Good afternoon, everyone, and thank you for joining us at Needham & Company's 24th Annual Healthcare Conference, Day 3. My name is Ethan Markowski, and I'm a member of the Biotech Research Team here at Needham. It is my pleasure to have Immunocore's Head of R&D, David Berman, and Chief Financial Officer, Travis Coy, who will be joining for the beginning part of the session with me today. As a reminder, any viewers who are watching through our conference portal are able to submit questions via the Ask the Question feature below the video feed. Welcome, guys. Before we dive in, I do want to just spend a minute or two on the current marketing conditions we're seeing.
Obviously, there's a few key topics on everyone's mind right now, but maybe we could just start by addressing how the team at Immunocore is viewing the potential impact of tariffs. I know within the past day or so, there's talk of tariffs on pharmaceutical products. The follow-up question would be your view on recent changes at the FDA.
Yeah, thanks, Ethan. First of all, Ethan, thank you for hosting us and having us. We appreciate it. You know, with respect to tariffs, I think everyone is aware at this point that, at least initially, pharmaceutical products have been excluded from tariffs. We, you know, from an Immunocore perspective, have not seen an impact financially or from a supply perspective on KIMMTRAK. You know, that being said, KIMMTRAK is manufactured in Europe, both from a drug product and drug substance perspective. Moving forward, if tariffs were to be implemented in the future that impacted pharmaceuticals and impacted KIMMTRAK, we would potentially see a non-immediate impact to our cost of goods sold. It is something we are closely monitoring and paying attention to. You know, we'll continue to look at ways to mitigate those impacts, depending on, obviously, it's an evolving situation.
Depending on what ultimately that situation lands on.
Ethan, thank you. In terms of the FDA, I would say that right now, there's no impact to us. Our major FDA interaction will probably come at the earliest next year when we get our when TEBE-AM, our phase 3 trial, reads out. Other than that, we have, of course, the day-to-day interactions with the FDA. Right now, we haven't seen any issues with those. Certainly, we're going to keep our eyes open.
Great. Great. That out of the way, we can dive now really into Immunocore and the company. Maybe just a good place to start for people who aren't as familiar, and this one might be for David, can you just describe Immunocore's technological platform and how it's similar or differentiated from other T-cell engagers?
Yeah. The major invention from Immunocore was the use of a T-cell receptor as a targeting therapy. All other companies until then, all approved drugs that were biologics were antibody-based, which means that antibodies can only recognize cell surface targets, cancer targets on the surface of the cell, for example. With T-cell receptors, you can recognize peptide-bound HLAs, which essentially means you can look inside the cell and you can target proteins inside the cell that are normally hidden from antibodies. This allows you to have a very large group of targets that are more specific for cancer than those found on the surface. Immunocore was the first company to develop and get approved a TCR therapeutic that was KIMMTRAK in uveal melanoma. I'm sure we'll talk more about that.
What's different is, as a T-cell engager, we use a T-cell receptor as the targeting domain, whereas other companies use an antibody. We can target intracellular targets. It's validated in oncology. We have multiple development programs for other targets, including a novel target called PIWIL1 in colorectal cancer, the first time that protein has been targeted. Our company also can develop this and has programs in multiple therapeutic areas, not only cancer, but also in infectious disease. We had some HIV data earlier this year. We're going to start our autoimmune programs later this year.
Great. Great. I think that's a great overview. Obviously, we'll dive more into each of those topics as we progress through the conversation. While I do have you, Travis, I think it could be a good opportunity to focus on KIMMTRAK for the next few minutes. Obviously, sales have continued to show consistent growth over the past few years. What do you attribute to the successful launch thus far, and how do you continue to generate further growth?
Yeah, thanks, Ethan. As you appropriately highlighted, we've been very proud of the launch thus far, almost three years now on the market. We have seen 11 consecutive quarters of growth, which we're very proud of. We have launched in, I think, 14 countries now. Sorry, in 2024 alone, we had launches in 14 additional countries. We continue to expand there OUS and also continue to grow from a US perspective as well. I think you asked the question of reason for our success. Honestly, I think our success is from the data. Overall, a very strong overall survival benefit in the program has allowed us to be successful in the marketplace. I think that's been the number one driving aspect of that.
Clearly, we have to execute, right, which is, I think we've seen from the sales perspective, our commercial organization has been successful in doing so.
Great. Great. A question that I know you guys get a lot, and I'll try not to belabor it too much, but obviously, average duration on therapy is a key part of KIMMTRAK's success. It's about 12 months, I believe, is the latest figure. How do you expect this figure to continue to grow? Do you think it's sort of reaching its ceiling? Or is really the takeaway here that it's just exceeded what you've seen in the clinical studies? An interesting, encouraging sign. What are your thoughts?
Yeah, no, as you've highlighted, we've been in a very unique situation where we've seen duration of therapy in the real-world setting actually go beyond what we saw in the clinical setting, which is incredibly unique. I think it's a testament to the product's safety profile and also the efficacy that I mentioned earlier. We have reached 12 months of duration. We do continue to see that increase. It's very difficult to predict where that's going to ultimately sort of plateau. We do expect it to moderate, obviously, over time. For now, at least, it is a part of the growth that we think we'll continue to see throughout both the U.S. and OUS.
Great. One question that we have gotten from investors from time to time. You are also evaluating KIMMTRAK in cutaneous melanoma, slightly larger indication. Do you expect there to be any reason to potentially lower pricing or for any pushback from payers if you get approval on that indication given the larger size?
Yeah. I think you have to break with respect to how you think about pricing on cutaneous, I think you probably have to break it into two regions. What I mean from that is break it into US considerations and OUS considerations. From a US, sorry, let me start with the OUS first. From an OUS perspective, you know, if you just look at analogs in the industry, as additional indications and as you increase your eligible patient population, you expect to see some price decline. That's natural. We would expect some pricing declines there as we launched cutaneous in OUS territories. From a US perspective, I think we think we can hold the pricing fairly steady. Obviously, that's incredibly encouraging. Clearly, all of these comments will be dependent upon the data that we generate out of TEBE-AM and the strength of that data.
That'll inform, sort of, the ultimately inform the pricing dynamics that we're able to negotiate.
Ethan, I'll just add that the reason we believe what Travis said is because the phase 3 trial is a survival endpoint. Like the survival benefit in uveal.
Great.
I definitely plan on diving more into TEBE-AM and some of the other studies as well. Maybe one more for Travis, and then I'll move over to David. How do you continue to grow XUS? Or maybe another better way to put it is, what are the remaining territories that you think are important to either gain approval or gain reimbursement at this point?
Yeah. I'll actually comment on the US growth as well. XUS, it'll largely be additional launches, right? We have approval in more than 30 countries. Apologies, the exact numbers are escaping me. Maybe David actually remembers. We have approval in more than 30 countries. We have additional launches underway. You may recall, we got reimbursement with NICE at the end of last year. That's with the UK. That's certainly one of the important ones, as you're asking, that we've begun launching in and will expect growth from this year. As you think about US growth, we expect most of that growth to come from additional launches. It varies from country to country, but in many of those countries, we have incredibly high penetration. We are the standard of care across both US and XUS.
If you think about growth U.S., you didn't ask this question, but I'll share it anyway. If you think about growth U.S., we actually touched upon the duration of therapy aspect. We do continue to see some growth from a duration of therapy, so we expect that to occur to benefit sales. We also have about 65% penetration in the U.S. A lot of that, where we're really focusing our efforts and increasing that penetration even further, is in the community setting. We are putting a lot of additional effort there to really, obviously, as you launch a product, you start with your highest deciles, right? You kind of expand from there. That is where we're really focused now, getting into the community setting and continuing to increase the usage.
Great. Thanks for that, Travis. I do think I'll probably transition now more into the clinical development side of the company.
Thanks for having me, Ethan. I really appreciate it.
Yeah. Yeah, thanks, Travis. David, maybe staying on the topic of KIMMTRAK, and I know we talked about it briefly, but can you just remind everyone the timelines for TEBE-AM as well as the ongoing study in the adjuvant setting?
Sure. TEBE-AM is the cutaneous melanoma one. Enrollment is on track to complete in the first half of next year. The endpoints are, of course, event-driven. Right now, we're projecting the second half of next year would be when the endpoint, of course, event-driven. For the ATOM trial, it's adjuvant, so it takes longer. Here we're expecting three years for accrual and then 18 months to read out. It started in the fourth quarter of last year, which is 2024. Finish accrual in 2027. I think within the next 18 months to read out.
Great. Maybe shifting focus now to PRAME. That's obviously a big topic for you guys. Last year, you reported some data for brenetafusp in melanoma as well as ovarian cancer. How do those results compare to your expectations heading into the data?
Yeah. First of all, these were late-line patients who progressed on all therapies. When we saw the initial data in these patients a few years ago at ESMO, we saw durable PRs in that initial phase one data set. We did the expansions to further define what the efficacy signal was. I think in retrospect, when we saw this new data, which is essentially one of disease control more than RECIST response rates. The disease control picture, we call a closed umbrella spider plot where patients are hovering between +20% and -30%. The same shape of the spider plot was evident in the original data that we saw. In fact, some of the PRs we saw were at -30%, and there were some patients who had minor tumor reduction of -28% or so. It was clear that brenetafusp was active.
It's active in melanoma, and it's active in ovarian. It was clear also to us that there wasn't a path forward as monotherapy in these late-line patients. It was also clear to us that there is a path forward in earlier lines. That's what we've been focused on.
Yeah. I think following up on that topic, you also saw some indicators or showed some really interesting data regarding T-cell fitness as well as ctDNA. Maybe in terms of T-cell fitness, how did that data that you generated, how does that influence your strategy going forward in PRAME?
Yeah, the T-cell fitness insights, I think, were incredibly important. We're pioneering this new field of T-cell engagers, and we continually learn from what we see. We saw this T-cell fitness in the peripheral blood in KIMMTRAK, and we've been now applying it to IMC-F106C. What it tells us is not that we want to use it as a diagnostic, a companion diagnostic, but it really guides us to which types of tumors we should prioritize and which lines of therapy. For example, we see that late-line lung cancer has those patients, unfortunately, have the lowest T-cell fitness that we've seen almost in any tumor we've enrolled. That's probably why it's been harder to identify a monotherapy signal in late-line lung. It tells us that perhaps in earlier line, the T-cell fitness might be improved. That's how we're using T-cell fitness.
Sort of similarly, in ovarian cancer, you guys are looking at both platinum-resistant and platinum-sensitive populations. Is that similar rationale there?
Yeah. The activity we saw as monotherapy was in late-line platinum-resistant. The T-cell fitness tells us you need to probably move into earlier lines. That is why we are looking at the platinum-sensitive earlier line combination. With the platinum refractory, we saw some interesting chemotherapy combination data, which we shared at ESMO last year. It just said to us we need to expand that data set because there might be something interesting. Now, there are two reasons why I think chemotherapy combinations in the platinum-resistant or PROC are interesting. The first is we showed also at ESMO that chemotherapies can induce the target on the cell. They can induce and upregulate peptide HLA on the surface. That is reason number one. Reason number two is mechanistically, there is some synergy because if you reduce the tumor size, we know our platform does work better with smaller tumors.
There are two reasons why to follow up on the chemotherapy in PROC, and there was a reason why to study earlier lines in the platinum-sensitive setting.
Great. You guys also have an ongoing phase three study for brenetafusp in frontline cutaneous melanoma being conducted against Opdualag. Can you just help us, tell us a little bit more about the study design, timelines for the study, and kind of how much of an improvement over Opdualag that you're hoping to see?
The design of the study, just to clarify, it's nivolumab plus brenetafusp in the experimental arm. The control arm is actually a blend of nivolumab monotherapy and Opdualag. The investigators don't get a choice of which to use. We do it on a country-level basis. In some countries, like the US, the investigators have to use Opdualag. They don't get a choice. In other countries in Europe, they have to use nivolumab. They don't get a choice. What we predict is that a majority of the control arm will be nivolumab monotherapy, and a minority will be Opdualag. The study is powered against the blend of the control arm. We plan to enroll enough patients on or randomize to enough Opdualag so that we can draw a point estimate comparison.
Because we know commercially to be successful, we're going to have to show that we're superior to Opdualag. It doesn't have to be statistically powered, but has to be convincing that there's a point estimate. Now, what's the reason to believe? First of all, the reason to believe in the nivolumab monotherapy that we can beat nivolumab monotherapy is that we have monotherapy activity on IMC-F106C in patients who are refractory to PD-1. It's clear to us if you move IMC-F106C earlier and you add it on to nivolumab, you now have two drugs with at least additive activity. That's the reason why we believe Nivo plus brenetafusp will be better than Nivo. With regard to Opdualag, that's Nivo plus brenetafusp versus Nivo plus LAG3, the Nivo activity cancels out.
We have to believe that brenetafusp monotherapy is better than LAG3 monotherapy because everyone's getting nivolumab. The reason that I believe that is because I believe, first of all, brenetafusp monotherapy has more activity than LAG3 monotherapy. Moreover, if you compare brenetafusp monotherapy compared to Nivo plus LAG3, which was called study RELATIVITY-20, a similar population, the brenetafusp disease control was greater than Nivo plus LAG3. I believe now moving into first line, we get the three multipliers. We know brenetafusp activity will be better in first line. We know we're adding two drugs together, brenetafusp plus nivolumab, and we know that we have two drugs each with monotherapy activity.
I know that there's also an independent monitoring committee that's expected to select a go-ahead dose later this year. What type of data will be used to inform that decision, and what kind of disclosure do you guys plan on making?
Yeah. Ethan, we did not see big differences in doses when we did the phase one dose escalation. As part of Project Optimus, the FDA still requires some type of confirmation of the dose. We agreed with them that the initial part of the PRISM-MEL, the phase three study talked about, will include two doses of brenetafusp and the control arm. That will be the first 90 patients. The IDMC will look at that data and make a decision. They will recommend dropping one of the arms, and the go-forward arm will continue. In terms of the data that the IDMC will get, they are going to get efficacy data, and they are going to get safety data from both of the brenetafusp arms. That is 30 patients per arm, so they are going to be looking for large differences.
We did not see small differences or large differences in phase I, and we do not expect there to be. They are going to look at that data. They will make a decision based on the data that they see, and they will recommend dropping one of the arms and continuing one of the others. The efficacy endpoints will be RECIST-based endpoints, like response rate to DCR, those types of endpoints.
Okay. I know, obviously, you're studying your PRAME program in non-small cell lung cancer, like you mentioned. Can you just remind us timing-wise or where you're at in that indication and why also you took a slightly more selective approach to enrollment there?
Yeah. Where we are is still in the signal detection phase for lung cancer. We're still looking for the signal. Now, on the one hand, there's reason to believe that it should work because we have seen when we looked at patients' tumors early on, we saw PRAME peptide being presented on the surface. In theory, it should be targeted. We know that lung cancer is a T-cell-sensitive tumor. We know that T-cell therapies should work. On the other hand, lung is a very complex tumor. There are different subsets. Unfortunately, the patients that we enrolled in the initial monotherapy had very aggressive tumors. I've talked about they had low T-cell fitness.
When we discussed this data with the investigators, they said, "Based on everything that you're seeing and based on types of patients, it'd be better to look earlier and in combination to look to see a signal." That is what we're doing now. I think that we'll be able to determine, look at the data and have insights in the next 12 to 18 months.
Okay. Maybe one more on PRAME for me. You also have a half-life extended program in the pipeline. What kind of frequency of dosing are you hoping to achieve, and how will you decide whether to advance that program forward versus brenetafusp?
We think it has to be at least every two weeks or three weeks to be reasonable because we already have the weekly dosing from brenetafusp as a monotherapy. We know when we combine brenetafusp with another active therapy, we can space out the dosing to every two weeks. There has to be strong reason to believe. Our base case has always been that the half-life extended will give us more convenience. I talked about every two weeks or three weeks or perhaps even longer. The open question is whether you get better efficacy by doing a half-life extension. We're open to that. I mean, that's part of what the phase one study is being done. What we're going to be doing is we essentially have three experiments in parallel.
We have the PRAME half-life extension as a monotherapy, which is ongoing now this year in 2025, in many of the same tumors that we've studied brenetafusp in. We have the brenetafusp for ovarian, bevacizumab combination, chemotherapy combination, and we have the brenetafusp in ovarian. In lung, we have brenetafusp plus docetaxel, brenetafusp plus osimertinib. We will be actually able to integrate all of those different arms to decide on what the next step is because all of the data we're generating with brenetafusp is translatable to our half-life extension, which is essentially the same as brenetafusp, except it has an FC fragment on it. We are going to use all of those data points to really determine what the next steps are. We will make a data-driven decision as to which program. We can mix and match. We could develop PRAME HLE mono.
We could take the data from ovarian and switch in PRAME HLE. It is going to be a data-driven decision.
Sounds like you have a lot of optionality there. I do want to move on to some of the data you presented in infectious disease recently. Before I do, there is actually a question in the chat that I want to relay to you. Someone asked, just to clarify, is the phase three study, assuming for cutaneous melanoma, not powered to show superiority over Opdualag?
Yeah, correct. It is powered for all of the patients in the control arm are treated as one. What we will do is present point estimates. Like you see in a tornado plot, we'll present point estimates to compare to Opdualag. It is not powered because there will not be enough patients. We have identified the minimum in order to have a reliable estimate to draw a conclusion because we know that has to be drawn for us to be commercially successful.
Okay. I think that's helpful. Back to HIV, presented some data recently. Can you talk a little bit about the activity you saw and what you're ultimately hoping to achieve with that program?
Yeah. It is the same general idea as KIMMTRAK. For KIMMTRAK, we have a TCR targeting peptide specific for cancer, and then we are recruiting T-cells. Here in the HIV program, we have a TCR targeting an HIV peptide, and we are redirecting T-cells to kill infected cells. The current standards of care are antiretroviral drugs, which will suppress viral replication, but they do not eliminate the reservoir. When a person stops taking antiretroviral, the virus will rebound within two weeks. The current HIV other companies are focused on less frequent antiretroviral treatment, whether it is every other month, six months, or once a year. Our approach is radically different. Our approach is to eliminate the viral reservoir so that the person can be off all therapy for a long period of time, one, two, three years. That is what the goal of the study was.
Initially, in the multiple ascending, we really wanted to, of course, we want to get to a dose, but we want to ask, can this mechanism actually work? Because it's a huge unknown. Can you actually impact the viral reservoir, and can you actually alter the kinetics of rebound? We believe that the data that we showed suggests that we are on the right track. Now, we haven't reached our TPP with this initial data, but it's incredibly exciting to us in the field that we've actually seen alterations and reductions of the reservoir and alterations of rebound. We are incredibly excited by that. We continue to dose escalate.
Great. The safety profile looked good overall. There was some transient grade 1 CRS reported in the highest dose cohort. What degree of CRS do you think physicians would find acceptable in an indication like HIV versus oncology, for example?
Yeah. It is clear, I think, with oncology, they are going to accept some low, some severe CRS, usually less than 5%. It is likely in HIV, they will probably have to have grade 2 CRS very, very low. Grade 1 CRS is essentially fever. It is what you get when you get a COVID vaccine or if you have the flu or something. The CRS that we have seen and are likely to see is very predictable. It is within a few hours of dosing. Right now, at 300 micrograms, that has been perfectly tolerable, which is why we are going to dose escalate. One interesting thing we did learn, if I can mention scientifically what was fascinating, is we were giving a regimen of 20, 40 micrograms, and then 300 micrograms without steroids here.
If we gave those doses in a cancer patient, for example, PRAME or gp100, you would see severe CRS even at the 20 micrograms. The fact that we're not seeing any CRS at 20 or 40 micrograms was so exciting to us because it confirms that the CRS we are seeing is likely target-mediated. It's not just randomly activating T-cells in the blood because we would see it then regardless. With HIV, the key point is that the target density is so low compared to a large solid tumor. There was some scientific excitement about why the CRS was so low.
No, that's a good point. Thanks for bringing that up. I think that is an important clarification. You also have ongoing study in HBV. Are there any takeaways from the HIV dataset that you think are pertinent to that ongoing study, and what data do you expect to report there?
Yeah. It is a very similar idea here. The goal is to eliminate the HBV-positive hepatocytes. The HIV MAD study, I think it went faster than—sorry, the HIV MAD study went fast. The HBV SAD study, unfortunately, has taken longer than we wanted. Here, the critical question that we in the field had is, can you thread the needle of efficacy and safety? Can you actually eliminate the virus by killing infected hepatocytes without causing massive liver toxicity? You do expect to see what is called productive transaminitis, which is LFT, AST, ALT increases because you are killing hepatocytes, but then those should go back down. What you do not want to see is synthetic liver damage. You do not want to see changes in albumin or clotting times. We were really trying to see, can we thread the needle?
Can we see early signs of activity in the absence of severe liver toxicity? The caution here is, of course, this is a single-dose study that we'll be reporting later this year, not multiple doses. That is the question that we're set out to answer.
Okay. And then in general, for your infectious disease programs, I know that obviously a lot of your, well, KIMMTRAK and then a lot of your pipeline is in oncology. Do you plan on progressing these for yourselves, or are you open to partnering them?
Yeah. Our general sense is to partner if it makes strategic sense for us. The HIV, HBV programs, we can run phase one and probably phase two, likewise maybe with the autoimmune. I think late-stage programs probably would make sense to partner. I think we'll have to see where the data goes. Yeah, I think we're open to partnering.
Okay. You did mention autoimmune, which I do want to spend a few minutes on that because I think it's interesting technology. Can you just provide a little more background on those programs and their ability to accurately target specific tissues?
Yeah. The current standards of care for autoimmunity are essentially systemic immune suppression. You can try to suppress inflammation in the target organ, but you also end up with global immune suppression. Our vision was, could we get tissue-specific immune suppression or organ suppression? The way we decided to do that is to use our T-cell receptor technology. In cancer or HIV, we target the infected cell with our T-cell receptor. In autoimmune, we target the specific organ or tissue by using the same approach by targeting peptide HLA that are specific for the tissue. For example, the beta cell in the pancreas is the site or the place where type 1 diabetes occurs.
The major difference with our oncology program is on the effector arm because here, rather than activating T-cells, we have an effector arm that will turn off T-cells, which is the PD-1 agonist. The idea is to tether the bispecific to the target that's inflamed and then use the effector to turn off the immune system.
Great. I know your CD1a program is a little unique in the sense that's not HLA-restricted. Can you just talk about the significance of that and if you have other non-HLA-restricted programs teed up in the pipeline?
Yeah. The HLA non-restricted nature is we're quite excited about it because this is our we don't have to do HLA screening, which certainly helps. Atopic dermatitis is a large opportunity also. We have studied other non-HLA-restricted oncology programs. For example, we've looked at HLA-E. We've also talked, and we will talk more about a gamma delta receptor program, which is HLA unrestricted. I think HLA unrestricted in oncology is just a little more challenging. We've also talked about HLA unrestricted for tuberculosis. We've actually developed a T-cell receptor program for that. We recently published about HLA unrestricted for HIV. It certainly is something that would make a lot of sense, but it is technically still a challenge in oncology.
Okay. I do want to take this time to remind viewers that we are getting closer to time here. If you do have any questions, you could please forward them in the chat, and I will relay them on to David. We do actually have one question here. It's more of a broader question, but I think you'll be able to give your thoughts on it. Are there any thoughts or outlook on the potential changes in the frontline setting across oncology given development of PD-1 VEGF bispecifics recently?
Yeah. Certainly, there's been a lot of investment and excitement on the PD-1 VEGF. I think we're waiting for the survival update this year to see the PFS look promising, and I think we're waiting to see the survival. My sense is that the PD-1 VEGF will replace PD-1s where the PD-1s are approved. I think it's yet to be seen whether they can expand where PD-1s are not active. If that's the case, for us at least, the approach would be we would need to combine with PD-1 plus VEGF rather than just with PD-1. For us, it doesn't matter what the combination partner is, whether it's PD-1 VEGF or whether it's PD-1 monotherapy.
I think probably the challenge to the field in general is sometimes you get caught up in an inflection point where trials are ongoing, and you have to make decisions without knowing if the PD-1 VEGF is going to be approved in that setting. That's probably the challenge for everyone in the field is that it's a place in flux right now.
Great. I did get another one related to your HIV program. I think you touched on this a little already, but could you foresee that program ultimately being used in combination with other agents to achieve a functional cure?
Yeah, absolutely. I mean, right now, we are using it on top of antiretroviral, which is, of course, standard. But we could easily see it being used also with broadly neutralizing antibodies or with any modality that would make scientific sense. In fact, one of the amazing things with this platform is no matter what we've studied in combination, the safety has always been acceptable. That's because we have most data in oncology, of course, but I fully expect the same to be in HIV. That's because almost all the adverse events we see are within hours of the first three doses. With repeated dosing, there doesn't appear to be any new AEs forming. Typically, with combination partners, the AEs are cumulative. You don't see them in the first few weeks. They typically occur later. Absolutely, we can combine them.
There may be scientific reasons to combine them with certain therapies also.
Great. I know we are getting close to time here, but I do want to give you the floor for the last minute or two, maybe touch on I think we covered a lot, but maybe touch on any other programs in the company that you want to highlight or aspects that are being potentially underappreciated by investors at the moment.
Yeah. I think, first of all, the fact that we have two KIMMTRAK lifecycle management programs in the same tumor, melanoma, is something that's missed. Lifecycle management programs typically have a higher probability of technical and regulatory success. We're going to get the first readouts of the cutaneous next year and the adjuvant study in a few years. I think people understand where we are with IMC-F106C from PRAME, HLA, and we hope to have some data in the next 12-18 months to afford the next step. Behind that, PIWIL1 is our first foray into colorectal cancer, and then the two autoimmune programs that are entering the clinic that we touched on. I do, and then HIV expansion will be in the next 12-18 months.
I do think the next 12 to 18 months will be a data-rich insight into where this company is going.
Great. With that, I do not see any further questions in the chat. I think we are just about up on time. I want to thank you again, David, for attending the conference and for talking a little bit about Immunocore.
Thank you very much, Ethan. Have a nice day.