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

Welcome, everyone, to the 41st Annual JPMorgan Healthcare Conference. My name is Tessa Romero. I'm one of the senior biotech analysts here at JPMorgan. I'm joined by Taylor Hanley and Adhiraj Chauhan from the team. Our next presenting company is Sana, and speaking on behalf of the company, we have CEO, Steve Harr. Before I turn it over to Steve, I just wanted to highlight that for Q&A after the formal presentation, there is an Ask a Question button in the portal, which should allow you to submit your questions, and I'm happy to ask the question on your behalf. We are also taking live questions here in the audience. So just wave your hand and we'll get your question in. So with that, I'm going to hand it over to Steve.

Well, thank you, Tessa, and thank you, JPMorgan. Thank you everybody here in the audience as well as online for joining us. We're thrilled to have a chance to tell you a little bit about what we're up to, the progress we've made. We're quite excited, hopefully, you'll be as well. We have a lot of information hopefully coming out that will help you understand our company better in 2023 and beyond. And before we do that, though, of course, you know we will be making forward-looking statements. So please take a look and peruse our regulatory filings, 10-Qs and 10-Ks for risk factors. We spent a lot of time on them and there's a lot of good information in them. So with that, Sana's purpose is to change the possible for patients through the power of engineered cells. And we went about trying to do this by really tackling 2 of the most fundamental challenges in actually making that vision a reality. First and foremost, every time we transplant a cell into another person, there have been challenges and problems with allogeneic rejection. And so overcoming that, we think, can have a very significant impact. And the other is it's pretty possible today to do anything you'd like to a cell in a petri dish. The real challenge in terms of modifying the genome and controlling the genome has been delivery in vivo. And so we have a technology, our fusogen technology for in vivo delivery, where we're able to really deliver the genomic modification reagents, gene editing, base editing and others in a cell-specific manner. We've made a lot of progress there, but we really want to focus today and we're going to talk about that later on the hyperimmune platform. Overcoming immune rejection, as I said, has the potential to really change the way we approach and actually utilize cell therapy. I think most people recognize the opportunity and promise of autologous CAR T cells and also some of their challenges. And we've been -- the field has been working on allogeneic CAR T cells, but really struggling to overcome immune rejection. And we think if we have allogeneic CAR T cells that perform like autologous cells, we can really transform the treatment of a whole host of blood cancers, lymphoma, leukemia, myeloma, and have the opportunity to treat tens of thousands of patients per year. Additionally, really, if you're going to look at stem cell-derived therapies such as pancreatic islet cells, we have to overcome this allogeneic rejection issue. And then we think we're making real progress there. The beautiful thing is, this year, we have 2 opportunities for really clear clinical proof of concept of what we're doing. SC291, which is an allogeneic CAR T cell targeting CD19, we'll have -- the IND has been filed. We anticipate having substantial data as we move through the year. And something we haven't talked about until today is we've been working on hypoimmune-edited primary islet cells, which we can transplant into patients with type 1 diabetes and really understand can we overcome allogeneic and autoimmune rejection in patients. We think this will not only -- these will not only provide insights for our portfolio broadly, but it also really will hopefully highlight that we have a number of drugs which can move forward towards the market. So we have a lot of drugs we'll talk about in a second. And we have a balance sheet with over $500 million to hopefully see this through at least through the next phase of clinical development. So this is just a little screenshot of our pipeline. As you can see, we've got an IND. We filed for SC291 when we'll file shortly for these hypoimmune primary islet cells, which I'll describe later. You begin to see data readouts this year from a couple of programs. And with 2 to 3 INDs coming this year and next year, you can see that the data readouts begin to really pile up as you move through 2024 and 2025. We'll show -- we'll talk about the rest of this pipeline at another time. Today, we're going to really focus on the allogeneic CAR T cell portfolio as well as what we're doing in type 1 diabetes. So since the advent of cellular medicine and really transplant medicine, the problem of allogeneic bone marrow rejection has been at the forefront of challenges for the industry to really tackle. And cell-based medicines have the same problem as organ transplant. The only real path to date to overcome this has been very significant immune suppression, and there are challenges with that. Patients end up with severe infections. They are at higher risk for cancer, and there are all kinds of other idiosyncratic problems with each drug. We've tried to overcome it with allogeneic cells. To date, the genetic modifications have been incomplete. I mean I think that's pretty transparent. And it hasn't really worked as well as we hope. I think people recognize autologous cells have really had challenges to scalability and they only work for a few types of cells that exist in suspension. And in fact, there's only one, and I remember this, there's only one allogeneic cell that's widely used today, and that's red blood cells, right? And they have been used broadly in millions and millions of patients really successfully. I'm going to come back to that in a minute. But we think overcoming this immune rejection has the potential to really unlock not just what we do at Sana, but really a host of drugs across the field. So how do we approach this? And one of our -- my core learnings over time has been when you're faced with a complex scientific challenge, see if mother nature solved it and if she has exploited that system. And it started really around the paradox of pregnancy. And the paradox of pregnancies is that we're each half mom and half dad. And the only reason that we're in this room together today is our mothers didn't reject us in utero. But our DNA and proteins are different enough that really none of us would be good organ transplant donors to our moms. So what we set out was to really understand what was different about that maternal fetal border. And you have to overcome 2 aspects of immunology to really make this work. There is the adaptive immune system of B and T cells. It's actually relatively easy to deal with. People figured this out a long time ago. In some way, we need to disrupt Class I and Class II MHC. And you do that, the challenge is it's easy enough that cancer cells and virus has figured it out a while ago. And so we evolved the innate immune system, things like natural killer cells. And they will kill cells that are missing that. And that's been the challenge. What we figured out is that with overexpression of CD47, we can both turn -- and knocking out Class I and Class II, we can both turn off the adaptive immune system and also turn off the innate-immune system. And remember, I told you this has only been that there's only one place that you really are successfully able to transplant allogeneic cells, that's red blood cells. And it turns out, and this was not why we went down this path, but it turns out red blood cells have no MHC Class I and Class II on their cell surface and they markedly overexpressed CD47, and we have been able to successfully transplant them in humans over and over again for decades now. So when we started this, this is just a little bit of the in vitro data that we did. The first challenge is overcoming T cell killing. And what we have is across the top, knocking out Class I and Class II MHC, HLA I and II. And then there are various strategies that we and others have tested for trying to grapple with this innate immunity, doing nothing, and you can see the T cells actually do fine, knocking in some other things which may impact T cells. But as you do this, what you -- on the bottom, what we plated are just regular cells and we put on top of it regular natural killer cells. And what you see is that for every example here, except for overexpressing CD47, the natural killer cells will rapidly chew up and eat these modified cells that overexpress some other protein or just knockouts of Class I and Class II. So we know these other systems don't work. We believe that what we're doing is working. This is in vitro. So we tested this in mice. We've tested this in human (sic) [ humanized ] mice. And the next real test was to figure out what happen, we put them into normal immune nonhuman primates. So here, this is an experiment of 8 nonhuman primates, 4 in each arm. In 1 of -- in 4 of these animals, we put in hypoimmune cells, hypoimmune, again, have these 3 gene modifications. And the other, we just transplanted regular unmodified cells. And at the bottom, what you see is with unmodified cells, they're killed within a matter of a couple of weeks. And what you see across the top is that our cells thrive and survive for as long as we watch them in this study, which is about 4 months. So that was exciting for us and it was a real transformation in our understanding our belief because no one that we're aware of has ever transplanted allogeneic cells into a normal immune nonhuman primate with no immunosuppression and seeing them live. And so it was a big step for -- we wanted to see what happened, we went into other cell types. And so this is an example of transplanting pancreatic islet cells. And what you see on the bottom is, again, that these cells are killed very rapidly, really within a week, if you have not made any genetic modifications. And we transplant our gene-modified cells. What you see is cells were living at this point were out to 10 months and the cells are still doing quite well and thriving. So not only can we transplant iPS cells, we can transplant real thriving cells like islet cells, and you're seeing them live for a prolonged period of time. We've now done this across multiple cell types. Here you see iPS cells, islet cells, retinal pigmental epithelial cells, cardiomyocytes. And so our general take is, if you're a nonhuman primate, we've solved this problem. Unfortunately, none of us are, right? We're people. And so the most important step for us is to get this into humans and see really what happens. So to do that, the first place we're going is into allogeneic CAR T cells. And just to set the pattern, the table a little here, I think sometimes this is a marketplace that can be very confusing for people. It's lymphoma leukemia, multiple myeloma, and it feels like there are so many drugs that are coming after them. And it feels like with particular CAR T cells, maybe these problems are already solved. But what you see here on the left is if you look at just the U.S. and EU5, there are 250,000 people annually who are diagnosed with these diseases. There are 100,000 people a year that are still dying from these diseases. There are only mid-single-digit thousands of people that are treated with CAR T cells, and now there's only 30% to 40% benefit. So that little blue dot is the only thing that the market is currently satiated in. The rest of it is available for us to go out and hopefully transform the way these cancers are treated. And we know the problem with autologous CAR T cells. They're hard to make, right? They're hard to scale. Sometimes people fail in making them. And even when they get them, the majority of patients actually will relapse and will not have a durable complete response or cure. The allogeneic cells to date, they do work. People have made them. The challenge is that they have people -- we have not overcome immunologic rejection. The cells die quickly and the cancer recurs at a very, very high rate. And so we have to make these cells work really overcome the limits of CAR T persistence. And with that, we think we'll have really great efficacy. So we know the opportunity. We know the targets. We know the efficacy and safety bar. And so really, it's up to us to go forward and make this happen. So how do we do this? The first thing we do is we take just white blood cells from healthy donors. We choose them based on some immunologic criteria and other things. We then select out the T cells, and we modify the genome with our 3 gene edits we talked about. And that will prevent something called host versus graft disease, your cells trying to kill my T cells. We also have to make one other modification to the TCR alpha gene, and that will prevent my cells from trying to kill your body, something called graft-versus-host disease. And that provides a construct from which we make all of these allogeneic CAR T cells. We then can insert in different CARs, CD19, CD22 BCMA, GPRC5D. And with the first 3 of those, what we have chosen to do is we're taking forward clinically validated best-in-class CAR T cells. So I hope to convince you is if it works in one, it's going to work in 3, right? This is going to be relatively straightforward. And then we make them at scale, so we can make these cells in the hundreds of doses per batch. You translate that, that's going to be relatively straightforward we think, to be able to treat thousands or tens of thousands of patients annually. We make very high-quality CAR T cells, and we are off to the races. So the first question, really, when you're dealing with this is and you're making all these gene modifications of have I heard efficacy. In some way, have I made it so these cells don't work as well. And this is a mouse model that everybody uses in making the CD19 CAR T cells. It's called the Nalm6 model. And a little bit differently, we left the mouse and we put in a human immune system into these mice to see what would happen. So on the left-hand side, what you see is you put in the tumor and that it overwhelms the mouse, that the red is just cancer everywhere. In the middle, you see the unmodified cells on the right, you see our HIP-modified cells. Typically, people run these experiments for about 4 weeks. And what you see in the short term is there's no real difference between ourselves and regular CAR T cells. But what you see is you watch longer, and the unmodified cells are rejected as the cancer recurs in the unmodified cells and it doesn't in our cells. And then we did something that really has never been done before. We actually reinjected CAR T -- we reinjected tumor cells to you see what would happen. And you see in the bottom is that, that really does still -- they're still around, and they still kill the cancer cells. And that was something that when we presented this just about a month ago at the ASH meeting really kind of caught the eye of scientists and investigators in the field because we haven't seen it. So we're optimistic that these cells will work quite well. We filed the IND. We expect to see clinical data this year. And it's actually really straightforward, we think, to understand what we have. There is a direct correlation between CAR T cell persistence and the durable long-term complete responses. Hopefully, they'll turn into cures that patients receive. And we think you can figure this out really quickly with some data. If our cells last in a month, they're going to look like a lot of the other allogeneic CAR T cells today. That's really what the field is showing. If our cells last 2 to 3 months, you probably have a best-in-class allogeneic program. If the cells last 3 to 5 months, 3 to 6 months, we'll be comparable than anything you've seen from the autologous CAR T cells. If they last more than 6 months, there's a -- really we're optimistic we can be better than what the field is seeing today. And that's data we can generate in very short order. So we're quite excited to really understand what we have. And if we do, we're ready to move forward with this drug really rapidly in lymphoma and leukemia, CLL and ALL But we won't be done. If you look today, a number of patients who receive CD19 CAR T cells fail. And the market estimates are that in the next 5 years or so, about 12,000 people a year will be getting these CD19 CAR T cells. So about 35% of them will have a durable complete response and the others will relapse. So you're looking very shortly at a market of around 7,500 to 8,000 patients per year. And here, what we have chosen to do is move forward with a CD22 CAR to treat these patients. CD22 is another target that's overexpressed. That's expressed highly, I should say, on these B cell malignancies of lymphoma and leukemia. And all we're doing is swapping out that CD19 CAR and we're putting CD22 in here. And fortunately, we've licensed the CAR T cell -- the CAR that has been really utilized across the field and generated best-in-class data. So in the autologous setting, what you see is over 50% of patients who have failed a CD19 CAR T cell who have treated with a CD22 CAR are generating a long-term durable complete response or complete remission. We'll file that IND this year, like we have data next year for you. Hopefully, that corroborate that what we see in CD19 really pulls forward into CD22. We won't be done that either because I think because I think everybody recognizes the potential and power of targeting BCMA with autologous CAR T cells. And when we were at ASH having our meetings with clinicians in the field today, it was really exciting to see the data that's being generated with these drugs and CAR T cells are moving earlier and earlier into patient populations. Those are bigger and bigger market opportunities. Unfortunately, even today, what clinicians say is that for every 25 patients in their practice for whom they have a real need to give a CAR T cell, they're getting a slot for one. So even as access improves, that market will not be satiated for a long time. And what we have here is this is a CAR that again, in the autologous setting has generated at least as good a data as anything in the field. This is a 100-patient study. And what you see is, the best marker of long-term complete responses is MRD negativity, meaning you cannot find the cancer by the most sensitive genetic test. And 95% of patients are reaching MRD negative. This is in patients both who have received prior CAR T cells and those who haven't. And about 80% of them remain in MRD negative out a year. So we're really excited about the opportunity for this drug in myeloma as well. We've done a lot of preclinical work. We have only so much bandwidth. So this is an IND, we'll file next year. Hopefully, we have data coming not too distant after that. So really set up, we think, with the CD19, CD22, BCMA and beyond to build something. So what we have is we have validated targets, right? You've got validated CAR constructs. We're not building these things from scratch. We're taking things from the autologous setting. You have the opportunity to treat over 100,000 patients. You know exactly what we need to do. And we have a HIP platform or hypoimmune platform that's very well understood and validated in preclinical models. So now what we need to do is show that works in humans. Hopefully, we'll do that for you over the coming quarters. And then you unlock everything in that blue box on the right. And we move past that, we have the potential to move into lupus, where we're really excited by some data that's been generated in the field, in particular, in lupus nephritis and other -- we can go into other autoimmune disease and then solid tumors. So stay tuned. This is something that we think can be very powerful and really excited about. I'm going to switch tacks for a second and move to type 1 diabetes. Type 1 diabetes is a disease where the immune system attacks and destroys the pancreatic beta cells inside of a patient. The patient can no longer make insulin. And they are able now to be controlled with glucose -- sorry, they're now able to be controlled with endogenous insulin. Even with the best care, a type 1 diabetic will live about 15 years less than you and I will on average. And it's a very large unmet need with about 4 million patients between the U.S. and Europe. Their lives are really challenged, even within those -- when they do live with a number of issues like stroke, blindness, kidney failure. And our goal is really simple. So with a single treatment to allow patients to live in euglycemia, normal glucose, with no exogenous insulin or immunosuppression. That's the goal. So we know that transplanting pancreatic islet cells can cure patients with type 1 diabetes. It's been done a couple of times by others in the field from stem cells, but patients -- people have been doing this with primary islet cells derived from cadavers now for thousands of patients. Unfortunately, because you have to overcome the allogeneic rejection, the autoimmune rejection, patients get a lot of immunosuppression. And there aren't that many patients for whom lifelong substantial immunosuppression is better than lifelong insulin. But it does work. We know what works. So our goal on the right, what we will do is from a pluripotent stem cell, make the genetic -- the HIP modifications. We will then make those cells into pancreatic islet cells and transplant them in the patient with no immunosuppression and hopefully, protect them from both allogeneic and autoimmune rejection as well as return them to normal glycemia. So we showed you earlier nonhuman primates that we can overcome the allogeneic rejection with these cells. We're out 10 months-plus now in transplanting islets into nonhuman primates. So that's the allo side. There isn't -- hasn't been historically a great model of autoimmune rejection. But this is something where some of our capabilities came together to create a unique model. So we took a type 1 diabetic, got informed consent in their blood, took part of the blood and made it into a -- transplanted a humanized immune system into a mouse. So now you have a mouse who has a diabetic immune system that will attack its own islet cells. We then took some of the other blood cells and reprogrammed them back into pluripotent stem cells. We then gene-modified half of them with our hypoimmune edits, and we left the others alone. We then grew them into or differentiated them into islets and transplanted them into diabetic mice. So what you see on the right-hand side is it worked. So -- when you -- these are mice where we give them diabetes, they have a diabetic immune system, and we put in their islets derived from their own cells. Their immune system will very rapidly kill these cells. You see that within a matter of a few days, and the diabetes is not controlled. So this is an autoimmune model that really shows you how the immune system kills these cells. And our gene-modified cells, what you see is it also worked. So here, we transplant the cells. The cells live, survive, they thrive. And the animal's glucose comes under control, and they no longer have diabetes. So this is a model that's never been utilized before. We think it's about the best way we could preclinically test autoimmune rejection. So I feel really excited about how we've done preclinically in testing allogeneic and autoimmune rejections. So the next key is to get into humans. So we've never talked about this, but about a year ago, we started working on a way to do this. We told you that -- we talked a little bit about earlier that patients have been getting primary islet transplants for years. There have been thousands of patients who have gotten them. And so our -- what we've devised is a way to gene-modify these islets and hopefully transplant them into type 1 diabetics. So we'll do this very soon. We'll file for regulatory approval shortly. And our goal is to have data in 2023 that will help -- will allow us to understand, can we overcome autoimmune and allogeneic rejection? And it transforms a cure from -- for type 1 diabetes to something that we think about as being possible to something that's absolutely inevitable. That will be inevitable if this works. It's really straightforward, too. You see that cells will die within a matter of days if they're not gene-modified. And if we can do this, transplant cells with no immunosuppression and see them live and thrive. We'll know within a month if this is really working like we hope we do. So we're excited and this will give us insight into our ability to make SC451, which is stem cell-derived islets, as well as really help us understand how well our stem cell therapies broadly are going to work in overcoming immune rejection. So that's where we are. I talked a little bit about the hypoimmune platform today. We've got a couple of shots on goal this year to really understand exactly what we have in humans. If it does work, we'll be moving forward very rapidly with an allogeneic CAR T franchise in oncology as well as in autoimmune disorders. We'll understand what we have with stem cell-derived therapies, hopefully this year through type 1 diabetes and push forward. And we're going to come back and don't forget about the fusogen platform. This is something that, we think, is going to be really powerful over time. We absolutely aimed for cell-specific delivery of the gene modification reagents. And we think we can do gene-specific modification in a cell-specific way, and that will unlock a whole host of treatments across the field for, in particular, genetic disorders. So with that, you can take questions. I think some other people are joining me on stage.

Yes. Yes. Thanks, Steve. So I'd like to invite the rest of the Sana team up on stage with me, and we'll take a couple of questions. And just a reminder to just wave your hand at me if you have a question. So the IND for SC291 was filed. So what can you tell us about a potential Phase I trial design there? And will the trial allow for investigating the potential for redosing?

I'll take the last question, and I'll turn it over to Terry because the redosing question is easy. If we have to redose, it hasn't worked like we thought it will, right? We think that these cells will persist and they will be there to kill tumor until it is gone. I don't see any need to redose. So that really -- we'll cross the bridge of exactly what the design is. But you should know as you think about it, if we're redosing things haven't worked we thought they do. Terry, you want to take the kind of just what our Phase I trial design looks like, but maybe break it into Phase Ia, a little bit about Phase Ib?

Yes, sure. So the Phase Ia portion of the study is a fairly standard Phase Ia design, dose escalation with the goal of understanding safety. But we certainly expect at the doses that we're using, including really the first dose level that there's -- that we'll be able to look at biologic activity and certainly cell persistence. The diseases we'll go after will be CAR-naive patients will include lymphoma, but will also include CLL as an additional indication in the Phase Ia portion of the study. And then when we go beyond the Phase Ia once we establish the dose, then we'll look at multiple expansion cohorts to be able to understand efficacy better in preparation for the pivotal study.

Yes. So for those of you who don't know, Terry, Terry Fry runs our T Cell Therapeutics Group, formerly was a Head of Pediatric Hematology at the NCI. And the number of the CAR T cells that are in development and even one that's approved came out of Terry's labs. He's been doing this for a long time, and hopefully, it will be there to help us navigate it. We really do think that the key out of the Phase I studies, you're going to want to see complete responses. That's very clear because you want to see these cells work. And then you're going to want to see how long these cells persist because that will directly tell you, we believe, how -- what percentage of your patients are you really going to get to a durable complete response, which is the only thing that really matters, right? We're really not looking to make patients better for weeks. We're looking to make them better for years and years.

And I think, Steve, I think you had a slide on this in your presentation about kind of what the bars for success are on persistence. So maybe it makes sense because I know we get this question from time to time just to dig in a little bit there on what the bar for success is on persistence and then maybe on response rate.

So persistence we kind of laid out in the slide. So just a reminder, you can look at data across the field, and it's really transparent, I think, around what the expectations are and the implications. So if we have cellular persistence, it's less than 1 month, we're going to be like all the other allogeneic CAR T cell players. They are important. I'm not saying these are worth these drugs, but there is, we think, a too high of a rate of relapse. If we're able to beat that and be a couple of months, 2 to 3 months, we'll have a best-in-class allogeneic product. And if we're able to kind of get more towards 3 to 5 months, something like that, we really start to look like autologous CAR T cells. Because that's how long they're lasting. And we can do better than that, we'll do better in autologous. The reason we could do better is autologous CAR T cells do actually often generate an immune response. People recognize this. As the T cells recover and the immune system recovers, you will see that a number of patients develop a T cell response to the mouse in the CAR, in particular with CD19. And those CARs then disappear. And you see that when you try to redose patients. When patients are redosed with autologous cells, they have a very blunted early expansion. It's just the immune system. So if we are able to truly hide cells from the immune system, our goal is to be able to really take care of any CD19-positive tumor cell. Again, we still have a problem or a potential problem that some cells may stop expressing CD19. And then we'll just add our CD22.

Just as a segue from the CAR-T duration and persistence. So in the setting of an islet-cell transplant, you would need potentially indefinite or lifelong -- in the setting of islet cell transplantation, the duration there would need to be [ sensitively ] indefinite or lifelong, you couldn't redose or retreat. So how do you think about that 10-month nonhuman primate data?

Hopefully, 10 months will be longer. So a couple of things to know, right? One, you'll know if you've overcome this auto and allo rejection within a handful of days, right, or a handful of weeks. Then your question really gets at clinically how long would be really meaningful. And a couple of things that I'd say. First off, beta cells do die, right? So there's natural beta cell turnover in our pancreases every, call it, 4 years or so. And so we may need -- we may overcome that. That's kind of the idea of the whole islet coming in there, and we may have challenges. Our goal -- if -- I would say, if you can give -- treat patients once a year, it would be transformative, assuming that we have a cost of goods and a price point that's consistent with that. Our goal is not to do that. Our goal is to be able to give patients this once a decade, maybe once in life and really have them kind of not worry about needing to come to physician and monitoring their glucoses and getting insulin injections. So our goal would be it lasts for decades. Transformative would be a decade. I would argue that a year or 2 will -- if you had to take one injection every year or 2, it becomes our problem. But I think the patients would really like that. So even working on this for a long time...

I agree. I mean if I look from the solid organ transplantation field, for example, we do we transplant there as well. So I think it's acceptable to think about retransplantation if it's necessary from the islet biology perspective. From the immune perspective, that we are hiding the cells from the immune system, that should be stable. There shouldn't be anything that can break that because as long as we have the edits, we should be able to hide them. But the islet biology we can't control.

[indiscernible] subsequent transplant will be rejected [indiscernible]

That's the nice thing about the...

Can you please repeat the question. There are people who are listening. Yes, go ahead.

So your question was with our hypoimmune product, we would sensitize recipient and then couldn't retransplant. So the platform is based on an MHC class I class II knockout. And therefore, you're not sensitizing against those molecules anymore. That's the biggest issue in transplant medicine that we sensitized against the MHC molecules. But our product is a knockout, so there is no sensitization.

And maybe just to give you just a little data, we didn't take this -- we have the date we took it out of this. So one of the things we have -- we've done a couple of things in these nonhuman primates to really get at this question. One, we showed you we transplanted hypoimmune cells and wild-type cells. We then follow them. And in the other leg, in the wild-type side, we then -- we've seen that they have a robust B and T cell response to those cells. In the other leg, we then injected our hypoimmune cells, and they were not recognized at all, and they continue to live and thrive. In the monkeys that had -- nonhuman primates that had the hypoimmune cells, after a few weeks, we actually injected wild-type cells into the leg. And we saw, again, a very robust immune response that eliminated those cells, but that B and T cell response eliminating the wild-type cell left ourselves alone, and they continue to live and thrive. So we've tried to test that notion in nonhuman primates and feel good that we are not sensitizing these patients and that we can redose them. That's where we can -- particularly to your question, we can redose them if we need to. And that we can also really hopefully -- it was the first time we started to get very excited about overcoming autoimmune disorders because with a preexisting immune response to that cell, we did not see any evidence of immune rejection.