Welcome, everyone, to the 43rd Annual JPMorgan Healthcare Conference. My name is Tessa 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, Tessa, and thank you, J.P. Morgan, 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. 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 in 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, non-human 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 the place where we can have the biggest impact, is type 1 diabetes. You may have seen last week that we put data out showing that we can transplant beta cells or pancreatic islets into a patient with type 1 diabetes with absolutely no immunosuppression and see no immune response and see these cells survive and function over time. I think it's the first example in the history of humanity of somebody doing that.
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. It's a broadly applicable platform over time. 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. We're going to spend a good bit of time today talking about Type 1 diabetes. It's a really important unmet need, but we'll go through that. We have a drug called SC451 that we're developing. 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. But 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 fusion platform. And it's something we use to drive cell-specific delivery inside the patient of genetic materials.
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 non-human 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. We have the balance sheet to go for multiple data readouts.
We also have the assets to help us really finance the company. How we approach this problem of allogeneic rejection, there are two arms to the immune system. There's the adaptive immune system of B and T cells, and there's an 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 killer cells will eliminate those cells. Sana's real insight here has been that overexpressing CD47 in that context 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. 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 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, and it's growing relatively rapidly, and it's expected to double over the next 15 years.
Too high of blood sugars in patients that have all kinds of complications like amputations, blindness, heart attack, stroke. Too low of blood sugars, and you can have comas or 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're going to hear me talk about islets. An islet 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 transplanted into a patient.
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 the product quality very predictable. Patients have to be on lifelong immunosuppression. There just aren't that many people for whom this strong level of immunosuppression is better than lifelong insulin. Over the course of the last few years, if you look at number two here, we've seen several parties show that you can make these pancreatic islets from stem cells. That has been a major advance. 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.
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. We've done that in non-human primates. We've shown that we can cure a non-human primate of this disease. The really critical question is, can we do this in humans? I think I'm going to show you today that we've checked that box as well. In order to go forward in this, what we designed is an investigator-sponsored trial with some partners in Sweden. The goal of this study was relatively straightforward.
It was to take cadaveric islets, and the number one in here, to gene modify them with these Hypoimmune 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 was to see, number one, safety. Number two 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 proinsulin, 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 one 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 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 said after two 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 this 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. I'm going to walk you through now some of the other data points that we have. The most important element of function is actually just looking at C-peptide. This is a patient who had no C-peptide, and it was known for many, many years he'd never made C-peptide. You see that at baseline, it's undetectable. 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 and 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 one 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 what happened. 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.
Those arrows highlight a white opacity. And that white opacity is consistent with the cells. That's right where we put the cells and what we put in there. You can 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 the 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, we 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, and 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're 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 two weeks because all those were past the barrier. But you can see that very rapidly those cells lead to killing. Wild 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 two weeks into an IgG response as the patient develops memory to the allogeneic transplanted cell, so those cells are gone. You then look at the double knockout 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. 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 that doesn't happen, but what you see, unfortunately, is that natural killer cells, even at baseline, rapidly kill those cells. Those cells are gone within a day or two, probably, of transplant and then you have our hypoimmune or hip islet cells.
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. 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. What we have here in green is the actual cell types from the drug products. On the left-hand side, you see wild type islets. In the middle, you'll see these double knockouts. On the right, you will see the HIP islets. What we did here is very simply pour blood, more or less, onto these and see what happens.
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 two different cell types. We can confidently say that we have, in humans, overcome autoimmune rejection of type 1 diabetes. 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. 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. You see in the middle, 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's 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 four 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 one 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. And that single cell will be our drug product forever. We're just going to grow it.
So you have 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're 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 one process. The left-hand slide 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 our endocrine 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 are 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. And it's 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 five 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 depth of B-cell depletion correlates directly with the clinical effect. Turns out there's a drug called autologous CAR T cells, or CAR T cells more generally, are the best B-cell depleters that humans have ever made.
A group in Germany led by Dr. Georg Schett has shown that you can treat patients with a whole host of these different diseases. 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. An autologous CAR T-cell is one where they take your cells, ship them to a factory, genetically modify them, and send them back for treatment. It's a long process. It's very difficult to scale. It's probably more complicated in the autoimmune setting than it is even in oncology, whether you've been around. 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 that completely evades the patient's immune system, and we hope that can be the future. 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 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, just to give you a sense, with an autologous CAR T-cell, if you do 100 runs, you can treat at 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. We have a best drug.
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 that you can see with CAR T-cells. There were no cases of grade 2 or higher CRS. There were three 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.
Now, knowing that we can safely get deep B-cell depletion in the oncology setting, what we want to see is that translate into autoimmune and then see that become clinical benefit. We have a trial called the GLEAM study. It's a phase 1 study right now in patients with lupus and ANCA-associated vasculitis. It's a dose escalation study. It has fast-track designation. 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'd be 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. 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. 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 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 in vivo CAR T-cells. So if you look at this, I want to just kind of describe for you what the general concept is. So our medicine is a 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 its genetic content, which is that little minus sign. And 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 or an activated CAR T-cell will do two 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 an F component. The G is, I think of 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.
Our medicine inside of it or the CAR is a CD19 CAR. Around a year and a half ago, we did a GLP tox study with this. The Fusogen is designed to cross-react with non-human primate, but the CAR does not. What you can see is really the pharmacokinetic effects. Where does this go? 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. That's very good. On the right-hand side, you see something that's even more important. That is that this drug goes nowhere except to CD8-positive cells. 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 does not 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've changed the payload. And we put a CAR in that will cross-react with the non-human primate target, the non-human primate B-cell. And that, we call this 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 about 35%-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 non-human primate or sorry, in the autoimmune setting, is complete depletion or aplasia in the periphery of B cells. 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. On the right-hand side, absolutely no B cells in lymph nodes. So you see deep tissue depletion. In the middle, it's actually what we see in that first monkey was that they had a very rapid depletion. They were starting to come back. And this is evidence it's 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 because 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. We'll be pretty quick. This is a drug 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, it 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 one 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 four-to-six 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.
We think this Hypoimmune platform can be broadly applicable across many, many cell types. It is broadly applicable 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. 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 substantive 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 two people, Dhaval Patel, who's our Chief Scientific Officer, and Sonia Schrepfer, who really is the architect of the entire HIP platform and the foundational scientist of the company who's driven really the field forward. So Tess, go ahead. Great.
Steve, thank you so much for the presentation and welcome, team. I thought I would start our conversation on your recent phase one 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?
Yeah, that's a very simple question. So you and I, we probably have C-peptides in the range of 200 to 300 when we're 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. So we transplanted around 4%-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 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? It's really straightforward. It's been done now by thousands and thousands and thousands of patients. The question was, can you get rid of the immunosuppression?
That is something that we've clearly shown.
OK. Can you talk a little bit about your plan monitoring this patient longer term? What are you hoping to see data-wise as you take this patient out further from the four weeks?
Yeah. Sonia, do you want to start that one?
Sonia.
Happy to. Thank you. Yeah, 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 already overcame that allogeneic response.
OK.
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 to publish it. 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.
OK. 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 two things: documentation and sterility. So the difference between research is that it allows 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's there. Anything you'd add to that, Dhaval?
Probably a little more complicated than that.
Simple to articulate, hard to do. Yeah, but we're working on it. Yeah.
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 a research one.
So yeah, the simple is not meant to describe the process. The simple is meant to describe what needs to be done: documentation and purity, sterility.
OK. What is a reasonable timing framework to get into the clinic with SC451?
We've been really clear. We're not going to tell you. And I think what I want to do is not sacrifice accuracy for precision. And I've already proven myself to be not so good at this. And we've actually said in the past a couple of times. And it's been more challenging to make this master cell bank than we assumed. So we'll know. We'll tell you when we've heard about six months. Anything beyond that is really unpredictable because of what we need to do. So I can tell you confidently it will not occur in the next six months. And anything beyond that, I'm just going to leave for the future.
OK. But it sounds like you're confident you're ultimately going to be able to get to the clinic.
Absolutely. 100%.
OK. Steve, what does "in the not-too-distant future" mean for your GLEAM and VIVID study updates?
Sorry, say that again. What does?
What does "in the not-too-distant future" mean?
For when?
Timelines to your GLEAM and VIVID study updates. I think you said that on the podium for both those.
Oh, again, I think one of the things that we're trying to build is a long, durable, sustainable company. If your goal is to try to figure out exactly what day we're going to release data, you're probably not the investor for us. If your goal is to understand how we're going to make progress over time in building these medicines, because this is really hard stuff, I want to help you understand how long it's going to take us and what we need to do. We will have data as we go forward from these clinical phase one clinical programs. It's inevitable. We enroll patients. We treat patients. But we're not going to litter you with data that we don't think changes your ability and our ability and the clinical and patient community's ability to understand our probability of success.
So when we think we have something that meaningfully gives you the opportunity to understand, for good or for bad, how well we're doing, we will tell you, just like we did last week with this Type 1 diabetes patient.
Just as a follow-up, last question for me. What does really meaningful mean to you for each of these studies in terms of the data you'll like to present to the community? Can you give us a little bit more of a framework for both of the programs?
Tess, I love that you're trying to really try to box us in. And one of the things I'm going to do is I'm going to back away from you. So meaningful is that you understand the drug product, right? And so if you think about something like type 1 sorry, if you think about this type 1 diabetes, for us, we really wanted to see could we do cell survival and function without immunosuppression. We did that. That's meaningful. I think that if we were to go into the autoimmune setting as an example, you already know from the oncology setting that we can safely deplete B cells. So that's not meaningful to show that in the autoimmune setting. What is meaningful is to see that translate into a clinical benefit of seeing patients off therapy and doing really well and returning to their lives.
And so that's what I would view as meaningful in that setting is seeing the deep B-cell depletion. And again, more than just in the blood, seeing the things that are really consistent with whole body B-cell depletion, including a reset of the B-cell repertoire, which you are not always seeing in some of the studies that are being done by commercial companies, which means they're probably underdosing, just to be clear. You want to see a complete reset of the B-cell repertoire and see patients off therapy, immunosuppressants, and doing very well. And so that would be meaningful. Or it would be meaningful to say we can't. But that's a little bit of how we think about it.
Very helpful, caller. I think we actually have to close the session now. Thanks, everyone, for joining.
Thanks, everybody. Appreciate it.