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

Welcome, everyone, to the 43rd Annual JPMorgan Healthcare Conference. My name is Tess Romero and I'm one of the senior biotech analysts here at JPMorgan. We're pleased to welcome to the stage our next presenting company, Sana. And presenting on behalf of the company, we have CEO, Steve Harr. Steve?

Thank you, Tess, and thank you, JPMorgan for having us. And my gratitude to everybody who's joined us online and in the room. I think you guys know, we'll be making forward-looking statements. You can take a look at our 10-Q and other SEC filings for our risk factors. So at Sana, our goal is to change the possible for patients through engineered cells. I'm really excited today to have the opportunity to tell you about the progress we're making and untangling fundamental and really important biology to make therapeutics that we believe will have a meaningful impact for patients and build an important and enduring company. Since the advent of transplant and cellular medicine, a major limitation in the impact has been the rejection of allogeneic cells. If you put someone else's cells in your body, you will reject them quickly and every single time. Our scientists have been working to try to figure out how to overcome this now for many years. And we've kept you and the scientific community updated with many publications in nature, cell and science journals and we've shown an ability to overcome allogeneic rejection in mice, humanized mice, nonhuman primates and even in our first-in-human study for an allogeneic CAR T cell. But we really have viewed the most important and highest bar and a place where we can have the biggest impact is type 1 diabetes. You probably -- you may have seen last week that we put data out showing that we can transplant beta cells or pancreatic islets into the patient with type 1 diabetes with absolutely no immunosuppression and see no immune response and see these cells survive and function over time. And I think it's the first example in the history of humanity of somebody doing that, and it's a fundamental insight that's likely to change the course of cellular therapy going forward. We think we can use this in some really important medicines that we're going to talk about today. But it's a broadly applicable platform over time. And it's likely something that we believe can be a little bit like the Intel chip was where it goes inside of every single computer. So we're going to spend a good bit of time today talking about type 1 diabetes. It's a really important unmet need if you ever -- we'll go through that. We have a drug called SC451 that we're developing. And the goal of this therapy is to give a patient a single treatment and allow that patient to live the rest of their life with normal blood glucoses, no insulin and no immunosuppression. We're taking the same technology and we're applying it to B-cell mediated autoimmune diseases, things such as lupus, multiple sclerosis, vasculitis, myasthenia gravis. And the goal, again, is to take a drug we call SC291 and do a control, alt, delete in some regards to the patient's immune system and allow that patient to go back to the life they used to have off all medicines going forward without symptoms and without the disease. We're applying it as well to blood cancers with a drug called SC262 which is also in human testing for patients who have failed CD19 CAR T cells. That's not all we've been doing. And today, we're excited to talk a little bit about something you haven't heard from us for a while around. That's a fusogen platform. And it's something that we use to drive cell-specific delivery inside the patient of genetic materials. And we will show you data for the first time showing that we can make an in vivo CAR T cell and get deep B-cell depletion with cell specific delivery in a nonhuman primate. It has the potential to make really potent CAR T cells with absolutely no conditioning chemotherapy, which we're going to talk about, and an opportunity to really transform the autoimmune landscape and something that we think can have a big impact in oncology as well. Doing this always takes money. I think you know that. We own 100% worldwide rights to all of our drugs. We will partner them going forward. We wanted to get to a place where we had the right proof of concept and the ability to draw the path with a partner of how we come to market. So we have the balance sheet to go from multiple data readouts. We also have the assets to help us really finance the company. So how we approach this problem of allogeneic rejection? There are 2 arms to the immune system. There's the adaptive immune system of B and T cells, and there's innate immune system of things like natural killer cells. It's actually relatively straightforward to deal with the adaptive immune system, you disrupt something called MHC Class I and MHC Class II. Unfortunately, when we do that or when anybody does that, what you see is that natural killers will eliminate those cells. And so Sana's real insight here has been that overexpressing CD47 in that context will -- of knocking out MHC Class I and Class II will turn off both the adaptive and innate immune system and you get true immune evasion. And we're going to walk through a number of human examples of that, but I want you to know we've shown this and published it across many, many different animal models over time. So I talked about where we think we can have the biggest impact over time and with this technology, and that is type 1 diabetes. If you happen to know anybody with type 1 diabetes or you have a family member or a friend or you have it yourself, I think you know that this is a very difficult disease, where most of your -- a lot of your life is spent managing your glucose and your insulin and your exercise. And while insulin has been a major advance for these patients, it is far from a cure. It's a very large and unmet need, about 8.4 million people worldwide suffer from this disease. Unfortunately, it's growing, it's growing relatively rapidly and it's expected to double over the next 15 years. Too high of blood sugars and patients that have all kinds of complications like amputations, blindness, heart attacks, stroke, too low of blood sugars and you can have comas and even death. There's a lot that needs to be done to make progress here. The good news is that we kind of know what we need to do. So type 1 diabetes is a disease of missing pancreatic beta cells. You can hear us talk about islets. And islets is alpha beta and delta cells all put together in a little cluster. And so over the course of the last 20 years or so, the community has made progress with transplanting primary islet cells. These are islets that come from a cadaver and are isolated and transplant into a patient. And what we've seen is that people can live for well over a decade off of insulin actually doing quite well. The challenge with that is that cadavers are neither a scalable supply nor is a product quality very predictable. And patients have to be on lifelong immunosuppression and there just aren't that many people for whom the strong level of immunosuppression is better than lifelong insulin. Over the course of the last few years, if you look at number 2 here, we've seen several parties show that you can make these pancreatic islets from stem cells. And that has been a major advance in what you see is that it's more predictable in its outcome, and you probably have a more scalable supply source. Unfortunately, though, nothing's really been done to deal with a chronic immunosuppression. So our goal is really simple. A single treatment that leads to normal blood glucose for patients with no immunosuppression and no insulin therapy going forward. And we've done that in nonhuman primates. We've shown that we can cure a nonhuman primate of this disease. And the really critical question is, can we do this in humans, and I think I'm going to show you today that we've checked that box as well. So in order to go forward in this, what we designed is an investigator-sponsored trial with some partners in Sweden. And the goal of this study was relatively straightforward. It was to take cadaveric islets, in the number one in here, to gene modify them with these hypoimmune edits, I talked about, knocking out MHC Class I, knocking out MHC Class II and overexpressing CD47. And then to transplant those into a type 1 diabetic with absolutely no immunosuppression. It's a very simple procedure. We actually are just putting it into the forearm of the patient. And the goal is to see: number one, safety; number 2 is could we evade the immune system. And we had some hope that we would see cell survival and actually function. And function can be measured by something called C-peptide. When a beta cell makes insulin, it actually makes pro insulin. And it's secreted by the cell as insulin and C-peptide. So C-peptide is a one-to-one measure of the amount of insulin that a patient is making. As we went forward here -- so that was our goal. We wanted to see C-peptide. So it's a Phase I safety study, so just -- in difference from the monkey, we were dosing at a dose that was about 5% or so of what you would normally dose a patient with to get true insulin independence. So we wanted to see was would this survive. And I'd ask our team, how long do these cells need to survive to really know we've overcome the immune system. And they gave -- they said after 2 weeks, they're going to open a bottle of champagne. I asked them to just have a beer, and I thought maybe we could have the champagne after a month to build in some cushion. And what we're going to show you are our results. I'm thrilled to say we met all primary and secondary endpoints of the study. The patient is doing well and making his own insulin for the first time in over 30 years. It's pretty profound. There were no safety events from the study to date. And I'll walk you through now some of the other data points that we have. So the most important element of function is actually just looking at C-peptide. And this is a patient who had no C-peptide and it was known for many, many years. He's never made C-peptide. And you see that at baseline it's undetectable. And as we follow this patient now, over the first month on a weekly basis, you can see that it's very stable and the patient is now making his own insulin. Importantly, there's something called the mixed meal tolerance test or MMTT and what that looks at is a patient's ability to respond to make insulin with a glucose bolus or with food. And you see the little gray line at the bottom, confirming that the patient had absolutely no insulin and no response in making insulin from a meal. And what you see on the top is that the patient actually increased C-peptide by about 70% with a meal at 1 month. And I think this is the result that really convinces the people who really know this field in the type 1 diabetes space. So we then took an MRI image, and we have serial MRIs to watch it happening. So what you're looking at here is a cross-section of the forearm of the left arm of the patient. And if you take that yellow box and look on the right-hand side, take a look at those arrows. And those arrows highlight a wide opacity. And that wide opacity is consistent with the cells. That's right where we put the cells and what we put it there. You could never say they're definitively pancreatic islets, we're not testing for that, but you can say definitively that there is new tissue that's residing there. And then they C-peptide levels beforehand show that those really are pancreatic beta cells. So we've really shown for the first time in a human being that you can transplant cells from an allogeneic donor with zero immunosuppression, not even any steroids, and in this case, you put even a higher bar. The patient had a pre-existing immune response from type 1 diabetes to kill these cells and it didn't happen. They have survived, they have functioned. So I'm going to walk you through some of the immune-evasion data. it's transformative. And so what you see here is when we make this drug because it comes from a donor, that's not our final product, by the way, but within this experiment, we're pretty good at gene editing cells, but we don't get everyone edited. And so the HIP islet cells, they were around half of the cells, and that's just on the top, we'll show you through. Sometimes we knock out both genes of HLA I and HLA II, but we don't overexpress CD47. And you'll see people in the field do this. And what I told you before is the natural killer cells should kill those. And then we also transplant some just normal islet cells, what everybody else does all the time, right? And that's what people in the field have done to date. And we can now take the product that we transplanted and test it against the blood of the patient to see what really is happening inside the body. So unmodified islets. This is what everybody does in the field. And what you see is a very rapid T cell response to kill these cells. It peaks at about a week. And our team tells me that means they're right. They could have had the champagne at 2 weeks because all those we were past the barrier. But you can see that very rapidly, those cells lead to killing of -- the T cells will kill the wild type. You also see on the right-hand side, they generate antibodies. And for those of you who are immunologists, you'll have fun with this, you see an initial IgM response, and it translates over about 2 weeks into an IgG response as the patient develops memory to the allogeneic transplant itself. So those cells are gone. If you then look at the double knock-out cells type 1 and type 2. And you see on the left-hand side, T cells, don't see them. They shouldn't. There's no HLA, right? In the middle, you see they don't make antibodies. Again, they shouldn't because the parts that tell you that -- your body that it's foreign, the HLA is gone. So it doesn't happen. But what you see on [indiscernible] is the natural killer cells, even at baseline, rapidly kill those cells. So those cells are gone within a day or 2 probably of transplant. And then you have our hypoimmune or HIP islet cells. And what you see here is that throughout this time, the patient generates no T cells that recognize these cells. What you see in the middle is the patient generates no antibodies that recognize these cells. And what you see on the right is that natural killer cells are unable to recognize these cells as foreign and leave them alone. Sometimes though, a picture is worth a thousand words. And what we have here in green is the actual -- these cell types from the drug products. So on the left-hand side, you see wild type islets. In the middle, you'll see these double knock-outs. And on the right, you will see the HIP islets. And what we did here is very simply pour blood more or less onto these and see what happens. And what you see happen very, very rapidly is that the other cells are killed and our wild type -- sorry, our HIP islets are left alone, completely consistent with what we've seen. So I think we can confidently say that we now have clear evidence in humans that we have overcome allogeneic rejection. We've done this now across 2 different cell types. We can confidently say that we have in humans overcome autoimmune rejection of type 1 diabetes. And I hope that you can have the confidence that I have around that little triangle I showed you that we now have all of the component parts to have a curative therapy for patients with type 1 diabetes, and that it becomes inevitable that patients will have the opportunity to have normal blood glucoses with no insulin and no immunosuppression. So how are we going to do this at real scale? So we have a drug called SC451. It's really meant to go for the broad population and it starts with a stem cell on the left. We then put in those HIP gene edits. And you see in there, we knock out MHC Class I and Class II and overexpress CD47. We actually also put in a safety switch just in case something goes wrong, so we can kill those cells. And we grow them into that green cell, which is the pancreatic beta cell. We do that at scale and we can cryopreserve that so that hopefully, there is in every hospital around the world or maybe every endocrinologist office, there is, over time, a supply of these islets that they can then deliver to a patient in their arm with a single needle injection. So what does it take to really make this happen? And we've kind of articulated 4 distinct important scientific challenges. First and foremost, you have to overcome immune rejection without immunosuppression. I think we've done that. The second thing you need to do is be able to take these pluripotent stem cells and grow them and differentiate them at the things -- the words we use in manufacturing purity, potency and yield to be able to run a Phase I clinical trial. We've done that. Many others have too, by the way. That's not the most complicated thing. This third thing you need to be able to do is generate -- what you do is you start with a single cell. That single cell will be our drug product forever. We're just going to grow it. So to generate a gene-modified master cell bank that is GMP-compliant, that is genetically stable and that does so over -- as we go through many, many passages or divisions and differentiates over time. That's been really, really hard for us. And for those of you who've known us for years, it's something that we've struggled with over a few years. We've now done it. We've done it in a research bank. We can hopefully make that into a GMP bank. We're also in parallel making it in GMP conditions. I think this has been the major hurdle to us getting into humans and making progress, and it's something that we believe is now something we will do. The fourth is you have to manufacture enough drug to treat the patients that need it. And when we -- at number two, we're manufacturing drug where we're making billions, many billions per manufacturing run. To give you a sense of the scope of the challenge to treat 1% of the population or around 100,000 patients will probably require around 100 trillion cells. So we do have work to do to get there and it will be a scientific challenge. And I think it's important that we recognize that there's a lot to go to make that happen. So just to show you a little bit of why we can do this. This is some of the early data from what we've done with what we'd call kind of maybe a Phase 1 process. The left-hand slide (sic) [ side ] is just single cell sequencing of all the drug -- of all the cells in this. And the yellow are the beta cells. And the product is about 60% beta cells very consistently. The product is, if you look at this consistently made up of the islets and neuroendocrine cells and we have, if you know how to read this, no residual pluripotent stem cells in there. So we're excited about that. In the middle and right-hand column, our data from an in vivo study, where we've transplanted these cells and you've seen them survive and function now out over 15 months with really continued potency and importantly, as well, no evidence of any tumor, which is something that you always worry about in products like this. So we're excited about where we are. Stay tuned. We think this has the opportunity to be really one of the more transformational medicines our industry has created. We have a long way to go to really make that vision a reality. So I don't want you to feel like this is going to come immediately overnight. But I kind of view it as simply someone's built the electric car, and it really works but it has to be plugged in. So it's not that useful. We just showed you that we can make a lithium battery. So now all of the component parts are there to be able to build a scalable solution for patients. It's just going to take us some time, and it's going to take us some capital, and it's going to take some patience from both patients and you, but we are going to get there. And we're going to do more. So I think many of you know, B-cell mediated autoimmune diseases are a big problem. There have been about 75 different autoimmune diseases where the underlying pathology seems to be from B cells. That translates to well over 5 million patients. When I was trained in medicine the way those diseases were treated was generally given some kind of toxic suppressor of the immune system, and it was a battle between what was worse, the medicine or the actual disease. Over the last 20, 25 years, I think you've seen a lot of progress in being able to turn off single cytokines or other factors. And these diseases have turned into chronic diseases that patients can manage, but they're still challenging. In that time, what we learned is that if you deplete B cells, patients will often do really quite well. And importantly, the B-cell depletion correlates directly with the clinical effect. It turns out, there's a drug called autolog -- the autologous CAR T cells or CAR T cells more generally, are the best B-cell depleters that humans have ever made. And a group in Germany led by Dr. Georg Schett has shown that you can treat patients with a whole host of these different diseases, and patients will last for years off of any medicine and remain in remission. Others have noted this, there are a number of different companies that are going forward, in particular with these autologous CAR T cells. For those -- an autologous CAR T cell is one where they take your cells, ship into factory, genetically modify them and send them back for treatment. It's a long process. It's very difficult to scale and it's probably more complicated in the autoimmune setting than it is even in oncology, where they have been around. So what we're hoping we can deliver with the exact same gene modifications that we use in the type 1 diabetes study you just saw is an allogeneic CAR T cell that is scalable. It's available off the shelf. They completely evade the patient's immune system, and we hope that could be the future. So what we do here is, again, we knock out MHC Class I and Class II. We overexpress CD47 and we knock in a CAR. I mean, that's basically what we do. We've already -- we already have done this. We manufacture this where we get hundreds and hundreds of patient batches per manufacturing run. If you take the middle of that and just say we get $500 million, just to give you a sense with an autologous CAR T cell, if you do 100 runs, you can treat up most 100 patients. If we do 100 runs, we can treat around 50,000 patients. This is something that's available, hopefully to deal with the scale of the challenge. So we have the best drug and it's actually been in an oncology study over the course of the last 18 months. We haven't shared these data before. And what we saw, we're not moving forward in oncology, we're really going to focus on autoimmune, is that we treated 16 patients. Patients actually tolerated the drug really quite well. There were no cases of ICANS or the neurotoxicity you can see with CAR T cells. There were no cases of Grade 2 or higher CRS. There were 3 cases of Grade 1 CRS and what that is, is just a fever that happens. So what you see importantly on the right-hand side in the oncology setting is that we have -- and this is a dose-dependent effect, which makes you really clear around where this is. A deep B-cell depletion is consistent in the periphery at least with what we need to drive clinical benefit. So now knowing that we can safely get deep B-cell depletion in the oncology setting, what we want to see is to see that translate into autoimmune and then see that become clinical benefit. So we have a trial called the GLEAM study. It's a Phase I study right now in patients with lupus and ANCA-associated vasculitis. It's a dose escalation study. We started -- it has fast track designation, and we enrolled the first patients around the middle of last year. I think we're really optimistic about what this drug can deliver for patients. We're pretty surprised if it doesn't work. I think what we have to do is see how well it works in the context of a very competitive marketplace. And I think if it does work reasonably well, given the scale and the ease of delivery, we think it will be a really important medicine for patients. So stay tuned, we should have data for you in the not-too-distant future that we're ready to share. But when you look at this, one of the elements of these autologous or allogeneic CAR T cells that can limit their utility is actually the fact that they need -- patients need to get something called lymphodepleting chemotherapy at the outset. And I mentioned we've been working in other areas. We've been working on an in vivo CAR T cell. So what -- if you look at this, I want to just kind of describe to you what the idea -- the general concept is. So we have -- our medicine is the fusosome on the left-hand side. And it has a cell-specific delivery capability that will drive it to just go to T cells in the patient's body. It then will deliver a genetic content, which is that little minus sign. And that -- the genetic content will make a CAR. That's kind of the yellow y. That CAR will recognize B cells, and when it does, it will activate and an activated T cell -- an activated CAR-T cell will do 2 things: It will divide; and it will kill that target. So the goal is to make a therapy that is really off the shelf and available. So the way we do this, it's called a fusogen. It's got a G component and F component. The G is, think of it as guide, the F is fusion. We manipulate the guide so that we'll only recognize the cell we want. And that will drive fusion of the medicine and the cell membrane. So you get cell-specific delivery of the genetic content that goes directly into the cytoplasm. So our lead drug here is a CD8-targeted fusogen. So we'll go to CD8-positive cells, in particular, T cells. And our medicine inside of the CAR is a CD19 CAR. So around 1.5 years ago, we did a GLP tox study with this. And the fusogen is designed to cross-react with nonhuman primate, but the CAR does not. So what you can see is really the pharmacokinetic effects. So where does this go. And you see a dose-dependent delivery, at the high dose you get into about 15% of the T cells in circulation. Again, because there's no lymphodepletion, it's actually a lot higher level than what you'd see with normal CAR T cells. And that's very good. And on the right-hand side, you see something that's even more important. And that is that this drug goes nowhere except the CD8-positive cells. And I would challenge you for anybody who's in this field to see anything close to this. It does not go into the liver. It is not going to go into gonadal tissues and it does not go anywhere else. And that gives us the opportunity to have a really differentiated both safety profile and scalability. So you couldn't see though, really what the drug did. And so over the course of the last few quarters, what we've done is we changed the payload, and we put a CAR in that will cross-react with the nonhuman primate target, the nonhuman primate B cell. And that is called the surrogate SG299. We put an additional little bell and whistle on it, that's its new IP, which is really nice. And what you see here is really beautiful transduction and expansion of the CAR in the T cell. You can get up to 35% to 50% of the circulating T cells are CAR positive. What you see on the right hand, and this is, again, what we're looking for in the nonhuman primate -- I'm sorry, in the autoimmune setting is complete depletion or aplasia in the periphery of B cells. And importantly, what you see here, and this is where you really, really want to go is, on the left-hand side, absolutely no B cells. On the right-hand side -- sorry, left-hand side, tons of B cells in the control, right? On the right-hand side, absolutely no B cells and lymph nodes. So you see deep tissue depletion in the middle. It's actually what we see in that first monkey was it they had a very rapid depletion that they're starting to come back, and this is evidenced as just starting to come back. So we're really optimistic that this is a therapy that can change the landscape in autoimmune. I can tell you it's one that has gotten the field really excited as you can do scaled delivery of a CAR T cell in vivo with no lymphodepletion and that gives you all of the benefits of the CAR T space and really the convenience and safety, particularly in the early setting of some antibodies and T cell engagers. So stay tuned around that one. I don't want to forget about SC262 pretty quick. This is a drug for -- that we have in human testing that's targeting patients who have failed CD19 CAR T cells. It's a growing market because CD19 CAR T cells do continue to be used. With CD22 in the autologous setting and academic setting has shown really nice efficacy. We use the same CAR construct, we licensed it that is in the Stanford study, if you're familiar with the field, and you get about a 50% complete response rate. So similar to what we do with the CD19 CAR, we knock out the same genes. We knock in CD47 and we knock in a CD22 CAR. There's an ongoing Phase I study. We treated the first patients last year. Stay tuned. We'll have data to you in the not-too-distant future around what that looks like, and we're excited that, that can be an important therapy for a very large unmet need in a patient population that probably has about 4 to 6 months to live right now. So I hope you see it's actually been a pretty exciting 2025 for us already with showing that we can overcome allogeneic and autoimmune rejection in the type 1 diabetes setting. We've shown that as well with the CAR T cells, and we think this hypoimmune platform can be broadly applicable across many, many cell types, and it is broadly applicable against -- across a broad patient population. In type 1 diabetes, we think we put the component parts together now to really show the community that we are as an industry going to be able to deliver for them a curative therapy where we can keep them for many, many years off of insulin with no immunosuppression and normal blood glucoses. We're making progress in B-cell autoimmune diseases where we think the control, alt, delete, of resetting the B-cell compartment will also lead to a curative therapy for patients where they can be off medicine. And we've got an opportunity to do this with no lymphodepleting chemotherapy going forward with our in vivo CAR T cell. And finally, we'll continue to go after what we see as really substantiative high unmet needs where you have a population such as CD19 CAR T cells where patients can die really within a couple of quarters. It's going to be an exciting year. We're going to deliver -- we've already delivered, hopefully, one important piece of clinical data. We'll get you some more. And I hope you see we have a really exciting future, and I look forward to sharing updates with you going forward. And with that, I think we're going to take some questions. I'm going to be joined on the podium by 2 people. Dhaval Patel, who's our Chief Scientific Officer; and Sonja Schrepfer who really is the architect of the entire HIP platform and the foundational scientists of the company who's driven really the field forward. So Tess?

Great. Steve, thank you so much for the presentation and welcome, team. So I thought I would start our conversation on your recent Phase I IST data, which you just showed everyone here. A question we've gotten from a few investors on the backside of the data was how to interpret the magnitude of C-peptide change? And what is considered normal? Could you opine a little bit on that for us?

Yes. That's a very simple question. So you and I -- we probably have C-peptides in the range of 200 to 300 in this setting. And what we showed here is something that is in the range of, let's call it, 10 to 12, something like that. But that is exactly consistent with what we did. We transplanted. So we transplanted around 4% to 5% of the dose that we thought would be curative for a patient. So what we see is what we should see. And we're quite confident that there really is -- there is no challenge. There is no scientific question, can you dose enough of this drug and get patients off of insulin. That's just putting more cells in, right? Really straightforward. It's been done now by thousands and thousands and thousands of patients. The question from -- was, can you get rid of the immunosuppression? And that is something that we've clearly shown.

Can you talk a little bit about your plans monitoring this patient longer term? What are you hoping to see data-wise as you take this patient out further from the 4 weeks?

Yes. Sonja, do you want to start that one?

Sonja?

Happy to. Thank you. Yes. So it is a gene-edited product. The patient will be followed for 15 years. It's a safety trial. From the immune perspective, you have seen it in the data we already passed that fulminant allogeneic response. So I wouldn't expect anything there. Of course, I cannot look into the future but knowing the transplant immunology and the data, the preclinical data we have, I would be surprised that we learn anything there because we overcame that allogeneic response.

And just a reminder, a couple of things. One, it's a gene therapy product. So a patient will be followed for 15 years, right? Two, we do intend to publish -- put this into a scientific forum and a publisher -- the patient, everything that we have will be updated at that time, and we will continue to follow this immune system and the beta cells for a long time.

Okay. Can you talk a little bit more about what is exactly involved in the process of converting from a research to GMP master cell bank?

It's really simple. It's just 2 things, documentation and sterility, right? So the difference between research is that it allows you -- the operator to do a few more things. They may have been exposed to something in the air or in the material, and we have to make sure the documentation is there. Anything you'd add to that, Dhaval?

Probably a little more complicated than that.

It's simple to articulate, hard to do. But we're working on it.

Anything else you wanted to add?

Look, I'm really excited by this project. It's the reason I joined Sana. I do believe that we will be able to convert with regulatory help, the RCB to an MCB. But in case, we're also in parallel doing new ones under GMP conditions. And they're not easy to make but I think we have the research one...