Great. Good morning, everyone. My name's Jess Fye. I'm a biotech analyst at JPMorgan, and we're continuing the 44th annual healthcare conference today with Immunocore. First, you're going to hear a presentation from the company, and then we're going to go into a Q&A session. So if you're in the room and want to ask a question, just raise your hand, someone will bring you a microphone. And if you're listening online, you can submit questions to the portal, and I'll read them off the iPad up here. So with that out of the way, let me turn it over to Immunocore's CEO, Bahija Jallal.
Good morning, and thank you, Jess, for having us. It's always a pleasure. This is our forward-looking statement. Our mission at Immunocore is to bring transformative medicines to patients. We are a commercial-stage biotechnology company that pioneered the first soluble TCR bispecific platform. This platform is validated clinically and commercially. And what's really interesting about this platform is very modular. So it can upregulate the immune system by redirecting the T cells to kill tumor cells and infected cells. And that's useful, obviously, in oncology and infectious disease. Or it can down-modulate the immune system in autoimmune diseases. 2025 was a year of execution for Immunocore. 2026, 2027, 2028 is really where things will come together, as we're going to have several data catalysts. But let me focus on 2026 today. Our priorities are very clear in the company.
One is to grow KIMMTRAK and prepare for potential new melanoma indications. The second is to expand beyond melanoma into other tumor types. And third is to unlock the value of the opportunities beyond oncology. I will walk you through all the three. So let's start with the first one. KIMMTRAK was approved five years ago as the first treatment for metastatic uveal melanoma in 40 years. And this was done with a landmark or a gold standard of overall survival. It was absolutely necessary for these patients. But the question is, how did it do really in the real world? And here we have the data to really see that, actually, in the real world, did even better. So we have the duration of treatment. So the mean duration of treatment is 14 months. It surpassed what we've seen in clinical trials.
We published the three-year survival data. It was also very, very important data but the latest data that we've just said in ESMO I-O showed in real world, now taking a registry from France with 150 patients, a median OS of 28 months, and we can see that translating into the commercial arena. We have 70% penetration in all the major markets. We have some markets where we have 90% penetration, 80% penetration, and so on, so that tells you that there is a real need for this drug, and it's working, and of course, it translates into the commercial arena, where we have 30% revenue growth this year. We have, since we launched, 14 consecutive quarters of growth so what's next for KIMMTRAK?
We will be publishing this year, in the first half of the year, the five-year OS data, and we believe the biggest potential opportunities for KIMMTRAK are yet to come and still ahead, so how are we looking ahead into 2026? One is to continue the US penetration into the US market and the global expansion in MUM. So basically reaching it will come. My coffee is not kicking in. So the expansion is into more and accessing more patients around the world. The second is the expansion into second-line cutaneous melanoma. Now we're starting to look at the life cycle management with two phase III trials. The first one is the TEBE-AM, and I'll talk to you about it, and the second is the adjuvant uveal melanoma, so let's look at the cutaneous melanoma. We know that the market opportunity is around 4,000 patients, HLA-A2 positives.
There is an unmet medical need for population beyond PD-1, basically resistance or refractory to PD-1. What's the reason to believe? We had a trial, a phase 1B trial with 60 patients that showed that for this population, the one-year OS was 75% compared to one-year OS of 55% for the benchmark. We started the phase 3 trial in second-line plus cutaneous melanoma. The design is the following. We had KIMMTRAK, KIMMTRAK plus anti-PD-1, or straight to follow-up, or if you will, the investigators' choice. The endpoint is the overall survival. Where are we with this trial? This is the next milestone for us. We are on track to finish the enrollment of this trial in the first half of 2026 with data that could be as early as the second half of 2026.
Now looking at the adjuvant uveal melanoma, so what happens after the primary tumor is the final treatment, if you will, for the primary tumors. The patients with metastatic uveal melanoma, 50% of them will develop metastasis in the next, basically, three years. There is nothing for these patients right now except for basically what we call the watch and worry. So it's just surveillance, and our value proposition with KIMMTRAK is to bring and impact the disease at earlier point, hopefully delaying or eliminating even the metastasis for these patients. So this trial is ongoing. If you look at the market opportunity, it is 1,200 patients. It's ongoing right now in collaboration with EORTC. We are enrolling patients in Europe very actively and will start enrolling patients in the US as well.
So you can see with this life cycle management, we can go from 1,000 patients in metastatic setting today that we are serving today up to 6,000 patients with the two trials that I just talked to you about. And we don't stop there for melanoma. We have another in cutaneous melanoma, we have another shot on goal, as we call it. And that's with PRAME. So first, let me introduce PRAME to you. It's a great target for different reasons. One is highly expressed in cutaneous melanoma. It's also a negative prognostic marker. So that means the tumor does not like to lose it. It's target is clinically validated across multiple modalities by us and others. And we have demonstrated monotherapy activity and that it combines very well with checkpoint inhibitors.
So we've shown, as I told you, we've shown that there is a monotherapy that is active in cutaneous melanoma. And we started the phase III trial. This is PRISM-MEL, a phase III trial in cutaneous melanoma. But now we are going into first line. So we have KIMMTRAK in the late lines and PRAME in first line. So there were two milestones for this trial. One was the safety run-in, if you will, which was very successful. The second one for this trial was part of the Project Optimus for the FDA. So that means we had two doses going into the trial. And the independent data monitoring committee was to look at which dose to take forward and which one will drop. We achieved all that in November 2025. And the IDMC chose the highest dose.
And so this trial right now is continuing with dropping one dose. It's all over the globe. So we have 200 sites open. It's enrolling very nicely. And if we continue on that trajectory, we anticipate to finish enrollment by 2027. The market opportunity here is 10,000 patients that are HLA-A2 positive. So as you can see, in melanoma, we have multiple shots on goals. And we can go even beyond melanoma. So that's the second focus right now, is again looking at PRAME. So PRAME is interesting. I told you, as a target, not only because it's expressed in melanoma, but it is expressed outside melanoma in ovarian and non-small cell lung cancer, among other tumors as well. So we already showed monotherapy activity in ovarian. And we showed that it combines very well with chemotherapy. We presented this data at different times, either in melanoma or ovarian.
But what was really important for us now is we know that to explore even more in ovarian, not only in platinum-resistant ovarian cancer, but also in platinum-sensitive ovarian cancer, either as monotherapy or in combination and move even earlier. We are doing the same thing in non-small cell lung cancer so that we have basically the signal searching in non-small cell lung cancer. So this data is being generated and will be developed into this year. And I'll tell you that by the second half of 2026, we'll be presenting this data. But what's also really exciting is we have the PRAME half-life extension that's in the clinic. We put it in the clinic at the end of last year. So in 2025 and in 2026, we'll continue those escalations.
So we hope that by the second half of 2026, and we plan for the second half of 2026, we'll have data for all these three experiments, if you will, that will allow us to basically plan what's in the next step and which molecule to take forward. And last but not least is PWIL. So PWIL is a novel target that was basically discovered by us. It's also a really important target because it's expressed very widely in 25% of colon cancer. Basically, 75% of tumor cells are positive for PWIL. It's expressed in other GI cancers like pancreas and others. But we're very much focused right now on colon cancer because of the unmet medical need. So we have 20,000 colorectal and 15,000 other tumor patients that are positive for PWIL.
But you know that there is a huge unmet medical need right now, and especially where checkpoint inhibitors have not worked as well as in colorectal cancer. So where we are with this program, we get it into we started the end of 2024, literally in December. So we are in dose escalation. It's going very well. And we hope to have data either this year or 2027. But this platform, like I told you, is modular. So we have opportunities beyond oncology. The first one is in HIV. So we know that HIV is very well served with antiretroviral. What we are really looking for is a functional cure. And they're going where nobody has gone there before. Because you know antiretroviral do very, very well. However, when you stop, you have to take them all the time.
When you stop, you can see less than two weeks. You can start having the viral rebound, and if you look at over 500,000 patients HLA-A2 positive today or people living with HIV are currently on antiretroviral. So we showed the single ascending dose with our MTAV, the first compound for HIV, and what we're trying to do is really you see the rebound because there is basically the virus hides in a reservoir. So our value proposition is to go and actually attack that reservoir and then see if we can actually basically have an antiviral effect or. So what we've done, the single ascending dose showed that it is safe, and we can continue into the multiple ascending dose. At the beginning of 2025, in the CROI, we showed the first data of our multiple ascending dose, and there are really two things.
It was very well received by the KOLs, I have to say, and we had two important points. One is that it's very well tolerated, and the second is we saw dose-dependent antiviral effect. If you look at the blue lines at 60 micrograms, which is the lowest dose, you can see when you stop everything, our compound plus the antiviral, everybody takes off, and then you can see in the orange, as you get 120 and 300 micrograms, you have delay the viral rebound. That's what we're really looking for. We don't believe that we are at the most effective dose yet, so we are continuing the dose escalation into much higher doses, and we hope to get this data at the end of 2026, the second half of 2026. What's really close to my heart and I think absolutely exciting is in autoimmune diseases.
I think it's an area where we absolutely need more innovation. And instead of really looking for systemic immune suppression, what we're trying to do is to go very much organ-specific down modulation of the immune system. Right? And we do it because in our, we can have the tissue-targeted molecule, the TCR. And on the other side, the first one we're starting with is the agonist, PD-1 agonist. So we chose to go into Type 1 diabetes because there is first an unmet medical need. You still have 50,000 patients that are newly diagnosed with Type 1 diabetes every year. And we made basically a construct that binds to the preproinsulin on the beta cells that are specific. Just the preproinsulin is expressed only in beta cells. So we're bringing our molecules to bind to the preproinsulin.
And on the other side, basically switch off the autoreactive T cells with PD-1 agonist. Very, very quickly on this one, just to show you how specific it is. These are pancreatic slices from human beings, if you will. So you can see the beta cell marker. And you see that when we put our construct, it's specifically binding to the beta cells. But not only that, on my right, you can see that not only we bind, but we also rescue the beta cells from killing. And then the question is, if you rescue from killing, is it functional? I'm not showing the data here. But it is functional. It's the secrete insulin. So we have a real rich data package preclinically that convinced us to move into the clinic. We filed the CTA in December.
And I think we have really very good experiments that can be done that we can find out early in the clinic, phase 1 and phase 1b, basically if it's working or not, which I think is very, very exciting. And then you can imagine if this works, that opens up any T cell-driven diseases that we can go after. And not only that, we can go even beyond with autoimmune. So with that, I'm just going to show you. I told you to really focus on 2026. It's going to be a very busy year. The first half is very much focused on continuing to enroll the TEBE-AM and finish that enrollment. And then we are in the autoimmune diseases in type 1 diabetes to start the trial. The second half is much busier. And we hope that we'll have data there for TEBE-AM.
Then you can see, as I walked you through some of the data readouts that we'll have with the PRAME and other things. It doesn't really stop in 2026. As I told you, we're now looking forward to 2026, 2027, and 2028, where we're going to have data catalysts coming after the labor of the last three years of enrolling, especially phase three trials and so on. I'm going to leave you with three key takeaways. We have validated product in the real world, in commercial. Not only that, we have actually a 30% increase in revenue and 14 consecutive quarters of growth that really sustain. It actually speaks very highly of the drug, the KIMMTRAK. We have three phase three trials in melanoma that are ongoing with data readouts starting in 2026.
And then we have a diversified pipeline, as I showed you, one that we believe we have shown proof of principle in infectious disease, but can be the unlocking the value in autoimmune disease is the next step for us. So with that, I just want to thank you and thank all the teams in Immunocore. And we'll call my team to come answer all the tough questions.
Great. Thank you. So it looks like there's a lot going on with the pipeline this year. But I did want to start out with KIMMTRAK. We turn the page and enter 2026. What are the key growth drivers from here?
Yeah. I think I'm happy to start with that, Jess. So thank you. Thank you for having us, by the way. So if you look at KIMMTRAK and the current uveal melanoma indication, as Bahija highlighted, we are greater than 70% penetrated in all major markets and even 80 and 90% penetrated in some European markets. That strong penetration has allowed us to grow in the first three quarters of 2025, 30% year on year. So as we move into 2026, what we do anticipate, and this is our fifth year on the market, so naturally, we do anticipate some growth to moderate. But we expect that growth to come from increasing the penetration in the US community setting and as well as further global expansion outside the US. So that's for the current uveal melanoma indication. Beyond that indication, we have two life cycle phase three trials ongoing.
One is TEBE-AM, the advanced cutaneous melanoma indication, which Bahija highlighted. We anticipate completing enrollment in the first half of this year with data as early as the end of the year. That life cycle management indication has the potential to increase our current eligible patient population from about 1,000 patients to an additional 4,000 patients. So it's a significant inflection point potentially for us. Then the second life cycle management indication is the ADAM study, the adjuvant uveal melanoma trial. That trial is ongoing. We just started that late last year. It's enrolling well. That has the potential to add in an additional 1,000 patients. So if you look across the horizon of the current uveal melanoma indication that we have alongside the two life cycle management indications, that could take our eligible patient population from 1,000 to up to approximately 6,000 patients over time.
Recognizing that kind of the next big tebe readout is in cutaneous and not uveal, if that hits, does that create an additional halo around the product that could help deepen your penetration in uveal?
I think if you look at where we're at, so we have two objectives with increase in the US community penetration. One is increasing the patient starts, and the second is, and it's tied to the first, is bringing that treatment closer to patients' homes. We've made good strides in that already, in that we have about 50% of our patient starts coming from the US community currently and about 70% of the prescriptions, and what has allowed us to do that is the drug's profile. Patients are living longer. We hear from patients all the time. They not only live longer, but they feel better, and obviously, that's driven by efficacy, but it's also driven by the safety profile that we have. It's predictable. It's manageable.
That is a testament, again, to that drug's profile, which has allowed us the success in pushing it into the community that we've seen thus far today. I think all of that translates into the cutaneous melanoma indication as well.
Yeah. So, Jess, I think just to add, so when we look at markets like France, we are 90% penetrated already. Germany, 80%. I think we still have some room to go in the U.S. That's 70%. But I think the other for cutaneous melanoma, to your point, we're not going to be starting from scratch because 50% of the patients who are treated for cutaneous melanoma are treated in centers that are familiar with KIMMTRAK. So just to add to that.
Is it a structural phenomenon that kind of accounts for why the U.S. penetration is a little bit lower than some of those European countries?
Yeah. Yeah. Community centers, if you think about Europe, you're very, very centralized payer systems, right, reimbursement systems. U.S. is very dispersed. So there's very low density of patient populations in that dispersion. And so what we do to help achieve those objectives that I mentioned earlier is we use advanced analytics and AI because we have a very fit-for-purpose footprint given the relatively small indication that we have today. So we leverage those advanced analytics to help achieve the objective in that penetration in the U.S.
For the ATOM adjuvant trial, where do you stand with kind of progress on site activations? And what's the best thinking on timing for that data?
So the EORTC is running that trial. And they have it activated in Europe. And we should have sites activated in the U.S. now. I think this year is the year we'll probably reach steady state accrual. And right now, we've penciled in a three-year timeline for randomization started in the fourth quarter of 2024. So I would imagine by the end of 2027, we can finish accrual or early 2028. And then it's event-driven. So it's probably 18 months or so after that would be the events. But it's certainly too soon to have a fine-tuned projection of events, better certainty on the enrollment.
OK. And maybe shifting to brenetafusp for the PRAME asset, after selection of the high dose to continue in the phase III trial, have you been able to refine your projections for enrollment completion and top-line data?
Yeah. So we are now down to two doses, which is good. It helps the trial accrue. We have, as Bahija mentioned, over 200 sites globally enrolling, and it's enrolling pretty well, actually. So right now, what we're projecting is to complete randomization at the end of 2027. It could bleed into 2028, but we're trying to push for 2027, and then, of course, it's event-driven after that. Typically, in these first-line phase III trials, PFS usually reads out not that long after all the patients have been randomized, but in terms of event prediction, I think we'll have a better sense next year.
What specifically gives you confidence in phase III success with this asset?
I think there were multiple factors that led us. First, when we enrolled brenetafusp monotherapy in late line, we saw some durable partial responses. So we know the drug is active. But we also saw pretty high disease control, which was this closed umbrella type plot. In fact, the disease control rate for brenetafusp monotherapy was higher than the disease control rate for the combination of nivolumab plus relatlimab or LAG-3 in the same population. That was relatively steady 20. So on monotherapy, brenetafusp had more activity than the combination of the both. The second piece was we've done a lot of work into understanding T cell fitness in blood. And we found that T cell fitness improves as you move into earlier lines. And the activity goes up with better T cell fitness.
We projected that there would be higher activity in earlier lines, including first line. And this is not unusual in immunotherapy. And then the final point was we knew that if nivo plus LAG-3 beat nivo in first line, we felt that adding nivo plus brenetafusp, so two active agents, each with a different mechanism of action, would be better than nivolumab and also would be better than nivo plus LAG-3 because of the monotherapy data. So those were the data points that led us to launch the phase III trial.
I will just add, so I think looking at the mechanism of action and two actives will have at least an additive effect. We'll see, the trial will tell us if there is a synergistic effect as well because they're two different MOAs.
It sounds like we're also getting more data in other indications outside of melanoma for brenetafusp coming up. As the ovarian and lung data continue to emerge, how could DCR and kind of response durability influence future pivotal planning in those indications?
I look at ovarian and lung in two different ways. For ovarian, we saw monotherapy activity for brenetafusp in late line. In late- line ovarian, although it wasn't enough to advance given the rapidly changing landscape, but we know the drug is active, and so knowing about the mechanism, we realized that we should try to move earlier, which hence the platinum-sensitive cohort with bevacizumab. First time ever a T cell engager with beva is being tested, and then we also wanted to expand on the chemotherapy combination in platinum-resistant. In both of those cases now, we're going to look at the data later this year, and the strength of that data will determine what the next step is. We'll be looking at is there further reduction when you add brenetafusp on top of bevacizumab because this is a maintenance setting.
With chemotherapy, is there a higher response and a more durable response in that combination? The strength of that data will determine what the next step is. It's likely a randomized trial. The strength of data determines, is it a randomized phase II? Is it a phase II, three, or is it a phase III? We also have the PRAME half-life extension, which is moving in parallel. We can talk more about that. For the lung, it's more of a signal detection because lung in this late line is a very difficult tumor.
Just to kind of keep picking at lung there, though, if you do see the signal that you're hoping for, then what does the next kind of development step look like?
So depending on the strength of the data, I think we would choose the partner, the combination partner where we saw the strongest signal. And we would probably do a randomized trial because in this case, we're adding two active agents together. And although you can see signals above a background of one of the agents, you never know until you run a randomized trial. So we would likely need to run a randomized trial.
OK. And when you say combo partner, you mean combo drug?
Yes.
Not combo partner.
Biotech company.
Oh, yes. Yeah. Sorry. Correct.
Is it the chemo or is it the beva, or that's good?
Osimertinib, chemotherapy, anti-PD-1, yes.
OK. Great. So what's the next update we should expect for the half-life extended PRAME product? And how do you think about the next development plans for that asset? What data that you generate with brenetafusp kind of factor into how you advance that product?
Yeah. So that's why we're lumping it, if you will, with the totality of the data because one thing for the half-life extended is the molecule is almost the same except for the FC. So we believe whatever we see with brenetafusp is going to be relevant if we choose to continue with the half-life extension. So for the half-life extension, we are really two things. One, is it for convenience? Right? So that's our first hypothesis. And then the second, does it increase the ORR and other things? We know. But we can swap that. I do believe that we can use the data from brenetafusp if we want to continue with the half-life extension. So we'll have the data first. I think most of the, even in the dose escalation, we have cutaneous melanoma, ovarian, things where we have already data with brenetafusp.
What's the difference in dosing frequency between the two?
The traditional is every week. With the half-life, it's actually flexible. It could be every two weeks, three weeks.
Thinking ahead to the potential phase III melanoma readout for brenetafusp, what kind of regulatory interactions could streamline a potential approval there in melanoma?
Yeah. We always take really advantage of whatever pathway we have with the FDA. So there are several points where you can actually interact with the FDA. One is on the statistical analysis plan. You can do that on the narratives, on the clinical side. You also can, once you finish the PPQ batches on CMC, you can interact with them. So all these can be done before you actually have the data. And we found that out to be very, very useful, actually, getting the guidance from them. And we're very grateful that they give that guidance before.
So you're not the only company who thinks PRAME is an interesting target. So what other products are you watching competitively? And how is brenetafusp kind of differentiated from them?
Yeah. No, definitely. I think the data from Immatics looks really very promising. It's always good to see different modalities on the target, basically, that just brings you even higher confidence in the target, right? So that basically what we've seen either with TCR-T for what they produce or the bispecific, that PRAME is definitely a good target as we started a few years before. I think it's the early data. So I think it's very, very promising.
So maybe shifting to the pipeline, you mentioned you're particularly excited about the efforts for Type 1.
Yeah.
As that moves into the clinic here, what marker do you look at in phase I to help assess the tissue-specific immune modulation?
Yeah. So we chose that Type 1 diabetes because you don't have to go all the way to a big phase IIb to find out if it works or not. We're not that kind of company. I think we have, with the single ascending dose and the multiple ascending dose, we can address two questions. In the first one, the first basic one, does the drug hit the target, basically? And that, I think we can do a lot of exploratory things. But one very solid biomarker there is the soluble PD-1. We know that there is soluble PD-1. If it increases, then you know that it binds to that. On the multiple ascending dose, we can actually start addressing at least a biomarker of activity, if you will.
So if everything is working as we believe, then you can do the C-peptide levels, basically, after the mixed meal test, if you will. And we know that the FDA is even considering, or at least Sanofi is trying to have the C-peptide as a marker. But you can.
Yeah. I just want to add one other set of assays that we're looking at, which are immunologic autoimmunity. So first of all, autoantibodies, which are known to be reflective of disease activity, we would look for those to go down potentially in the SAD. And then the second is our scientists have developed assays to measure autoreactive T cells and whether they're exhausted or not, which is the exact mechanism of action that we're looking at. So we can follow those autoreactive T cells, the T cells that kill the beta cells. We can follow them over time. And we would expect, based on the mechanism, for those to become exhausted. And we could potentially see that even in the SAD, which we think will complete this year.
Does that mean we see the data this year?
Probably next year, I would say, 2027.
Beginning of 2027.
Yeah.
OK, and I guess what's the ultimate kind of target product profile here? Let's say you see something on C-peptide. Is there a certain kind of threshold that tells you this is full steam ahead versus we need a different dose or kind of more work?
Yeah. You can go.
Yeah. So C-peptide, preventing progression of Type 1 diabetes, is still in the early stages. There's only one trial, really, the Sanofi trial that had reduction of C-peptide. And we'll see whether that is going to be the regulatory endpoint. Our target profile is going to be patients who are newly diagnosed with Type 1 diabetes. So they still have a beta cell mass to protect. In late stage T1D, there's no more beta cells left. It's to protect those beta cells to give a finite dosing regimen so that we can induce exhaustion in the autoreactive T cells. And after that finite dosing regimen, we hope to have a disease-modifying effect so that the patients can stop treatment and potentially beta cell regrowth can occur or at least no more decrease. So C-peptide is the marker of beta cell activity.
You can also look at use of insulin, hypoglycemic incidence, and so there are other endpoints, but we are trying to have a disease-modifying effect with a finite duration of treatment.
You also talked about the PIWIL-directed asset. Following dose escalation, what do you want to see for safety, PK? What's going to inform your decisions about advancing that further?
It's really we'll be looking at activity. We know enough of the platform now that the safety is not an issue, right? That also the PK is not an issue because we see the OS that has a ratio of 0.51 with the Tebi that has a very short half-life. So we'll be looking at the characteristics that we see in our platform. Do we have durability, the DCR, the ORR, everything? And we know if it hits the target, we look at cytokines and things like that. But we'll be looking at activity, basically.
Just to add one thing, even if PIWIL1 is a KIMMTRAK-like drug with a low response rate and very good survival, it has a direct path forward in late-line colorectal where the current survival is very dismal. The response rates for therapies there are less than 10%. Much interest in PIWIL1. We'll complete dose escalation this year with data next year.
Oh, question on that? Are we out of time?
You've got obviously KIMMTRAK's now generating more revenue than you guys, I'm sure, expected at the beginning. You've also got a lot going on in the clinic. I mean, roughly what are your funding requirements now for the next couple of years?
Yeah. Yeah. Thanks .
Yeah. Actually, please. So year-on-year, we actually increased our cash. We ended the year with unaudited, but about $860 million of cash on the balance sheet. At this time last year, we were about $820 million. So I think the more important thing is the capital allocation strategy. We're investing in the phase III, phase III studies. We're continuing to advance the portfolio. And we're doing so from an R&D investment perspective. We're doing so in a data-driven manner with our R&D expenses. And we're staying very disciplined with our SG&A expenses. And that's the philosophy that we have with respect to the capital allocation.
Great. Great. We're out of time. So we'll stop there. Thank you.
Thank you.