Great, good morning, everyone. My name's Jess Fye. I'm a senior biotech analyst at JP Morgan, and we're continuing the 42nd annual Healthcare Conference today with Immunocore. I'm joined on stage by the company's CEO, Bahija Jallal. She's gonna give a presentation on the business, and then we're gonna go into Q&A. If you have a question in the room, you can raise your hand, and someone will bring you a microphone, or you can submit questions via the portal. So with that, let me pass it over to Bahija.
All right. Good morning, everyone. Thank you, Jess, for having us. I would like to start with a patient story. You know, a few days ago, we met this very vibrant CEO. She was diagnosed seven years before with uveal melanoma, metastatic uveal melanoma. Her doctor said, "You know, and only a few months to your daughter's graduation, but actually, you're not gonna make it to that graduation." She enrolled into KIMMTRAK, and she lived seven years to tell her story. This is always, that reminds me why we come to work every day and what a privilege to be doing what we do. So let's get started. This is our forward-looking statements. Our aim is to bring immunomodulating medicines to patients by pioneering the modality, a new therapeutic modality, an off-the-shelf, bispecific soluble T-cell receptor.
In the last five years, we transformed the company from an R&D company to a fully integrated biotechnology company that brings value to patients and to shareholders. A company that saw the first ever TCR to be approved in solid tumor with OS as an endpoint. The first ever, product to be approved in uveal melanoma after four decades where nothing has worked in this indication. We have the industry-leading TCR pipeline spanning three therapeutic areas, and our, innovation engine in the research continues to bring novel targets and expand on our technology. We are also revenue-generating company, but even with that, we continue a very careful, capital allocation and watching our expenses. So how we did all that is really focusing on three strategic priorities. The first one is to maximize the potential of KIMMTRAK.
We believe there is still growth in KIMMTRAK, and I'll share with you how we can expand even more. The second is to focus on advancing the clinical portfolio, and we announced the first phase III PRISM that I will share as well. The third thing is to continue and really have a sustainable pipeline by bringing and encouraging more innovation coming from our laboratories. Today, I will, I'm really happy actually to bring you a new, or showing how our we can push the boundaries of science and our technology to get into autoimmune diseases. I'm gonna talk about each one of these, pillars, and I'm gonna go through what have we achieved in 2023, in 2023, and what we will be, doing in 2024. So first, let's start with KIMMTRAK.
So today, you know, thanks to really an amazing job done by our commercial organization, it will go in history as one of the best, you know, launch in a biotech, and I'm very proud of that. In less than two years, we are already approved in 38 countries. We are reimbursed and launched in 10 countries and looking at a growth, QoQ growth, that culminated this year in three, just from Q1 - Q3, to $160 million, and still going. And KIMMTRAK, we believe, can help even more patients. So we have announced the first phase II/III trial in cutaneous melanoma. This trial is enrolling very well, and we should be expecting to have a top-line data by Q4 2024.
The second trial that we announced only six weeks ago is the adjuvant trial, and that's basically focusing on the patients that are more at risk of developing or highest risk of developing metastasis after the first tumor is removed. And so we are really happy that we collaborate now with the EORTC. It's a European organization that has done the last 14-16 trials and in adjuvant trials in melanoma. So very happy about that, and we are anticipating to start the randomization, or they start the randomization in the second half of 2024. So to actually summarize where we see KIMMTRAK and the opportunity, we see, you know, today, still growth definitely in the U.S. and outside of the U.S. We are at 1,000 patients.
If we add then the cutaneous melanoma and also the adjuvant, we can go from 1,000 patients to all the way to 5,000-6,000 patients. So really a big opportunity, and most importantly, even more patients to be helped by this fantastic drug. So the second thing is the clinical portfolio, and I'll start with PRAME. So why we believe PRAME is an exciting target? So PRAME is expressed in multiple tumors. It's a negative prognostic marker. We like that because the, you know, tumors don't like to get rid of it, if you will. And we have shown in ESMO last year that in phase I, we've seen signal in multiple tumors. And you can see the number of patients, like a really wider patient population that can be treated with PRAME.
We spent 2023, a big portion of that, to really interrogate that monotherapy and do expansion in multiple tumors, in ovarian, non-small cell lung, endometrial, and so on, to address the monotherapy activity. At the same time, we expanded the footprint for these trials and for the combination trials, combinations with multiple chemos, with checkpoint inhibitors, and so on. And the first what came from that expansion, the first is what we announced, is the PRISM-MEL, which is the first phase III in cutaneous melanoma. So for this trial, we announced in July, and I'm really proud of the clinical organization because already in December, we initiated the first site, and we intend to have to randomize the first patients in Q1 2024. There is more to come from PRAME.
We decided early on to build the franchise around this important target. So we had two molecules that we announced last year. One of with the half-life extension that we believe we would like to test for patient convenience, and the PRAME-A24, which is another allele that's not only, you know, present in the West, but also dominant in Asia. So these two molecules, the IND was filed, will be filed in 2024. So we're on track for that. Then I move to the HIV. So in the HIV, we showed in the beginning of the year, last year in 2023, the single ascending dose, and we started then the multiple ascending dose. And as you know, the goal there is to look at for functional cure.
But I would like to go through what are the data. We are on track. It's unrolling really well, and we expect the data by the second half of 2024. I would like to just emphasize and go with you through the sets of data that we expect from this trial. So as you know, the first portion of the trial that's gonna have also the data that's really important is where we put the antiretroviral and ImmTAV on top of the antiretroviral. And so there, we're asking the question: you know, "Can we touch the reservoir?" You know, the reservoir that stays even on the presence in the antiretroviral is the reason why these patients have to take medicines all their life. They can't stop because otherwise you get the viral rebound.
So this is really important. Are we gonna bring that to 50% or 100%? We don't know, because nobody has done it before to really have an impact on the reservoir. So on itself, that's gonna be an important question to answer. And on the second part of the trial, that's very, very important, is to answer the question: if we bring the reservoir to 50% or 100%, what does it translate to? You know, do we see a delay in viral rebound? Do we see a complete, you know, inhibition of the viral rebound? And so these two sets of data are gonna be really important, and we will be sharing that with you in the second half of 2024. Then the last point is, you know, really that continuing that innovation and bringing more.
This is a lot of efforts that went into looking at targets and other things. But today, it is something really close to my heart, is bringing the first autoimmune targets as well. So let's start with the first PIWIL1. So PIWIL1 came from our efforts. We have what we call the ImmTAX. That's years of efforts of looking at, you know, targets that are expressed only in tumors or in tissues and things like that. So PIWIL1 is the first in class. We like these targets for, you know, you'll see this, there are some things that are in common with PRAME. It's. When it's expressed, it's homogeneously expressed.
It's also a negative prognostic marker in multiple cancers, and it's expressed in CRC, which is really important because CRC has historically been insensitive to IO. So we announced that last year, and we said we'll file the CTA, and that's exactly what we've done. We've filed the CTA in December, and we believe we are on track actually to having the phase I start in Q3 2024. So now to something really exciting, at least for me, is the autoimmune. So here, the concept is you know, how can we go from systemic immune suppression to down-modulation of the immune system in a very specific and tissue specific? You know, because we know inflammation happens in certain tissues.
So how we do that, I'll just walk you through that. So we take the tissue of interest that's inflamed, and we mapped actually what are the targets that are expressed only in that tissue. So we know how to do that, so we'll have the peptide. We know how to make a TCR against that peptide. That's what we've done. And then on the effector side, here is a PD-1 agonist. This is a nanobody for PD-1 agonist. So this is the yin and yang from cancer. You know, in cancer, we wanna take the foot off the brake. Here, we wanna go all the way to really stimulate this inhibitory receptor, that then reduces the T cell activation and hopefully drives them to exhaustion.
So the first application was in β-cells in Type 1 diabetes. We know that β-cells are, you know, basically killed by the autoreactive T cell, to the point where the disease progresses, you have to provide insulin. And so we identified a very, very good peptide from preproinsulin that's extremely highly expressed in β-cells . We have shown that it's actually it binds only when we do the clinical candidate, it binds completely just to the β-cells . You see it in the red there. We've done a lot of experiments to convince ourselves that it's doing what it's supposed to do. It localizes where it needs to localize into the synapses. And this is just one representative of the...
Ultimately, what we saw is that basically in the purple, when you put β-cells with autoreactive T cells, you can see it, basically, there is a killing, there are no growth. But if you add the ImmTAAI, that's the molecule, if you add the ImmTAAI to the β-cells plus autoreactive T cells, you actually rescue these β-cells , and you can see it's going all the way as dose-dependent. So really, really excited about that. This is a program that now is going into GMP, CMC. The second is taking another tissue, which is the skin. And we know in the skin, this is basically the antigen, the APCs are the culprit in the skin for the skin inflammation. So we have identified a target we have not disclosed.
It is a universal target, unlike what I just showed you, that's HLA-A2 positive restriction. This is a universal, our first one. This is antigen, so it's expressed on antigen-presenting cells and inhibits the autoreactive T cells on the skin. So we, again, we can see the localization, we can see the inhibition. We've done a lot of experiments there. And suffice to say that the opportunity could be really huge here because you have anything that's inflamed in the skin, atopic dermatitis, psoriasis, you know, scleroderma, other things as well. So this is also starting the GMP CMC, and we hope to be in the clinic by 2025, or at least do the IND by 2025.
So as you can see, I hope I showed you how busy the 2023 and productive 2023 has been. And really, the goal is always, you know, to continue to bring to bring the pipeline. So as you can see here, I think I've been the whole time while my team is doing this, and I said I just started the talk, and it's actually there is a delay between the computer and which slide you see. So now I got it. All right. So, you know, two things to see from our pipeline is, first of all, really happy about it's starting—you know, you can see almost three programs in late stage.
We have a sustainable pipeline with more coming from the early phases, and it's now officially, I can say, it spans three therapeutic areas. So we have multiple milestones looking into 2024. I think I shared them with you as I was talking, so I'm not gonna go into each one of them. But suffice to say, a very data-rich 2024 to look forward to. And before I finish, I just want to say nothing really can happen without an amazing team. I'm very grateful to their dedication to really bringing and helping patients every day in and day out. And I would like to thank you all for your support, and most importantly, thanking our patients. Thank you very much. Go ahead.
Great. Thanks for the-
You can stand up.
... presentation. Maybe starting out with the, autoimmune efforts, on the recently announced, IMC-S118AI. Can you, can you talk about the, encouraging data in that IO Insight paper from 2021, and just, I guess, what gives you confidence in this approach? Maybe compare and contrast a little bit to, say, just a PD-1 agonist and kind of the advantages you've got there.
... Yeah, I'll let David talk about that.
Yeah, so, Jess, the major advantage of our platform is it's tissue-specific. So there are PD-1 agonists out there. Some have been shown to have some preliminary data in rheumatoid arthritis, but those are systemically active, and so they will systemically turn off T cells everywhere. Our approach is tissue-specific, so it should only inhibit T cells in the-
Working more
... tissue that's inflamed. That's probably the major advantage. And then, as Bahija mentioned, we can use that T cell receptor approach to target almost any tissue. The lead program, the one you talked about, is for type 1 diabetes, so it is a super specific PD-1 agonist that will only be active near and around the β-cell of the pancreas.
Great. Maybe switching to KIMMTRAK. You know, obviously, very successful launch, I think you highlighted, but thinking about kind of 2024, where's the growth going to come from, from here?
Go ahead.
Yeah, so just to recap, 2023, we achieved over $60 million per quarter. We continue to see that in the fourth quarter. We continue to see growth. We haven't flashed the earnings number yet. Jess, you'll be happy that in 2024, we'll be a domestic filer and report everything in dollars, so we have to go back, and Jess has been asking us for years to do dollars—so we'll be doing that. So yeah, so we'll give earnings in February in dollars, but pleased to see growth continue in the fourth quarter. Into 2024, we expect sequential growth as well. We're still growing globally in terms of countries, but from a revenue perspective, the U.S. is still the significant driver. So still more to penetrate in the U.S., Jess.
We have about 65% penetration there, so the team is still expanding. And I think for KIMMTRAK, one of the what we're focused on as a team, as Bahija went through, that the existing patient opportunity is 1,000 patients a year. We think that patient population by 2030 will be 5,000 patients a year. So later this year, we'll have KIMMTRAK data, top-line data, in late-line melanoma. And then, we'll see what that data is, and it'll inform us to move into a phase III. And then we also, in 2024, are starting an adjuvant trial that we mentioned that'll take about 3 years to randomize. But we think that with this mechanism and this platform, we want to move earlier in the disease progression. We know that the earlier you go-
Yeah
... the better the efficacy.
Maybe sticking with that, kind of post ipi/nivo in a cutaneous melanoma trial, can you just talk a little bit more about what we should expect to learn from the interim phase II later this year?
Right. So the phase II design, as a reminder, is KIMMTRAK monotherapy versus KIMMTRAK plus pembrolizumab versus the control arm, and it's an innovative control arm, which we can talk about later. The dual primary endpoints of the phase II are circulating tumor DNA reduction, so that's going to give us our early surrogate of activity, and then survival. And so those are the two endpoints we'll be looking at. Now, to be transparent, the survival will probably likely not be fully mature at this analysis at the end of the year, but we believe it will be directional and allow us to make some early decisions about, for example, should we continue both of the KIMMTRAK arms, or should we drop one of-- You know, perhaps we want to drop the KIMMTRAK plus PD-1 if there's no significant difference in survival in ctDNA.
So that's primarily what we're going to be doing at this end-of-the-year analysis.
Adjusting the power of the phase III-
Yes
... which for me, the de-risks really the phase III.
Yeah, that's correct.
I guess, how are you thinking about the competitive landscape in that kind of second-line plus cutaneous melanoma market? And related to that, how do you define success when phase III eventually reads out?
Yeah. So let's talk about current and future. The current is there's nothing really available for these patients, and that's why when we designed the control arm, it had to be carefully designed. Doctors did not want to be forced to use something that doesn't work, and so that's where we came up with this idea, this innovative idea of essentially randomizing to a real-world registry. So the patients randomized to the control arm, they get discharged from our study, and they go to follow-up, and that allows them to enroll on other clinical trials or get treated however they- doctor would like them to treat. So that's- that was the design to reflect the current standards of care. Now, in every therapy, there are always new therapies that come out.
The nice, advantage for our trial is that everyone else who's studying therapies in this setting are doing single-arm response rate for accelerated approval. If our study reads out positive, and we can talk about what positive would be, this would be the new standard of care in second plus line because it would be the only therapy to show a survival benefit in that line of therapy. And I think then your other question was, about what does success look like or... So the current, survival, and I use one-year survival as a landmark in this setting, the one-year survival is around 50%. And that doesn't-- It's independent of what-- whether it's an observational trial, whether it was an experimental clinical trial. No one's really been able to move the needle.
In our phase I, II trial for KIMMTRAK that a few years ago, that was a combination with checkpoints, the one-year survival was about 75%, just as a comparison. So for us, success would be a statistically and clinically meaningful survival benefit versus the control arm.
... And Jess, we can do that because at least for that, the control is because it's an OS endpoint that you can do that basically. Way to follow up.
Right. If you had a PFS or response rate endpoint-
You could not do it.
You couldn't, follow them on someone else's clinical trial, but you always follow survival-
Correct
... even if they go to another clinical trial.
Right.
What about adjuvant uveal melanoma? What gives you confidence in the ultimate success of that trial?
Yeah, Jess, I think a couple of things do. One is if you look at the subset analysis from the phase III first-line metastatic trial, patients with the smallest tumor burden, that's M1a, it's that those are patients whose tumors are less than 3 cm in size, had a survival hazard ratio of 0.36. And actually, that was the largest subset in the phase III trial. And so if you have a hazard ratio of 0.36 with small tumors, then we said, imagine what this benefit would be if you don't see any visible tumor. That's the adjuvant setting. Number two is the platform observation that we've seen throughout, which is as you move into earlier line of disease, we see better activity for our platform. We see that with circulating tumor DNA.
You see, the rate of clearance triples as you move from second line to first line, and there's probably various reasons why that's the case. And so we think in an adjuvant setting where there's no visible tumor, the immune system is gonna be better. And then finally, I would say the control arm here, there is nothing. Patients do watch and worry- and so we're randomizing against just, you know-
Observation.
Against observation, yeah.
Yeah.
You know, but that's an extremely low hurdle because there's no therapeutic intervention.
Jess?
Right.
From the previous comment, could you explain a little bit more about how the randomization works in the control arm? Like, they either go on, you know, checkpoint PD-1 or, like, what does the placebo arm do?
Yeah. So... Right. So, all right, so the question was, can I explain more specifically the design of the phase III trial in terms of the control arm in the cutaneous melanoma KIMMTRAK trial? So in a typical trial, what you would do is you would randomize to a control arm. In a cancer trial, you, we wouldn't use placebo, but you would randomize to, let's say, investigator choice or a chemotherapy. And then once the patient progresses on the experimental arm or on the, let's say, chemotherapy control arm, they then leave your study, and they can get enrolled on another study, right? You progress on the current study, so you're eligible for other studies. Now, when patients progress and go on to other studies, sponsors always follow them for survival. So you can follow them for survival.
If they go on to 10 other clinical trials, you still follow them for survival. So when we came up with a design, we said to investigators, "What do you want on the control arm? Do you want us to have dacarbazine? Do you want IL-2? What do you want?" And to almost everyone, they said, "The only thing that we want for these patients is clinical trials." So when you do this, when you have something like that, the design is if they're randomized to the control arm, we tell them, "Okay, you're discharged from our study. You can go and get treated however you want. You can get best supportive care. You can go into another clinical trial.
The only thing we ask is that we still can follow you for survival. So you can only do this type of innovative design if your primary endpoint is survival. Obviously, if it's PFS or response rate, you can't do it.
It can be confounding, yeah.
Yeah. Does that make sense?
They're still kind of in your trial, but kind of out of it.
Yeah. Yes, they're still being followed in follow-up, and it's called survival follow-up, standard for every trial.
Mm-hmm. Yeah.
Which is why, by the way, we did the survival update in our phase III first-line trial. Even though they had progressed-
Yeah
...and gone on to something else, we did a survival update. But that's why we came up with the three-year survival update in the first-line uveal trial.
Okay.
You follow them for survival.
Are they able to... The only question is, could they try to get KIMMTRAK commercially, which would kind of mess up the survival calculation?
Yeah, I mean, in theory, but it's not approved in that setting, so yeah.
Okay.
Also, it's a global trial, and so outside the U.S., it's very difficult. You know, it's more controlled outside the U.S., and I think most of the randomization will occur outside the U.S.
Okay. From the phase I, II, where you said you had a 70% survival-
Mm-hmm
... is that this exact same group that you're rolling into the phase III cutaneous?
Yeah, so we actually went back and defined the eligibility for that retrospective phase I, II analysis. We came up with the 60 patients who I believe would match the patients who were enrolling into this trial. So yes.
Okay. Okay, great. Okay.
Sorry, and how big is the cutaneous trial? Let's see.
Yeah, so currently, it's about 120 patients in the phase II, and it's about 340 patients in the phase III. That's assuming we only take two arms forward because we're likely to... Remember, it's a three-arm trial, so it's 170 patients per arm in the phase III. What we're gonna do in the phase II is we're gonna look at the treatment effect, and we could alter the size of the phase III. We could make it smaller, for example, if the treatment effect is very large. So right now, it's 170 per arm, but that could change based on the data.
Okay. Which it sounds pretty. Is that more for safety? 'Cause it sounds pretty, with the kind of survival difference that you've described, that's a pretty highly powered trial, 170 per arm.
Yes. Yeah, no, you're exactly right. So, we put a placeholder of 170 per arm. But if the treatment effect is really what we expected to see, I don't think you need 170 patients per arm. So we wrote the trial that it could be adaptive.
Yeah.
We'll get the data, and then we'll adapt the size exactly as you point out.
Okay. But to enter the trial, then what are they failing? Are they failing a frontline PD-1?
Yeah, so they must have progressed on PD-1.
PD-1.
They must have had ipilimumab.
Yeah.
And then if they're BRAF mutant, they must have had a BRAF targeted therapy.
... That's the whole point of doing it phase II, phase III, so you de-risk a little bit before you get into phase III. So that's the data we're talking about.
Great. Thank you.
Another question in the room?
Hi there, Lucas De Breed, the American Cancer Society. I have a question around health equity because of the haplotype specificity of your products. So it's very encouraging to see that you're thinking about additional haplotypes. Can you talk a little bit more about the larger strategy behind that? Because also there's gonna be a trade-off between market size and cost of development.
Yeah, definitely. And I think that, you know, we've shown that, for instance, in uveal melanoma, this is more, mostly a Western, you know, disease. So there was, you know, looking at other haplotypes is not as, as big or as, prevalent as a disease. When we look at, for instance, in PRAME, there is a substantial, it's an, 30% more, you know, patients overall that you can add to the numbers that's already big for, for PRAME. And there, I think it's, it's worth going after, and definitely, it, it serves Asia. And that's, I think, from the health equity, is a really good one, and that's what we're gonna do. You know, I think, you know, molecule by molecule and disease by disease, where it is prevalent and where we can do that.
I think, you know, we have still every time you do that, you have a new peptide, a new program, basically, because you have to go. But we believe, you know, what you have to do is the phase I, 'cause you need to, to know the dose and the safety and all the stuff. But then after that, you can, you can go more, you know, faster, if you will, because you don't have to do signal searching. So there are other ways. I think we, we will be looking with the regulators, you know, how to, to speed up that, that program even more. But yeah, it's gonna depends, but.
Great. Thank you.
Thank you.
So, obviously, you guys are in a very nice position in terms of growing revenue and, and to some extent being self-financing. But it, it's quite obvious that you've got some very exciting new activities, getting lots of clinical trials. These are expensive. Could you just talk about the cash flow implications as we move into the, this next phase?
Yeah, I can, I can, speak to that and ask Brian to, to say something as well. So I think we're in a great position right now. I think if we look at, you know, 2024, 2025, we are fine. You know, if we—of course, it's a great problem to have if we have to do multiple phase IIIs. We have also the opportunity to go back to the market. But, yeah, we're, you know, we'll continue to push the sales, but at the same time, continue to bring great drugs to the market.
Yeah, I'll just, I'll just add that in 2023, our cash position increased without raising any money. So, Julian, thanks for noticing we're sustainable. We expect that to continue as we head into 2024, 2025. But you are correct, as we move into large randomized trials, they'll be more expensive, so I think it'll be data dependent. But we're funded for the foreseeable future, and we'll look to raise money opportunistically, as, as we move forward.
Maybe we can talk about PRAME a little bit. I think you outlined kind of the cadence of expansion cohort updates throughout the year, with lung coming later. What's your latest thinking on kind of where you want PRAME to go in lung or where it could have the greatest impact?
Yeah, I think we have to be data-driven, and I'll ask David to talk about that. I think we the cadence of what we said last year, we said that we're gonna start bringing data at the beginning of the first half of the year, and now we have more granularity as we look at the enrollment, you know, and what we had. You know, as we said at the beginning, we had to go really away from a phase I to a global sites. I think on the lung, it's really important you cannot go into lung. We chose, anyway, not to go into lung as all comers and then come back and look at you know, where the signal. It's heterogeneous.
We know it's a little bit where breast cancer was a long time ago. I think you see it now in lung. These are different biologies going in there, and we decided to go, you know, cohort by cohort, different cohorts to interrogate. And so that's, you know, when we anticipate the enrollment and everything, we said by the fourth quarter, we'll be bringing the data.
Just to make sure I understand, when you talk about heterogeneity, is that heterogeneity within lung, and is there any kind of hypothesis going in kind of prior to data about where a therapy like this could have the best impact?
Yeah, definitely heterogeneity in the lung. For instance, you see, you know, the responses to checkpoint inhibitors in kinase mutant versus non-kinase mutant is very different, right? For us, really, the... You know, we have two things. You know, we know that the T cells, wherever the T cell mechanism works, we should work as well, right? So we know in some of the lung, you know, T cell mechanism works. But also what we saw with uveal melanoma, where checkpoint inhibitors don't work, we see our mechanism working. So I think we have to interrogate all that and not just go for where checkpoint inhibitors are sensitive there or not. That's exactly what we're doing.
Great. Maybe switching gears to your infectious disease efforts, can you just talk about when we could see additional updates for HBV and HIV, and kind of what you're trying to learn with those programs kind of at this stage?
Yeah, go for it.
Yeah. So, with HIV, there's been a lot of enthusiasm from the sites and from the participants. And so there, we're asking two questions. The first is, during the treatment phase, can we reduce the reservoir? Currently, the reservoir is essentially one out of every million CD4 T cells are infected with HIV, despite antiretroviral. So can we have a biomarker to show that we're reducing that reservoir during the treatment phase? No one's been able to do that. That's question number one. Then we interrupt treatment, and then you're looking for, can you delay viremia? Can you delay the viral rebound? And that's looking at the HIV RNA in the plasma. So we'll be looking at both of those. One is the reservoir question, and then one is the functional output, about how fast the virus...
We'll have several cohorts worth of data, both the reservoir and the treatment interruption, and we'll be presenting that in the second half of this year. HBV has been enrolling a little bit slower, and there's probably a variety of reasons for that. It was our first foray into infectious disease. I think HBV, people with HBV are just not as familiar and comfortable yet. But we have taken some updates to the protocol to speed up the accrual, including adding an HCC arm of HBV-positive HCC. We're hoping this year to be able to treat more patients to see whether this bispecific can decrease the surface antigen in patients with HBV.
Great. I think we're out of time, so we'll stop there. Thank you.
Thank you, Jess.
Thank you.
Thank you very much.