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

Good 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 Nicky 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. And thank you for hosting us, and thank you to everybody who's listening for joining. And before we begin, I presume everybody knows, we'll be making forward-looking statements, and we spend a whole bunch of time on our risk factors internally. So please do peruse at your leisure. So Sana was founded under the belief that one of, if not the most important transformation that will occur in medicine over the next 10 to 20 years, is the ability to modulate genes in use cells as medicine. So we call engineered cells. And our goal is nothing less than to build one of, if not the sustainable, leading company out of that era. And 3 aspirations really drive us. And to be clear, we'll never get to any of them, probably, but the closer we get the more, the larger impact will be. And 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 kind of performed the work that we wanted to do. And that's to replace what's missing. And the third is to broadly expand access to cellular and genetic-based medicines. And we're not -- our strategy has been, from the beginning, is to figure out what are the biggest hurdles to reaching that -- those goals and aspirations, and they 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 is right today as it was when we founded the company. I'd say the technologies that we brought in to go -- to prosecute the strategy are working. That's a long way from them 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. But I do think it's very reasonable to think about as early as next year, starting with a 2 to 4 new medicines entering human testing each year. That's kind of the scale, which we're building the company. So when we started the company, and I get in the strategy for a second. The key initial decision that we made was not -- we didn't want to be a cell therapy company or a gene therapy companies. Ultimately, you're just trying to engineer the cell. It's just where are you doing it. And 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 to attract better people because the best people want to have the biggest impact. The other is that for in vivo and actually a cell engineering, it turns out, the risks are actually idiosyncratic in the near term. So 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. And it struck us that you can do more or less anything you want in a petri dish. And the real challenge is to in vivo delivery. And so we set out to be able to do -- to deliver any payload to any cell on a specific and repeatable way. And every time you do one of those 4 things, you create a whole new category medicines. And one of the platforms that obviously 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 can 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, right? So if you distill it down to just a couple of key principles, 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 4, right? You don't get away with even 3 out of 4, they're not. So what we went after first here was cellular persistence and, in particular, immune rejection. So since the admin a transplant in cellular medicine, the biggest issue has been, if you put my cells into you, your body will see them as foreign and reject them. And so really figure out how to cloak or hide cells from the immune system. And then we will apply that hopefully, where others have figured out some of these other key risks already. That's kind of how we started building and thinking about the company. And we've made a good bit of progress. And I'll start by describing the cell-specific delivery technology at this highest level. And if I have one learning in the last decade is, if you're faced with a complex biologic problem, see if mother nature is already solved it, and if she has, exploit that system. And viruses 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. So great examples would be COVID. If you look at that the evening news and you see those red spikes singing outside, that's actually a viral fusogen that leads to cell-specific delivery only to cells that express the H2 receptor, right? Another example is actually human egg and human sperm. So human egg will traverse its way and not stop anywhere along the way until it gets to human egg. And there, it will deliver a genetic payload. Those are both fusogens. And that's a system we exploit. And at the highest level, I'd just say we've figured out how to modularize the system to go after various cell types. And we've now kind of gotten this to work against over 40 cell surface receptors for over 14 different cell types. And the real key then is getting it to work really well. So the first 3 places we're going after are T cells, CD8 and CD4 positive T cells, HSCs, hematopoietic stem cells and liver cells or hepatocytes specifically. And we can get into this, but what we've shown is that the system does work in vivo. And for example, with a CD8 targeted fusogen, we can use that to use the to make a CAR T cell inside your body. So 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 with just a single IV infection -- sorry, intravenous injection, where your body becomes a bioreactor and the CAR T is made as a simple process. And the system does work. I mean, we've shown -- if you're a mouse, we can give you a tumor, and we can then give you our medicine 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 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. And that -- so the system will work. I think the question is, does it work well enough, right? And no, that's what we'll see as we go into human testing. So 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. And the key insight, biologic insight here was mother nature has solved that. And mother nature is solved it most specifically in the paradox in 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, you call, together is our mothers didn't reject us in utero. But pretty much none of us would be good transplant donors to our mom because we have dad's proteins. So the real question is what's the difference between the fetal maternal border? And I think it really was eliminated down to a few things. And 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. So the adaptive immune system is B and T cells, is kind of what we hear a lot about. It turns out that's actually a little bit easier, and people have done this for a long time. You eliminate something MHC class 1 and class 2. The more challenging aspect that is cancers and viruses figured out a long time ago. And so our bodies developed the innate immune system, so things like natural killer cells to kill those cells, right? And that's been the real challenge. I think that's really where the insight is. And so we've shown is that we can across species, including in a nonhuman primate. We can transplant allogeneic or foreign cells into a normal immune animal with no immune suppression and see it work as these cells will thrive and survive. So we're going to move forward with this. And the real question is not -- no longer does it work in animals is does it work in humans. And so the first place we'll go is an allogeneic CAR T cell. I mean there are a couple of -- you kind of have the odd stacked in your favor. You are going into the immunosuppressed patient from cancer, right? It's -- and you only really need these cells to live for, call it, 6 or 9 months, you don't need to live forever. And it's obviously a competitive field, and there are a number of companies there. But what we think -- I think we have unprecedented data in animals. You have to see, does it translate to real clinical efficacy in humans. And so we'll go forward there with, again, a CAR T cell that we hope will be in human testing next year. The thing -- 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. So 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 modified to hide it from the immune system, grow that up, transplant that into patients with Type 1 diabetes. And we know that transplanting these islet cells can be curative for patients with diabetes. It's been -- the disease itself is just an immune response that kills all of your pancreatic pilot cells, right? There have been over 1,000 patients who have received cadaveric -- ground up cadaveric pancreatic islet cells and then have been immunosuppressed, and it works. So the real question is, can we really reproduce at high scale make high-quality islets and hide them from the immune system. And that's -- we've done all these things in animal work. So now we need to scale up and get the engineering done. It will take a little longer. It's more like a 2023 INDs, a few years. But I think that's another one that's very exciting. And so that's a 10-minute overview. With that, maybe we can go to you, Salveen, to start jumping into some Q&A.

Yes. So Steve, you do have a vast portfolio. I think you have 11 preclinical assets across 12 indications and growing and 2 platform technologies. So how do you think about portfolio management and asset prioritization in terms of how many IDs you could file in a year and which ones you start with?

Yes. Well, I'd start with whatever you think science has an amazing way of humbling you. And so 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. So to start with, we need to have more than just a -- we have to assume there's some just natural attrition, right? Second is, I think of the area where the biology and -- both on the disease front and on the clinical development side is most straightforward is with T cells. I always think about risk is like you've got 4 big categories of risk and drug development when you're making a new platform. One is platform risk. So my platform really works. The second is disease biology risk because my platform interceding really important biology. The third is clinical trial risk. Can I show it in a human? And the fourth is commercial risk. Is it something that will impact the world more broadly? And 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. And when you get the platform working well enough, you have the privilege of taking on more disease biology risk. So one of the things I really like about what we're doing in T cells, 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. And so we'll continue to modulate the platform. Then if and when it works, we get the privilege of going after it. So I think about those as that from a portfolio perspective is run hard and fast to them because we understand kind of the -- we understand the risks so well. So that's -- and then I think about big impact, right? So those 2, though, are what we put at the top of the list. And as platforms, right, the allogeneic and the fusogen. And then underneath that, bringing forward several different CAR T cells once we get it going. It is something that is, again, relatively straightforward for us and something that we would put in as being high-risk -- sorry, high priority for the company because it is a risk profile. I don't know if I answered your question, but that's...

No, that makes a lot of sense. So maybe jumping to the technologies. 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? And b, what's the optimal? How do you identify the optimal fusion for a given target?

Yes. Maybe I'll take them in reverse order, right? Because the first thing is you have to identify a great fusogen. So what -- there are a couple of elements to the fusogen that are really important. First is potency. We get -- so what we do just to be really clear of how this system is, so think of a viral fusogen like nature's logic gate. It's a 2-protein system. One recognizes a cell surface receptor and it binds to it. And when it does, it tickles this other protein that drives fusion. So now you get merging of the genetic -- you get dumping on the genetic payload into the cell cytoplasm. And you get 2 things with that. You get cell-specific delivery, and you get endosomal escape. So most gene-delivery technologies, LNP is great example. The biggest problem is they go into the endosome, and endosome choose up 99-point something percent of your content, right? So it's a very efficient system. So the first thing that we're doing is that we need to get a binder that is potent enough, right? And then we need to modify the system to optimize potency, right? So that's the first thing. So 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. So a really great example of a virus within novel fusogen on it or different fusion is just lentivirus. Lentivirus is HIV, right? Where some -- there's been some change to the genetics sit to the payload. And then it's got a different fusogen. Instead of binding to CD 4 cells, they put something on it called PSPG, and it binds to LDL, which is -- LDL because it brings in cholesterol is basically on every cell, which is why such a -- lentivirus is so great at going into all kinds of cell types, right? So we know you can make lentivirus at reasonable scale. So it's a nice benchmark for us to have to see how well are we doing against lentivirus in terms of potency, right? That just kind of gets you -- that's a good way to kind of like think about for us, is it potent. So we go into specificity, right, after that. So 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. It's basically how we go about is it good enough, right? How do we know will translate into humans in what we're doing? Like we don't. We know that these viral fusogens are utilized and 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, not human primates. And what we've done, I'm very confident that the system works. The real question is, does it work well enough, right? As you go into humans, might you have other challenges that prevent it from working well enough. It's why those first experiments are so important. It's because you begin to understand how translatable are your animal models into your human efficacy? Just to be really clear, again, I would be very surprised if this doesn't work. I just may not work well enough. And I think that's really where the risk is. And the risk around that are threefold. One, can we make enough of it? So can we scale manufacturing? Two, do you have some unanticipated or anticipated safety event, right? We go through what the anticipated ones would be is a risk. And three, is it enough, right, is cancer is tricky. And we're going to be putting this into cancer patients. And when you get into a human with cancer, the cancers clearly play with our immune systems in ways that are difficult to predict from preclinical models. But we've done the most rigorous preclinical test you could do, right? We've done everything that an autologous CAR T cell has done and more.

And then of that, your in vivo versus your ex vivo oncology approaches, right, which overlap in terms of your target cells and indications, how are you deciding which whether -- which one will be best suited for which targets?

Yes. I'll start by saying I would love to have that choice, right? One of the first things is we want to -- if both of them work, we're going to be like quite happy. If one of them works, we're going to be actually quite happy, right? So we'll start with -- there is some element of kind of risk management around having a couple of different ways to go after this. But ultimately, if they do both work, I think that we believe they have a chance of doing that. Then they will serve different purposes. So the in vivo fusogen system, 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, right? You're doing it in its natural environment. And if that works, one would think it would naturally move very quickly towards an upfront treatment, single shot, potentially curative, right? The allogeneic, your basic hope here is that you take the efficacy of an autologous CAR T cell and you match it, right? That's ultimately what you're trying to do. You may be able to theoretically get a little bit better. But you're ultimately -- so you're ultimately not trying to move to frontline because you have the same issues around lymphodepleting chemotherapy and some other complexities. Well, 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 gene edits will be necessary. I wouldn't be comfortable out that doing tons of gene editing 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 gene edit, it's already inside the body, right? And so you can't go back and do the quality assay. I would be very comfortable doing that analog genetic setting and we're making a lot of doses per patient, and we have time, and we can do all the quality assays we need. So I kind of think of that as where the -- if everything worked 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.

And what are the gating factors to your 3 to 4 potentially IND filings in 2022?

Two things, just really simple. Manufacturing, GMP manufacturing scale-up and pharm tox studies. And so pharm tox studies, there are a couple of elements, one of which is probably less recognized and has become a bigger issue. We want most -- everything we're doing, it requires nonhuman primate pharm tox studies to get into human testing. And there is a global shortage of nonhuman primates. And with the fusogen system more broadly -- more specifically, I should say, we can only utilize a certain species of monkeys. And so that limits -- it puts some risk and start ability to get all this test done at the right time. None of the normal things is something unexpected pop up. It's a problem, right, both to chase it down and figure out if it's really a problem. The second element probably -- in all these things, we've already done nonhuman primate studies. So it's not -- we're not going in blind. And as if this is some like risk that we don't have some visibility into. I feel pretty good. The second then is manufacturing scale up, right, in there and making GMP quality materials. And there are a couple of elements to risk there. One is GMP supply chain. So supply chains are very complicated in these novel areas. You have multiple suppliers, and each of them has their own risk and issue, right? The second is, does our process actually scale up in the way that we wanted to. And the third is -- so the way we have thought through manufacturing, as we own our own -- and we built our own pilot manufacturing plant. That's where you develop your process, right? You transfer your process out. We're building our own late-stage clinical and commercial, early commercial facility. And we're using CMOs or contract manufacturers for Phase I studies. And you just have to get -- to make sure you get the right slot at the right time, right? So that's the third risk. So the elements would be, is the supply chain come together, does our process really work? And it could we like CMOs are a risk, per se. There are risk in like a month or 1 quarter or 2, right? So that's how it could fall into be 6 months later than we hoped, we just don't get the spot we want to. So those are the 3 elements of like what we have to get through to get all these INDs done. The other stuff, it's internal. We'll take care of it. Like we won't -- like we'll write the INDs, the FDA interactions. I think we have a really experienced team that can grapple with these things.

And you explained the need to understand the biology risk, right, with your initial targets, you get the biology. So you're really trying to optimize for the platform. And so it makes sense that you've gone after BCMA and CD19 initially in CAR Ts. Help us understand what your liver-targeted fusogen? OTC, is it -- did you choose that indication just based on understanding the biology aspect there,, truly and then just being able to kind of optimize the platform and then open it -- open up the liver vertical? Like how are you thinking about that?

Yes. So hepatocyte targeted fusogen, it's -- there -- it has 2 kind of ways to move forward. One is with this first thing, well, we're delivering a gene and inserting it into the DNA. The second is to utilize this cell-specific delivery for gene-specific modifications, right? So let's just say, we use it to deliver a CRISPR or like base editing or prime editing or something else, right? And so the first element is understanding, can we get to enough liver cells to really matter, right? And just the math, just take a step back. CAR T cell dose, autologous CAR-T cells, it's call the circa 100 million cells, right? That's basically what people use. We have 200 billion liver cells in normal adult liver. And so if you want to modify half of them, that's $100 billion, right? So you're looking at orders of magnitude, more product that you have to deliver. And so first thing is, can we deliver something efficiently to deliver, right? That's like a real risk change for us, right? And then the second is what diseases to go after. Why do 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 there's a very severe disease that is a problem at birth, right? And so 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, right, because it's just -- it's hard to get an in -- some people argue your ability to get an informed consent from a child, right? And no different than the COVID vaccine development, right? And then to be able to go forward, to go backwards into the early development with these kids, it gets something that AAV can't do, right? So AAV is a really -- it's 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, I have to see, but it carries a risk that as liver cells divide, you dilute out the effect. So if you put that into a baby, take a little baby's liver and all of a sudden it grows into adult liver, you just don't -- you can't keep up, right? And so it gives us a chance to go -- start in adult and go back into early patients where really the system that we have is uniquely valuable. We don't need to -- if someone else can do it, our view has always been let them, right? We want to go where we're uniquely valuable. And so we thought OTC kind of threaded that really nice line for us. But very quickly, we're going to move to where we're doing gene-specific fixes, right? That's like that the system does work. And so how we go forward and what's next is something that stay tuned we'll chat about going forward.

And then I'm just curious, are you comfortable now with the specificity of payload integration, given you're using a lentivirus based on kind of all that Bluebird just did and yours?

No. I'm very comfortable in T cells. So what do you know about T cells? 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 kind of de novo T cell tumors you've got. The second is, you've got all -- you've got 10,000-plus years of patient safety data from CAR T cells, right? And you actually -- if you were to say, I want to use a targeted, I want to use CRISPR as an example, you've got like 7 years of human safety data in aggregate from the whole field, right? So it's -- 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 -- that you will integrate in ways that are totally benign to that cell type. And so I think this is one of the things that we have to really be careful on. 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, and maybe that is having your cake and eating it, and it may be that we need to move quickly into more targeted gene modification. I think those are -- that's a question that we kind of ask ourselves all the time. But definitely, you have a higher, in my mind, safety bar as you're going into these 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 in vivo therapy.

You mean started in humans?

Started [against ].

Yes. So -- because you have 2 elements here, right. The first element is delivering your payload to the right cells and be because what we're trying to get rid of the way the system works today, right? I use it whatever system you locate -- we're really going at gene modification. There is mobilization of HSCs. Mobilization is challenging because it can cause a sickle cell crisis, right? You then have -- they 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, and then the cells are transplant. 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 and of the patient goes, right? So it has all kinds of safety, maybe efficacy and definitively convenience advantages, right? If we can get it to work. So the first thing is we have to ensure that we are getting into all the right -- enough of the right cells, right? And I think this is a place where we've made a good bit of progressive of late. So I think the second is we have to incorporate and deliver the right gene modification material. And that is the next step for us to really make sure we're doing. So 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. And there, again, the biology has to work with both delivering to the right cells and modifying the cells, and we have to be able to scale and manufacturing, right? So those are things -- it won't be the next 12 months, but it's not that far away, right? And I do think if it does work, what we would want to do is utilize what we think is the best in modification system because the in vivo delivery is so transformative. And in particular, when I would prefer to do cell-specific delivery because you really don't want to be delivering a whole -- it's creating the risk every time you're modifying genome in cells that don't need to be modular. So we need to make sure we get into the enough of the right cells.

And then switching to your hyperimmune 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 -- is it neuro is a vertical? Or what is it?

Type 1 diabetes. And so the reason is you already know, right? So first of all, what's the problem in Type 1 diabetes. You're missing the cells that we're putting back. So the biology hypothesis is crystal clear, right? So you already -- the other is there have been over 1,000 transplants that have been done in the United States, a ground-up cadaveric pancreatic islets, where the patient is immunosuppressed, and the islet is transplanted. And 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 and modulate. And the cells will last somewhere from a few years to they've last as long as a decade, right? So 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 was how do you get these cells to engraft and what are the right cells that you need to really make this function, right? So then 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. So that's why I think it's really straightforward. And I think it's the 1 that if we happen to get right, we'll 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 kind of portfolio today that you see. So I think it's both very biologically straightforward. It's actually relatively execution straightforward, right? Right now, we kind of -- we know we can make really good cells. We know we can -- 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. And so we didn't transmit this into this disease, right? It's an engineering problem. So 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. But if things went well, we'll be in human testing in 2023.

And SanaX, what is the vision for that division at the company? And what projects are you working on?

Yes. So SanaX is a -- it's 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? So if you -- very few -- struck us a very few companies are able to win them now and win the future. One of the real problems is almost all your best people and your resources in time go to win them now or you don't get the privilege of paying out the future, right? And so we wanted to create a specialized group of people who were kind of taking and really developing the really the next thing. So that we are -- this field is moving so quickly around cell and gene therapy, that we will be disrupted, and we will be disintermediated. So we want to do that ourselves rather than have someone do it to us, right? And so it's really a -- I think it was like a SWAT team group of really just technically great scientists across a couple of areas going after kind of the next thing. And so 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? So it's a little earlier stage around kind of exciting new platforms. So they work 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 antibody making machine, think of it like that. And they kind of figured this stuff out and how to do this. And then we want to be able to tune 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? And so these are a couple of really simple examples of things that they are working on. And yes, 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?

Yes. Thanks, Salveen. We feel good about our cash position. I mean we had over $980 million of cash on hand at the end of the first quarter. And we remain confident that, that will last us 3-plus 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 hyperimmune platform as well as investing -- 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 with their favorite child is. Would you -- you can't do that, right?

You can say they are all. You can talk about something in the near term.

Yes. I think the thing that if we have it right, it is most disruptive is this hyperimmune technology's ability to cloak cells broadly. It's the issue that has been holding back the broad field. I think its implications are so important across some many different areas. And we've now shown in multiple species, including, again, normal immune nonhuman primates that this system works. I think that is the thing that I think is most transformative to how the whole field develops over the next 5 to 10 years. So I guess, I really like where that child is right now in its life, maybe a favorite child. That's like an unfair question.

Well, with that, thank you so much. Really appreciate the time, Steven and Nate and Nicky.

Yes. Thank you, Salveen, and thank you to everybody for listening. Take care.

Bye.