Sana Biotechnology, Inc. (SANA) September 2026 Conference Transcript

Great. Hello, everyone. I'm Max Skor, a biotech analyst with Morgan Stanley. And before we get started, for important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com forward slash research disclosures. And with that, I'm happy to introduce Steve Haar, CEO of Sana Biotechnology. Thank you very much for joining me today.

Max, thanks for having us. I appreciate it.

So maybe just to get started, we'll give you the stage. introduce Sana's story, maybe set up recent progress, and what we should focus on going into the end of the year.

Sure. I'm sure everybody here recognizes we'll make forward-looking statements, and like you, I have my own little risk factor. Please read our 10-Q for looking at those risk factors. We started the company around the idea that one of the most important transformations that will occur in medicine over the coming 20 years or so is the ability to engineer self. And we wanted to do this in a way that allowed us to go after diseases that are highly prevalent with scalable platforms that could access patients broadly. And we chose to go after two problems and excited to say shortly we should be getting going on studies for them and really understanding their impact on human health. So the first one is, you know, if you transplant someone else's cells into your body, your body will see them as foreign and try to reject them, or will reject them. And it's been a major limitation for transplant medicine for decades. And we went after the idea of trying to hide allogeneic cells, a transplant from immune recognition. It turns out that the technique we use seems to hide them, at least in some cases, not only from allogeneic, but also autoimmune rejection. And probably the most visible and potentially most important program that we're working on is a one-time functional cure for type 1 diabetes. And type 1 diabetes is actually a pretty simple disease from far away, which is the immune system gets confused and attacks and kills the pancreatic beta cell. And the beta cell is the only cell in our body that makes insulin. And before the advent of endogenous insulin about 103 years ago, patients just starved to death. Their cells couldn't get any sugars over the course of several months. Since then, people have done a lot better, but it's still not great. And so even with the best therapy today, your average type 1 diabetic will live about a decade shorter than someone without it. And to put that into perspective, that's about the same for a 20-year-old being diagnosed with type 1 diabetes as being diagnosed with breast cancer or HIV. And during that time, it's a very complex life, right? Every meal, every time you exercise, every time you get a little bit sick, you're trying to adjust your insulin. And so these people deserve something better. So if you take a step back and say, okay, the missing cell is the pancreatic beta cell. I'm going to go back and forth between beta cell and islet. Just think of it as an islet is the beta cell plus its support structure. About 25 years ago, a guy named James Shapiro and others have followed started isolating pancreatic islets from recently deceased people's pancreases. And it turns out it works very effectively. They're transfused in the liver, and people have lived for decades without any insulin. So normal blood glucose is no insulin. The challenge is that it's not a very replicable supply source, right? There's a lot of variability. It's not very scalable. And people have to be on extraordinary immunosuppression, like an organ transplant. And there just aren't that many people for whom the risks of immunosuppression are less than the risk of diabetes. But there are thousands of people around the world who have gotten this. So over the last several years, others have begun to show that you can take pluripotent stem cells, either embryonic stem cells or induced pluripotent stem cells, iPSCs. and you can grow them and mature them into pancreatic islets. And there seems to be a more replicable outcome, which is kind of working on almost everybody. Two, it seems to be that it's probably more scalable, although I don't think we've answered that question for sure. But people are still on lifelong immunosuppression. And again, so the limit, the impact. Over the last several years, what we've shown is we can make some gene modifications. First we showed in vitro, then in mice, and then in non-human primates, and we showed it in people. We actually did this in Type 1 Diabetic, published in the Journal of Medicine, that we can gene-modify these islets, transplant them into a person with Type 1 diabetes, and they will survive and function. And the last update in the England Journal of Medicine is at 14 months. So no immunosuppression, cell-tuned really well. So now you have all the component parts together for a one-time curative therapy for Type 1 diabetes. And what we have is a gene-modified IPS cell-derived islet. So we made a handful of gene edits. We made a master cell bank. We've grown them, and then now we'll differentiate them into islets. We've been working hard at this. I think we're almost there. Our goal is to get the IND cleared this year and start our praise one study this year. I'll go through this, but you should know pretty quickly if this works or not. I'm sure you'll ask me questions. I think it's probably worth the second question, but people get bored with me rambling. We have another platform, though, and that is our goal at that point was to go after another big problem, which is you can do more or less anything you want to a genome in a petri dish. The hard part has been delivering it into the cells in the body. And so we wanted to develop a platform that would allow us to go after the challenge of being able to deliver it to any cell in a specific repeatable and with any payload way. And, you know, we seem to have made some real progress on that. And so our most advanced program is in vivo CAR T-cell. We've been at this, you know, for a while. You know, we have a platform that we believe gives us some very specific advantages we can get into versus others. They've gotten a little bit ahead of us, so I hope, you know, it does play out that it's been worth the time to make a best-in-class therapy. I'm quite confident if you were a non-human primate this would be the best-in-class therapy, and whether or not that's true with a human, we'll have to see. But, again, our goal is to get that study started soon and start generating data and get that out in the not-too-distant future.

Okay, great. Let's start with the type 1 diabetes program. Stepping back, you talked about the New England Journal of Medicine paper. The follow-up UP421 data showed continued islet cell survival and insulin production without immunosuppression through 14 months. What do you expect the October presentation to add to investors' understanding of durability, immune evasion, or cell function? zero.

I said this from the beginning. There's nothing that will get you after about a month from the immune system. So these cells are going to live until they die. When they die, it will be because of something related to these cadaveric islets, most likely. And so when they live, it doesn't mean that our cells, which are stem cell drive islets, will live in the long run. If they die, it doesn't mean our cells will die. We got immune evasion, And now we need to put these stem cell dry violets in and ensure that they last for hopefully decades for people. So unless something really surprisingly came up, like there's some new twist in the immune system that killed these things, I don't think you'll learn anything as you watch this for longer. I've kind of been pretty clear on that for a while. I don't view any update around us learning that things are still alive as being material. I wouldn't view it if they died, and that was because of immune response to the material, we would tell you. But otherwise, just assume they're doing fine.

Then let's fast forward then to progress towards starting the SC451 Phase 1-2 trial. We could break it out. I can ask specific questions. But what are the gating factors? What are the challenges? If you could lay that out for us.

Historically, the biggest challenge for us, it took us years to figure this out, was trying to make a genomically stable GMP master cell bank. I'll explain what that all means. So it turns out, so you're going to start, so we gene-edited a pluripotent stem cell. We knocked two genes out, we knocked two in. And as we did that, what we'd find is we grew these in, because you start with one cell, and you're going to grow every patient. Let's just say it's around a billion cells as a dose. Every thousand patients is a trillion. To go after a disease of 10 million people, you need quantrillion cells. So as we grew up the number of cells, we would start to see mutations arise. And essentially it's DNA repair enzymes because you put things in growth media that selects for cells that grow quickly and the cells that grow quickly are those that don't stop to fix their genome. So the biggest challenge is doing that and we did it. So once we did that, it's actually been pretty rapid. And we had three work streams we're working our way through. Number one is just being clinically ready. You have the clinical trial protocol aligned with everybody outside the company, regulators, physicians, others. And then in this case, because we're delivering this product, we send some live cells into a hospital where they have to be stored, processed, and then actually put into the muscle of the We need to make sure that was replicable and good. So that was part one. We feel very good about where we are there. And particularly, we had a collaboration we signed earlier this year with the Mayo Clinic. They've been quite helpful in ensuring we did that in a replicable and hopefully reproducible way across sites. Number two is there's all kinds of non-clinical studies that get done. The things that are normally done, GOP tox studies, biodistribution efficacy, some things that are specific to what we do, genomic stability. You don't want cancer-causing mutations in these cells. And then another one is we have a safety switch we put in so that in case something did go wrong, we could kill the cells. That's preliminarily all done. We don't have the final study reports in our hands yet, but I think that can be off all of our worry lists. The third thing is manufacturing. So these are complex medicines, and we need to both block a process and then transfer it in from our research labs into a GMP, or Good Manufacturing Practice, manufacturing suite, and then have it done by their hands, not our scientists' hands, but their employees' hands. So we're finishing that. So hopefully that goes very well. We'd like to believe we're going to file this IND, get it cleared and start our phase one study this year. We don't know if we'll dose anybody this year. I think that's another question. Like, we want to make sure it's the right patient. It's the end of the year around the holidays. But, you know, we'll hopefully get all that done soon.

Can you talk about the trial design, the number of patients you anticipate enrolling, and just timelines in general?

I think that there are, you know, three things you're trying to learn. Well, let's just say you're always trying to learn safety. That's the most important aspect of a Phase I study. So let's put that in. And there are two main safety things to be worried about, at least as far as we know from afar. One is when you put in these stem cell-driven violets, some of them don't live. They don't engraft. That's what always happens when you put cells in. And they're full of insulin granules when they release. We need to make sure we don't have severe hypoglycemia or low blood sugar in the short term. Super easy to deal with if you haven't, hopefully, which is just IV sugar. right? The second thing is in the long run tumors, right? That's going to take many patients. So safety particular. So then what we want to know is first off, does the technology or what we've seen, the immune evasion in this end of one study we did, transfer into these gene modified stem cells? If that occurs, I would argue the majority of the risk is out of the program, right? Because we're going to transplant cells into a patient with a pre-existing immune response against beta cells or islet cells, right, with no immunosuppression, they should be rejected in a matter of days. And if they're not, if these cells are living, let's just use it as a marker a month out, they're probably going to live for years and years and years. So that's question one. Does that happen? I think that that will be super important, and if it does happen, it will be a very important event for our company. The second is we're not just trying to make a great technology. We're actually trying to make a drug, right? And the goal of the drug is normal blood sugars or euglycemia with no more insulin shots and no immunosuppression. If we use the experience of others, that may take us a quarter or two to ensure we have potent enough cells and we get the efficacy we want. So that could happen again pretty early in the year. The third thing is, is this a consistent result? Is this going to happen in more or less everyone? Is it going to be some subset of patients? And, you know, that may take us a bit longer to figure out, but we like to think we can figure that out maybe as we move through next year. So, you know, our phase one study set up is around a dozen patients. You know, we can kind of flex it in a new direction. And, you know, we want to make sure we have a good, solid dose and that these things really work. And I think then it's pretty straightforward to move into a registration study, assuming it all works as we hope it does.

And how have interactions gone with regulators, everything on track in that regard?

Yes. It's an important field, I think, from a regulatory perspective. They understand the unmet need. It's a very vocal patient group because they haven't had anything really novel in a century. And I think with the human data that we have in this N of 1 experience, there's a lot of curiosity about how well that will translate to people. So we found that regulators around the world in many jurisdictions have been helpful in helping us navigate questions and the path forward.

And maybe you can comment a bit more on the... That does not mean they're easy.

It means they're transparent, right?

The deal you signed with the Mayo Clinic earlier in the year, the implications of that, and maybe looking out further, any strategic partnership you think would be valuable, valuable, or are you interested in that?

I'll start with the Mayo Clinic has been a tremendous partner to date in the collaboration with them. I have to say, from my perspective, it's exceeded at least my expectations. And in the very near term, they were trying to help us with two challenges. In the long run, we hope they can help us with more. one is really de-risking this period, this black box from the time the drug product leaves our hands until when the patient leaves the hospital and there are elements of product storage there are elements of product preparedness we're sending it in a media that has to keep it alive for a while you have to concentrate the cells down so you don't put all that media into your muscle there are elements of kind of delivery, getting the cells into the right muscle at the right time and with the right needles and all that stuff, then elements of taking care of the patient. We wanted to make sure we're standardized in a way that it could be reproducible across many sites. It's been really great for that. They also then came with a bit of cash for us. There's a $25 million investment in the company at a premium which is helpful because we're an early stage company where our cost of capital is high and that was quite helpful. Well, those are two things that came with it to date, and I think we're both optimistic there will be more as we go forward.

And then view on potential strategic partners going forward.

We'll have to see. I mean, I always kind of think of this. If you knew to answer these four questions, you would know how this movie plays out with this drug. One is, does it work? And you'll learn that very quickly. Two is, can we figure out how to scale manufacturing? This is a disease of 10 million people. There are 500,000 new patients a year. I mean, if we somehow, like, cure 100,000 people per year, the prevalence pool will still be growing. So we have to figure out scale. And then the third is, can we figure out a commercial model for a curative therapy of a highly prevalent disease? I mean, those are the three big, like, giant macro questions. And the fourth one is, how do we sign up and answer a company to all that, right? So we know big pharma partners can help with the latter, right? And I don't know if they can help us answer the question, does it work, because the drug is kind of being made, right? The kind of cards are on the table. We haven't been able to flip them over yet. And so we'll have to see if they can help us with these others or if it's just, you know, again, never say never because you never know what the financial conditions are of companies. Certainly if they can grow the pie for us, that's very, very attractive. If they can de-risk these, like, you know, kind of existential questions for us, that would be very, very attractive. It's not clear yet that anybody can. The questions haven't been answered, not that we're better than they are. It's just the questions haven't been answered. And then it would be great to have a bigger pie with lower risk and more capital. Those are all good things, but we'll see if anybody can ever do that. I kind of like the idea of taking this forward a while on our own, but that isn't always the right answer for patients, and we'll do what we think is the right thing for the therapy and for all of our stakeholders.

Not pressing you to look too far ahead, But the cadence of updates, should we expect by the end of the year we'll get a press release that the Phase I trial has started? And then first quarter?

I think investors have been very clear to us that IMB clearance is material on their mind, just given the complexity of this medicine and how hard it's been for us to make it. Above and beyond that, we'll figure it out when it happens. But I think that's something that's very material to us, so we'll make sure that that's something.

If it happens, they get to make sure. So we'll be waiting for that press release.

All right. I don't think we want to give a blow-by-blow of everything that happens because it just takes away, it puts unnecessary pressure around things. Sometimes the better answer is a week later. Right. That's fair. We want to make sure that we get the best answer.

Okay, maybe we can pivot to the rest of your platform. SG293, if you can introduce it where you're at, and I can ask some specific follow-up questions.

This is an in vivo CAR-T program, leveraging a platform we call the Fusogen Platform. This particular drug makes a CD19 targeted CAR-T cell, which we intend to initially develop in the setting of blood cancers, in particular, non-Hodgkin lymphoma out of the gate, with a goal of things, a safety profile allows it to move into things like autoimmune disease, where I think it could be, if a safety profile allows it, really, really transformative. We did three things that are different than the field in making this platform. And, you know, we'll see how they play out as being clinically important. The first assumption that we made was that you want exquisite specificity in delivery, meaning you only want to go to T-cells. I think many others have taken a different view. I would tell you one of our board members had a different view around this, And so it's not like it's crazy, which is you just want to get enough of the genetic material into your target cell, the T cell, so you can make enough CAR T cells, and that's your major thing. Our view has been, though, that for safety reasons, for reasons around immunogenicity, and even just for manufacturability, just because T cells are a small number of cells in your body, that you want to be exquisitely specific. And I think we confidently can say we've established that within the context of the technologies that are out there. I can get into why if you want. The second is that you want to have a signal that integrates into the target cell. So what that means is we put in the cell DNA, and that DNA goes into the chromosome of the target T cell. And so when you car T cells, you know, you might make 100 million of them, right, if you're really good at it in a patient. But you have, you know, you and I have probably 100 billion B cells. And if you tie it with B cells plus tumors, you have hundreds of billions of cells that have to be killed. Therefore, your CAR T cell is going to have to go through multi-logarithmic expansion or growth to kill all of the cells. And if you don't integrate it into the chromosome, the signal won't go to the progeny cell, right? So mRNA, there's a lot of really smart people who have spent a lot of money, and they could be right. I'm not saying we're right. These are just assumptions we made, right? Specificity matters. You want to do integration over mRNA. Smart people are making a different bet, and they, you know, we make, and integration has its own safety issue, right? It's got at least a theoretical idea that could go in the wrong spot of your genome. And the third thing that we made a bet on is that you wanted to dissociate entry of your genetic material from activation of the T cell. And so what you've seen is that all the other people who are doing these virus-like particles, more or less, are trying to use CD3 as the way that they get to T cells. And that has led to a new toxicity, which is a peri-infusion toxicity, which in some cases has put people in the ICU on blood pressure and has actually led to people getting, around the time of infusion, very high-dose steroids, 20 milligrams of dexamethasone, which if you've ever taken steroids, it's a lot of steroids. And so with these three things, we think because we've dissociated those two things, we can get entry without overactivation. We can get, you know, the DNA going into the progeny cells, and we only go into T cells, and that will give us a clinical advantage. We need to see that that's true in humans, right? And so the next step is to get into humans. We've been working towards starting an investigator-initiated trial in China imminently. We had some things that slowed down a bit. There was some adverse publicity around in other studies, some people who died in China. And I think that that just led to people dotting their I's and crossing their T's. I don't think in any way it's going to impact our ability to get this done. But last week we told people, instead of data later this year, it's probably going to be in the first half of 2027. So it's still coming at us. If that works in the lymphoma setting, we will expand to other cancers. If the safety profile allows it, we will go into the autoimmune space where I think, again, the benefits can be profound. There's no lipid depleting chemotherapy. There's all kinds of things that are maybe different than other. And if that also works, we have a second drug targeting BCMA that's ready to go into human testing. But we're a capital-constrained small company, and we figure we don't need to do two drugs in the same platform until we see the first one work.

Okay, that's fair. Could you just comment on what would constitute meaningful early proof of concept across the CAR-T generation? Is it safety, durability? kind of set the stage for what we can expect in the first half of next year?

I think you want to see a reasonable safety profile with complete responses, like elimination of the tumor.

And I think we have something better.

So for those of you who don't know, I was in the CAR-T space for a while, like an old company that did this. And one of the things that we weren't always sure, particularly in a lymphoma setting, was whether a complete response would translate into a durable complete response or maybe like a functional cure. And it turned out that if people's CAT scans or PET scans, PET CT scans, were negative at six months, they almost never recurred, right? That's a long time to wait as you're going through dose escalation studies to figure out if you're at the right dose. We have a new technology. It's, you know, it's a CT DNA or it's kind of tumor DNA, circulating tumor DNA. And this really allows you early to understand, And is a patient likely at a dose with a therapy that's likely to lead to a durable, complete response? And so I think we can learn pretty quickly. Do you have complete responses with undetectable ctDNA in a drug that is reasonably safe? And if you have that, it's going to be a really important drug. You know, the bar is probably you want to do as well as autologous CAR T cells, right? If you're that air bar of that, the ease of use of this, the lack of lympho-depleting chemotherapy, which comes with a lot of toxicity, is probably pretty attractive, right? If it's better, that's a no-brainer. If it's, you know, moderately worse, maybe you compete with T-cell engagers or you have to figure out if you really have a drug, right? I mean, that's kind of at least an air bar of what to think about.

Before moving on to maybe some macro questions, I wanted to pivot briefly back to diabetes and just ask, if SC451 data are positive, what would regulators need to see before SANA could transition into a registrational program, particularly around patient population, safety database, efficacy, durability, et cetera?

I don't know the answer to that question is the clear answer. We haven't engaged any regulator on the planet around what a registration study will look like. I think that from my own perspective, what we would want to see is a few things. One, I kind of think we kind of outlined there would be three different periods of manufacturing. There's good enough for phase one. We have that, but just barely. I mean, then there's good enough for what we call like an early commercial launch. And to do that, that gets in the number of patients, and you want to have reasonable gross margins. You have to have that in place at the start of your registration cohort. You're not going to be able to change your manufacturing process meaningfully while you're doing that. And we have some work to do to get there. We've made a lot of progress over the last six months. I'm way more optimistic than I was at the beginning of the year that this is going to be readily doable, but we're not done, to be clear. And the third will then be, you know, like tens and tens of thousands of people, hopefully at very attractive gross margins. The, you know, to get to the process lock on that phase in that registration study is likely the rate limit or the registration cohort, right? You're going to have, as I said, do you have any short-term safety issues to deal with? As far as we know, which, again, you never know until you know, the major thing we need to ensure is that we can deal with the short-term risk of severe hypoglycemia. As soon as we can do that, which seems readily doable, then, at least as I think about it, the other risk would be long-term these things ever cause tumors. You need lots of people for long-term follow-up. I think the registration study should be relatively limited. I don't know if that's true or not. with, you know, pretty meaningful post-marketing follow-up, but we'll have to see. And then it's a manufacturing question. So I don't think there's a lot in there that we need to grapple with. Now, what we want to make sure of is that we have a consistency of result, and if it's an inconsistent result, that we understand what patients it's more or less likely to work in. We want to get the dose reasonably right. I mean, it's hard to imagine you can overdose this stuff. I mean, it's glucose-sensitive, insulin secretion. But because we will be capacity limited for years and years, if we give people 2x a dose, we will help half as many patients as we might otherwise do it. So that's not helpful. We need to make sure we get the dose kind of right. We want to make sure we have a manufacturing process. In terms of patient population, patient population we're looking at is very broad. It's not everybody, but it's most people over 18 with type 1 diabetes. You know, we may add, you know, change most to, you know, even more as part of our phase I'd like to think we'd get into a pediatric population if this works in a relatively urgent fashion. You know, start with 16 plus, 12 to 12 plus, and then you get a little more. It's clearly parents and those kids really want something like this. It's a big burden for them. So we're going to go through all that, but I don't think any of them are gating necessarily the starting of a registration study.

And then just in regards to financials, could you just talk about your cash runway, capital allocation, any color around that?

Yeah, so at the end of the second quarter, we had $160 million. We said that gets us in the middle of next year, assuming we continue to run the business as we do today, which is our goal. I don't think you can cut your way into making these things work, right? The goal, I'd just say, we'd like to bring more money in the company in the not-too-distant future. We're not urgent about it or anything like that. I'd like to think with reasonable clinical data, it's a good time for us to be thinking hard about financing the company and our partnerships, everybody that understands kind of where we're allocating that cash, what we need, and what the inflection points are. We have the capital we need to get to the next set of value inflection points, which is, do these drugs work? and again if they do we're going to need to make sure we do more if they don't it's going to be messy neither one do but we'll figure that out if it happens and our goal is our hope is that they both do in terms of capital allocation today the vast majority of it goes to this type 1 diabetes project it is an enormously complex drug this is an aggregation of novel transplant immunology, CRISPR gene editing, stem cell biology, and kind of really difficult scale manufacturing, right, kind of in one drug. And it has to be done. We can't outsource these things, right? These things are done inside of the company. But we've done it now, hopefully, and at least we can turn the card over, and if it works, we'll get the privilege of playing out the next hand.

Great. So with about four minutes to go, if you can entertain a couple of macro questions, how is the rise of China innovation changing your competitive positioning, your thoughts on R&D, or maybe how BD plays out long-term?

Well, we've developed these medicines ourselves, and they're enormously complicated. So we're just going to stick to our knitting and do what we do, and we're not looking to bring in other molecules or anything else in their term. And I presume that China has been wonderful at kind of innovating on the sciences of scale and manufacturing, that as we go through it, if this thing happens to work, that we'll have to kind of make sure that we continue to focus on scale and cost of goods so we can deliver this at a reasonable value to patients and payers around the world. I think they've been very thoughtful in innovating around how to get proof of concept in humans at a reasonable level of regulatory burden and cost. Some of those things, I think, are being applied in the United States. We're in the process of trying to figure that out. More of them need to be, but we will never be able to apply them all. And then we have the challenge in that there are, you know, many of these companies have subsidies and things from them. And, you know, we have the other benefit, which is why we're here, right? It's this really robust and rich and deep capital markets expertise that resides in the United States. And so that's part of what we hopefully have the opportunity to leverage in making an important medicine.

Great. And then question number two, AI implementation. Is SANA taking on AI, leveraging it internally? What are your thoughts on the future?

We're not taking it on. I mean, it's pretty powerful.

Sorry, bad choice of word.

Yeah. Leveraging it. I mean, we do. I kind of divide it into three major categories as we think about it. One is just knowledge extraction. I think it's super powerful for that. I think most people use it. There's kind of no excuse for showing up to a meeting and saying, I don't know what we're talking about today. I haven't heard or learned about this. you can always show up with a reasonable level of knowledge. They can also help people accelerate their understanding of complex things with what's known in the field pretty rapidly, right? The second would be operating efficiencies, and that's kind of in areas that relate to how we run our business, right, whether that's in finance. There's a lot of the GNA functions. There's some elements of clinical trial work. I think we're getting some of that, right? It's helpful. I don't think it's like mind-boggling helpful, but it's helpful on the margin. And third are things like creativity enhancements, like really making novel therapies and things because of it. That's not an area we currently have really kind of gotten much out of it, partly related to we kind of have what we think we need, and we just need to understand it in humans, and so that's a, you know, we're exquisitely focused on that. So that's kind of how we've divided it and kind of where we're getting what we can out of it.

In the last minute, anything?

Please don't send me any AI-generated emails like that kind of stuff. Those are just to delete it, right?

Anything I missed?

They're not true productivity enhancers because no one reads them, right?

Last minute, anything I missed or anything you'd like to call out?

I'd like to just highlight, we've been at this for a while. we went out when I started the company the goal was to do something that if it happened there were two goals and we decided what to do broadly one was if it happened to work we wanted it to be transformative not something incremental and the second is for it to be complex and complicated and that had to do with just the type of people that are attracted it's also just what's worth doing and I think we nailed finding those things and it's been hard And we've made a lot of, we've had some setbacks along the way. We've made a lot of progress. And we're now sitting here, and I was saying to somebody, like, sometimes it's spelled a little like we're waiting for Godot. But Godot is going to show up. And, you know, we will be in a position, we believe, to deliver to you, to patients, and all our stakeholders an understanding of what these drugs do over the next several quarters. You know, most importantly, you know, we're really focused on trying to understand And is the technology that we've really proved in humans already to work translate into this gene-modified stem cell drive islet? Because if it does, a cure for people with type 1 diabetes becomes absolutely inevitable. And that's our focus. That's what we really want to deliver for patients. We want to deliver for others. And we're hopeful we can do it.

Well, thank you very much for joining us today, Steve.

Thank you, everybody in the audience.