Excellent. Good afternoon, everyone, and welcome to the JMP Securities Hematology and Oncology Summit. It's my pleasure to introduce Sana Biotechnology. Presenting for the company is Nate Hardy, the Chief Financial Officer. Welcome, Nate. Thank you very much for joining us. as I've, as I've probably mentioned, you know, and you've, you've had these fireside chats before, I have no idea who's in our virtual audience right now and how much they know about Sana. And so I always ask, you know, for the presenters to maybe take 2-5 minutes kind of summarizing the company for us before we dive into, you know, some specific, detailed questions. Absolutely. And And thank you, Ran, and thanks, JMP, for including us. We're happy to be here. You know, before I jump in, I do want to mention I'll be making some forward-looking statements as we go through this, and just want to highlight that we spend a good deal of time on our risk factors, and so encourage people to take a look at those as they're looking at the company. And so with that, you know, just for those that don't have as much background, you know, Sana, you know, we've been at this a bit over five years now, and really, our ambition has been: how do we use engineered cells to transform the possible for patients? And as we looked at what was the biggest challenge that we saw to making that happen was allogeneic stem cell rejection. And how is it that, you know, if you take a donor-derived cell or a pluripotent stem cell, and you want to use it as a therapeutic, but you put it into the host, the host's immune system is going to recognize it, and their immune system is going to kill the cell. And so, you know, one of the keys that we see to being able to truly use kind of cells as therapeutics is overcoming that. And, you know, we've made progress over the last few years with what we call our hypoimmune technology, where we make a number of gene edits, which I'm happy to talk through. And those gene edits have shown in mice models, in humanized mice models, and in non-human primates that, you know, we are hiding these cells from the immune system, and we're hiding them in different microenvironments, and we're hiding them kind of out, you know, ten months in certain cell types. And so obviously, the real benefit and what we're hoping to do is to use this hypoimmune technology to benefit patients. And, you know, we're at a really exciting time for the company. as we're going to learn a lot about how this works in multiple programs in the next year. And, you know, we could be in a place where, you know, a year from now, you know, we're talking about patient data on 30-60 patients across, you know, four platforms and multiple diseases. This is the pipeline chart that you have up here. You know, the first program that we have is a CD19 allogeneic CAR-T that leverages the hypoimmune. You know, we released kind of one patient's worth of data last week, and we'll continue to, you know, release data as we progress through next year. We also have that same drug product we're using, and we have an IND that's been allowed for three indications in autoimmune disorders that are B-cell mediated. We think that's a really kind of unique opportunity, particularly for an allogeneic therapy, where we can make a lot of it and perhaps have some safety benefits. We also, just sticking with Allo T, have our SC262 program, which we'll file an IND this year, and against a CD22-targeted program to go after CD19 failures. And then finally, stem cell-derived programs, and you can see a few here. The one that we're pushing forward is SC451, which is, you know, the goal is to take a stem cell-derived product, make our hypoimmune edits, and put it into a type one diabetic patient with no immunosuppression. You know, we haven't talked specifically about the timeline for that IND. You know, we will in time. But the most important thing for us in the short term is, you know, can we hide these cells in the immune system? You know, we just announced a few weeks ago that a CTA had cleared where we're doing a study with a university in Sweden, where we'll take primary islet cells, we'll modify those with our edits, and put them into a type one diabetic with no immune suppression. So, you know, expect the data on that in the, in the near term. So Ran, hopefully, that's an overview for people that are less familiar. Yeah. No, thank you very much for that. Let's jump into, you know, maybe some of the specifics. You mentioned gene edits, right? That makes your cell type clearly different than other ones that are out there. Can you, you know, A, talk about that, and then, B, you know, you did mention the, the first ever, sort of clinical data. Granted, it's from one patient, but nonetheless, it is groundbreaking in that, you know, it is the first time that we're seeing these data. You know, from the program you just reported on, can you maybe take us through, you know, the key findings, if you will? I understand it's preliminary, but, you know- Yeah ... there's always a good case scenario and a bad case scenario. I'd love to hear, you know, kind of what, what was your key, key takeaways from it? Yeah. No, absolutely. So, you know, first, to talk about the edits that we make as a reminder for everyone, you know, we knock out Class I and Class II MHC, and I think that's kind of well-known that that takes care of the adaptive immune system, T cells, B cells. But then the challenge is once you do that, the innate immune system, specifically NK cells, recognize the cells and quickly kill them. And so we're also, in addition to those two edits, overexpressing CD47, and the combination of those edits has again shown the ability to hide these cells from both sides of the immune system, both innate and adaptive. And so, you know, the first place that, you know, we've talked about results in the clinic on this is SC291. And again, this is a hypoimmune allogeneic CAR T program. And, you know, there's a few things we want to see. The first one we want to see is, do these cells kind of survive, and are we seeing kind of no immune kind of activation, when we put them in? And what we, what we shared last week, was, I think, early data that, that provided a few things, all of which we were hoping to see. The first is, you know, it is safe and well-tolerated. Again, this is one patient. The second is in an in vitro assay, where we're basically taking blood samples from the patient at different time periods and kind of putting them against the drug product. You know, we can see, based on the later points, that the person's immune system is intact, and, you know, that they are hiding from the immune cells, that the cells that are fully edited are hiding. And so, you know, it's exactly what we wanted to see kind of at this stage. Obviously, it's one patient, and, you know, we'll dosing more patients, and we'll share that in time. Yep. So, it is early. You know, you have additional dose escalations that you will undergo. And we'll talk about, you know, maybe how we should expect the cadence of these milestones, you know, into next year. But I guess just sticking with, you know, sticking with this, you know, the hypoimmune platform, clearly, you can extend that to other areas, right? And you had mentioned, you know, SC451, but before that, there is this IST that's ongoing. Somewhat different cells, right? Because these are cadaveric, you know, islet cells. You know, would love to kind of get your thoughts on, you know, A, what kind of expectations do you have for this program, right? Ultimately, how does it kind of help you transition, or how do you take the learnings from this program to your SC451 program? Yeah, absolutely. So, if we take a step back, I mean, I think what we have seen over kind of the past few years is that there are a number of institutions, you know, primarily in Canada and Europe, which do cadaveric islet transplants. And what they do is they take islet cells from a person that's recently died, and they kind of harvest those specific islets, and then they put them into a Type one diabetic patient, and they also heavily immunosuppress the person. And, you know, that patient, and many of them are able to become euglycemic over time, and as long as they can tolerate the immunosuppression, their diabetes remains under control. And so our thought is we're partnering and doing an IST with this institution that's done kind of hundreds of these cadaveric islets. And the difference is we're going to take the islets again from the donor. We are going to make our hypoimmune edits that I mentioned previously to them, and then we'll put them into a Type one diabetic patient with no immune suppression. And when we do that, we hope to see two things. One, we hope to see that the cells survive and are there, and that there's no immune reaction to those cells. So that's one. The second is C-peptide. Given these are Type one diabetic patients, they will have kind of no C-peptide prior to the transplant, and so if we are detecting C-peptide after, we both know that the cells are there, kind of from the first test that I mentioned, and second, that they're functioning and creating C-peptide. You know, there is a possibility, but we don't expect it, kind of in the initial patient, kind of due to the number of cells they'll get, glucose control. You know, obviously, I think from a valuation perspective, it would be great to get that, but from a risk perspective, if we see C-peptide, we know they're functioning, and so we'll feel quite good about what that is. You know, that's something where, you know, we've again said the CTA cleared. You know, we've also said that, you know, given, you know, the importance of this and how it kind of translates to how hypoimmune is working in people, you know, it's likely not a long period of time before we share the data. You know, we know that if you transplant an allogeneic cell without kind of these edits, they're going to die kind of within, you know, I don't know, before two weeks. And so if all of a sudden this gets out a month, it starts to get in the period where we would likely to share it. ... Excellent. I guess, you know, so obviously there's the underlying platform, right? That's being applied not just to, on the oncology side, but here- Yeah -on the autoimmune side. But the pipeline is gonna expand, right, to other neuronal diseases. You know, we sometimes get asked, and then we sometimes wonder ourselves, right, does the failure of one program impact the rest of the pipeline, you know, en masse, right? So basically, if this study winds up showing that, I don't know, the cells don't last that long, does that suddenly impact your oncology platform or the other programs? Yeah, it's a good question, and I mean, I think it's not gonna be a great answer because I definitely think it's one of these where it depends, you know? I mean, I think there are kind of situations where, you know, if one of those two arms of the innate immune or of the immune system is recognizing the cells in either one of these, you know, it probably does have some type of a read-through to the other program. But they're also quite different. I mean, you know, beta cells, you know, when you're talking about transplanting islet cells, you have to overcome both allogeneic and autoimmune factors. And so you know, you could argue there that the bar is much higher. Where on the CAR T side with T cells, you know, there's a lot of other factors, you know, the what the patient has gone through before with treatments, the lymphodepletion, and other items. So I think it's hard to get a direct read-through, but, you know, there are things that we could see, which I think there would be. And there are others where I think it would be harder to translate. So ultimately, a long answer to say it depends. I got you. Yeah. So, let me fire off a couple of questions that we typically get from investors- Yep ... and see, you know, and kind of get your answers. You know, one, right, the CAR T space is just, like, overhyped. It's too many companies all going after the same targets. Even if SC291 produces the same sort of results as autologous therapies, you know, ultimately, it can't become a commercial success, just given all the competition. How do you address that? Yeah, I would say a few things. I mean, one, I think we believe there's still a lot of opportunity here for patients. I mean, there's still 100,000 kind of people a year that are dying from kind of these B-cell malignancies, and, you know, that certainly means... If you think about how many people have been treated with a CAR T, I mean, it's, I think, certainly below kind of 20,000. And so there's a lot of opportunity to kind of grow and treat patients. Second is, I think allogeneic kind of needs to work, and, you know, we've said that if our allogeneic cells can persist, and they can start to persist kind of in this 3- to 6-month time period, we could see efficacy from an allogeneic product that looks a lot like autologous. You know, if the efficacy looks a lot like autologous, then we're in a place where, you know, with every manufacturing batch that we do, or every manufacturing run, we're making, you know, depending on the dose, you know, somewhere, call it 400 or 500 doses per batch. And I think that gives us two really good advantages. I mean, one, you know, the cost is naturally lower. Two, you know, the access in getting this to patients when they need it is better. And so I do agree with the statement that there's a lot of CD19 players. I think there's still a big unmet need, and I think if we have an allo CAR T that works as well as an autologous, we're gonna be in a position to really be disruptive there. Yeah. The this question we got, you know, is much more based on recent sort of events that have taken place, right? The cell therapy space got some negative news last week with the FDA, you know, starting some investigations as to you know, some of these autologous cell therapies and the potential for T-cell malignancies. You know, you know, and people have answered, like, "Well, when you're evaluating this in oncology, right, that you it might not be as a big an issue, but when you start moving to autoimmune, it can become a big issue." So I kind of wanted to get your thoughts on how that might be impacting your decision-making. Yeah, I don't... You know, first I'll say I'm not a physician or a scientist, so I mean, my view here is based on kind of what I've read and what we've discussed internally. But, you know, one, it hasn't affected the way we think about the certainly oncology nor autoimmune. I mean, I think we're continuing to move forward and, no change in thoughts there. You know, I think the risk-benefit, you know, trade-off, the benefit that CAR Ts have provided for a lot of patients is quite significant. You know, I know in the database there were 12, I think, patients identified, and I heard something that it's closer to 19. Mm-hmm. And so, you know, if you take that kind of on the denominator of, you know, 20,000 or whatever number you pick, I think there's a lot to learn, and, you know, we're not reacting to it yet, but this is T-cell malignancies, and, which is cancer, and that's serious, and so we'll, you know, we'll continue to monitor it and learn. Got it. The other question that we typically get is, is regarding the company's burn rate. And, and so while you weren't, you know, you're not a physician for the prior question. Mm. You're a CFO, so this is perfect. You know, it's, look, it's, it's significant, but you have a lot of irons in the fire, right? And you're moving a lot of things forward. I guess the question is, you know, can they focus resources even more? Because you, you did announce not too long ago, you know, the shelving of the Fusogen portfolio. But can you focus resources even more to kind of get through this, you know, biotech nuclear winter that we've experienced, which, which might be experiencing some thawing right now, but, you know, how, how you should manage that cash position? And you know, while you're answering that, what is the cash position? Yeah. I feel really good about where we are from a burn perspective at this point. I mean, I think we have, you know, said externally that, you know, we'll have burn below $200 million on an operating basis as we go into 2024. And I think one of the things that was important to us was to create a financeable business going forward. And, you know, we're going to be in a place where kind of with that burn rate, you know, as I said before, we're going to be able to get kind of clinical data on, you know, 30-60 patients, depending on how things progress, and you're going to get that across kind of four programs and, you know, a number of diseases. And so I think that really puts us in a place where, you know, we can deliver a lot of potential value and be in a place to access more capital. You know, too, I would say that, you know, we still own all of the rights to all of our assets, and, you know, we haven't partnered to date. But as you know, as you move into the clinic, things start to cost a lot more than they did before, and I think a partner can bring more, both in terms of capital, but also capability. And so I think that's also a potential for us as we go kind of through the next year. You know, our cash will last us into 2025, and, you know, that gives us a chance to see a lot of data from patients before we need to access again. So, you know, I think our decision to focus on the hypoimmune platform and kind of less in the near term on kind of Fusogen was a good decision that really helps get our burn to a place where we have a financeable company. So let's talk about, you know, the milestones. You hit a major one just recently with the reporting of initial data, right, from that study. You know, these are the ones that we have listed. It's primarily 2024 sort of centric of focus, so clearly it's going to be a big year for you. If you had to kind of rank order this, if you will, you know, into which milestones maybe you feel would drive the most shareholder value, would you be able to guide us to that? Yeah. I would say a few things, and I don't know if I would rank order them. I would say there's obviously a lot of attention and questions related to, you know, two pieces of data. One, kind of more data on our SC291 oncology program, and specifically the early data, which will tell us a lot about hypoimmune and are those cells surviving? And then the second is also related to that in the beta islet program, where we're editing the primary islets in type one diabetes. I think there's a lot of kind of near-term focus on that. You know, I think what we're really excited about is that, you know, we're going to have four clinical programs that we're pushing forward and we'll get data on. You know, while it's important and we believe that if hypoimmune works, it's going to have benefit, we're going to start to see, you know, how each of these are a therapeutic next year in multiple diseases. And, you know, we haven't talked a whole lot about autoimmune today, but you know, as you know, as I'm sure others know, the early data that that's come out regarding that is quite powerful for patients. And, you know, we think, you know, with an allogeneic product that you can make a lot of, if it works as we hope, it could be really unique, and there could be a lot of excitement around that as we get into next year. Excellent. Yeah, no, I'm looking forward to it, and you're right, the autoimmune component of, you know, cellular therapies is definitely generating some very, very, you know, intriguing data. You know, and so I look forward to seeing how you guys what kind of data you guys generate as well. Well, Nate, thank you very much. We've come towards the end of our time. Really appreciate, you know, you joining us, and look forward to the next data update from this program. Great. Thank you, Ran.