Afternoon, I'm Salveen Richter, Biotechnology Analyst at Goldman Sachs. Thanks for joining us. We're really pleased to have the Sana team here with us, of which we have Steve Harr, President and CEO, Nate Hardy, CFO, and Nikki Keith, VP of Finance. With that, I'm going to turn it over to Steve to make a couple of opening comments.
Thank you, Salveen . Thank you for hosting us. Thank you to everybody who's listening for joining. Before we begin, I presume everybody knows we'll be making forward-looking statements. We spend a whole bunch of time on our risk factors internally. Please do peruse them at your leisure. Sana was founded under the belief that one of, if not the most important transformation that will occur in medicine over the next 10 - 20 years is the ability to modulate genes and use cells as medicine. We call engineered cells. Our goal is nothing less than to build one of, if not the sustainable leading company out of that era. Three aspirations really drive us. To be clear, we'll never get to any of them, probably, but the closer we get, the larger our impact will be.
One of them is to be able to fix, control, replace the genes of any cell in the body, basically to repair what's broken. The second is to build from scratch any cell in the body and have it perform the work that we want it to do, and that's to replace what's missing. The third is to broadly expand access to cellular and genetic-based medicines. Our strategy from the beginning is to figure out what are the biggest hurdles to reaching those goals and aspirations, and to go after what we think are the most important and tractable of them. I'd say we're a few years into this, and the strategy that we chose is at least as right today as it was when we founded the company. I'd say the technologies that we brought in to prosecute the strategy are working.
That's a long way from saying they work, and we have a good bit ahead of us. We're a little over 300 people today. If everything went perfectly, we would have double-digit INDs over the next few years. To be clear, it won't go perfectly, and even if it did, we don't have the capacity to prosecute it. I do think it's very reasonable to think about as early as next year, starting with two-four new medicines entering human testing each year. That's the scale at which we're building the company. When we started the company, again, the strategy for a second, the key initial decision that we made was we didn't want to be a cell therapy company or a gene therapy company. Ultimately, you're just trying to engineer the cell. It's just where are you doing it?
That decision, it turns out that most of the capabilities you need to build are the same, and it's allowed us to build better scale and attract better people because the best people are going to have the biggest impact. The other is that for in vivo and ex vivo cell engineering, it turns out the risks are actually quite idiosyncratic in the near term. From a risk perspective, I think that's worked out very well. For in vivo cell engineering or what most people call gene therapy, ultimately, you're trying to deliver payload and modulate or control the genome. It struck us that you can do more or less anything you want in a petri dish, and the real challenge is the in vivo delivery. We set out to be able to deliver any payload to any cell in a specific and repeatable way.
Every time you do one of those four things, you create a whole new category of medicines. One of the platforms around which we started the company was a cell-specific delivery capability. With that, we got payload diversity so that we can deliver DNA or RNA or proteins. With ex vivo cell engineering, the great thing is you go after the diseases that most of our loved ones will die from. These are the big problems. The flip side of that is it's harder. If you distill it down to just a couple of key principles, say we want to manufacture a cell at scale that will engraft in the body, function as we want it to, and persist. In order to make a meaningful medicine, you have to do all four. You don't get away with even three out of four is enough.
What we went after first here was cellular persistence and in particular, immune rejection. Since the advent of transplant and cellular medicine, the biggest issue has been if you put my cells into you, your body will see them as foreign and reject it. Really figure out how to cloak or hide cells from the immune system. We will apply that, hopefully, where others have figured out some of these other key risks already. That's how we started building and thinking about the company. We've made a good bit of progress. I'll start by describing the cell-specific delivery technology at its highest level. If I have one learning in the last decade, it's if you're faced with a complex biologic problem, see if Mother Nature's already solved it. If she has, exploit that system.
Viruses a long time ago figured out how to deliver their genetic payload specifically to cells in our body. Our bodies figured out how to use that system to deliver payloads internally. Great examples would be COVID. Maybe you look at the evening news and you see those red spikes sticking out. That's actually a viral fusogen that leads to cell-specific delivery only to cells that express the ACE2 receptor. Another example is actually human egg and human sperm. Human egg will traverse its way and not stop anywhere along the way until it gets to human egg. There it will deliver its genetic payload. Those are both fusogens, and that's a system we exploit. At the highest level, I just say we figured out how to modularize the system to go after various cell types.
We've now kind of gotten this to work against over 40 cell surface receptors for over 14 different cell types. The real key then is getting it to work really well. The first three places we're going after are T-cells, CD8 and CD4 positive T-cells, HSCs, or hematopoietic stem cells, and liver cells, or hepatocytes specifically. We can get into this, but what we've shown is that the system does work in vivo. For example, with a CD8 targeted fusogen, we can use that to make a CAR T-cell inside your body. All of the complexity of making a CAR T-cell that people have heard about, where you take cells out of the body, ship them somewhere, isolate them, activate them, transduce them with a new gene, grow them, sterilize them, freeze them, send them back, lymphodeplete the patient with chemotherapy.
We want to change to just a single intravenous injection, where your body becomes the bioreactor and the CAR T is made in a simple process. The system does work. We've shown if you're a mouse, we can give you a tumor, and we can then give you our medicine and as a single shot, and it will create in vivo CAR T-cells, and it will eliminate the tumor. We've shown if you're a monkey without cancer, we can do the same thing and target and deplete your B-cells. What we haven't shown is that we can do this in a human and actually go after their cancer. The system will work. I think the question is, does it work well enough, right? That's what we'll see as we go into human testing.
I'm just going to very quickly, the next is this cloaking technology, to make sure we talk about. The ability to hide things from the immune system has been the rate limiter, really since the advent of stem cell medicine, and before that, the advent of transplant medicine. The key biologic insight here was Mother Nature has solved that, and Mother Nature has solved it most specifically in the paradox of pregnancy. Each of us is half mom and half dad, right? In terms of our DNA and our proteins. The only reason we're on this Zoom call together is our mothers didn't reject us in utero. Pretty much none of us would be good transplant donors to our mom because we have dad's proteins. The real question is, what's the difference between the fetal-maternal border? It really was eliminated down to a few things.
When you grapple here, what we're grappling with is you have to turn off both the adaptive immune system and the innate immune system. The adaptive immune system is B and T -cells. It's kind of what we hear a lot about. Turns out that's actually a little bit easier, and people have done this for a long time. You eliminate something, MHC class I and class II. The more challenging aspect is cancers and viruses figured that a long time ago, our bodies developed the innate immune system of things like natural killer cells to kill those cells. Right? That's been the real challenge, and I think that's really where the insight is.
What we've shown is that we can, across species, including in a non-human primate, we can transplant allogeneic or foreign cells into a normal immune animal with no immune suppression and see it work. These cells will thrive and survive. We're going to move forward with this, and the real question is no longer does it work in animals, is does it work in humans? The first place we'll go is an allogeneic CAR T-cell. You kind of have the odds stacked in your favor. You are going into the immunosuppressed patient from cancer, right? You only really need these cells to live for, call it six or nine months. You don't need them to live forever. It's obviously a competitive field, and there are a number of companies there.
I think we have unprecedented data in animals. We have to see does it translate to real clinical efficacy in humans. We'll go forward there with, again, a CAR T-cell that we hope will be in human testing next year. The next place we'll take that would be to gene modify stem cells, grow them, differentiate them into a differentiated cell, and transplant them. The first place to do that, I think, would be if it works, the thing that really transforms the way we think about medicine would be type 1 diabetes. We're taking an iPS cell line, gene modify it to hide it from the immune system, grow that up, transplant that into patients with type 1 diabetes. We know that transplanting these islet cells can be curative for patients with diabetes.
The disease itself is just an immune response that kills all of your pancreatic islet cells, right? There have been over 1,000 patients who have received ground up cadaveric pancreatic islet cells and then have been immunosuppressed, and it works. The real question is, can we really reproducibly, at high scale, make high-quality islets and hide them from the immune system? We've done all these things in animal work, now we need to scale up and get the engineering done. It will take a little longer. It's more like a 2023 IND. It's a few years. I think that's another one that's very exciting. That's a 10-minute overview. With that, maybe we can go to you, Salveen, to start jumping into some Q&A.
Yeah. Steve, you do have a vast portfolio. I think you have 11 pre-clinical assets across 12 indications and growing, and two platform technologies. How do you think about portfolio management and asset prioritization in terms of how many INDs you could file in a year and which ones you start with?
Well, I'd start with, whatever you think, science has an amazing way of humbling you. It's unlikely that everything we do will work as well as we think it does as we move through the last stages of testing, and that we can scale it. I think there is real risk still around manufacturing. To start with, we need to have more than just We have to assume there's some just natural attrition, right? The second is, I think of the area where the biology, both on the disease front and on the clinical development side, is most straightforward is with T -cells. I always think about risk as like you've got four big categories of risk in drug development when you're making a new platform. One is platform risk. Does my platform really work? The second is disease biology risk.
Does my platform intercede in really important biology? The third is clinical trial risk. Can I show it in human? The fourth is commercial risk. Is it something that will impact the world more broadly? When you start with a new platform, which we really want to do is isolate platform risk and go in where the disease biology and clinical trial risk are very low. That way, when things don't work, you know it's because your platform isn't working well enough. When you get the platform working well enough, you have the privilege of taking on more disease biology risk. One of the things I really like about what we're doing in T-cells, and in particular with CD19 and BCMA as targets, is they're validated. If they don't work, it's not because CD19 and BCMA don't work, it's because our platform isn't working well enough.
We'll continue to modulate the platform. If and when it works, we get the privilege of going after it. I think about those is that from a portfolio perspective, is run hard and fast to them because we understand the risks so well. I think about big impact, right? Those two, though, are what we put at the top of the list as platforms, right? The allogeneic and the fusogen. Underneath that, bringing forward several different CAR T-cells once we get it going is something that is, again, relatively straightforward for us and something that we would put in as being high priority for the company because of its risk profile. I don't know if I answered your question.
Yeah. No, that makes a lot of sense. Maybe jumping to the technologies.
Yes.
It sounds like you've done a lot of preclinical work here with the fusogen technology, looking at different cell types. How do you, A, I guess, how do you get confidence this is going to translate to humans? B, how do you identify the optimal fusion for a given target?
Yeah. Maybe I'll take them in reverse order, right? The first thing is you have to identify a great fusogen. There are a couple of elements to the fusogen that are really important. First is potency. What we do, just to be really clear of how this system works, think of a viral fusogen as like nature's logic gate. It's a two-protein system. One recognizes a cell surface receptor and it binds to it. When it does, it tickles this other protein that drives fusogen. Now you get merging of the genetic, you get dumping of the genetic payload into the cell cytoplasm. You get two things with that. You get cell-specific delivery, and you get endosomal escape.
Most gene delivery technologies, LNPs been a great example, the biggest problem is they go into the endosome, and the endosome chews up 99%-point-something of your content, right? It's a very efficient system. The first thing that we're doing is that we need to get a binder that is potent enough, right? We need to modify the system to optimize potency, right? That's the first thing. We want to get to something where you're getting to a potency level that will allow us to manufacture this at scale. Right? That's ultimately what you're doing. A really great example of a virus with a novel fusogen on it or a different fusogen is just lentivirus. Lentivirus is HIV, right, where there's been some change to the genetics, to the payload, and then it's got a different fusogen.
Instead of binding the CD4 cells, they put something on it called VSV-G, it binds to LDLR. Which is LDLR because it brings in cholesterol. It's basically on every cell, which is why lentivirus is so great at going into all kinds of cell types, right? We know you can make lentivirus at reasonable scale. It's a nice benchmark for us to have to say how well are we doing against lentivirus in terms of potency, right? That just kind of gets you. That's a good way to think about for us, is it potent enough? We go into specificity, right, after that. You want to just have it so that you want to make sure that you're getting into the cells you want to and not other cells. That's basically how we go about, is it good enough, right?
Now, how do we know it will translate into humans in what we're doing? We don't. We know that these viral fusogens are utilized, they go across species, right? We know that the fusogen we're using works in human cells, right, against human cells. We can run animal experiments in regular mice. We can run them in humanized mice. You can run them in monkeys, non-human primates. What we've done, I'm very confident that the system works. The real question is, does it work well enough? As you go into humans, you have other challenges that prevent it from working well enough. It's why those first experiments are so important, is because you begin to understand how translatable are your animal models into your human efficacy. Just to be really clear, I would be very surprised if this doesn't work.
It just may not work well enough, and I think that's really where the risk is. The risks around that are threefold. One, can we make enough of it? Can we scale manufacturing? Two, do you have some unanticipated or anticipated safety event? We go through what the anticipated ones would be. It's a risk. Three, is it potent enough? Cancer is tricky. We're going to be putting this into cancer patients. When you get into a human with cancer, cancers clearly play with our immune systems in ways that are difficult sometimes to predict from preclinical models. We've done the most rigorous preclinical tests you could do. We've done everything that an autologous CAR T-cell has done and more.
As you look at your in vivo versus your ex vivo oncology approaches, which overlap in terms of your target cells and indications, how are you deciding which one would be best suited for which targets?
I'll start by saying I would love to have that choice. One of the first things is, if both of them work, we're going to be quite happy. If one of them works, we're going to be actually quite happy. We'll start with, there is some element of risk management around having a couple of different ways to go after this. Ultimately, if they do both work, we believe they have a chance of doing that. They will serve different purposes. The in vivo fusogen system, where you're taking all the complexities of manufacturing and you're replacing it with a single intravenous infusion that should, beyond being much simpler and more accessible for patients, actually make better T-cells because you're not growing them outside the body. You're doing it in its natural environment.
If that works, one would think it would naturally move very quickly towards an upfront treatment. Single shot, potentially curative. The allogeneic, your basic hope here is that you take the efficacy of an autologous CAR T-cell and you match it. That's ultimately what you're trying to do. You maybe theoretically get a little bit better, but you're ultimately not trying to move to frontline because you have the same issues around lymphodepleting chemotherapy and some other complexities. Where I think it becomes really valuable is as you move into refractory patients from the current therapies and/or solid tumors where it's likely multiple genetics will be necessary. I wouldn't be comfortable out of the bat doing tons of genetics in autologous CAR T-cell because you can't do all the quality tests to ensure that you did what you said you were going to do.
I wouldn't be comfortable starting that with our in vivo platform because when you make the genetics already inside the body. You can't go back and do the quality assay. I would be very comfortable doing that in allogeneic setting where we're making a lot of doses per patient, and we have time, and we can do all the quality assays we need. I think of that as where if everything works out well, we will move to a model where the early stage definitive treatment becomes a fusogen. The place where you begin to really innovate in the field is the allogeneic cell.
What are the gating factors to your three - four potentially IND filings in 2022?
Two things, just really simple. GMP manufacturing scale-up and pharm tox studies. Pharm tox studies, there are couple of elements, one of which is probably less recognized and has become a bigger issue. Most everything we're doing, it requires non-human primate pharm tox studies to get into human testing, and there is a global shortage of non-human primates. With the fusogen system more broadly, more specifically, I should say, we can only utilize a certain species of monkeys. That limits or it puts some risk in. Are we going to get all this test done at the right time? The normal things, does something unexpected pop up that's a problem? We'll have to chase it down and figure out if it's really a problem.
The second element, by the way, in all these things, we've already done non-human primate studies, so we're not going in blind and as if this is some risk that we don't have some visibility into. I feel pretty good. The second is manufacturing scale-up. Making GMP quality materials. There are a couple of elements to risk there. One is GMP supply chain. Supply chains are very complicated in these novel areas. You have multiple suppliers and each of them has their own risk and issues. The second is, does our process actually scale up in the way that we want it to? The third is, the way we have thought through manufacturing is we built our own pilot manufacturing plant. That's where you develop your process. You transfer your process out.
We're building our own late-stage clinical and commercial facility. We're using CMOs or contract manufacturers for our phase I studies. You just have to make sure you get the right slot at the right time. That's the third risk. The elements would be, does the supply chain come together, does our process really work, and could we like CMOs aren't a risk per se. They're a risk on a month or a quarter or two. That's how it could fall into being six months later than we hoped. We just don't get the slot we wanted. Those are the three elements of what we have to get through to get all these INDs done. The other stuff, it's internal. We'll take care of it. We'll write the INDs, the FDA interactions.
I think we have a really experienced team that can grapple with these things.
You explained the need to understand the biology risk, with your initial targets, you get the biology, so you're really trying to optimize for the platform. It makes sense that you've gone after BCMA and CD19 initially in CAR Ts. Help us understand with your liver-targeted fusogen, OTC, did you choose that indication just based on understanding the biology aspect there truly, and then just being able to optimize the platform and then open up the liver vertical? How are you thinking about that?
Yeah. A hepatocyte-targeted fusogen. It has two ways to move forward. One is with this first thing where we're delivering a gene and inserting it into the DNA. The second is to utilize this cell-specific delivery for gene-specific modifications. Let's just say we use it to deliver a CRISPR or base editing or prime editing or something else. The first element is understanding, can we get to enough liver cells to really matter? Just the math, just take a step back. CAR T-cell dose, autologous CAR T-cells, that's called circa 100 million cells. That's basically what people use. We have 200 billion liver cells in a normal adult liver, if you want to modify half of them, that's 100 billion. You're looking at orders of magnitude more product that you have to deliver.
First thing is, can we deliver something efficiently to the liver? That's like a real risk change for us. The second is what diseases to go after. Why did we choose OTC first? One is, it's a disease where there are various phenotypes, meaning various clinical manifestations, some of which affects people later in life, and some of them, there's a very severe disease that is a problem at birth. When you're bringing in a novel technology and thinking through regulatory strategy, it's nice to be able to first to go into adults. Because it's hard to get an informed. Some people argue your ability to get informed consent from a child. No different than the COVID vaccine development. To be able to go forward, to go backwards into the early development for these kids, that gets something that AAV can't do.
AAV is a pretty good delivery technology to the liver. It doesn't integrate. It doesn't permanently become part of the DNA. That's maybe good from a safety perspective, have to see. It carries a risk that as liver cells divide, you dilute out the effect. If you put that into a baby, take a little baby's liver, and all of a sudden it grows into an adult liver, you can't keep up. It gives us a chance to start in an adult and go back into early patients where really the system that we have is uniquely valuable, but we don't need it. If someone else can do it, our view's always been let them. We want to go where we're uniquely valuable. We thought OTC kind of threaded that really nice line for us.
Very quickly, we're going to move to where we're doing gene-specific fixes. The system does work. How we go forward and what's next is something that stay tuned, we'll chat about going forward.
I'm just curious, are you comfortable now with the specificity of payload integration given you're using a lentivirus based on all that work Bluebird just did and yours?
I'm very comfortable in T -cells. What do you know about T -cells? You know, first of all, HIV, you've had billions of patient years, and you're using the same basically integrating system, and you don't have a problem with de novo T -cell tumors. The second is you've got 10,000 plus years of patient safety data from CAR T -cells. You actually, if you were to say, "I want to use a targeted, I want to use CRISPR," as an example, you've got seven years of human safety data in aggregate from the whole field. In our mind, as of today, it was safer to go with this because you have a lot more information. As you go into other cell types, I think the risk profile changes.
You don't have that same level of confidence that these cells will integrate in ways that are totally benign to that cell type. I think this is one of those things that we have to really be careful around, and we will. In our HSC-specific delivery. Our plan has never been to use random integration. Our plan has always been to utilize a targeted delivery system and a targeted gene modification system. In the liver, we kind of want to do both, maybe that is having your cake and eating it may be that we need to move quickly into more targeted gene modification. That's a question that we kind of ask ourselves all the time. Definitely you have a higher, in my mind, safety bar as you're going into those other areas, because you don't have the same level of information.
How quickly do you think you could get your beta thal and sickle cell programs started, just given the unmet need for an in vivo therapy?
You mean started in humans?
Started in humans, yeah.
Yeah. You have two elements here, right? The first element is delivering your payload to the right cells in vivo. What we're trying to get rid of, the way the system works today, right, wherever you're looking at gene modification, there is mobilization of HSCs. Mobilization is challenging because it can cause a sickle cell crisis, right? You take them out of the body, they're sent to a manufacturing plant, they're genetically manipulated, they're sent back. The patient gets transplant-level chemotherapy, right, which carries its own risk, then the cells are transplanted. Our goal is to replace that with a single shot where in vivo, the genetic material will be delivered to the right cell. You make the modification there, off the patient goes, right? It has all kinds of safety, maybe efficacy, and definitively convenience advantages, right? If we can get it to work.
The first thing is we have to ensure that we are getting into enough of the right cells, right? I think this is a place where we've made a good bit of progress of late. The second is we have to incorporate and deliver the right gene modification material. That is the next step for us to really make sure we're doing. How quickly we have it is on our chart as early as 2023. It won't happen before that. To be in 2023, things have to kind of work well for us in there, right? The biology has to work with both delivering to the right cells and modifying the cells, and we have to be able to scale in manufacturing, right? It won't be the next 12 months. It's not that far away, right?
I do think if it does work, what we would want to do is utilize what we think is the best gene modification system, because the in vivo delivery is so transformative. In particular, I would prefer to do cell-specific delivery, because you really don't want to be delivering a whole bunch. It's creating risk every time you're modifying a genome in cells that don't need to be modified. We need to make sure we're getting to enough of the right cells.
Then switching to your hypoimmune platform or the cloaking technology platform. Outside of cancer, what do you think has the least risk? Because they're all big markets that you're going after with riskier biology. What do you think is it, neuro as a vertical, or what is it?
Type 1 diabetes. The reason is, you already know, right? First of all, what's the problem with type 1 diabetes? You're missing the cells that we're putting back. The biology hypothesis is crystal clear, right? The other is, there have been over 1,000 transplants that have been done in the U.S. of ground up cadaveric pancreatic islets, where the patient is immunosuppressed and the islet is transplanted. You see these patients do amazingly well for some period of time, right? They get off of insulin. You see regression of a lot of the damage from diabetes. They don't have problems with hypoglycemia or hyperglycemia. Ultimately, patients break through their immunosuppression, or they end up with some kind of an infection that requires immunosuppression to be modulated. The cells will last somewhere from a few years to, they've lasted as long as a decade, right?
When you think about those things, manufacturing cells at scale that will engraft, function, and persist, right? The reason I like it so much is someone else already figured out how do you get these cells to engraft, and what are the right cells that you need to really make this function, right? The real question is, can we manufacture enough cells of the right cells at scale, and can we hide it from the immune system? Right? That's why I think it's really straightforward. I think it's the one that if we happen to get right, will transform the way people think about the art of the possible in medicine in the biggest way, of the things that are kind of in our portfolio today that you see. I think it's both very biologically straightforward. It's actually relatively execution straightforward, right?
Right now, we know we can make really good cells. We know where to put them. We know we can hide cells, including in monkeys, right, from the immune system, including when they have an immune reaction to those cells already. Right? We've shown you those data. We need to transmit this into this disease, right? It's an engineering problem. It won't be in human testing next year. It's just too complex to kind of put the whole supply chain together and scale it. If things went well, it will be in human testing in 2023.
Sana-X, what is the vision for that division at the company, and what projects are you working on?
Yeah. Sana-X is a small part of our research, but it's a really important part of our research, both because of what it says and what it will do. Right? It struck us that very few companies are able to win the now and win the future. One of the real problems is almost all your best people and your resources and time go to win the now, or you don't get the privilege of playing out the future. Right? We wanted to create a specialized group of people who were taking and really developing the next thing so that This field is moving so quickly around cell and gene therapy that we will be disrupted, and we will be disintermediated. We want to do that ourselves rather than have someone do it to us. Right?
It's really a, you can think of it as like a SWAT team group of really just technically great scientists across a couple of areas going after the next thing. Success for them is not making a drug. Success for them is making a platform and putting it into our regular discovery platform that turns it into a drug. Right? It's a little earlier stage around kind of exciting new platforms. Just to give you a couple of examples that we've talked about. One, they've been working on how to utilize viral vectors to turn your body into an antibody-making machine. You can think of it like that. They've kind of figured this stuff out, how to do this. We want to be able to turn that up and turn it down or turn it off. Right?
They have been working on immune tolerance. Right? Not just hiding from the immune system, but actually creating tolerance. Your immune system looking at something and saying, "I don't care about you. You're fine. You're just like me." Right? I'll use two really simple examples of things that they are working on. Yeah, there's more, but that's a good place to start.
Maybe a last question here for Nate. Nate, given the programs entering the clinic next year, where do you stand from a cash runway position, but also the ability, if you are able to unlock a technology or a vertical, be able to go broad in a certain area? I'm just wondering where the flexibility lies there.
Yeah. Thanks, Salveen. We feel good about our cash position. We had over $980 million of cash on hand at the end of the first quarter, and we remain confident that that'll last us 3+ years and really allows us to let the science guide us forward and get to multiple programs, first in human data readouts on both the fusogen and the hypoimmune platform, as well as the necessary investments in manufacturing.
Great. I'm going to ask one more last one to Steve. Steve, there's a lot going on at this company. If you had to pick one thing you're most excited about right now, what is it?
You would never ask somebody who their favorite child is, would you? You can't do that. Right?
You can say they're all favorite-.
Yeah.
You can talk about something in the near term. Yeah.
I think the thing that if we have it right that is most disruptive is this hypoimmune technology. The ability to cloak cells broadly is the issue that has been holding back the broad field. I think its implications are so important across so many different areas. We've now shown in multiple species, including, again, normal immune non-human primates, that this system works. That is the thing that I think is most transformative to how the whole field develops over the next 5- 10 years. I guess I really like where that child is right now in its life. Maybe, yeah, maybe not favorite child. That's an unfair question.
Perfect. Well, with that, thank you so much. Really appreciate the time, Steve and Nate and Nikki.
Yeah. Thank you, Salveen, and thank you to everybody for listening. Take care.