Immunocore at TD Cowen Conference: Strategic Growth and Innovation

On Tuesday, March 4, 2025, Immunocore Holdings PLC (NASDAQ: IMCR) presented at the TD Cowen 45th Annual Healthcare Conference, showcasing its strategic advancements and financial performance. The company highlighted its robust growth driven by KimTrak’s success and ongoing clinical trials, while also addressing potential expansion challenges.

Key Takeaways

• KimTrak sales reached $310 million in 2024, expanding to 24 countries.
• Immunocore is advancing Phase 3 trials for KimTrak in cutaneous melanoma and adjuvant uveal melanoma.
• The company holds over $100 million in cash, with a 99.6% gross margin on KimTrak sales.
• Upcoming data readouts are expected for HIV, HBV, and type 1 diabetes programs.
• Immunocore aims to quadruple the addressable patient population for KimTrak.

Financial Results

• KimTrak achieved $310 million in sales for 2024.
• The drug is approved in 39 countries, with plans for further expansion.
• Immunocore maintains a strong financial position with over $100 million in cash reserves.
• The gross margin on KimTrak sales stands at an impressive 99.6%.

Operational Updates

• KimTrak launched in 14 new countries in 2024, totaling 24 countries.
• The TB AM trial in cutaneous melanoma is fully enrolling.
• The ADEM trial in adjuvant uveal melanoma has commenced, sponsored by the EORTC.
• The PRISM MEL Phase 3 trial is ongoing, focusing on dose confirmation.
• HIV program is in the dose escalation phase, with data expected soon.

Future Outlook

• KimTrak lifecycle management data for cutaneous melanoma expected in the second half of next year.
• ADEM trial data anticipated after three years of enrollment and 18 months for the primary endpoint.
• HIV multiple ascending dose data expected in the coming weeks.
• HBV single ascending dose data expected later this year.
• CTA submission for the CD1A program planned for 2026.

Q&A Highlights

• KimTrak growth in 2025 will focus on increased U.S. penetration and ex-U.S. launches.
• The duration of KimTrak therapy is extending, attributed to its favorable safety profile.
• Approximately 65% penetration achieved in the approved U.S. population.
• The company targets a survival hazard ratio in the low to mid 0.7s for the KimTrak cutaneous melanoma trial.
• The HBV study aims to achieve biologically active doses without liver toxicity.

In conclusion, Immunocore’s presentation at the TD Cowen Conference underscored its strategic growth and innovation. For more details, please refer to the full transcript below.

Full transcript - TD Cowen 45th Annual Healthcare Conference:

Nick Larusso, TD Cowen: Good afternoon, everyone. My name is Nick Larusso, and thank you very much for joining us at TD Cowen’s forty fifth Annual Healthcare Conference. For our next session, we have a hybrid presentation and Q and A with ImmuniCore. And it is my pleasure to introduce David Berman, the Head of R and D, and Travis Koi, who’s sitting down right now, but will be with us for the questions. And so it’s a privilege to have you both here.

And with that, I’ll let you go ahead and start with the presentation.

David Berman, Head of R and D, ImmuniCore: Nick, thank you very much for inviting us to present today. Here’s our forward looking statement. I joined Immunocor 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 three pipeline which I’ll get into.

And we also have line of sight now to three to early stage three, therapeutic area clinical programs. And I’ll get into those three therapeutic areas. And, of course, this is supported by a very robust revenue stream from KimTrak. And 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, KimTrak, which is currently commercialized for metastatic u v l melanoma, two life cycle management phase three trials that I’ll review for you. With PRAME, we have a pretty large franchise including an ongoing phase three in first line cutaneous melanoma, signal detection in ovarian and lung and I’ll talk to you about our PRAME program. PWIL, the first immunotherapy TCR program for colorectal cancer and it’s a very interesting exciting target highlighting our unique discovery engine. HIV and HBV will be sharing our full m a d our initial MAD data for our h v HIV program later this month, and then the HBV Phase one single ascending dose later this year. And then we’re very excited now to have line of sight to autoimmune and I want to share to you why we’re excited about the autoimmune franchise.

First, I want to focus on KimTrak. Twenty twenty four was a very strong year. We had $310,000,000 in sales. We had 14 new launches, bringing it to 24 total countries. It’s approved in 39 countries and we’ll have continued expansion throughout this year and we can talk more about that during the Q and A.

This is the near term for ChemTREC. In the midterm, which is not that far away next year, we’re focused on ChemTREC lifecycle management in cutaneous melanoma. Now after PD ones, after checkpoints, there is no therapy demonstrated to prolong survival benefit. This is the indication where our phase three TB AM trial is currently enrolling. In fact, it’s the most advanced phase three trial, with a survival endpoint in second line melanoma.

We are randomizing these patients to KimTrak versus KimTrak plus pembrolizumab versus a control arm, and we expect to complete enrollment in the first half of next year to be followed by a readout, we believe, in the second half of next year. So not too far away. After KyMTrac in cutaneous melanoma, we’re very excited about KyMTrac in adjuvant melanoma adjuvant uveal. So after patients have their initial diagnosis of uveal melanoma in the eye, they get definitive treatment, which is either surgery, enucleation, or radiation. And 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 three trial in adjuvant u v l melanoma. And we’re randomizing patients to Kimtrac versus observation. The primary endpoint is relapse free survival.

The study just started last year, and it’s being sponsored by the EORTC. So currently, we believe our chemtrak and metastatic uveal melanoma has the potential for a thousand patients a year. Chemtrak in cutaneous melanoma could bring it that up, an additional four thousand patients. KimTrak in adjuvant by a thousand. And so we do believe that KimTrak has the potential to be delivered if these two trials are positive to up to six thousand patients per year.

And so we’re very excited about our ChemTraq franchise. Moving now into our earlier clinical stage pipeline, I want to focus on PRAME, P well 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, BRINITA Fest, last year showing very compelling disease control. And this, along with other data points, led us to initiate a randomized phase three and first line of brinetofest plus nivolumab versus either nivolumab monotherapy or nivolumab plus rilatlimab.

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 ninety patients to select the go forward dose. Either the forty micrograms of Bernadofest or the hundred and sixty micrograms of Bernadofest. We will continue enrolling the phase three trial and we expect it to be a three year Phase three trial. Beyond cutaneous melanoma, we are building on the initial signal for bonidifast 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 acimertinib in EGFR mutant and in combination with docetaxel. Finally, we have a PRIME half life extended molecule, which is essentially similar to brinetofusp, except it has an FC fusion for a longer half life. We’ll be integrating these three data points over the next twelve to eighteen 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 prunidifib, so those data are interchangeable. I’ll now move on to our next program, PWEL.

So PRAME and GP 100 were very well known TCR targets. PWEL is a exciting target that is expressed primarily in metastatic colorectal cancer and is not expressed in normal vital tissues. And the fact that we are the first to develop this highlights our novel and exciting discovery engine. CRC is increasing in incidence. PWIL is expressed robustly or broadly in about a quarter of colorectal cancer patients.

Colorectal cancer CRC historically has been insensitive to checkpoints. And so this, we feel, provides a unique advantage for us. And by the way, uveal melanoma where we had our initial phase three also was insensitive to checkpoints. And PWEL is also a negative prognostic marker in colorectal cancer, which we believe means that it contributes to the virulence. The more PWEL, the more aggressive the tumor.

And typically, tumors have a harder time immune editing out or losing genes that are involved in the aggressiveness. So we think this makes a very compelling target, and we are currently into dose escalation of PWol. Moving on from oncology to HIV. Now the current standards of care in HIV are daily antiretroviral treatment, which certainly can control the disease, but, it it requires a lifelong adherence. And, there is an unmet need to functionally cure these people.

That is to allow them to stop all therapy for at least two two or three years. And, 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. So this is the goal that we are intent on trying to achieve and the opportunity could be up to half a million people currently living with HIV. So a very large patient population. The challenge for the functional cure field is that when ARDS antiretroviral therapy is 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, very rapid proliferating virus.

By week eight, over ninety five percent 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 twelve, low single digit percentage of people are able to control the virus. Now the fact that, some people can control the virus by week twelve 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. And so, this is the trial called STRIVE that we are currently, going to that we are still dose escalating, but we’re gonna share the initial MED data.

We shared the single ascending dose data last year at Croix. This year, in the next few weeks, we’ll share the initial multiple ascending dose data of about 16 people. They’ll they are treated for twelve weeks with our bispecific, and then they are on the background of ART. And then both ART and our bispecific, which is m one one three, are then stopped and will monitor for viral rebound over a twelve week period given that context of the historical data that I just shared with you. During the twelve week dosing phase, we’ll be looking at can we reduce the viral reservoir in the blood.

And then 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. So 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?

So 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. And the way that we achieve this is with our M type 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 Kimtrac targets g p one hundred melanoma. The effector arm in purple here is the p d one agonist. This is the opposite of checkpoints, which are p d one antagonists, and the p d one agonist will turn off the T cell.

And then the third component is an FC, fusion for infrequent dosing. And the general idea is that we will only get PD one agonism or T cell immunosuppression when the Imtai is tissue targeted or tissue tethered. And that’s shown with our lead program called s one one eight for the delay or the prevention of progression of type one diabetes. Type one diabetes is a pernicious disease and is associated with high risk and morbidity. T one d 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.

S one one eight is designed to specifically bind or tether to the beta cell. And when doing so, it will turn off any auto reactive T cell that comes in to kill the beta cell. But interestingly, it will only protect the beta cell from killing when it’s tethered or bound to the beta cell. When it’s not tethered, there is no inhibition and the t cells can kill, the the tissue. So 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, c d one a. Langerhans cells and a HLA like molecule called c d one a expressed on Langerhans cells are both implicated in allergic inflammation. Langerhans cells are antigen presenting cells in the skin.

They’re their 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 CD one a to lipid sensing t cells, and the peptides are presented by HLA class one and two to, traditional t cells. So we believe a Imtai, a bispecific that can block both lipid presentation by CD one a and peptide presentation by HLA class one and two would be an exciting therapeutic approach for atopic dermatitis, where both Langerhans cells and CD one a are implicated, and potentially other immune pathologies as well.

And so we designed U one twenty, which is our I’m tie targeting CD one a for exactly this purpose. The targeting end of u one twenty binds to CD one a. And in binding to CD one a, it sterically blocks CD one a from presenting lipids to t cells and therefore will sterically block activation of lipid sensing t cells. By now binding to thousands of CD one a on the surface of long run cells, it will coat the long run cells in PD one agonists. So anytime a t cell comes in to be activated by a peptide HLA, it will be turned off by PD one agonism, and that’s shown in the in vitro experiment on the right.

Interestingly, our PD one agonist, once again, is only active when it’s tethered to the Langmuir cell. When it’s free floating in blood, there’s going to be no inhibition of the t cell. But interestingly, it’s more efficacious and more potent PD one agonism than parasolumab, which is another PD one agonist that was recently reported to have activity in rheumatoid arthritis. In fact, we think u one twenty and our type one diabetes program have the potential to be the most potent p d one agonist to enter into the clinic. This is a really exciting time at ImmunoCorps, and we believe we are twelve to eighteen months away from very important data.

For KimTrak, we want to expand on our current leadership in metastatic u v l melanoma. Our TeBI AM Phase three 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. And our ADEM phase three trial will continue to enroll. For the PRIME portfolio, our phase three 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 twelve to eighteen 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. And then we will finally realize our vision of being three therapeutic areas when we submit our CTA for Type one diabetes later this year and then for CD1A in the, in 2026. And as I’m sure Travis will be happy to talk about, we have a very enviable and good cash position and very nice revenues.

So I think with that, we’ll end and I invite Travis up.

Nick Larusso, TD Cowen: Great. Thank you very much for that detailed presentation. Before I get started on Q and A, if anyone in the audience has questions, feel free to speak up or raise your hands. And so thank you again. So to get started, let’s start with KimTrak and the revenues.

And obviously, you’ve generated over $300,000,000 in revenues last year, which was mentioned on the presentation. So what’s going to lead to growth in 2025? And what’s going to be the key drivers there?

Travis Koi, ImmuniCore: Yes. I think, Nick, we’re obviously incredibly proud of our commercial launch of KimTrak. We’ve had 11 quarters of growth, which has been terrific to see, and we expect that growth 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. And then further is we continue to see the duration of therapy increase.

This has been quite a remarkable thing and I think it’s a testament to ChemTraq’s safety profile and its efficacy. And 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. So, 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, continue 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 and 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 commercialize ex U. S.

Nick Larusso, TD Cowen: 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 eleven months or a little bit more than eleven months now in the real world setting. What’s driving that and what’s leading to this being better than the clinical trials?

Travis Koi, ImmuniCore: Yes. And I’ll David comment here too. But I think it’s just a testament to the patient, 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, you know, become very comfortable with it.

You know, it’s a CD3 arm, so there’s some CRS, and we need to monitor that. But physicians have become very comfortable with that, which also gives us leads us comfort into believing that we can continue to penetrate the community setting, beyond just the academic setting. Anything?

David Berman, Head of R and D, ImmuniCore: 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.

Nick Larusso, TD Cowen: It’s very interesting. What percent penetrated would you say you are right now for chemtrak in the approved population and the UBL population?

Travis Koi, ImmuniCore: Yes. In The U. S, approximately sixty five percent. So still some room to grow. Hence, why we believe we continue to grow there.

OUS, in some particular countries, we see penetration even higher than that. And that’s why I say when I say we expect more of the growth to come from additional launches, that’s the framing

Nick Larusso, TD Cowen: there. Got it. It makes a lot of sense. So you mentioned during the presentation that you’re going to be targeting another six thousand patients with the TBIM and the ERTC trials. So for that, what’s the bar to be in both the adjuvant and the cutaneous settings?

And I mean, you mentioned when we’re going to see data, but can you just mention it again, so everyone knows?

David Berman, Head of R and D, ImmuniCore: Yes. So for the in terms of timing, we expect, TBHIMTRAK and cutaneous melanoma probably in the second half of next year. So, you know, twelve to eighteen months away. And then for ADaM trial, we expect that’s the adjuvant UBL. We expect a three year enrollment and then eighteen months for the the primary endpoint.

So for the ADaM trial in terms of, what, you know, 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 three 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. So now if you can imagine patients who there is no visible tumor and that by the way was randomized against pembrolizumab and natalumab. Here we have tumors where there is no visible tumor and we’re randomizing against observation.

So you would expect there to be perhaps an even better hazard ratio than that. For Kimtrac in the cutaneous melanoma setting, this is a survival endpoint. And so typically in Phase three late line trials, I think you want to target a survival hazard ratio that’s in the low point sevens or better for it to be clinically meaningful, mid to low 0.7s.

Nick Larusso, TD Cowen: Great. That makes a lot of sense. So let’s move on past chem track to your very exciting pipeline, which is very extensive. Let’s start with infectious disease because you have that HIV data coming in Q1. So 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?

David Berman, Head of R and D, ImmuniCore: So Nick, we have 16 people across three cohorts and, the highest was three hundred micrograms. And we’re gonna 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 twelve weeks. And there, in addition to safety, we’re gonna be looking at the viral reservoir.

So what happens with HIV is when it infects, for example, CD four t cells, it gets integrated into the human genome. And so you can measure that reservoir that remains even when the people are taking ARTs. And the way we’re gonna measure that initially is by looking at the transcriptionally active reservoir. There’s other ways you can look at the reservoir too. So 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? 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, you know, less than five or ten percent will actually produce replication competent 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. And there we’ll monitor the patients for up to twelve 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. And the senior author there, Sarah Fiddler, is also the senior author of our phase one trial. So this becomes the best comparator for what you expect to see during the treatment interrupt and the treatment interruption phase. And 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.

And then by week eight, ninety five percent have levels of above transmission threshold, which is 200 copies per mil. By week twelve, the rate of viral control is in the low single digits. So it’s very, rare to see people actually make it out. In fact, it’s even more rare in the patient population where in the in the population we’re working on is the population we’re working on usually started their art later after their infection. And here, the rate of control at week twelve is zero point five percent.

So it’s let’s just call it very rare to see people control. So we’re gonna be looking at, can we reduce the reservoir and can we alter rebound kinetics and control?

Nick Larusso, TD Cowen: That would be fantastic. We have 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.

So what should we expect to see and how will that support continuation?

David Berman, Head of R and D, ImmuniCore: So 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? And so 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, you know, and you do expect to see transaminitis is called productive transaminitis.

But can you do that without seeing liver necrosis and liver toxicity? So that’s really the question that we hope to answer with the SAB, keeping in mind this is a single dose study. This is not a repeat dose study.

Nick Larusso, TD Cowen: It makes sense. Let’s move on to Brenny. First, you mentioned that let’s start with the PRISIMEL study, the Phase three trial that’s enrolling right now. Can you just quickly remind everyone why you chose the, rolatlumab as the potential comparator dose there?

David Berman, Head of R and D, ImmuniCore: Yeah. So the reason we chose it is number one, we believe we can beat it. And that comes from our, phase one data which we shared at ASCO where the disease control for our monotherapy, brinetofest, was higher than the Relativity twenty, apples to apples clinical trial which was nivo plus Rella in a similar population. So as a monotherapy we felt we were better than nivo plus LAG three. And we had reasons to believe that when we move into earlier lines, we will be more active and then now we’re going to be combining with another agent PD one.

So we felt scientifically we could do it. And then strategically, we felt it’s important to do it because nivo plus relo by the time we launch will be widespread and will have a lot of penetration in the community. And so we have to show that we’re better. The trial is designed where most patients will end up getting nivo monotherapy in the control arm and a minority nivo rela so that we can at least have a point estimate comparison, but the control arm will be heavily dominated by nivo mona.

Nick Larusso, TD Cowen: Got it. That makes sense. So 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?

David Berman, Head of R and D, ImmuniCore: Right. So with melanoma, we were able to extrapolate because we had a lot of experience in melanoma, and we saw signal that justified us moving into the first line Phase three. 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.

And 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 earlier 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 the patients are coming in with stable on bevacizumab, so they act as their own internal control. So we’ll be looking at responses on the background of stable bevacizumab.

So we’ll 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’re studying two active agents, but the type of randomized study will depend on the strength. If it’s very strong data, we could go to Phase three. If it’s interesting, but not strong enough, we could do a randomized Phase two.

Nick Larusso, TD Cowen: That makes sense. So I think we are almost out of time. But I want to ask about the cash and the gross margins. And do you need to explain that 99.6 percent gross margin and how fantastic that is as unseen and unheard of? So yes,

Travis Koi, ImmuniCore: any CFO likes that number. Yes. Okay, great. But no, we’re obviously, we’re incredibly encouraged by the revenue that KimTrak is and the success we’ve had as we just discussed. The thing that I think we’d and the CFO also thinks the company is undervalued.

But when you look at a company in our position that has over $100,000,000 of cash, has a strong revenue and continued growth from Chemtrack combined with three Phase 3s and then upcoming further advancement in infectious disease and in autoimmune, we have to think we have incredibly compelling story.

Nick Larusso, TD Cowen: Yes. Just ask you because you pretty much answered my next question, but what do you think is most underappreciated aspect of the story? Yes.

David Berman, Head of R and D, ImmuniCore: I think, you know, as as Travis said, I think that there right now people are focused on metastatic u v l melanoma opportunity and I think people are missing the fact that ChemTraq is in life cycle management in a different type of melanoma with data next year that could quadruple the size of the population. And the efficacy signals that I see for KIMTRAC in u v l melanoma are replicated in cutaneous melanoma, both of them being survival endpoints. I think that at a minimum is being missed. And then as Travis said, also in the next twelve to eighteen months, we’re going to have additional data with Pernodifos, HIV and PWEL. Awesome.

Nick Larusso, TD Cowen: With that, thank you very much.

David Berman, Head of R and D, ImmuniCore: Thanks, Nick.

Travis Koi, ImmuniCore: Thanks, Nick.

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