Okay, good morning. I'm Eric Joseph, Senior Biotech Analyst with JP Morgan. Our next presenting company is Lyell Immunopharma, and presenting on behalf of the company is CEO, Lynn Seely. There will be a Q&A after the presentation. Just raise your hand, we'll get a mic over to you. For folks tuning in via webcast, feel free to submit questions via the portal. So with that, Lynn, thanks for joining us.
Well, welcome everyone, and thank you to Eric and JP Morgan for inviting us. Lyell Immunopharma is a company focused on enhancing the extraordinary T- cell to develop novel cancer therapies for patients with solid tumors. I will be making forward-looking statements during this presentation, so see our disclosures and our securities filings and websites for additional information. Simply put, people with cancer need better therapies. I think we're all aware that T-cell therapies have been approved for and are benefiting patients with hematologic malignancies. But the fact of the matter is, more than 90% of cancers result from solid tumors, cancers which progress rapidly and in fact, become metastatic. And once a patient has a metastatic diagnosis, they live on average less thant three years. This is where the major problem lies, and this is where Lyell is focused.
We are developing transformative, individualized therapies, taking advantage of the extraordinary patient's own immune system. We're advancing T- cell therapies for solid tumors, two types of T-cell therapies. We have a CAR T-cell therapy program, as well as a tumor infiltrating lymphocyte or TIL program. So I want to walk through these. Each of our product candidates are wholly owned and addressing large patient populations. Our first and lead program in the clinic is LYL797. This is a ROR1-targeted CAR T- cell, currently enrolling patients with triple-negative breast cancer and non-small cell lung cancer. We expect to present data from at least 20 patients in the first half of this year, both clinical and translational data. We are also advancing our Epi-R, epigenetically reprogramming, reprogrammed TIL program in patients with advanced melanoma.
We have recently gotten orphan drug designation for this indication, and we'll also be expanding into non-small cell lung cancer and colorectal cancer. Here, we expect to present data from this clinical trial in the second half of 2024. Our scientists continue to innovate, and we're advancing a third program into the clinic this year, LYL119, which is a ROR1-targeted therapy, which incorporates all four of our genetic and epigenetic reprogramming technologies. Here, we expect to file the IND in the first half of 2024. We're very proud of the scientific expertise at Lyell, and we have developed multiple genetic and epigenetic reprogramming technologies, all geared to getting the T-cell function right, and I look forward to describing those to you in some detail today.
And of course, I would be remiss if I didn't mention that Lyell has a strong balance sheet with approximately $600 million in cash, enabling us to get through runway into 2027 and multiple clinical readouts, as well as continuing to invest in our new innovative technologies. Well, at Lyell, it's all about the cells. We believe, of course, that the target is important, but even more important is getting T-cell function right. And so we're generating T-cells that resist exhaustion and have durable stemness. Why? Because we believe these are the two key primary barriers that are preventing CAR T-cells and T-cell therapies to have the same success in solid tumors that we've seen in hematologic malignancies.
So let me walk through some of what I'm talking about, the two key primary barriers to successful cell therapies: T-cell exhaustion and lack of durable stemness. This illustration here really takes advantage of an accumulating body of both clinical and scientific evidence, talking about why cell therapies have not been as successful as we might have hoped for to date in solid tumors. As T-cells are infused into patients and encounter the very hostile tumor microenvironment seen in the lower bottom of this slide, they get exposed to repeated chronic antigen stimulation, which drive them down the path of exhaustion, ultimately rendering them dysfunctional and ineffective at killing cancer cells. So that's one key barrier. A second key barrier that you see at the top is this lack of durable stemness.
As T-cells go through the manufacturing process and are expanded, they become quite differentiated in the standard case. As these differentiated cells have to proliferate in vivo, they become even more differentiated, and they lack the durable stemness or this ability to self-renew, and so ultimately, don't have the persistence that we need to see success in solid tumors. At Lyell, we are busy developing new technologies to overcome these barriers. Currently, we have four reprogramming technologies in our clinical program or in our near-term clinical program.
Each of these are backed by strong intellectual property, and they really are encompassing both two genetic reprogramming technologies, taking advantage of viral transduction or gene editing, and then also epigenetic reprogramming that we use in our manufacturing protocols, really to alter the transcriptome, to influence gene expression without altering the underlying DNA sequence.... And so I want to talk about these in some detail, and I want to emphasize that these data have been published behind these technologies by Lyell scientists in top-tier peer-reviewed journals, including Science, Nature, and Nature Biotechnology. So our first technology is c-Jun overexpression.
This is being incorporated into our lead clinical program, and it comes out of work at Crystal Mackall's lab at Stanford, where we really began to understand that one of the key problems in T-cell exhaustion over time is with the AP-1 transcription factor pathway, and that we lose function in this pathway because of a decreasing in function of c-Jun. And so what we have done is, and what she showed in her work, and Rachel Lynn, who's a research director at Lyell, published in Nature, was that if you overexpress c-Jun, you can reverse this T-cell exhaustion. And so that's our number one technology. But the science has continued to advance, and we also now know that the NR4A family of proteins is a negative regulator of that pathway, in essence, puts the brakes on.
And so what we're doing now is knocking out NR4A3 as a complementary technology, and what that does is it makes the gene, AP-1, become more accessible, and it's yet another way to increase activation of the AP-1 transcription factor pathway, generating an even more powerful cells able to resist exhaustion. On the epigenetic reprogramming side, we have our Epi-R technology. This is incorporated in each of our clinical programs and is really developed to help the cells have this durable stemness that I've been talking about, this ability to self-renew. We recruited scientists from the National Cancer Institute and their TIL program, and they've helped us develop this proprietary Epi-R technology, which develops T-cells which have the right stemness, stem-like phenotype, so that they can persist and have that ability to self-renew in the patients, giving us the durability that we hope for.
Then finally, we have a novel way of activating T-cells. We call it Stim-R. These are lipid-coated silica micro rods, which are used to really control the duration, the intensity, the signaling that we use, to help our T-cells expand in manufacturing in a much more natural and physiological way than has been seen before. And it gives us really potency and characteristics that we haven't seen before. So very excited about each of these technologies. And this slide really tells you how we're incorporating them in this stackable way across our portfolio. We have two CAR T-cell programs in our pipeline and two TIL programs. You can see here our lead program, LYL797.
It's a ROR1-targeted CAR T-cell program, incorporates our c-Jun overexpression and Epi-R technology, and this trial is enrolling patients with triple-negative breast cancer and non-small cell lung cancer. Of course, there are other tumor types that express ROR1 that are possible as well. We have guided that we'll be presenting initial clinical data from this trial in at least 20 patients in the first half of this year. Coming soon is LYL119. This is the new CAR T-cell program, also using ROR1 as the target, which incorporates all four of our technologies, and we intend to submit the IND in the first half of this year. LYL845 is our TIL program, and here we have an ongoing phase I program. We're enrolling patients with advanced melanoma.
As I said, we have orphan drug designation for that indication, and we will also be expanding to colorectal cancer and non-small cell lung cancer. Here we intend to present initial clinical data from this trial in the second half of 2024. So a big year for clinical readouts. Then we have a second-generation TIL program, which we won't have time to talk about today, but which has both genetic and epigenetic reprogramming. Well, let's dive now a little bit more into the details, and we want to focus first on LYL797. Let me start by talking a bit about the target ROR1. ROR1 is expressed in a large number of solid tumors, including triple-negative breast cancer and non-small cell lung cancer. It is a target that's used by others, antibody drug conjugates.
It's been in the clinic in a study done at Fred Hutch, looking at hematologic malignancies as well as solid tumors. And to date, there hasn't been reported any significant on-target, off-tumor toxicity, including in non-human primate toxicity studies. So we believe it's a good target. What you can see here are data that we've had in our screening for our programs with our assay and our antibody. And what you can see is our data match very nicely what's in the literature, that about 50% of patients with triple-negative breast cancer are ROR1 positive and about a third of patients with non-small cell lung cancer. And ROR1 positivity, in general, has a tendency to correlate with a poor prognosis.
So this is an illustration of our program, again, taking advantage of the c-Jun overexpression and the Epi-R technologies, and you see the ROR1 CAR on our CAR T-cells in this program. And what are the key differentiators of this program? I'm gonna show you some data, but typically what we see with these reprogramming technologies is CAR T-cells that can provide great tumor reduction, enhance cytokine production, and tumor infiltration in a very aggressive non-small cell lung cancer syngeneic model with our overexpressing c-Jun ROR1 CAR T-cells. We get consistently with our Epi-R technology the stem-like phenotype that they're looking for—what we're looking for, bringing that durability and enhanced cytotoxicity.
And then when we bring it all together, combining these complementary technologies, we see really nice data in a xenograft non-small cell lung cancer model, which I'll show you. Let's start with this first, with this syngeneic non-small cell lung cancer model. It's a KP mouse model, quite aggressive. What we do is we use turn-on oncogenic driver mutations, mutant KRAS and p53, to really recapitulate human-like non-small cell lung cancer. We get multifocal tumors in the lungs of these mice, and it's in the setting of a hostile tumor microenvironment, which is unusual. Most people study animal models without that type of a microenvironment. And so we think this is a really strong test of our technology, and it's very well known that in this model, tumor regression is quite unusual. It doesn't respond well to chemotherapy or to checkpoint inhibitors.
But what we see with our ROR1 overexpressing c-Jun CAR T-cells is something quite, different. What you see here is, first in the left-hand panel, high levels of interferon gamma, indicative of enhanced intratumoral function. So our CAR T-cells are killing cancer cells in the tumor. We then see enhanced infiltration, and what a lot of people don't appreciate is that if you can get T-cells to resist exhaustion, they can infiltrate better, and that's one of our goals in solid tumors, and this is really shown nicely here in this slide. And then finally, we see tumor control in about 50% of the mice. Again, something that would be quite remarkable if it could be replicated, in the clinic. And so this is a really tough challenge, and we think our LYL797 really rose to the occasion.
Here you see a more standard xenograft non-small cell lung cancer model, where we're looking at LYL797's ability to reduce tumor burden. You can see at about 5 million CAR T-cells, that we very nicely are able to gain tumor control, and both shown here at a high and a lower dose. This, in turn, correlates with prolonged survival in these animals. So again, very robust data to underpin our LYL797 clinical program, and we're very much looking forward to bringing data in the first half of this year. Just to remind you of the clinical trial design, there are, it's a dose escalation trial with 4 dose levels, followed by dose expansion, both in triple-negative breast cancer and non-small cell lung cancer.
These are relapsed refractory patients, both in both indications, and they are ROR1 positive. The study objectives are standard: patient safety and tolerability, overall response rate, of course, durability, as much as we're able to achieve, and then we will be looking at a robust translational program as well. So now let's move to LYL119, which is our next generation program, incorporating all four of our technologies. We really believe this represents a step change in what we're able to do to fight T-cell exhaustion and to deliver more potent T-cells, more able to kill. We do this by incorporating not only c-Jun and Epi-R technologies, but NR4A3 and Stim-R. I wanted to spend just a moment talking about our new Stim-R technology because we believe it's quite a breakthrough in T-cell activation.
People have been activating T-cells for decades in a very similar way. But scientists and I would like to point out this technology is published in Nature Biotechnology by lead author, Dr. Alex Cheung, who's a research director at Lyell, have really developed a novel way to activate T-cells in a much more physiological way. And you can see here in the top panel, the way antigens are naturally presented to T-cells. And now with Stim-R, which are essentially lipid-coated, mesoporous silica micro rods, we can give the structure and with this lipid-coated membrane, the ability to activate T-cells more naturally and to control, in a very fine-tuned way, the way we present signaling molecules to the T-cell. And consistently, we get really nice activity from our T-cells with this way of activating them.
So let me show you some data to back that up. I want to—this is a xenograft model, quite similar to the one that I showed you before. Here I want you to know, when we're looking at our ability to control tumor, look at the doses here. At 1 million CAR T-cells, we can really totally control tumor growth, eliminate the tumors, in fact. Our scientists were so impressed with that, they then went to an even lower dose, 100,000 CAR T-cells. You see here, again, great potency. It's not just the ability to kill, but look at the in vivo expansion. Really superior expansion using all four of these technologies together, and that's a log scale you're looking at. So this is not a trivial increase in expansion.
And this correlates very nicely with the prolongation and overall survival. So we're really excited to get this program into the clinic. And so now let's spend a few minutes on our other program, our Tumor Infiltrating Lymphocyte program. As you know, in these programs, we harvest the patient's cancer sample, we send it to our Lyell manufacturing facility, and expand the tumor-infiltrating lymphocytes in the cancer specimen into billions of cells, which we then give back to the patients. And what we do is we use our very special Epi-R reprogramming technology during the expansion phase. And this really is what our key differentiator is, this Epi-R technology, and it allows us not only to robustly produce TIL in advanced melanoma, but also in other cold tumors, non-small cell lung cancer, and even colorectal cancer.
And we can do that generating the right phenotype, cells that have the right durable stemness and, and cytotoxicity. And we know what those right phenotypes are from data and clinical data in the literature showing which patients have previously responded well to melanoma. Importantly, we don't just make a lot of cells, we make cells with the right polyclonality, because that really is the power of TIL. And you need to preserve the polyclonality of the tumor-reactive cells as you expand them to get the best effect, and I'm gonna show you some data on that. And then finally, I'm gonna show you some data from a novel in vivo model we've developed for TIL. So first, a moment about our Epi-R technology. Some people are a little bit confused about exactly what this is. This is a protocol we use in manufacturing.
It consists of proprietary media, the optimized cytocomposition, cytokine composition that we use to expand our cells, and a really well-defined activation and expansion protocol. And what you can see here is it's quite distinct from the standard method that was developed at the National Cancer Institute, which is depicted on the bottom here, which, as the cells are expanded and differentiated, they tend to become predominantly short-lived effector cells. They're ready to kill, but they don't necessarily have the ability to persist as we might like. We've specifically developed our protocol to enable a nice mix of cells. Yes, we have some differentiated effector cells ready to kill, but also many more of the purple cells that you see represented here as the longer-lived cells with the ability to self-renew and persist. And so let me show you some data to back up those statements.
This is a really elegant experiment showing transcriptomic data from TIL generated from 5 donors using either standard or our Lyell Epi-R, our Lyell 845 Epi-R process. And really, these consist of data from 4 melanoma and 1 non-small cell lung cancer patient. And what you see is on the left-hand side, you see a Lyell 845 in teal, and what you can see that the TIL here is sort of clustered up in the upper right-hand corner of this U map. And what that tells you is this is an area where TIL express genes associated with a stem-like phenotype, and you can see this very specifically in the bottom panels, where we show TCF7 and cell or CD62L. Again, you see this clustering in the upper right-hand corner.
That's very distinct from what you see in gold, which is TIL made with a standard prep. And there, the clustering really comes in the lower right-hand corner, where you see genes associated more with exhaustion, and that you can see down in the bottom panel, looking very specifically at TIGIT or PD-1. And so I think this is very strong data, again, suggesting that our TIL have a very defined phenotype, which is what we believe is gonna be necessary for good clinical outcomes. And we know this from the literature, and patients with advanced melanoma have been published in a paper in Science, where they looked retrospectively at the cell phenotype that was associated with clinical responses. And what they've shown is that you wanna see, of course, CD8 positive effector cells, but you also wanna see cells with stem-like features.
What we've done here is to show you the difference between our cells in teal and standard prep cells in gray. Each of these dots represents an individual donor sample that was sort of split. What you can see here is the nice increase in percentage of CD8 effector cells, and very importantly, an increase in CD27 positive T-cells, as well as the very important double negative, or CD39, CD69 double negative T-cells. This is the phenotype that we believe is important and that we, our Epi-R technology has really been designed to achieve. What about polyclonality, right? You've got to generate cell numbers, you wanna have the right phenotype, but you also need to preserve polyclonality.
So our scientists did a very interesting set of experiments where we took malignant tumor tissues, and we used very sophisticated bioinformatics and computational biology to look at the high-frequency clones and the exhausted clones, because what we know from the literature is the intersection between those two is where the predicted tumor-reactive clones are, right? That makes sense, because those are the ones that are the, the clones that are present in high frequency and are exhausted from fighting the cancer. Then we looked at our clinical scale product, and you see here representing 9 donors, mostly melanoma, but some non-small cell lung cancer and colorectal cancer. We wanted to see what percentage of the predicted tumor-reactive clones were present in that clinical scale material. Here you see the range, 88%-100%.
So we were very pleased with this result, and we think, again, is very, very promising. And then finally, we worked very hard to develop an in vivo model for TIL, and this is an example where we can use melanoma tumor-bearing mice to look at the difference between the standard TIL prep and our LYL845 TIL prep. And so what we did is we took two refractory melanoma patient donor samples. We split them into two. We made TIL from either LYL845 done in TIL or in the standard prep. And what you see on the graph on the right is the tumor growth, with no TIL at the top, with 4 million standard TIL, and then with the LYL845 TIL, 4 million, completely eliminating tumor growth.
So very robust data, which gives us great excitement about our clinical program. We look forward to bringing data to you in the second half of this year, the initial data from this program. You can see here that we are treating patients with advanced melanoma. We will also expand out into LYL845, non-small cell lung cancer, as well as colorectal cancer. We're looking at relapsed refractory patients, of course, and you can see that safety and tolerability and overall response rate will be the key study objectives. And let me just sort of begin to close by acknowledging that manufacturing is critical. We can talk about a lot about science and clinical data, but we all know the manufacturing strategy is absolutely critical.
We're very fortunate to have our own internal manufacturing center, where we make our phase 1 clinical supply. We have capacity and capability, both for CAR and TIL, as well as making our own viral vector. But we are also planning for the future, and we want to have a scalable manufacturing process for down the road, and we have partnered with Cellares to do proof of concept and to develop the technology for an automated TIL process. And they have a Cell Shuttle , which can make up to 800 doses of our LYL797 product a year. So something that we're, we're working hard on.
And so let me close by saying I hope I have convinced you of why we're excited about the clinical data that will be coming out this year, the preclinical, robust preclinical data that underpin these programs and the novel innovative technologies. And would like to just close by saying we believe Lyell is well-positioned to deliver on the promise of cell therapy for solid tumors. Thank you. And why don't I bring up Gary Lee, our Chief Scientific Officer, and Charlie Newton, our CFO, and we'll take some questions.
Great. Well, thanks, Lynn. Yeah, I can start out. I mean, so, you know, I'm sure the focus both internally and externally is gonna be on the first data readout with LYL797 in the first half year. Maybe just, you know, you set the stage a little bit in terms of patient numbers. I guess, how can you sort of round that out a little bit in terms of what to expect in terms of the balance of histologies between lung and triple-negative breast cancer, and, you know, how to think about the, you know, where patients are in their treatment journey, I guess, you know, number of prior lines of treatment?
Sure. So we began the dose escalation in triple-negative breast cancer patients, so the majority of patients we'll be seeing will have triple-negative breast cancer. All the patients in these trials, as you might imagine, are quite relapsed refractory patients, have failed multiple lines of therapy, so they are quite sick.
Okay. And just in terms of the type of data that you expect to present, you know, in addition to, you know, safety, I guess, can you just talk a little about what to anticipate in terms of efficacy and what you would view as a promising or compelling efficacy signal?
Sure. So these are, as I just mentioned, relapsed refractory patients. We will be looking at safety, but also overall response rate, which I think is what the field is looking for. We, quite frankly, are looking for data that can get the drug approved, and the bar is very low in these patients. It would be 25%-30% overall response rate with durability in the 4-5-month range. Of course, anything better than that is fantastic, but I like to point to this bar for approval because that then gives us the opportunity to move to even earlier lines, and I think everybody believes cell therapies, you know, yes, we need them to work in late line, but the earlier we can move them, the more likely they are to have greater benefit.
So I think that that's what you can expect to see.
You made a comment earlier in the presentation about sort of the anticipated safety profile or therapeutic window in targeting ROR1, and that, you know, to date, there haven't been any on target off-tumor toxicity events observed. Was that a comment about observations in your trial, or is that for the field more broadly? And maybe just kinda speak to perhaps the level of ROR1 expression, I guess, on a target tumor cell that allows for that discrimination or a well-tolerated activity profile.
... Yeah. Well, first and foremost, when I made that comment, I was referring sort of to the field at large, and I think this is something that, ROR1 CAR T-cells have been explored in a clinical trial at the Fred Hutch, and so I think data, come from that trial. There are others who are developing antibody drug conjugate. Merck has a program in the clinic, as we speak, that's moving forward in hematologic malignancies and, solid tumors as well. And then there's also been a published, non-human primate, study, toxicity study, looking at this. What I would say is, with respect to what level of ROR1 expression, this is something, again, we are learning more about as we run our clinical trial.
We're using a cutoff of 10% ROR1 positivity in our clinical trial, and then, of course, we'll learn very specifically about that over time.
Can you talk a little bit about manufacturing? Well, really, I guess there's two components here, right? When it comes to manufacturing, then kind of matriculating into treating a patient, right? Successful manufacturing a product, and secondarily, you know, call it vein to vein time, I suppose, to make sure that you're getting product to patient in a time where they're fit enough to receive it, benefit from it. Can you talk about sort of your success rate in the clinical trial that speaks to both of those parameters?
So we're not talking about data specifically from our clinical trial today, but what I can tell you is we're working very hard to reduce the time, particularly for our TIL program, and we've said publicly that we're introducing a new process in our TIL program this year, which will reduce the manufacturing time to 21 days. So that's a substantial decrease from the standard, and I think it's something that, again, we've worked very hard on. Our CAR T standard time is consistent with others at this point.
Okay. All right. Got a question here submitted via the portal, kind of, asking you to elaborate on, assess the competitive landscape. What do you think of the Oncternal ROR1 readout, or at least their, their asset? I guess, I believe they have both a CAR T program and an ADC as well, targeting ROR1.
Yeah. So I think, Oncternal put out some data at the very end of the year. They did report a patient death from ICANS and CRS. They are studying hematologic malignancies and reported some partial responses, I believe, or some responses in their patients. I think maybe the question is alluding to, do we think there's any read-through to our program? And I think, you know, Gary can comment further, but I think we know that our construct is different from theirs, and at this point, we don't see any read-through from their program to our program.
Yeah, I think I agree with what Lynn said. I think it's important to note that I think there's now continuing evidence to suggest that ROR1 can be an appropriate target in the heme malignancy case. Certainly, ICANS and CRS is a fundamental clinical challenge that any CAR T deals with in heme malignancy. We will have to learn more to see exactly what happened in this particular case, but I think there's continuing evidence to suggest that ROR1 is a good target in heme malignancy, for sure, and we believe potentially in solid tumor as well.
As you're looking to iterate on top of 797 with 119, I guess if we're fast-forwarding to when you sort of, you know, have evaluated it in the clinic, I guess first question really is whether, whether, putting 119 into the clinic might be kind of conditional on sort of the activity you're seeing of 797, that would justify sort of the parallel investment. And then ultimately, you know, if you do go forward with that, sort of, you know, how much of a difference in clinical benefit do you think would justify sort of promoting that?
Yeah.
Yeah.
Perhaps-
Yeah, yeah.
No, it's-
Prioritizing one or the other.
It's a great question, and I want to sort of address that, and certainly happy for Gary and others to add on here. I think we are doubling down on ROR1 as the target. Why? Because we actually are interested in getting T-cell function right. We believe that once we get the T-cell function right, then our platform basically can be used across targets, right? Across TIL, across TCR, across CAR T. And so getting the T-cell function right is really the fundamental problem in getting T-cell therapies to work for solid tumors. And so we've moved forward. LYL797 with c-Jun overexpression and Epi-R, we're very enthusiastic about that program. But our scientists continue to innovate, and we're looking for that next step change.
What you can see is our scientists interrogate our products very robustly in the preclinical world, and not just the technologies that I showed you, many others, and they've selected these as the next step change to test T-cell function. So, yes, we want to lead, and then we want to continue to be the leader in this space, and that means we have to continue to innovate and get really the optimal T-cell function out of these cells. So I think that's what we're doing. We're data-driven. We're gonna make data-driven decisions as the data continue to accumulate. But right now, there are a lot of ROR1 positive tumors, and that we think these two programs give us great optionality.
As I said before, these technologies, as we prove their potential, can be used in a variety of different programs. Gary, anything you or Charlie want to add to that?
Yeah, I think on top of that, as Lynn mentioned, there are many different tumor types that are ROR1 positive, including ones that are particularly more challenging, such as pancreatic cancer. So we believe that there's opportunity to execute both programs, potentially targeting a different indication as a path forward as well.
Okay, great. Maybe just a final question on 845. You know, the heightened or higher polyclonality of your product versus other TIL programs being a key feature, is it—Do you kind of see uniform potential to get a high polyclonal product independent of histology? You have a lot of data in melanoma.
Mm-hmm.
Is that also supported in non-small cell lung cancer, colorectal, other indications where you see it?
Sure. Gary, do you want to take that?
Yeah, so we continue to develop a body of evidence to support that. So far in the analysis that we've done across different tumor types, with our TIL program, we do continue to see a high level retention of the tumor-reactive clones, as well as the stemness feature, which is a consistent features that we develop in our program.
Okay. All right. Well, I think we'll leave it there. Let me just see if there are any questions from the room. All right. I think we'll leave it there for time. So thanks so much to the Lyell team, thanks for joining us.
Thank you for having us.