Immunocore at Needham Conference: Strategic Growth and Innovation

On Wednesday, 09 April 2025, Immunocore Holdings (NASDAQ: IMCR) presented at the 24th Annual Needham Virtual Healthcare Conference, offering a comprehensive overview of its strategic initiatives and future outlook. The company highlighted robust growth prospects, driven by advancements in its T cell receptor technology and product pipeline, while also addressing potential challenges such as tariff impacts on pharmaceutical costs.

Key Takeaways

• Immunocore's T cell receptor technology distinguishes it from antibody-based therapies, offering unique targeting capabilities.
• Chemtrec has achieved 11 consecutive quarters of growth, expanding into 14 new countries in 2024.
• The company is optimistic about future growth, with significant data expected over the next 12 to 18 months.
• Immunocore is exploring partnerships for later-stage programs, especially in infectious diseases and autoimmune disorders.
• Financial strategies focus on expanding sales and maintaining stable pricing in the US market.

Financial Results

• Chemtrec Sales and Growth: Immunocore has experienced steady growth since Chemtrec's launch, with a strong presence in the US and international markets. The therapy's success is attributed to compelling overall survival data.
• Pricing Strategy: While potential price declines are anticipated in some territories, US pricing aims to remain stable, supported by data from ongoing trials.

Operational Updates

• Chemtrec Expansion: Immunocore is focused on launching Chemtrec in approved countries and increasing US market penetration. The UK is expected to contribute significantly due to NICE reimbursement.
• Clinical Trial Updates: Key trials, including TEBY AM and ADAM, are progressing as planned, with crucial data readouts anticipated in the coming years.

Future Outlook

• Pipeline Expansion: Immunocore is prioritizing combination therapies and early-line treatments, particularly for brunetifas. The company is also advancing programs in HIV and HBV, with potential for strategic partnerships.
• Strategic Focus: Leveraging T cell fitness insights, Immunocore aims to optimize tumor prioritization and therapy selection, enhancing the efficacy of its pipeline assets.

Q&A Highlights

• Cutaneous Melanoma Study: The phase three study is designed to provide comparative data, though not powered for superiority over existing treatments.
• HIV Program Potential: Promising initial safety profiles suggest potential for combination therapies aimed at functional cures.

Readers are encouraged to refer to the full transcript for a detailed account of Immunocore's strategic plans and developments.

Full transcript - 24th Annual Needham Virtual Healthcare Conference:

Ethan Markowski, Member of biotech research team, Needham and Company: Good afternoon, everyone, and thank you for joining us at Needham and Company's twenty fourth Annual HealthCare Conference day three. My name is Ethan Markowski, and I'm a member of the biotech research team here at Needham. It is my pleasure to have Immunocor's head of r and 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. So welcome, guys.

And before we dive in, I do wanna just spend a minute or two on the current market 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 Immunocor is viewing the potential impact of tariffs. I know within the past day or so, there's talk of tariffs on pharmaceutical products. Then this follow-up question would be your view on recent changes at the FDA.

Travis Coy, Chief Financial Officer, Immunocor: Yeah. Thanks, Ethan. Well, first of all, Ethan, thank you for for hosting us and having us. We appreciate it. You know, with respect to tariffs, I think everyone is aware of at this point that at least initially, pharmaceutical products have been excluded from tariffs.

So we you know, from an Immunocore perspective, we have not seen an impact financially or from a or from a supply perspective on on Chemtrak. But, you know, that being said, Chemtrak is manufactured in Europe both from a drug product and drug substance perspective. So moving forward, if tariffs were to be implemented in the future that impacted pharmaceuticals and then and impacted Chemtract, we would potentially see a non immediate impact, to our cost of goods sold. So it is something we are closely monitoring and paying attention to. And, you know, we'll continue to look at ways to mitigate those those impact depending on obviously, it's an evolving situation, so depending on what, ultimately, that situation lands on.

David Berman, Head of R&D, Immunocor: In term, 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 TEBY AM, our phase three trial reads out. Other than that, we have, of course, the day to day interactions with the FDA. But, right now we haven't seen any issues with those.

Certainly we're to keep our eyes open.

Ethan Markowski, Member of biotech research team, Needham and Company: Great. Great. So that out of the way, we can dive now really into Immunocor and the company. So maybe just a good place to start for people who aren't as familiar, and this one might be for David. Could you just describe Immunocor's technological platform and how it's similar or differentiated from other T cell engagers?

David Berman, Head of R&D, Immunocor: Yeah. So, the major, invention from Immunocor 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, say cancer targets on the surface of the cell, for example. And with T cell receptors, you can recognize peptide bound HLAs, which is essentially means you can look inside the cell, and you can target proteins inside the cell that are normally hidden from antibodies. And this allows you to have a very large group of targets that are specific, more specific for cancer than those found on the surface.

And ImmunoCor was the first company to develop and get approved a TCR therapeutic that was chemtrac in uveal melanoma, and I'm sure we'll talk more about that. So what's different is as a T cell engager is we use a T cell receptor as the targeting domain, whereas, other companies use an antibody. So we can we can target intracellular targets. It's validated in oncology. We have multiple development programs for other targets, including a novel target called p well one in colorectal cancer.

The first time that protein has been targeted. And then we can also 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. And then we're gonna start our auto our autoimmune programs later this year.

Ethan Markowski, Member of biotech research team, Needham and Company: Great. Great. I think that's a great overview. And, obviously, we'll dive more into each of those topics as we progress through the conversation. But while I do have you, Travis, I think it could be a good opportunity to focus on Chemtrac for the next few minutes.

Obviously, sales have continued to show con 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?

Travis Coy, Chief Financial Officer, Immunocor: Yeah. Thanks, Ethan. As you appropriately highlighted, we've been very proud of of the launch thus far, almost three years now on the market. And, you know, we've seen 11 consecutive quarters of growth, which we're, you know, very proud of. And we've we've launched in, I think, 14, countries now.

Or sorry. In in 2024 alone, we had launches in in 14 additional countries. So, you know, we continue to expand, their OUS and 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.

You know, and overall, a very strong overall survival benefit in the program, has allowed us to be successful in the marketplace. And that's I think that's been the, you know, the number one driving aspect of that. And and, clearly, we have to execute, right, which is is I think we've seen from the sales perspective, our commercial organization has has been successful in doing so.

Ethan Markowski, Member of biotech research team, Needham and Company: Great. Great. And then a question that I know you guys get a lot, and I'll I'll try not to belabor it too much. But obviously average duration on therapy is a key part of, Chemtrex success. And it's about twelve 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 and just an encouraging sign? What are your thoughts?

Travis Coy, Chief Financial Officer, Immunocor: Yeah. No. As you 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 the clinical what we saw in the clinical setting, which is is incredibly unique. And I think it's a testament to the product's safety profile, but also the efficacy that I that I mentioned earlier. You know, we we have reached 12 of duration.

We do continue to see that increase. We we can it's it's very difficult to predict where that's gonna ultimately sort of plateau. You know, we we do expect it to moderate, obviously, over time. But for now, at least we it is it is a part of the growth, that we think we'll continue to see throughout the both US and, US and OUS.

Ethan Markowski, Member of biotech research team, Needham and Company: Great. And then one question, that we have gotten from investors from time to time. So you are also evaluating Chemtrec and, 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?

Travis Coy, Chief Financial Officer, Immunocor: Yeah. I think you have to break in with respect to how you think about pricing on Cutaneous, I think you probably have to break it into two regions. And and what I mean from that is break it into US considerations and OUS considerations. From a US per sorry. Let me start the OUS first.

From an OUS perspective, you know, if you just look at analogs in the industry, as you as additional indications and and as you increase your eligible patient population, you expect to see some price decline. That that's natural. So we we would expect some pricing, you know, some pricing declines there as we the launch cutaneous in in OUS territories. From a US perspective, I think we we think we can hold the pricing fairly steady. And that's, you know, obviously, that's incredibly encouraging.

Clearly, all of these comments will be dependent upon the data that we generate out of WAM, and what the the strength of that data, and and that'll inform sort of the, ultimately inform, the pricing dynamics that we're able to to able to negotiate.

David Berman, Head of R&D, Immunocor: Ethan, I'll I'll just add that, the reason we believe what Travis said is because the phase three trial is a survival endpoint. So, you know, like the survival benefit in UVAIL.

Ethan Markowski, Member of biotech research team, Needham and Company: Great. And I definitely plan on, you know, diving more into WAM and some of the other studies as well. But maybe one more for Travis, and then I'll I'll move on over to David. How how do you continue to grow ex US? 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?

Travis Coy, Chief Financial Officer, Immunocor: Yeah. So I'll I'll actually comment on The US growth as well. So ex US, it'll largely be additional launches. Right? We we have approval in more than 30 countries.

I have apologies. The exact number is escaping me. Maybe David actually remembers. But we have approval more than 30 countries, and so we have additional launches underway. We actually got you may recall, we got reimbursement with NICE at the end of last year, so that's with The UK.

So that's certainly one of the important ones, as you're asking, that we're continue that we've begun launching in and and we'll expect growth from, this year. So from a as you think about US growth, we expect most of that growth to come from additional launches. We we have it varies from country to country, but in many of those countries, we have incredibly high penetration. We are the standard of care, across, across both US and ex US. If you think about Growth US, you didn't ask this question, but I'll I'll share it anyway.

Mhmm. You think about Growth US, we we actually touched upon the duration of therapy, aspect. We we do continue to see some growth from a duration of therapy, so we expect that to occur, to benefit sales. We also, you know, we have about 65% penetration in The US. So and a lot of that where we're really focusing our efforts and then increasing that penetration even further is in the community setting.

So we're putting a lot of additional effort there to to really, you know, you obviously as you launch a product, you start with your highest decile deciles. Right? And then you kinda ex expand from there. And that's that's where we're really focused now is getting into the community setting and continuing to to increase the the usage.

Ethan Markowski, Member of biotech research team, Needham and Company: Right. Thanks for that, Travis. And I do think I'll probably transition now more into clinical development side of the company.

Travis Coy, Chief Financial Officer, Immunocor: But Thanks for letting me, Ethan. I really

Ethan Markowski, Member of biotech research team, Needham and Company: appreciate it. Yeah. Thanks, Travis. So, David, you know, maybe staying on the topic of of Chemtrac, and I know we talked about it briefly, but, can you just remind everyone the timelines for TEBY AM as well as the ongoing study in the adjuvant setting?

David Berman, Head of R&D, Immunocor: Sure. So Tebi AM is the cutaneous melanoma one and enrollment is on track to complete in the first half of next year. And then the endpoints are, of course, event driven. But right now we're projecting the second half of next year would be when the, endpoints, of course event driven. For the ADAM trial, it's adjuvant, so it takes longer.

And here we're expecting three years for accrual and then eighteen months to read out. So it started at in the fourth quarter of, last year, which is '24. So finish accrual in '27, and then I think within the next eighteen months to readout.

Ethan Markowski, Member of biotech research team, Needham and Company: Great. And that maybe shifting focus now to PRAME. That's obviously a big topic for you guys. Last year, you reported some data for brunetifas in melanoma as well as ovarian cancer. How do those results compare to your expectations heading into the data?

David Berman, Head of R&D, Immunocor: Yeah. So, first of all, these were late line patients who progress in 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. And so we did the expansions to further define, what the efficacy signal was. And I think in retrospect, when we saw this new data, which is essentially one of disease control more than resist response rates, and the disease control picture, we call the umbrella we call a closed umbrella spider plot where patients are hovering between plus 20 and minus 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 minus thirty percent, and there were some patients who had minor tumor reduction of minus twenty eight percent or so. So it was clear that Brenny was active. It's active in melanoma, and it's active in ovarian. And 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.

And so that's that's what we've been focused on.

Ethan Markowski, Member of biotech research team, Needham and Company: Yeah. And 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. But maybe in terms of T cell fitness, how did that data that you generated, how does that influence your strategy going forward in print?

David Berman, Head of R&D, Immunocor: Yeah. The the T cell fitness insights, I think, were incredibly important. You know, we're pioneering this new field of of TCR T cell engagers, and we continually learn from what from what we see. We learned this we saw this T cell fitness in the peripheral blood in Kim track, and we've been now applying it to brunetifest. So 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, and that's probably why it's been harder to identify a monotherapy signal in late line lung. But it tells us that perhaps in earlier line, the T cell fitness might be improved. So that's how we're using, T cell fitness.

Ethan Markowski, Member of biotech research team, Needham and Company: And sort of similarly, in ovarian cancer, you guys are looking at platinum resistant and platinum sensitive populations. Is that similar rationale there?

David Berman, Head of R&D, Immunocor: Yeah. So the activity we saw as monotherapy was in late line, platinum resistant. And so the T cell fitness tells us you need to probably move into earlier lines, and that's why we're 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, and 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. So that's reason number one. And reason number two is, mechanistically, there's some synergy because if you reduce the tumor size, we know our platform does work better with smaller tumors. So there's two reasons why to follow-up on the chemotherapy in PROC, and there was reason why to study earlier lines in the platinum sensitive setting.

Ethan Markowski, Member of biotech research team, Needham and Company: Right. And guys have also have an ongoing, phase three study for brineon frontline cutaneous melanoma, being conducted against Abdulaleid. Can you just help us, you know, tell us a little bit more about the study design, timelines for the study, and kind of how much of an improvement over Abdulaliq that you're hoping to see. So

David Berman, Head of R&D, Immunocor: the design of the study, just to clarify, it's nivolumab plus brinadifusp in the experimental arm.

Ethan Markowski, Member of biotech research team, Needham and Company: Right.

David Berman, Head of R&D, Immunocor: Then the control arm is actually a blend of nivolumab monotherapy and obdulag. And the investigators don't get a choice of which to use. We do it on a country level basis. So in some countries like The US, the investigators have to use Abdulleg. They don't get a choice.

In other countries in Europe, they have to use nivolumab. They don't get a choice. And what we predict is that a majority of the control arm will be nivolumab monotherapy, and a minority will be Abdulleg. The study is powered against the blend of the control arm. Now we plan to enroll enough patients on or randomized to enough Abdulaleg so that we can draw a point estimate comparison.

Because we know commercially to be successful, we're gonna have to show that we're superior to up to a lag. 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? Well, first of all, the reason to believe in the nivolumab monotherapy that we can beat nivolumab monotherapy is that we have monotherapy activity of brunetifest in patients who are refractory to PD-one. And so it's clear to us if you move brinadipus earlier and you add it on to nivolumab, you now have two drugs with at least additive activity.

So that's the reason why we believe nivo plus brinne will be better than nivo. With regard to Abdulag, so that's nivo plus brani versus nivo plus LAG-three, the nivo activity cancels out. So we have to believe that branetifest monotherapy is better than LAG-three monotherapy because everyone's getting the volume out. And the reason that I believe that is because I believe, first of all, brunetifest monotherapy has more activity than LAG-three monotherapy. And moreover, if you compare brunetephus monotherapy compared to nivo plus LAG-three, it was called study relativity 20, a similar population, the brunetephus disease control was greater than nivo plus LAG-three.

So I believe now moving into first line, we get the three multipliers. We know Brinetipus' activity will be better in first line. We know we're adding two drugs together, Brinetipus plus nivolumab. And we know that we have two drugs each with monotherapy activity.

Ethan Markowski, Member of biotech research team, Needham and Company: And then I know that there's also an independent monitoring committee that's expected to start to 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?

David Berman, Head of R&D, Immunocor: Yeah. So, Ethan, we didn't see big differences in doses when we did the phase one dose escalation. But as part of Project OPTIMAIST, the FDA still requires some type of confirmation of the dose. So we agreed with them that the initial part of the PRIZMAL, the phase three study you talked about, will include two doses of brunetifest and the control arm, and that'll be the first ninety patients the IDMC will look at that data and make a decision. They'll recommend dropping one of the arms, and the go forward arm will continue.

In terms of the data that the IDMC will get, they're going to get efficacy data, and they're going to get safety data, from both of the brunetifest arms. And now that's 30 patients per arm, so they're going be looking for large differences. We didn't see small differences or large differences in phase one, and we don't expect there to be, but, they're going to look at that data. And, so they'll make a decision based on the data that they see, and they'll recommend, dropping one of the arms and continuing one of the others. And the efficacy endpoints will be resist based endpoints, like response rate to DCR, those types of endpoints.

Ethan Markowski, Member of biotech research team, Needham and Company: Okay. And then I know, obviously, you're studying your 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?

David Berman, Head of R&D, Immunocor: Yeah. So where we are is still in the signal detection phase for lung cancer. We're still looking for the signal. Now there's 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 brain peptide being presented on the surface. So in theory, it should be targeted.

And we know that lung cancer is a T cell sensitive tumor, so we know that, T cell therapies should work. But on the other hand, lung is a very complex tumor. There's different subsets. And unfortunately, the patients that we enrolled in the initial monotherapy had very aggressive tumors, and I've talked about they had low T cell fitness. So when we discussed this data with the investigators, they said, you know, 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.

So that that's what we're doing now. And I think that we'll be able to determine, look at the data and have insights with it in the next twelve to eighteen months.

Ethan Markowski, Member of biotech research team, Needham and Company: Okay. And then maybe one more on Prem for me. So 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 brinee?

David Berman, Head of R&D, Immunocor: So 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 brunetifest as monotherapy. And we know when we combine brunetifest with another active therapy, we can space out the dosing to every two weeks. So there has to be strong reason to believe. Our base case has always been that the half life extended will give us more convenience. You know?

So I talked about every two weeks or three weeks or perhaps even longer. The the open question is whether you get better efficacy by doing half life extension, and 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 pream half life extension as a monotherapy, which is ongoing now, this year in '25, in many of the same tumors that we've studied brunetifest in.

We have the brunetifest ovarian, bevacizumab combination, chemotherapy combination, and we have the brunetifest in ovarian. And in lung, have brinettifest plus docetaxel, brinettifest plus Tagrisso. And so we'll 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 Brinenafusp is translatable to our half life extension, which is essentially the same as Brinenafusp, except it has an Fc fragment on it. So we're going to use all of those data points to really determine what the next steps are, and we'll make a data driven decision as to which program. And we can mix and match.

We could develop PRAME HLE mono. We could take the data from ovarian and switch in PRAME HLE. So it's going to be a data driven decision.

Ethan Markowski, Member of biotech research team, Needham and Company: Sounds like you have a lot of optionality there. I I do want to move on to some of the data that you presented in infectious disease recently. But before I do, there is actually a question in the chat that I want to relay to you. So someone asked just to clarify, is the phase three study assuming for cutaneous melanoma, not powered to show superiority over Abdulag?

David Berman, Head of R&D, Immunocor: Yeah, correct. It is powered for the, you know, the all of the patients in the control arm are treated as one. What we will do is present a point estimates like you see in a tornado plot. We'll present point estimates to compare to up to a leg. But it was it's not powered because there won't be enough patients.

But 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.

Ethan Markowski, Member of biotech research team, Needham and Company: Okay. I think that's helpful. So 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?

David Berman, Head of R&D, Immunocor: Yeah. This is so it's the same general idea as KimTrack. For KimTrack, we have a TCR targeting peptide specific for, cancer, and then we're recruiting T cells here in the HIV program. We have a TCR targeting an HIV peptide, and we're redirecting T cells to kill infected cells. So the current standards of care is antiretrovirals drugs, which will suppress viral replication, but they don't eliminate the reservoir.

And when a person stops taking antiretroviral, the virus will rebound within two weeks. So the, current HIV other companies are focused on less frequent antiretroviral treatment, whether it's 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, you know, a long period of time, one, two, three years. So that's what the, goal of the study was.

And initially, in the multiple ascending, we really wanted to of course, we wanna get to a dose, but we wanna ask, can this mechanism actually work? Because it's 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 tells us suggests that we are on the right track. Now we haven't reached our TPP with this initial data, but it's incredibly exciting for us in the field that we've actually seen alterations and reductions of the reservoir and alterations of rebound.

So we're incredibly excited by that. And and so we continue to dose escalate.

Ethan Markowski, Member of biotech research team, Needham and Company: Great. And, you know, the safety profile looked good overall. There was some transient grade one 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?

David Berman, Head of R&D, Immunocor: Yeah. So I think with oncology, they're gonna accept some low, some severe CRS, you know, usually less than five percent. But it's likely in HIV, they want will probably have to have grade two CRS very, very low. Grade one CRS is is essentially fever.

It's it's what you get when you get a COVID vaccine or, it's, you know, if you have the flu or something. So the CRS that we have seen and are likely to see is very predictable. It's within a few hours of dosing. So right now, at three at three hundred micrograms, it's been perfectly tolerable, which is why we're going to dose escalate. One interesting thing we did learn is if I can mention scientifically what was fascinating is we were giving a regimen of twenty, forty micrograms, and then three hundred micrograms without steroids here.

And if we gave those doses in a cancer patient, for example, PRAME or g one hundred, you would see severe CRS even at the twenty micrograms. The fact that we're not seeing any CRS at twenty or forty 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. So there was some scientific excitement about why the CRS was so low.

Ethan Markowski, Member of biotech research team, Needham and Company: That's a good point. Thanks for bringing that up. I think that is an important clarification. You also have, you know, ongoing study in HBV. So 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?

David Berman, Head of R&D, Immunocor: Yeah. So it's very similar idea here. The goal is to eliminate the HPV positive hepatocytes. And, the HIV MAD study would just I think it went faster than than sorry. The HIV MAD study went fast.

HPV SAD study, unfortunately, has taken longer than we wanted. But here, the 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's called productive transaminitis, which is LFT, AST, ALT increases because you are killing hepatocytes, but then those should go back down. What you don't wanna see is synthetic liver damage.

You don't wanna see, changes in albumin or clotting times. And so 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, but that's the question that we set out to answer.

Ethan Markowski, Member of biotech research team, Needham and Company: Okay. And then in general, for your infectious disease programs, you know, I know that obviously a lot of your well, Chemtrac and then a lot of your pipeline is in oncology. Do you plan on progressing these forward yourselves, or are you open to partnering them?

David Berman, Head of R&D, Immunocor: Yeah. Our our 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. But I think, you know, late stage programs probably would make sense to partner, and I think, you we'll have to see if the data you know, where the data goes.

But, yeah, I I think we're open to partnering.

Ethan Markowski, Member of biotech research team, Needham and Company: Okay. And then you did mention autoimmune, which I do wanna 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?

David Berman, Head of R&D, Immunocor: Yeah. So the current standards of care for autoimmunity are essentially systemic immunosuppression. So you can try to suppress inflammation in the target organ, but you also end up with global immune suppression. And so our vision was, could we get tissue specific immune suppression or organ suppression? And the way we decided to do that is to use our T cell receptor technology.

So 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 in the pancreas is the site or the the place where type one 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 p d one agonist. So the idea is to tether the bispecific to the target that's inflamed and then use the effector to turn off the immune system.

Ethan Markowski, Member of biotech research team, Needham and Company: Right. And I know your CD one a 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?

David Berman, Head of R&D, Immunocor: Yeah. The HLA non restricted nature is we're quite excited about it because, this is our you know, we don't have to do HLA screening, which certainly helps. And atopic dermatitis is a large opportunity also. We have studied other non HLA restricted oncology programs. For example, we've published on we've looked for at HLAE.

We've 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, and we recently published about HLA unrestricted for HIV. So it certainly is something that would make a lot of sense, but it is, technically still a challenge in oncology.

Ethan Markowski, Member of biotech research team, Needham and Company: And I do wanna take this time, to remind viewers that we are getting closer to time here. So 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 one VEGF bispecifics recently?

David Berman, Head of R&D, Immunocor: Yeah. It's it's certainly there's been a lot of investment and excitement on the p d one VEGF. I think we're waiting for the survival updates this year to see you know, the PFS look promising, and I think we're waiting to see the survival. My sense is that the p d one VEGF will replace p d ones where the p d ones are approved. I think it's yet to be seen whether they can expand where p d ones are not active.

So if that's the case, for us at least, the approach would be we would need to combine with PD-one plus VEGF rather than just with PD-one. So, for us, it doesn't matter, what the combination partner is, whether it's PD-one VEGF or whether it's PD-one 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-one VEGF is going to be approved in that setting. That's probably the challenge for everyone in the field is that it's a it's a it's a place in flex right now.

Ethan Markowski, Member of biotech research team, Needham and Company: Great. And then I got I did get another one, related to your HIV program. So 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?

David Berman, Head of R&D, Immunocor: 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 can that 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. And that's because we have most of the 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 formings. And typically with combination partners, the AEs are cumulative. You don't see them in the first few weeks. Typically occur later.

So absolutely, we can combine them. There may be scientific reasons to combine them with, certain therapies also.

Ethan Markowski, Member of biotech research team, Needham and Company: Right. And I know we are getting close to time here, but, do wanna give you the floor for the last minute or two, maybe touch on, you know, I think we covered a lot, but maybe touch on any other programs in the company that you wanna highlight or aspects that are being potentially underappreciated by investors at the moment.

David Berman, Head of R&D, Immunocor: Yeah. I think I think, first of all, the fact that we have two Chemtrac lifecycle management programs in the same tumor melanoma, is something that's that's missed. Life cycle management programs typically have a higher probability of technical and regulatory success, and we're going to get the first readouts of the cutaneous next year and the adjuvant study in a few years. I think, you know, people understand where we are with Prunetifest from pre m h l and we hope to have some data in the next twelve to eighteen months to afford the next step. And then behind that PWL one is our first foray into colorectal cancer and then the two autoimmune programs that are entering the clinic that we that we touched on.

So I do and then HIV expansion will be in the next twelve to eighteen months. So I I do think the next twelve to eighteen months will be a data rich insight into where this company is going.

Ethan Markowski, Member of biotech research team, Needham and Company: Great. Well, with that, I don't see any further questions in the chat. So I we're just about up on time. So I wanna thank you again, David, for attending the conference and for talking a little bit about Unicore.

David Berman, Head of R&D, Immunocor: Thank you very much, Ethan. Have a nice day.

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