Good afternoon, everyone. Thank you so much for joining us. Really pleased to have Steve Harr, President and CEO of Sana, here with us. Steve, to start here, could you provide a high-level overview on the key programs where they stand, how the company's positioned heading into the second half of this year, given you have a slew of catalysts coming up, and where you're most focused over the mid to long term? Yeah. First off, thank you, everybody, for joining us. It takes a brave soul to put on the jacket and maybe even a tie in the sweltering heat and humidity of Miami in June, so very much appreciate it. And thank you, Salveen, for and Goldman Sachs for inviting us. Thrilled to be here. So I think you probably know as well, we'll be making forward-looking statements along the way, so, you know, please do take a look at our risk factors in our 10-Q. We spent a good bit of time writing them, and hopefully they can be helpful in navigating the rest of the company. So where are we? What are we up to? What are we excited about? You know, you know, we have four different drugs in human testing right now, in seven different indications. Hopefully we'll have data from all four of these therapeutic candidates this year. You know, each of them, in certain degrees, to a certain degree, are built off of the foundation of one of the company's technologies, which is something we call hypoimmune cells. Hypoimmune cells have been gene-modified to hide them from allogeneic rejection. So we put my cells into you, you're gonna recognize them as foreign and kill them. We've seen that in transplant. So it's kind of flummoxed the scientific field for years. We've made a lot of progress, we think, in being able to hide cells from allogeneic and potentially autoimmune rejection. And we've shown this now across many, many different species, in many different settings, and including in the, you know, a host of non-human primate studies that have been published in journals like the Nature journals and Cell and things like that. So take a look if you're interested. So I might kinda walk through them in maybe even order of when we might see data, and maybe the inverse order to when they started, you know, in the human. So we have it type 1 diabetes is a relatively simple disease in some regards. You know, unfortunately, a patient's immune system gets confused and obliterates pancreatic beta cells. And so the patient no longer is able to, you know, secrete insulin in a glucose-dependent fashion. And 100 years ago, up to 100 years ago, that person died pretty quickly. 100 years ago, there was the invention of insulin. The goal of what we're doing is to take a stem cell, gene-modify it so that it has these edits that will allow it to hide from the immune system, and then grow it into a pancreatic beta cell and transplant that. Hopefully you have a patient who has normal blood glucoses, euglycemia, for life, without any immunosuppression. The first part of us understanding if we've really nailed this in people is we're kinda taking a shorthand to get there. For the last about 20 years, some diabetics around the world have been transplanted with cadaveric islets or primary islets from people who donate their pancreas. And what we're doing and they tend to work. There are a number of people walking around who are off of insulin, but they have to be immunosuppressed as if they'd gotten an organ transplant. What we're trying to do is gene-modify these primary islets and see if we can hide them from allogeneic and autoimmune rejection. If we can, then I would argue that a cure for type 1 diabetes becomes inevitable. Now, we may not be the one who actually nails it and takes it to market and figures it all out. At that point, you will have figured out all of the component boxes that you need to kinda make this happen. We should know that very soon, right? I mean, we've said our goal is to have data in the first half of this year. I won't promise you that won't slip into 3-Q. It could still be now, in the first half of the or it could slip. But it's coming up very soon. And the goal is very simple, right? The field's already proven that transplanting an adequate number of cadaveric islets will lead to euglycemia for these people. So what we're trying to do in the phase 1 safety study is show that we can transplant these gene-modified cells and that they live and function without any immunosuppression. And there'll be kind of 3 layers of efficacy you could get. 1 is that you see these cells survive and there's no immune response to them. And you see them survive on a radiographic, like an MRI. And that's a good outcome. We're gonna feel really good about it. But we'll always be a little bit nervous if those are really the cells we think they are, right? And so the best outcome, I think, that's realistic is that we see something called C-peptide, and it's stably expressed over time. So when a beta cell makes insulin, it actually makes proinsulin, and it's secreted as insulin and C-peptide. And so when you see stable C-peptide, you know the cell, the beta cell's functioning and making insulin in a stable way. That's the goal of the stable C-peptide. And again, we hope to have data very soon. In some ideal world, the patient could have, you know, normal blood glucoses and, you know, either decrease or even off insulin. I wouldn't expect that from a phase 1 study. And since we've described this, our first in human study, you know, we've said if that's your investment thesis, you should probably hold off and invest later. It could happen, but it's unlikely. And so that's really the three levels of efficacy and should be coming soon. The second drug, and I, I was probably longer-winded than you wanted me to be, so I'll be relatively quick with these other ones, and then you can ask questions. And when things might come, the B-cell-mediated autoimmune disorders. And those are diseases like lupus, vasculitis, multiple sclerosis, myositis, a number of them. And we have a study in that started in three different indications: lupus nephritis, extrarenal lupus, and ANCA-associated vasculitis. And for some of you who are older like me, you may have learned that as Wegener's granulomatosis. That's, that's the old name for it. What we've, you know, what we've seen, or the field has seen, is that at least in, you know, some people's hands, autologous CAR T-cells targeting CD19 when given can be curative, potentially curative. That's probably the best word to say for these diseases. You know, for the last 20 years, there have been B-cell depleting agents being developed, for autoimmune disorders. What's become clear is that the more the therapy depletes B-cells, the better the patient does. What it looks like with these CAR T-cells is you may be eliminating the pathogenic B-cell that makes antibodies, and you get, you know, an effective cure. I don't know, we don't know how long that will last, but at least it seems like you can get durable remissions with no medicines. So we started a trial. Our goal is to see can these allogeneic CAR T-cells that we make, work as well as autologous CAR T-cells. We dosed the first patient, a while ago, a few months maybe a few weeks ago. I think it was 4, 5, 6 weeks ago. And, you know, we'll begin to get data as the summer progresses. So we should have something by the end of the year. Reasonable place to be would be something like the American College of Rheumatology or American Society of Hematology. We should, you know, you're not gonna be determinative if the drug works, but you can really begin to see does this smell if we're at the right dose, does this begin to smell like an autologous, the real benefits we're seeing from autologous cells. But we've done this in a way that's readily scalable and very predictable and off the shelf and ready for patients. The last, so we have two studies in different blood cancers, lymphoma and leukemia, with a CD19 CAR T-cell. And we also have a CD22 targeted CAR T-cell for people who failed a CD19 CAR T-cell, like Yescarta. The CD19, the trial started over a year ago. We should have a good bit of data by the end of the year. You know, I think most people are looking to yeah, the field has been a little disappointed by progress of, these CD19 CAR T-cells. I think we think it's been pretty clear why they fail, and that is immune rejection of allogeneic cells. So, you know, our goal is to put transplant these hypoimmune cells and that the immune system won't see them and that they will provide a patient benefit that's at least as good as what you see with autologous CAR T-cell. You know, the best measure of that to date has been six-month complete response rates. I think that's kinda the hurdle that everybody's looking for us to clear. We'll begin to have some data like that before the end of the year at something like ASH. Then there's the CD22 CAR T-cell just getting going. You know, it will have a handful of patients, again, probably towards the end of the year. So that's where we are. I can go into more detail on any of those. Let's start with the IST study for type 1 diabetes and help us understand how many patients you'll report data on as well as the translational risk of using cadaver cells? Yeah. So IST is investigator-sponsored trial. So because we're not trying to commercialize these cadaveric islets, it's being done in partnership with an academic center. And so if you kind of just take a step back, we're trying to prove whether or not the gene modifications we make hide these cells from allogeneic and autoimmune disease recognition. I've asked a lot of people to come up with how you can come up with a false positive, meaning that it looks like you hide these cells, but it's not really true. And I haven't heard from a single person a single reason how you could get a false positive. So I think an N of 1 is plenty, right? If you have an N of 1 where you've done that, that's gonna be in this for everybody, but it's gonna be broadly applicable, in a type 1 diabetes population. So, I mean, 1 patient is adequate. In terms of duration of follow-up, if you transplant any organ or cell into somebody without immunosuppression, it will be rejected in about a week or under a week. In patients who no longer tolerate immunosuppression and it has to be withdrawn, their cells will be killed within about 7 days. So our transplant team would argue that within 2 weeks, you pretty much know if it works or not. We might wait a little longer than that before we chat about it just to make sure that you see that it's working. But an N of 1, I think, is plenty to tell you if the technology's working. Vice versa. If you see robust immune rejection of those cells, again, I would say an N of 1 is telling you that it's inadequate, and it's unlikely that it's going to be working broadly. I think it's one of those things that doesn't take a lot of data. If you see positive data here, just walk us through your own trial that you would take forward and. Yeah. How you would think about changes that need to be made or what you do on the floor there. Sure. So, again, just so we're kinda all speaking with the same playbook, the study that we're doing is gene-modifying beta cells or pancreatic islets in the aggregate that have been isolated from a cadaver and transplanting them into a patient. That's a really good proof of concept. And, you know, but it's not a readily scalable solution for patients. So what we've been developing are gene-modified pluripotent stem cells that we differentiate into islets, pseudoislets full of beta cells that we can hopefully make at, you know, significant scale and transplant into, you know, a disease that has 8 million people and growing around the world. And so there are four real scientific challenges for that real drug. We call that SC451. One is can you overcome the immune rejection of these cells? We should know that imminently, right? The second has been getting comfortable with the genomic stability over time of these cells 'cause you divide many times. And just for context, you know, we kinda make one or two mistakes in our genome every time we have a cellular division. And, you know, so much of our body is set up to deal with and get rid of those cells. Here, what we're doing is we're putting cells into a media that enriches for cells that grow quickly. And so what you really don't wanna do is have clonality 'cause clonality over time could lead to some kind of a tumor, right? And so it's taken us more time than we thought it would to get really comfortable that we have controlled the genomic stability of this master cell bank. We think we're there. When we went if you look back at when we went public a few years ago, we would've told you we'd be dosing the first patient about now in this study, and we're not ready. It took us a few extra years to get there. So that's problem number 2. We think it's in the rearview mirror. Problem number 3 is making cells at enough purity, potency, and yield to run a phase 1 study, phase 1/2. I think that we've got that. I mean, I wouldn't, again, guarantee it. You gotta do the long-term tox studies. That's kind of what we're waiting for. That's what we'll need to do for the IND to ensure you have the purity where something doesn't pop up unexpectedly. But I think we got that. The fourth challenge is making this at enough purity, potency, and yield to be able to treat, and I make a number up, 100,000 people per year. We're not close, right? We have a lot of work to do. And that's something that is gonna be a real scientific challenge. No, it's not yet a scale challenge. It's still a scientific challenge, for the next, you know, at least a number of years. So that's kind of where we are on the journey. You know, we kinda went to a something where we put out INDs if they're gonna happen, you know, this year. So we don't have any if it's not gonna be this year. We would've told you if it were. You know, hopefully, it's not too far beyond that. Pivoting to the autoimmune program here, you know, clearly with CD19 in these disorders, it seems validated to a degree as a target. But with regard to your platform, help us understand the ability to kind of de-risk with your own asset, but then how you would? I would say sorry, how do we what? De-risk with your own asset. Yeah. Given the technology, but then also your outlook in terms of what is commercially relevant given it's a very different population from cancer. The different platforms that are out there? Mm-hmm. Yeah. So first off, these B-cell autoimmune disorders, they're just—it's a gigantic field. And unfortunately, there are still a number of people who are suffering from these diseases, you know, you know, majority of which are women and many of which are young women. And so there's a lot of; there's a big unmet need. And I think what we've learned over the last 25 years is that there are lots of ways to turn off and turn down B-cells. And the better the therapy is at doing it, the bigger the therapeutic benefit has been. And that's true for antibodies. That's true probably for ADCs, and it's almost certainly going to be true for these T-cell engaging bispecifics. Now, the challenge is that antibodies, while they're very good, don't get into tissue. And where you have these pathological B-cells. You know, the antibodies are made from basically B cells and tissue-resident plasma blasts. These tissue-resident plasma blasts, antibodies can't reach. They don't have the volume and distribution to do that. So they're unlikely to ever be curative. In every case to date, they've actually required some additional immunosuppression, right? They're almost never used alone. So they're gonna be important. We're gonna have to grapple with them, but I don't think they're category killers. You then have other modalities, other cellular therapies, right, which are trying to take out B cells and plasma blasts and B-cell. So the question for any cellular therapy you have to ask yourself is what kind of evidence do you have around its biodistribution? And does it get into the tissues where these tissue-resident plasma blasts reside? They do in these tissue-resident germinal centers you have. And really, to date, the only cell that's shown itself to do that readily has been a T-cell. So I'd expect that a number of different type of T-cells, autologous CAR T-cells will work. Allogeneic CAR T-cells may or may not work. We have to prove they do. You know, I think one of the things we've learned from cancer is persistence of a CAR T-cell or how long it is around the body is really important in being able to clear out every single last cell of cancer. And the challenge for the field in allogeneic CAR T-cells has been getting CAR T-cells that stick around long enough, like an autologous cell. We think we've done that, but we have to prove that to you. Within these B-cell-mediated autoimmune disorders, we don't even really know if persistence is a feature or a bug, right? And so I think you'll see a number of different companies trying to develop allogeneic CAR T-cells, some of which are really good at hiding from immune rejection, some of which aren't. And they may or may not those ones that aren't may or may not be adequate. They may be better for all we know. So I get why they're doing them. So it will be a field where we learn for a while. I'm, based on our cancer data and our preclinical data. I mean, I'm pretty confident we'll get rid of B-cells. I don't know if we'll do it in a way that you have the efficacy you've seen from autologous CAR T-cells yet. I mean, they've just been really surprising to me how great the data are. And I would love for our therapy to work that well. And we can deliver. I mean, if the dose is similar to what it is in autologous CAR T-cells, you know, our current manufacturing process will make over 700 batches per run. So to put that into context, I think sometimes that number is hard to fathom. If an autologous CAR T-cell does 100 manufacturing runs, their best-case scenario is they treat 100 patients. If we do 100 manufacturing runs per year, we treat 70,000. And so the ability to really commercialize this and make a broad impact for patients is just on a different level. It will be very, very different. I think we can deliver. It's off the shelf and ready to go tomorrow for the patient and the physician. So fingers crossed. On a more technical side here, is it understood why when autoimmune B-cells are depleted with CAR T, the B-cell population that repopulates comes back as non-self-reactive? Why it comes back what? As non-self-reactive. And it's, it's not reacting to the auto so really yeah. So I think there's no real understanding of this too but I think there are some hypotheses. So you have the B-cell lineage, you go just very simply, kind of like a pre-B-cell, B-cell, memory B-cell, plasma blast, plasma cell, right? And that's kind of how things go. So plasma cells sit in your bone marrow, right? And they make a little bit of antibody, and they turn back on when generally when you see the stimulus again. And so there's some hypothesis around there, and they're usually CD19 negative, that those cells will stick around like a vaccine because the antigen is no longer there to stimulate it. So they become plasma cells, and they sit in there, and that isn't impacted at all by a CD19 CAR T-cell. So then all of the, when you have persistent stimulus, you continue to express CD19 in the B-cell receptor, and you get rid of all of those cells. And you don't really, you know, you have to get rid of every single pathologic cell. And if you do, then there's no, then it's just, then you're just back into randomness. Will the patient develop an autoimmune disorder again? Right? Will they get exposed to something like a virus where a B-cell gets confused and has molecular mimicry for, you know, its own organs? And so, you know, your, your but your B-cells come back. They just don't have any of the memory of what they used to have. So if you look at Sonja Schrepfer data, so the way that our B-cells we, you know, we make IgM. That's how every B-cell is. And you class switch into IgG or IgA or IgE, right? And that's based upon the stimulus. And what you see is when the cells come back, it's all IgM, meaning they got rid of all of the things downstream that, you know, kind of are going against anything. So if you actually had an ongoing infection and you got this therapy, it wouldn't be a good thing, right? So that's you don't wanna do that, you know, but that's a little bit about why I think you're getting back a, it just think of it as control alt delete of your computer. It works a lot of times. I tell you, like, I've stopped calling IT until I at least tried the control alt delete, and, you know, that's really what you're doing to the B-cell population. Given your approach and the homogeneity of the cell type, can you do a basket trial in autoimmune? Say it again? What? Can you do a basket trial in autoimmune disease? Yeah. So, we have a, an IND that's open for three different indications in the B-cell-mediated autoimmune disorders. First one is extrarenal lupus. Second one is lupus nephritis. And the third one, as I mentioned, is ANCA-associated vasculitis. And we can add more indications to that, as we go. And so, it, it gives us more. I think we were allowed to do that because we have a safety database that's evolving and emerging in the cancer setting. And it's the exact same drug, right? And in fact, the first patients treated are with the exact same manufacturing batch, right, to just decrease risk. And, and then we'll modify that as we go forward. So, we're, we're able to. We, we still have to wait until we find our dose. There's still that really, like, you know, it's like watching paint dry sometimes in the CAR T space where you can only treat a patient every 28 days. And that, all that never is, it always turns into six or seven weeks as, you know, you get to day 28, and the patient then gets lymphodepleted, and then they get scheduled and all that stuff. But every six or seven weeks, we'll treat someone. And then once you clear a dose, we can really kinda get going across many, many indications. Pivoting over to the oncology programs here, help us understand when we see the 291 data later this year, how you're thinking about next steps if the data looks strong? How do I? What you're thinking about with regard to next steps if the data looks strong? In oncology? Yeah. It's a great question. I think that's a source of a lot of internal dialogue. We actually just brought in a new head of this space for us at blood cancer. It's a guy named John Gerecitano, who ran lymphoma and leukemia at J&J. I wanna make sure that, you know, he has a chance to really weigh in. So the B-cell cancers, right? You've got all these non-Hodgkin lymphomas, right? Follicular, a lot of indolent lymphomas, and then the more aggressive things like large B-cell lymphoma. You then have the acute leukemias and chronic leukemias. And they work really to varying degrees in all of these different indications. So our challenge is this stuff will probably work at least to some degree. It's how well it works. And then you already know the first few patients, we had some complete responses, right? So our challenge is navigating a field with a number of different competitors, including autologous CAR T-cells, where you're seeing, you know, survival data that's continuing to evolve and is evolving in a nice way. And these T-cell engagers, right, bispecifics, which, you know, create a very crowded marketplace. And most likely, we'll go into some the broader things, you know, like second- and third-line lymphoma as well as CLL. That's kind of the base case. Right now, most so the autologous CAR T-cells have shown a benefit against in head-to-head trials against autologous transplants in the second-line setting. Still, the vast majority of uses in the third-line setting. But in transplant centers, you're seeing them displaced more and more in the second-line. And so we probably have to develop broadly because most of the community and most cancer patients aren't gonna get these in the second-line. If that's the only place your label is, it can be a little limiting. So we'll, but at the same time, in the places that do the most volume, they're moving to the second-line. So we'll do both. So I think that's probably where we'll end up. And, you know, the way the rate limiter there is both data and manufacturing. So when you begin a registration study, really with these, particularly with these cellular therapies or gene therapies generally, where the product characteristics are less well understood than a pill, right? You really need to begin your registration study with your commercial process. And so, we are in the throes of launching. Oh, sorry, of locking our commercial process. And then we'll tech transfer it into manufacturing. And, you know, that's kind of a late next year kind of thing. So we've got some time. It's not, you know, we've got some, you know, to run more studies to understand where we go. Just manufacturing's a rate limiter. Okay. Great. Let Let me open it up to the audience for any questions. Let me, let me keep going here. Talking about business development and partnering strategy, you've talked about, well, you have about $300 million in cash and guided to a specific cash burn this year. How are you thinking about just overall cash runway and BD aspects with regard to your portfolio? I'll start by saying I think we think about it a lot, right? I mean, it's you know, developing these cellular therapies is expensive. And there's no way around that, right? And one of the beautiful things of you know, something like an allogeneic cell is the scale that you can do it. But one of the challenges of that is the very early investments that you have to make in that scale and product comparability. And even things like GMP-grade guide RNAs, mRNA, you know, plasmids, all these things. So, we burn a lot of money. We do own 100% worldwide rights to all of our assets. That includes things that are in human testing that we already talked about as well as whole platforms that we have aren't getting into, like our in vivo delivery capability. It's unsustainable for us to do that. I've generally kind of taken the view that small companies, we have one competitive advantage, and that's that we can make faster and better decisions, just 'cause we're focused and small and nimble. Big companies will beat us, you know, on everything related to resources, capital, even people, geographic reach. So the challenge of most partnerships is you get, you know, big company decision-making with little company resources, and particularly early in development. So we've really been trying to get to is past the periods of proof of concept in humans where we really understand the drug product. The critical decisions are gonna be on things that are very long tail, like your phase 3 development plan and your commercial regulatory strategy. At that point, it makes more sense to have a global partner. We will not be able to launch these drugs everywhere in the world, right? So, we're not that far away from when we might consider a partnership, you know, and that would be in all of these areas: in type 1 diabetes, B-cell-mediated autoimmune disorders, and cancer, and oncology. So, you know, most likely, we'll continue to raise money as well through the equity markets. But it will not be the gross burn will be a lot lower because we'll have partnerships coming in both to bring cash and to phase some of the spending over time. But we're not gonna rush it. It's a long-term commitment that you're making. These partnerships and the wrong partner and the wrong structure can be, you know, the death knell for a company. We're in no urgency to do that, assuming that, you know, you guys in the investor community continue to help us support, develop these drugs. Steve, one last question here. You touched base on the other platform that you have as well as you as Sana X, which is a vertical working on kinda novel approaches here and in cell therapy. Help us understand how you think about prioritizing the efforts to those other two verticals when the in vivo might move into the clinic. So you like the in-vivo delivery and things? Yeah. So prioritization's been really challenging for us in many regards. You know, we've had the good fortune of, you know, several things working, right? And so and even things have dropped into our lap, like these B-cell-mediated autoimmune disorders, which are gonna be very capital-intensive. And we're in the middle of a land grab, right, to get to really to get a number of different indications and, and develop these drugs as quickly as we can for patients. And so that's, you know, something that both is a great opportunity and it's been limiting in some of the things we can do. So, you know, we, we started the company with two main kind of platforms or ideas. One was to be able to to develop technology that would allow us to hide cells from allogeneic rejection 'cause that would allow us to really scale the cell therapy, which, you know, to date has been either limited by autologous delivery or the toxicity of immunosuppression. The other is to was for in vivo delivery. So you can kinda do whatever you want to a cell in a Petri dish. The challenge is getting the material into a cell in vivo. And we, you know, we have a cell-specific delivery capability that can deliver a bunch of different payloads. It can do gene editing reagents, base editing reagents. It can integrate DNA. It can do proteins, mRNA, that kinda thing. So, we actually the lead drug there goes targets CD8-positive T-cells. And we were moving forward with an in vivo CAR T-cell. We went through GLP-tox studies last year, which showed, you know, very nice delivery to circulating T cells, and really no off-targets. And it was quite encouraging. We did the GMP tech transfer, and we were ready to go. We just couldn't really execute. We didn't have the bandwidth to do five INDs last year. And so we kinda put it back into a research phase where we're trying to make them a little bit, you know, better, more potent, and such. And so, you know, that's something we would like to bring forward. I don't know. You know, we have one or two kind of killer experiments we're doing right now. And assuming they work, I don't know if that will be, you know, by the company as a partner. You could even see us spinning it out into a new co., but we need to move it forward. We can't just leave it on ourselves. We'll figure that out. And some of the, I think we would all like to do it ourselves. In vivo delivery with no lymphodepletion, to make a CAR T-cell in the autoimmune setting in particular seems like the killer app. And so we'd like to do that ourselves, if we can. But we may or may not have the wherewithal to do it. So that's kind of that platform. It's also in development for delivered HSCs, or hematopoietic stem cells for diseases like sickle cell. And we've had some success there. We've shown you guys some data that animals did about a year ago. You'll see us publish, you know, some really good information, I think, showing the ability to either gene edit or base edit into HSCs in a cell-specific way within the context of really flawed animal models. So I put that caveat. And we'll publish that in a really nice in a good journal, as the year progresses, most likely. So stay tuned for that. It's a nice platform. We will develop it at some point. We can only digest so much right now, though. Great. Well, with that, thank you so much, Steve. Thank you for the time and your attention. Take care.