disclosures, please see the Morgan Stanley research disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. So with that, I'd like to introduce Steve Harr. And for those in the audience who aren't familiar, maybe Steve, if you can give us an introduction on Sana and key takeaways.

Sure. First of all, thank you for having us. Thank you, Morgan Stanley. Thank you everybody for joining us, both here in the room and online. I'm sure you recognize as well, we're making forward-looking statements. I'll do my end of the disclosure, which is take a look at our most recent 10-Q filing for risk factors. So look, Sana, so we're approaching now about 6 or 7 years old. And we were founded under the idea that one of the most important transformations that will take place in medicine over the next several decades will be the ability to modify genes and use cells as medicines. And our aim is to build a defining company of that era. I don't think there's anything despite a really difficult operating environment in the cell and gene therapy space, which we get into why I think that is there and what we need to -- how we grapple with it. There's nothing that's dispelled that idea. And we set out with really 2 important goals or ideas. The first is we want to be able to transplant cells. And since the advent of transplant medicine, the major issue that has held the field back has been allogeneic rejection. And the way people have gotten around that has been either autologous cells, which are not that scalable and they don't work for every cell type or really, really significant immunosuppression. You put someone else's cells into your body, you will reject them. And that's been the history of the industry. And so part one was we wanted to overcome allogeneic transplant rejection. And I'm going to show you or tell you a little bit about it. I think we've done that. I think we've now proven that multiple times in people, and it's been published in places like New England Journal of Medicine and Cell and things like that. The second thing we wanted to be able to do was to repair ourselves. And so the goal there is to be able to deliver genetic material, either DNA, RNA, even proteins to cells in a specific, repeatable way. And really, what we have shown is that we can do this clearly, at least in nonhuman primates, delivering a genetic material in a very cell-specific way. And I think it's pretty clear that at least with preclinical data, we have a best-in-class asset. Now others are starting to make a little bit of progress in humans, and we need to show that as well in people. But -- so really substantial progress. And so if you take a step back where we are with the cell delivery or cell replacement, the most important and exciting area we're looking at is type 1 diabetes. Type 1 diabetes is a relatively simple disease to understand. It's about -- it's the patient or a person's immune system attacks and kills the pancreatic beta cell. The beta cell is the only cell in your body that makes insulin. And so up until 101 years ago, it was a death sentence. And then there was the invention of -- discovery of exogenous insulin. And exogenous insulin helps, but there are 9 million people today with type 1 diabetes, and that's growing, and it's supposed to be about 15 million people within 15 years. A person diagnosed with type 1 diabetes has on average with the best care 10 years or less of life expectancy. In most of the world, that's 20, 30 years less life expectancy. During that time, they have risks of amputations, blindness, heart attacks, stroke, kidney failure, and then if the sugars get too low, coma or death. And if you talk to anybody with type 1 diabetes, they'll tell you that it takes over their lives, right? It's every moment of every day. You're thinking about my insulin, my sugar is, what am I -- my exercise, what am I doing? So we have a really rare opportunity to move forward with what looks like a transformational curative therapy. So our goal with this is very simple. A single treatment that leads to euglycemia or normal blood sugars, with no more insulin, no more monitoring, no more immunosuppression for life. And I think we can comfortably say now this will happen. And so what -- again, we may not do it. We can make a mistake, or we have safety issues or time, but it will happen. And so why are we so confident? So as I said, the disease is super simple to understand. It's a missing pancreatic beta cell. And so about, let's say, 25 years ago, starting with James Shapiro's group in Canada, people started to transplant pancreatic islets from cadaver. So think about an islet as the pancreatic beta cell plus some support cells around it, right? So they could isolate islets and transplant those into people with type 1 diabetes. And what you saw was, you're now seeing people out 15, 20 years off insulin and doing quite well. But it's not a really scalable or replicable supply source. And you also have the challenge that there aren't that many people for whom lifelong immunosuppression is better than lifelong insulin. So over the last few years, you've seen several different groups show that you can take stem cells and grow them or differentiate them into pancreatic islets. So now you have what looks like a more scalable and definitely more replicable supply source. But you still have the challenge of immunosuppression. And so just with -- this year, what we've shown is that we can gene modify with the edits we make and get into what they are and why. These cadaveric islets. And patient -- the first person is making his own insulin for the first time in over 40 years. And that data from that patient was actually just published in the New England Journal of Medicine. And the official like print version came out last week as editorial as it goes through the mechanism of the drug. And it's a transformational finding, right? It's very rare that anyone gets into New England Journal of Medicine. And so I think that now you have all the component parts together to create this curative therapy. So what is our goal is we've made a gene-modified pluripotent stem cell, and we will grow that into islets. And so the most challenging part of that for us has been making that first cell that's your drug product forever, the master cell bank. We've now accomplished that. We get into that. And this drug is called SC451, and I'm very optimistic that this has -- is a therapy that can reach our goal for people with type 1 diabetes, which is a single treatment with new glycemia and no immunosuppression and no insulin for life. So that's the major part of the company. I'm sure we'll get into the other parts. So we have the in vivo delivery capability. And we also apply the same hypoimmune technology, which is what we use to hide cells from immune system to make allogeneic CAR T cells. There are a couple of different drugs in development there. But that's a little bit of overview of what we're up to.

That's great. Thank you very much for that introduction and congratulations on the New England Journal of Medicine publication. So maybe just to level set on -- in regards to the data you've demonstrated to date, how UP421 has been formed or translated to the stem cell-derived SC451. So maybe just walk us through the clinical relevancy of what you've shown so far and maybe some of the safety issues that you've overcome.

Well, I guess -- let's take a step back. So this UP421 that you referred to, this is -- so what we did -- what we wanted to figure out was -- so what we're trying to do is gene modify a stem cell. And that one single cell, you will grow into over time, quadrillion-plus cells, right? It's trillions and trillions because it's 1 billion cells per patient, right? So you figure 100 -- 1,000 patients a trillion cells, and there are -- 15 million people with the disease, right? So it's a lot of cells. And so the most challenging aspect of that has been is, every time we divide the cell, you get a mutation or 2 or 3. And usually, it's on noncoding regions and it doesn't matter. But what we're doing here is putting cells in growth media that selects for cells equal quickly. And so what we found was some clonality would emerge typically in DNA repair enzyme. And we didn't want to -- a good example of this is like people love I think it's like a TP53 mutation. You don't want to transplant patients in cells that have a p53 mutation. I think that would just be a bad idea. And so we spent a lot of time, energy and dollars figuring out how to make these cells and grow them through many, many, many new divisions without seeing problematic mutations emerge. So that has been the most important safety aspect that's taken us a long time and a lot of time and energy to overcome. And while we were doing that, and now I go to your question, we want to figure out, hey, this thing, this hypoimmune technology where it's shown its work in some humans in CAR T cells. And it's shown that it works in every preclinical model we've looked at, does it translate into the type 1 diabetes space. And the type 1 diabetes, you have 2 problems. They have to overcome, one, allogenic rejection, again put someone else's cells into you, you will reject them. So we have to figure out how do we hide it from your immune system. The second is you actually already have a preexisting immune response to the cells we're transplanting even an autologous cell would not work, the patient would just kill it. They have an autoimmune disease. So we wanted to ensure that worked in people. And while we were playing -- not playing around, working hard on the master cell bank, we did this investigator-sponsored study in Sweden, where we took cadaveric islets, so islets from recently deceased person, isolated them and did our gene edits. And to see, hey, could we see here that these cells would survive and function. That's all that we were looking for. So it's a safety study, a relatively low dose. And what we also want to see is can we do this and deliver the cells in a different way than what's been done historically? Because historically, most islet transplants, what happens is they are injected into the portal vein of a patient and then the cells are shot up into the liver. And the challenges with that is, first of all, it has to be done under interventional radiology. So for a disease with 15 million people, it's not that scalable. The second is that when they go into the liver, they tend to cause clots. And because of that, patients are anticoagulated. So about 5% of patients actually end up in the hospital either from a clot or a bleed. And again, those are things we don't want. We're trying to really do something that is scalable. The third is a bunch -- you're not supposed to have cells in your body and your bloodstream. And so your immune system will kill them, right, pretty quickly. So you want to get on. So we put the cells in the arm. So we do gene modified stem cells -- sorry, gene-modified islets from a pancreas of a recently deceased person and put them into the muscle in the arm of a person with type 1 diabetes. And the person is now out, we've shown data out 6 months. He's making his own insulin for the first time since 1987. And he's doing really well. It's a really exciting outcome. That's not a scalable solution. And so we're making sure we're working on our scalable solution, which is the stem cell derived. But it -- I think it solves -- it answers the question, is type 1 diabetes a cure? Will somebody get this curative therapy? The answer is yes. Like we need to be the ones that put the pieces together. We should be the ones. It's our technology, but we need to actually execute and get it done. There are reasons because we have the real safety issues and things like that and time and capital, we have to make it happen. We can go through what all those are. But it was a super important study, I think, for the field of type 1 diabetes. It's a super important study for the field of transplant. I mean it's the first time you've seen really something like this ever, right, you can transplant a cell with no other treatments. In no way they they're suppressed immune system at all, and you see the cells survive and thrive. And it's a super important study for Sana.

That's great. And so thinking about the next phase of innovation at Sana SC451, I believe you guided to filing an IND next year at some point. But just thinking about the learnings you've taken so far, how are you going to evaluate durability? Are you going to be doing any imaging? How are we going to understand the viability of these cells going forward?

Simplest way to understand the viability is the physical outcome of it. The outcome for the person. So -- and there are ways to measure what you're doing. So when a pancreatic beta cell makes insulin, it actually makes something called pro insulin. And when pro insulin is secreted from the cell, it's cleaved into C-peptide and insulin. And so first of all, C-peptide is relatively stable and measurable in your blood. So the amount of C-peptide is a 1:1 direct measurement of the amount of insulin your body is producing. And when you inject insulin, there's no C-peptide, right? And so the first way you're going to follow this is what happens with C-peptides. You actually can find it? Is it at physiologically relevant levels? Does it go up when you eat? Does it go back down when you're not eating, all of those things. The second thing is we want to see these people off insulin. There's no way you get off insulin. You'll die if you stop getting insulin as a patient pretty quickly, right? So you're not getting off insulin. That's super easy to measure, right? But the third is we will do little sub studies where you can look at the images of the patient. It doesn't need to be done in every patient. It's a lot to ask them to keep coming in. We'll do PET/MRIs, and some of them, we showed that where you can actually label -- put -- you can actually find beta cells, and we see them. It's in New England Journal of Medicine article. You see them and it's actually left arm of the person with type 1 diabetes. So we will do all of those things to -- to be able to measure this. It should be relatively straightforward. And the durability is something where you're putting terminally differentiated cells that should live a long time to a long, long, long time. Like we have the beta cells we have. And so hopefully, this last 3 decades, you're not going to learn that in phase -- you're going to learn it over time. You're not going to learn it early. I think it's a clinically very relevant drug with relatively short survival. Let's say, I think you ask a patient, they said, well, you have this happen once a year, that's no problem. That would be awesome, right? I can get rid of the injections of insulin. I can get rid of monitoring my glucose. I don't think that's a good business. We have to -- scaling these medicines is not simple. We're in no way do we have a direct path to being able to treat all the people in the world with type 1 diabetes yet. We also have to do it at a cost that makes sense for society, it makes sense for the patient and it makes sense for our investors, right? So all of that has to happen. So that's dosed to the patient every 6 to 12 months. I don't see that circle being square. I think that will be a -- not a viable business. But clinically it would be super viable.

Okay. So in regards to the IND filing for SC451, what are the gating factors right now, if you could just level set expectations on the trial design? And any feedback you've gotten from regulators?

Yes. So simple, IND, you have to do 2 major things. We have to do a number of things, but one of them is a nonclinical package, which includes GLP toxicology studies and efficacy studies to justify what you're doing. We have to complete all of that we would call representative material, right? We've done it. We've actually transplanted with the exact cell line we're using, the exact same cells, starting cell and with a research product, we've done this in mice and seen them 15 months out. It looks great. No histologic abnormalities. They work really well. We have to do that now with kind of what we would term representative material, finish doing that with representative materials better ways. That's track 1. Track 2 is GMP manufacturing, right? You move from making it at a research scale and with research quality reagents into making it with the GMP -- in a clinical trial scale with GMP quality reagents. So those are the 2 things. You got to get them both done. The latter will happen. It probably just has some time risk to it, right? The safety studies you have to make sure that adverse things don't happen. So the second part of that is a clinical study. I kind of like to think that if you're a good clinical development is super rational and you're changing as fewer variables as possible over time. Like a good way to think about the way to start this is has worked with the Swedish study. Why wouldn't you start and try to replicate that? Well, the only really difference is the product itself, right? And that's a very broad patient population, but it's not all type 1 diabetics, right? There's a certain exclusion criteria in there. Over time, we will work to expand that into younger people, this is 18 and over, into older people. There was an upper limit of age. There are elements. If you have had a recent heart attack, you don't really want to -- you really don't want to start with that person. If you had a recent cancer because if it comes back, that will complicate our understanding, does that happen from our drug or from something else. So relatively healthy people who just look at their individual medicine paper. That's probably the way to start. It may be a little bit different, but it should be more or less the same. Third, interactions with regulators. I think they've been really constructive. And those are both with the FDA and I think our very early experience in other parts of the world. And I think there's generally a recognition that this is a different therapy than anything that's been out there, and there's generally a recognition that it can be very transformative. And so it's different than the interactions we have, for example, the allogeneic CAR T cell, which are fine. But this is a much more productive. It doesn't mean it's easy, but I think it's transparent around what it is that we think we need to do.

And before moving on, could you comment at all on the competitive landscape? I think the Vertex is also in the space. Anything you'd call out there?

Well, I think for right now, we're kind of in our own competitive landscape. In that, we're getting rid of -- having a simple -- if you define the therapy is what we want is we want to be able to get patients to have normal blood sugars with no immunosuppression and no insulin. I am sure others are going to figure it out. There are a host of other companies that are playing around this space. I'm confident that many of them are really great science companies and someone else will figure some of that. But for right now, I think we have a very unique place and we need to really work urgently to get this into humans and continue to have that. That's kind of where things are. The other thing that we've done, I think, is different than maybe what some others have done is, one of the challenges of immunology is there are many aspects of immunology that you have to protect against. And we actually do have an Achilles' heel, right? We have an Achilles heel. If you have preexisting neutralizing antibodies. And the most common thing for that is blood type. I think that's common really, if you look across all these places. And so we worked really hard to go forward with an O-negative line because that allows us to be -- that's a universal donor. I think a lot of the other cell lines that people are working with are limited by blood type because it's just so hard to find these O-negative donors or lines. We have to make some ourselves, we brought -- we licensed them in. And so I think we have a number of areas of competitive advantage. I presume others are going to work really hard because there have been -- there are a lot of really great companies that have been playing around this space for over 10 years. That will, at some point, make some progress. But I'm -- for right now, I'm optimistic that we get the chance to at least figure this -- figure out if our stuff works in, for the first time, in people. And then we've got a really leverage and execute on that lead time advantage. But other people are doing important things for patients. It's just slightly -- some of those things will be in smaller patient populations, right, or sicker patient populations and for the ones that we're going after, I think we have a pretty unique perspective.

Yes. Just doubling down a bit on that because you hinted at inclusion, exclusion criteria for the potential Phase I trial. Could you just give us some thoughts on what the target patient population would be initially? And then how you expand that addressable population?

Well, over time, I want every person who has type 1 diabetes to get this drug. And I've yet to meet a person who has type 1 diabetes who if this hits his clinical profile says, no I don't want it. No, I want to see 15 years of data, I want to see that. It's a very unsatiated patient population. And so early on, we'll start with adults, right? They will quickly move into adolescence, and it will take longer to get into young children. Early on, we will probably again, not have people who've had a heart attack and things like that. But over time, you want to get this to them. I mean people who have cardiovascular disease, it's so clear that if you get their sugars under control, they benefit dramatically. People -- so we will expand it stepwise through clinical development. But we're not looking for -- we're looking for all comers. It's not like it's people who have poorly controlled type 1 diabetes. Why would you punish somebody? They'll just make it fully controlled, right? They will. I mean if you say, hey, you have to have an elevated hemoglobin A1c. I will guarantee you that people will have that hemoglobin A1c within 3 to 6 months. But if you said, hey, if there's a certain number of hypoglycemic events, that seems like a bad idea, but we won't go down that path. But they would find a way to make that happen. I mean it's a pretty unsatiated group of people. And I would like to make this available to all of them over time.

So Steve, I think you noted this at the beginning. Maybe you can talk about why it's been so challenging for companies in the cell and gene therapy space of late? And what potentially could be a tipping point or an inflection point near term?

I don't know the tipping point. I think there are 2 challenges that we're all facing. One is the capital intensity of this space, right? And the capital intensity is something where it's not only expensive to make these therapies, but so much of it relates to manufacturing that you are investing a lot of those dollars at risk before you have clinical proof of concept that says, hey, this definitely works. So that's part one. And part two is, we still haven't exactly figured out as a society how or whether we really want to pay for curative therapies, right? You look at the simplest and best example of a scaled cure would probably be Gilead's hepatitis C drug. And if you guys -- if you were -- and that was one where through a very short bolus of time, they were able to treat many, many people with a very, very grievous disease. And society really struggled with it, right? And it wasn't -- in the grand scheme of things, it wasn't that expensive at the end of the day, right? Just a lot of people. And so right now, so much of cell and gene therapy has been for niche populations, our goal here is to go after a population as big of a hepatitis C, right? I mean this is 15 million people. If we have to go and take care of all type 1 diabetes, this will be really helpful for a lot of type 2 diabetics, too, right, who are very brittle and poorly controlled diabetes. We have to figure out as a society how, and we're going to pay for this. And I think those are the 2 things that sit back and hold you back. And there isn't like some handful of examples where you look and you say, man, they built an unbelievably great business so far. And I think that's the other challenge. So to me, the tipping points come when people begin to make real money from this, investors wake up and say, I don't want to miss that, right? Because the science is moving pretty quickly. I don't think this is a science problem right now. This is a capital problem.

Okay. That's helpful. So beyond type 1 diabetes, you have a lot of other things going on in the pipeline, advantages of fusogen platform? Anything you'd like to call out or key near-term readouts that we can expect?

So fusogen platform, what this is, is it's a capability to do cell-specific delivery of genetic material in vivo. And so we chose to go after a couple of cell types early. We did T cells, where I think what I already described to you is probably a best-in-class nonpreclinical data set in nonhuman primates things like that. The second is we went after HSCs and be able to deliver gene editing agents and things like that. I think we have maybe the only thing that's really kind of working there. The third is we did hepatocytes and tons of things work there, so we stopped doing it, right? And so within the in vivo CAR T, we made 2 really big assumptions. One is that cell specificity on delivery matters. And we think it matters for 2 reasons. One is safety, right? You don't need to go into other cells because it just can create toxicities or immunogenicity and things like that. The second is manufacturability. You don't have that many T cells. So it turns out if you go into every cell in your body to get into enough T cells, you're going to have to make a ton of drug that's going in, for example, your liver as well. And so it's both safety and manufacturability. And we've done it. We've done this now. We've shown very clearly in nonhuman primates as an example, the ability to make a CAR T cell that only goes -- more or less only goes through T cells. It goes to the target -- cell surface target we pick. But it's not -- you can't find that liver. You can't find it in gonadal tissue. You can't find the lungs and things where other technologies show up. And we get, as an example, deep B-cell depletion, clean lymph nodes, a B-cell reset to all naive cells, right, afterwards. And we can predictably get that now in nonhuman primates. Maybe showing you a bit of data on that, we'll show you more. I think I can convince you with the data we have that this is something that is pretty good or really good. So you've seen a lot of strategic activity happening in this space of late. Our biggest Achilles' heel in that is that all the strategic activity that is taking place is taking place with assets that have a bit of human data. And we don't have -- we have a good bit of nonhuman primate mouse data, but not human data. So we most likely need to get that across the goal line. Our challenge is that we're pretty capital constrained as we talked earlier. And I think the type 1 diabetes is such a rare opportunity with such a high risk-adjusted return. It's not that a guaranteed return, but a high risk-adjusted return that it believes us to make sure that we're allocating our capital efficiently to that. And right now, we don't know how we're going to push forward this fusogen platform to get the human data. That's -- it may be that we do a bit more work and wait until our cost of capital is lower. It may be that some -- we end up partnering the asset. And I could even see that we kind of spin it out into mostly Sana-owned or partially investor-owned where they can -- an investor can solely invest in that. And we get the data and either we buy it back or we sell it, the whole thing to someone else. And so we'll figure out a way to get the right money to it. It is a really promising platform. And what you have is this chance from, again, a single therapy as an outpatient, for example, to deliver and make CAR T cells, no lymphodepletion, no chemotherapy, right? And a relatively scalable manufacturing process. I don't know if it's fully scalable yet because we don't know the dose with something that we think can have a really meaningful clinical benefit for people. So we got to figure that out.

So just touching briefly on capital allocation. I know you raised recently extended your runway. Any commentary around capital allocation beyond what you've said previously and just your overall runway?

Yes. I'll start. We need more money. I mean just to be very clear, we're not across the goal line for what we really need. I presume progress will lower our cost of capital over time, but we'll need to raise more money. And whether that through partnerships, I'd say nontraditional things or things that haven't been done before, which I think are may be available to us. We're working hard on some of them and/or equity with shareholders will figure that out. From a capital allocation perspective, as I said, we will focus what we need to get type 1 diabetes across the goal line. We will do that. I would really like to find the capital to push forward the in vivo delivery because I think it's a space that has a lot of important progress being made. There's a good bit of strategic activity. And to the extent we just sit on this asset, it's probably using value, right? We then have a couple of clinical stage allogeneic CAR T programs. And I think it's pretty clear that they work at least to some extent, right? We -- they evade the immune system. Actually, we just published this 2 weeks ago in a Cell journal showing in the human data set, our ability to evade the immune system. And they do work. I mean as an example, you can -- you see B-cell depletion, right? They need to see -- do they -- are they -- I kind of always say are they okay, good or great? We'll start with that, with the autoimmune study. To me, okay. Yes, it works, but it's probably not quite as good as an autologous CAR T cell. And good is it works and we have a much simpler and more scalable process for both the clinician -- for the clinician, the patient and manufacturing, right? And great is it's better. The challenge with that is, as I look at the outside world and what you guys are doing, I think there are only 2 publicly traded, maybe there are 3, stand-alone CAR T companies that have a positive enterprise value. So our challenge is then saying, okay, can we create a data set that both makes investors rerate the space and declare us the winner from Phase I. The odds are pretty low on that, right? And so we've been very focused on finding a partner because I think that's the best way forward for this asset. I think we can pull it off. And so if we don't, we may not even go forward with it because I'm not sure the capital allocation is going to make sense in a time period where we have a couple of other very high, we think, risk-adjusted return investments to me. But it is something that we're optimistic about. I think it would be good for people and good for patients, and if we can do this. It's a scale process. It works. It's a lot cheaper to make than an autologous CAR T. But we need to kind of figure out where this is going relatively soon.

Okay. So we have been asking a couple of just broader questions to all of our companies. In regards to China's rise in biotech innovation, how are you thinking about your competitive position here? And will this influence your R&D or BD strategy at all?

I'll just start with type 1 diabetes. We just need to get it right. I think we need to focus on our own knitting and not get too distracted by what happens in the outside world. So there are 2 main -- I kind of think just broadly what's happening in China, interesting. One, sometimes it's cheaper, right? And that cheaper can relate to people cost and just being a bit more scrappy. And I'd like to think we can be at least as scrappy. And two is, there are elements on the regulatory side where they're able to move much faster, right? And that's a lot with nonclinical or GLP tox studies as well as some of the manufacturing. And then you get into people, right, again, it's the same thing, where it's like something is cheaper, right? And right now, our -- I think we just need to get our own stuff right. I don't know if anybody -- there's some faster or, I'd say, lower bar process that we'd want to embark on related to these -- particularly the stem cell-derived therapies. I think this works outside of safety issues. Right now, we've proven all of the components of efficacy. And so we need to replicate those components that are super important for efficacy and not run into a safety issue. And the best way not to turn into a safety issue in a person is to get it right in the preclinical setting first, right? And I think you also have to remember, we're putting a gene-modified stem cell-derived therapy into a patient population that, but for our therapy, would live for decades, most likely, right? So we have a high bar we have to meet to justify doing that. And I think we need to make sure we test it early, and I don't think there's a faster, easier way to do that when you have such a novel technology. So a long-winded way of saying it's really not something that I think we nor our investors should be myopically focused on. We should be aware of, but not myopically focused on. It's different for other spaces, right?

Yes. That's true.

And even in the CAR T, every time you look up, there's like another -- there are -- there, you run the problem, what's the right target? If you have the right target, what's the right modality? If you have the right target and right modality, what's the right company, right? But because you don't know some of those answers, fast matters, fast and cheap matters, right? So you see all kinds of times where there's a target with multiple type modalities where people are moving quickly. And some of the Chinese companies are moving quite quickly. So in that space, it's very much a part of what we have to grapple with and think about because you see an ability to more rapidly move different modalities into human testing and see, hey, does this really work or not, right?

Lastly, from the regulatory side, is there anything you'd call out as being meaningful or impactful thinking specifically FDA, MFN or tariffs? I know we're early, but, yes.

I think that we're at a stage where the most important aspect of what we think about is the FDA, right? I think that -- I'd like to think that given the novelty of this therapy and the interaction to that debate that this will be a constructive relationship. I will tell you, it's not going to be an easy relationship, only in that I think there are a lot of very difficult assays and safety things we need to work our way through. But what makes it productive is it's transparent, right? And so I think that will continue to be the case. We have to make sure we hold up our end of the bargain on that, too. MFN, at the end of the day, I think it's a long ways away. There are a lot of things that could happen. And I like to think that we're developing a therapy that has a global price to it anyway. Tariffs, the supply chain is expensive. So adding cost to the supply chain is something that is complicated for us. So I hope that those are not permanent aspects of our cost structure. We'll grapple with that if that happens. This is a drug that likely needs to be manufactured at least somewhat proximal to the ultimate end delivery place, at least some end-stage manufacturing. So it will be done if there are tariffs that will end up being done in the United States regardless, but we have them, right, we'll do that for a while here. So I don't really worry about it too much. We think a lot about the FDA, and we'd like to maintain our relationship with them and see how that goes.

Well, I think that's time. Thank you very much, Steve. Really appreciate your time.

Thank you. Thanks, everybody.