Good afternoon, everyone. My name is Nick Lorusso, and thank you very much for joining us at TD Cowen's 45th Annual Healthcare Conference. For our next session, we have a hybrid presentation and Q&A with Immunocore. It is my pleasure to introduce David Berman, the Head of R&D, and Travis Coy, who's sitting down right now, but will be with us for the questions. It is a privilege to have you both here. With that, I'll let you go ahead and start with the presentation. Nick, thank you very much for inviting us to present today. Here's our forward-looking statement. I joined Immunocore about seven years ago because of the exciting science, and it's been an incredible journey since then. Over the past seven years, we've brought the first commercial TCR therapeutic. We now have a very strong late-stage, late-stage phase III pipeline, which I'll get into. We also have line of sight now to early stage three therapeutic area clinical programs. I'll get into those three therapeutic areas. Of course, this is supported by a very robust revenue stream from KIMMTRAK. All of this is helping us realize our vision of delivering transformative immune-modulating medicines for cancer, infectious disease, and for autoimmune diseases. We have a really deep pipeline. Of course, KIMMTRAK, which is currently commercialized for metastatic uveal melanoma, two life cycle management phase III trials that I'll review for you. With PRAME, we have a pretty large franchise, including an ongoing phase III and first-line cutaneous melanoma, signal detection in ovarian and lung. I will talk to you about our PRAME program. PIWIL1, the first immunotherapy TCR program for colorectal cancer. It is a very interesting, exciting target, highlighting our unique discovery engine. HIV and HBV, we will be sharing our initial MAD data for our HIV program later this month. The HBV phase I single ascending dose later this year. We are very excited now to have line of sight to autoimmune. I want to share to you why we are excited about the autoimmune franchise. First, I want to focus on KIMMTRAK. 2024 was a very strong year. We had $310 million in sales. We had 14 new launches, bringing it to 24 total countries. It's approved in 39 countries, and we will have continued expansion throughout this year. We can talk more about that during the Q&A. This is the near term for KIMMTRAK. In the midterm, which is not that far away next year, we're focused on KIMMTRAK life cycle management in cutaneous melanoma. Now, after PD-1s, after checkpoints, there is no therapy demonstrated to prolong survival benefit. This is the indication where our phase III TEBE-AM trial is currently enrolling. In fact, it's the most advanced phase III trial with a survival endpoint in second-line melanoma. We are randomizing these patients to KIMMTRAK versus KIMMTRAK plus pembrolizumab versus a control arm. We expect the complete enrollment in the first half of next year to be followed by a readout, we believe, in the second half of next year. Not too far away. After KIMMTRAK in cutaneous melanoma, we're very excited about KIMMTRAK in adjuvant melanoma, adjuvant uveal. After patients have their initial diagnosis of uveal melanoma in the eye, they get definitive treatment, which is either surgery, enucleation, or radiation. Currently, they enter a watch and worry period or a watch and wait, where there's nothing they can do. They just get monitored for metastases. This is the indication that we are currently studying. In fact, it's the only ongoing active phase III trial in adjuvant uveal melanoma. We're randomizing patients to KIMMTRAK versus observation. The primary endpoint is relapse-free survival. The study just started last year, and it's being sponsored by the EORTC. Currently, we believe our KIMMTRAK in metastatic uveal melanoma has the potential for 1,000 patients a year. KIMMTRAK in cutaneous melanoma could bring that up an additional 4,000 patients. KIMMTRAK in adjuvant by 1,000. We do believe that KIMMTRAK has the potential to be delivered, if these two trials are positive, to up to 6,000 patients per year. We are very excited about our KIMMTRAK franchise. Moving now into our earlier clinical stage pipeline, I want to focus on PRAME, PIWIL1, and HIV. PRAME is a very interesting target because of the breadth of expression and because it's a negative prognostic marker in many tumors. We shared our initial cutaneous melanoma data for monotherapy brenetafusp last year, showing very compelling disease control. This, along with other data points, led us to initiate a randomized phase III in first line of brenetafusp plus nivolumab versus either nivolumab monotherapy or nivolumab plus relatlimab. The primary endpoint here is PFS by a blinded independent review committee. The trial is accruing, and the goal for this year is for a blinded independent data monitoring committee or an independent data monitoring committee to review the first 90 patients to select the go-forward dose, either the 40 micrograms of brenetafusp or the 160 micrograms of brenetafusp. We will continue enrolling the phase III trial, and we expect it to be a three-year phase III trial. Beyond cutaneous melanoma, we are building on the initial signal for brenetafusp that we saw in ovarian cancer by studying earlier lines in platinum sensitive in combination with bevacizumab and by studying chemotherapies in platinum-resistant ovarian cancer. In lung cancer, we're continuing our signal detection in earlier lines in combination with osimertinib in EGFR mutant and in combination with docetaxel. Finally, we have a PRAME half-life extended molecule, which is essentially similar to brenetafusp, except it has an Fc fusion for a longer half-life. We'll be integrating these three data points over the next 12 to 18 months and determining what the next steps are. Now, the half-life extended molecule has very similar, almost the exact same specificity and the same CD3 as brenetafusp, so those data are interchangeable. I'll now move on to our next program, PIWIL1. PRAME and gp100 were very well-known TCR targets. PIWIL1 is an exciting target that is expressed primarily in metastatic colorectal cancer and is not expressed in normal vital tissues. The fact that we are the first to develop this highlights our novel and exciting discovery engine. CRC is increasing in incidence. PIWIL1 is expressed robustly or broadly in about a quarter of colorectal cancer patients. Colorectal cancer, CRC, historically has been insensitive to checkpoints. This, we feel, provides a unique advantage for us. By the way, uveal melanoma, where we had our initial phase III, also was insensitive to checkpoints. PIWIL1 is also a negative prognostic marker in colorectal cancer, which we believe means that it contributes to the virulence. The more PIWIL1, the more aggressive the tumor. Typically, tumors have a harder time immune editing out or losing genes that are involved in the aggressiveness. We think this makes a very compelling target, and we are currently into dose escalation of PIWIL1. Moving on from oncology to HIV. The current standards of care in HIV are daily antiretroviral treatment, which certainly can control the disease, but it requires lifelong adherence. There is an unmet need to functionally cure these people, that is, to allow them to stop all therapy for at least two or three years. If they were able to stop for two years and have viral levels below 200 copies per ml, this would justify achieving a functional cure. This is the goal that we are intent on trying to achieve. The opportunity could be up to 500,000 people currently living with HIV, so a very large patient population. The challenge for the functional cure field is that when ART, antiretroviral therapies, are interrupted, on average, virus is detected in the blood, which is 50 copies per ml is the threshold for detection, is detected in blood on average in two weeks, a very rapidly proliferating virus. By week eight, over 95% of the people will have virus above 200 copies per ml. This is the threshold for infection, for transmission from person to person. By week 12, low single-digit% of people are able to control the virus. Now, the fact that some people can control the virus by week 12 suggests that there probably is some immune component playing a role in these rare people and justifies or gives us reason to believe that an immunotherapy approach such as ours might be able to impact the viral reservoir that exists and therefore impact or delay time to rebound. This is the trial called STRIVE that we are currently going to, that we are still dose escalating, but we're going to share the initial MAD data. We shared the single ascending dose data last year at CROI. This year, in the next few weeks, we'll share the initial multiple-ascending dose data of about 16 people. They are treated for 12 weeks with our bispecific, and then they are on the background of ART, and then both ART and our bispecific, which is M113, are then stopped and will monitor for viral rebound over a 12-week period, given that context of the historical data that I just shared with you. During the 12-week dosing phase, we'll be looking at can we reduce the viral reservoir in the blood. As I mentioned, when we stop, we'll be looking to see whether we can delay or alter the kinetics of rebound. Now, we have shown that our TCR targeting platform can deliver a survival benefit in melanoma, in cancer. We know tissue targeting with our TCR platform works. We came up with the idea of using this tissue targeting platform for autoimmune disease, but rather than using it to activate the immune system, we thought, why not use tissue targeting to down-modulate the immune system? In other words, our vision for autoimmunity and inflammation is not systemic immune suppression, which is the current standards of care, but rather tissue-specific down-modulation of the immune system. The way that we achieve this is with our ImmTAAI platform, which has three components. The tissue tethering or the tissue binding arm is the TCR portion, much like the TCR, the T-cell receptor portion of KIMMTRAK, targets gp100 melanoma. The effector arm in purple here is the PD-1 agonist. This is the opposite of checkpoints, which are PD-1 antagonists. The PD-1 agonists will turn off the T-cell. The third component is an Fc fusion for infrequent dosing. The general idea is that we will only get PD-1 agonism or T-cell immune suppression when the ImmTAAI is tissue-targeted or tissue-tethered. That is shown with our lead program called S118 for the delay or the prevention of progression of type 1 diabetes. Type 1 diabetes is a pernicious disease and is associated with high risk and morbidity. T1D is caused when the beta cells, which are the normal cells in the pancreas that secrete insulin, are attacked by T-cells, and the T-cells will kill the beta cells. S118 is designed to specifically bind or tether to the beta cell. When doing so, it will turn off any autoreactive T-cell that comes in to kill the beta cell. Interestingly, it will only protect the beta cell from killing when it is tethered or bound to the beta cell. When it's not tethered, there is no inhibition, and the T-cells can kill the tissue. The general idea is that this immune suppression will only happen in the beta cell vicinity. In the blood and in other tissues, there will be no immune suppression. This program is on track for a clinical trial application later this year. Finally, CD1A. Langerhans cells and an HLA-like molecule called CD1A expressed on Langerhans cells are both implicated in allergic inflammation. Langerhans cells are antigen-presenting cells in the skin. They're the primary antigen-presenting cell in the skin, and they monitor the skin for any allergens, and they will trigger and initiate inflammation. It's one of the primary upstream modulators and triggers for inflammation. They trigger inflammation two ways: by presenting neolipids or abnormal lipids and by presenting peptides. The lipids are presented by CD1A to lipid-sensing T-cells, and the peptides are presented by HLA class I and II to traditional T-cells. We believe an ImmTAAI, a bispecific that can block both lipid presentation by CD1A and peptide presentation by HLA class I and II, would be an exciting therapeutic approach for atopic dermatitis, where both Langerhans cells and CD1A are implicated, and potentially other immune pathologies as well. We designed U120, which is our ImmTAAI targeting CD1A, for exactly this purpose. The targeting end of U120 binds to CD1A, and in binding to CD1A, it sterically blocks CD1A from presenting lipids to T-cells, and therefore will sterically block activation of lipid-sensing T-cells. By now binding to thousands of CD1A on the surface of Langerhans cells, it will coat the Langerhans cells in PD-1 agonists. Anytime a T-cell comes in to be activated by a peptide HLA, it will be turned off by PD-1 agonism, and that's shown in the in vitro experiment on the right. Interestingly, our PD-1 agonist, once again, is only active when it's tethered to the Langerhans cell. When it's free-floating in blood, there's going to be no inhibition of the T-cell. Interestingly, it's more efficacious and more potent, PD-1 agonism than peresolimab, which is another PD-1 agonist that was recently reported to have activity in rheumatoid arthritis. In fact, we think U120 and our type 1 diabetes program have the potential to be the most potent PD-1 agonists to enter into the clinic. This is a really exciting time at Immunocore, and we believe we are 12-18 months away from very important data. For KIMMTRAK, we want to expand on our current leadership in metastatic uveal melanoma. Our TEBE-AM phase III life cycle management trial in cutaneous melanoma is a year away. We expect to complete enrollment in the first half of next year to be followed by data in the second half. Our ATOM phase III trial will continue to enroll. For the PRAME portfolio, our phase III PRISM-MEL continues, and this year, the goal is to confirm which dose is the appropriate dose. Signal detection will continue in ovarian and lung, and we hope to have next steps in the next 12-18 months in parallel with our PRAME half-life extended molecule to confirm infrequent, less frequent dosing makes sense. For infectious disease, our second therapeutic area, the initial HIV multiple ascending dose data in the next few weeks, and then the final HBV single ascending dose data later this year. We will finally realize our vision of being three therapeutic areas when we submit our CTA for type 1 diabetes later this year and then for CD1A in 2026. As I am sure Travis will be happy to talk about, we have a very enviable and good cash position and very nice revenues. I think with that, we will end, and I invite Travis up. Great. Thank you very much for that detailed presentation. Before I get started on Q&A, if anyone in the audience has questions, feel free to speak up or raise your hands. Thank you again. To get started, let's start with KIMMTRAK and the revenues. Obviously, you've generated over $300 million in revenues last year, which was mentioned on the presentation. What's going to lead to growth in 2025, and what's going to be the key drivers there? Yeah, thank you, Nick. We're obviously incredibly proud of our commercial launch of KIMMTRAK. We've had 11 consecutive quarters of growth, which has been terrific to see, and we expected that growth to continue going forward. If I break that growth down into two regions, the U.S. versus OUS, in the U.S., we're focused on two things. One is further penetration in the community. We see just under half the starts occurring in the community today, so we believe we continue to improve and increase that utilization. Further, we continue to see the duration of therapy increase. This has been quite a remarkable thing, and I think it's a testament to KIMMTRAK's safety profile and its efficacy in that we're seeing the duration of therapy actually go beyond what we saw in the real-world clinical, sorry, in the clinical setting, something that's very rare for that to occur. Continue to expect growth, obviously in the U.S., and for the U.S. to drive the majority of the growth worldwide. From an ex-U.S. perspective, continuing to see launches driving that growth. We've got reimbursement in the U.K. late last year, so we'll have a full year of U.K. sales this year. Continuing to just drive those launches. I think David showed that we had 14 launches last year. Obviously proud of that, and we'll continue to continue to commercialize ex-U.S. Thank you. Appreciate that. Can you speak a little bit more to the duration that you're seeing, right? You said, or you've said before that I think you're at around 11 months or a little bit more than 11 months now in the real-world setting. What's driving that, and what's leading to this being better than the clinical trials? Yeah, and I'll have David come in here too, but I think it's just a testament to the product profile. The safety profile in particular is incredibly encouraging. I think physicians continue to get more and more comfortable with the initial dosing and then monitoring those patients and then actually becoming very comfortable with it. It's a CD3 arm, so there's some CRS, and we need to monitor that. Physicians have become very comfortable with that, which also gives us, leads us comfort into believing that we can continue to penetrate in the community setting beyond just the academic setting. The only thing I would add, Nick, is I think now that there is a therapy available, there is increased screening earlier, so there's increased detection of smaller, earlier lesions, and that might play a role also. That's very interesting. What percent penetrated would you say you are right now for KIMMTRAK in the approved population, the uveal population? Yeah, in the U.S., approximately 65%, so still some room to grow. That is why we believe we'll continue to grow there. OUS, in some particular countries, we see penetration even higher than that. That is why I say when I say we expect more of the growth to come from additional launches, that is the framing there. Got it. Makes a lot of sense. You mentioned during the presentation that you're going to be targeting another 6,000 patients with the TEBE-AM and the U120 trials. For that, what's the bar to beat in both the adjuvant and the cutaneous settings? I mean, you mentioned when we're going to see data, but can you just mention it again so everyone knows? Yeah, so for the, in terms of timing, we expect TEBE-AM, KIMMTRAK, and cutaneous melanoma probably in the second half of next year, so 12-18 months away. For the ATOM trial, we expect, that's the adjuvant uveal, we expect a three-year enrollment and then 18 months for the primary endpoint. For the ATOM trial, in terms of what would be a target hazard ratio there, so the hazard ratio is relapse-free survival. I think what I would call attention to is in the phase III metastatic trial in patients who had small but visible tumors in the subset who had tumors less than three centimeters, the PFS hazard ratio was 0.68. If you can imagine patients who there is no visible tumor, and that, by the way, was randomized against pembrolizumab and ipilimumab, here we have tumors where there is no visible tumor, and we're randomizing against observation. You would expect there to be perhaps an even better hazard ratio than that. For KIMMTRAK in the cutaneous melanoma setting, this is a survival endpoint. Typically in phase III late-line trials, I think you want to target a survival hazard ratio that's in the low 0.7s or better for it to be clinically meaningful, mid to low 0.7s. Great. That makes a lot of sense. Let's move on past KIMMTRAK to your very exciting pipeline, which is very extensive. Let's start with infectious disease because you have that HIV data coming in Q1. You've briefly touched on how this differentiates based on the current treatment options. Can you just get into a little bit more detail there and explain what we're supposed to see or what we should expect to see and how this will prove this differentiation in this data? Nick, we have 16 people across three cohorts, and the highest was 300 micrograms, and we're going to continue to dose escalate because it was so well tolerated. We just had to amend the trial, and we now have it amended, and we're continuing to dose escalate. During the treatment phase, we're going to be treating for 12 weeks, and there, in addition to safety, we're going to be looking at the viral reservoir. What happens with HIV is when it infects, for example, CD4 T-cells, it gets integrated into the human genome. You can measure that reservoir that remains even when the people are taking ART. The way we're going to measure that initially is by looking at the transcriptionally active reservoir. There are other ways you can look at the reservoir too. Can we reduce the reservoir during the treatment phase? You would think that would need to happen. Now, one of the questions comes up is how much do you need to reduce the reservoir? It turns out no one knows because there never has been a therapy to reproducibly, reliably, and meaningfully reduce the reservoir. We do know that most of the reservoir is not active. I think less than 5% or 10% will actually produce replication combined virus. So you don't have to eliminate the reservoir. You have to reduce it, perhaps to allow the immune system to take over. When we stop treatment, we'll enter what's called the analytical treatment interruption or ATI. There we'll monitor the patients for up to 12 weeks looking at viral rebound. Can you alter viral rebound kinetics? It turns out that there was a meta-analysis. In fact, the largest and most recent meta-analysis was just published a few weeks ago. The senior author there, Sarah Fidler, is also the senior author of our phase I trial. This becomes the best comparator for what you expect to see during the treatment interruption phase. Historically, what's seen is on average, when you stop taking, when someone stops taking ART, the virus is detectable at on average two weeks at 50 copies per mil. By week eight, 95% have levels above transmission threshold, which is 200 copies per mil. By week 12, the rate of viral control is in the low single digits. It's very rare to see people actually make it out. In fact, it's even more rare in the patient population we're in, the population we're working on, because the population we're working on usually started their ART later after their infection. Here, the rate of control at week 12 is 0.5%. Let's just call it very rare to see people control. We're going to be looking at can we reduce the reservoir and can we alter rebound kinetics and control? That'd be fantastic. You guys have HBV data coming up in the second half of the year. That's the next most pressing catalyst for you guys right now. What are your expectations for that? This is obviously earlier data. What should we expect to see and how will that support continuation? With HIV, the reservoir is so small, we just expected to see a little bit of CRS and really nothing else. With HBV, one of the questions we had is can you thread the needle of efficacy, that is, kill the infected hepatocytes without having massive liver toxicity? Can you thread that needle? That, I think, is the goal of the SAD study, which is to say, can we get to doses that are biologically active, that are meaningfully active, but where you have a, and you do expect to see transaminitis. It's called productive transaminitis. Can you do that without seeing liver necrosis and liver toxicity? That is really the question that we hope to answer with the SAD, keeping in mind this is a single-dose study. This is not a repeat dose study. That makes sense. Let's move on to brenetafusp. First, you mentioned that let's start with the PRISM-MEL study, the phase III trial that's enrolling right now. Can you just quickly remind everyone why you chose the relatlimab as the potential comparator dose there or comparator there? Yeah. The reason we chose it is, number one, we believe we can beat it. That comes from our phase I data, which we shared at ASCO, where the disease control for our monotherapy, brenetafusp, was higher than the RELATIVITY-020 apples-to-apples clinical trial, which was nivolumab plus relatlimab in a similar population. As a monotherapy, we felt we were better than nivolumab plus LAG3. We had reasons to believe that when we move into earlier lines, we will be more active. Now we're going to be combining with another agent, PD-1. We felt scientifically we could do it. Strategically, we felt it's important to do it because nivolumab plus relatlimab, by the time we launch, will be widespread and will have a lot of penetration in the community. We have to show that we're better. The trial is designed where most patients will end up getting nivolumab monotherapy in the control arm and a minority, nivolumab relatlimab, so that we can at least have a point estimate comparison, but the control arm will be heavily dominated by nivolumab mono. Got it. That makes sense. For the ovarian and lung updates, what are you looking for? I guess not updates, but what are you looking for there that's going to determine if you definitely go into the frontline setting, which one you move into, how fast you move into them? Right. With melanoma, we were able to extrapolate because we had a lot of experience in melanoma, and we saw a signal that justified us moving into the first line phase III. With ovarian and lung, it's a different story. We have to generate the data, reason to believe. With ovarian, we saw a signal as monotherapy, but it wasn't enough to develop. We had scientific reasons to believe why earlier lines should work better. In terms of what we want to see, here we're looking at early lines in combinations with bevacizumab and with chemotherapy. The chemotherapy has a low response rate by itself, and it's not very durable. For the bevacizumab, the patients are coming in with stable on bevacizumab, so they act as their own internal control. We'll be looking at responses on the background of stable bevacizumab. We will be looking at do we see increased efficacy, and the strength of the efficacy will lead us to determine what the next study is. It will need to be a randomized study because we are studying two active agents. The type of randomized study will depend on the strength. If it is very strong data, we could go to phase III. If it is interesting but not strong enough, we could do a randomized phase II. That makes sense. I think we are almost out of time, but I want to ask about the cash and the gross margins. Do you need to explain that 99.6% gross margin and how fantastic that is? That is unseen and unheard of. That's pretty amazing. Yeah. Any CFO likes that number. Yeah. I agree. No, obviously, we're incredibly encouraged by the revenue that KIMMTRAK is and the success we've had, as we just discussed. The thing that I think, we, and the CFO also thinks the company's undervalued, but when you look at a company in our position that has over $800 million of cash, has strong revenue and continued growth from KIMMTRAK, combined with three phase IIIs and then upcoming further advancement in infectious disease and in autoimmune, we have to think we have an incredibly compelling story. Yeah. I'll just ask you because you pretty much answered my next question, but what do you think is the most underappreciated aspect of the story right now? Yeah. I think as Travis said, I think that right now, people are focused on metastatic uveal melanoma opportunity. I think people are missing the fact that KIMMTRAK is in life cycle management in a different type of melanoma with data next year that could quadruple the size of the population. The efficacy signals that I see for KIMMTRAK in uveal melanoma are replicated in cutaneous melanoma, both of them being survival endpoints. I think that at a minimum is being missed. As Travis said, also in the next 12-18 months, we're going to have additional data with brenetafusp, HIV, and PIWIL1. Awesome. With that, thank you very much. Thanks, Nick. Yeah, thanks, Nick.