Per Norlen: Yes. I can give some more background. So there’s a lot of ERV DNA in all humans. And as I said before, these are more or less randomly expressed in some cancers when the machine — control machinery breaks down. That seem to be around, say, 10,000 or 20,000 different ERVs that can be expressed. So, finding they are very different from each — from patient to patient. And that said, there are sometimes in some patients that could be overlapping ERVs. But we are in this trial looking for producing a fully personalized vaccine towards ERVs, and that’s really where we are unique. So — and these ERVs, they are selected based on likelihood to induce a strong immune response, given that they are relatively long foreign peptides that can be actually quite a large number of epitopes on each Europe, so we can find a very, say, high-quality antigens whenever we find a strong expression of these ERVs in patients.
And it’s based more or less in the same way as when you select the new antigens that you look for how well they match the immune system of that patient. So, you need to predict the shape of the patients’ immune receptors and also the shape of the epitopes on the ERV, and then how likely they are to adhere to one another. That is one of the key factors we look at, but there are many more aspects to it.
Ahu Demir: Got it. Thank you very much for taking my questions.
Per Norlen: Thanks so much, Ahu.
Operator: Thank you. We will now take the next question. It comes from the line of Swayampakula Ramakanth. Please state your company name and ask your question.
Swayampakula Ramakanth: Thank you. This is RK from H.C. Wainwright. Good afternoon, Per. So, a quick question on EVX-01. So, on the Phase 1 portion of that study, you had presented some interim data on the nine patients. Is there going to be an additional data in the next update that you’re going to be presenting at the end of this year? Or is it mostly going to be initial data from the Phase 2 portion of the study?
Per Norlen: Yes. Thank you, RK, for that question. So, at ASCO this year, we presented the full data set. So, as you mentioned, we previously have shown interim data from nine patients. But at ASCO in June, we presented — and the slide that’s in the presentation today is actually on 12 patients, which is a full patient set where we do have eight responders. So there, we have already presented the data. We will likely publish the more scientific details later on, but we don’t intend to present additional clinical outcome data on these programs. So that’s already final. At the end of this year, we will focus on the interim data of the Phase 2 trial, which is a slightly different design, and it’s then sites in Australia and in Europe. So, it’s a multi-center trial.
Swayampakula Ramakanth: Really good. And then on the ERVs, I’m just trying to understand a little bit more on the ERV. Are the ERVs expressed uniquely based on the patient or are they expressed uniquely based on the indication?
Per Norlen: Yes. That question, I would say, is uniquely based on the patient. We think there could be some overlaps sometimes depending on the cancer. And maybe if you reason around how they’re expressed if the sort of — if there is a signal to express a certain part of the genes in a patient, then — if that signal is common between patients, there may be an overlap between those ERVs. But usually, the expression of that is completely independent. So, to answer your question a bit more simply, we think it’s highly patient-specific, but with the potential to find some overlap. We don’t — are not looking for overlap in the first trial. So, there is fully personalized. But it’s possible that you can find a subpopulation where there is some overlap and you can produce a common drug for several patients.
Swayampakula Ramakanth: So, one last question on the ERV again. Do you need — is there a certain threshold in terms of expression of the ERV for you to make a personalized vaccine against it? Or are you…
Per Norlen: That’s a very good question, I think, because this is really the key challenge with neoantigens that you need a lot of mutations in order to find enough high-quality neoantigens to make a vaccine. And that’s really why personalized cancer vaccines today are restricted to, say, melanoma, a few more indications, lung cancer and so on. And in other indications where there are a few mutations, maybe it’s just a few percent of the patients where you can actually make a personal neoantigens vaccine. With ERVs, we find a slightly different profile. It’s not the same indications where they’re highly expressed. It’s often expressed in patients with cold tumors. So, it really allows for treating — making a cancer vaccine for patients with a complete cold tumor without any neoantigens.
And — but in EVX-03, we actually plan to do both. We will sequence the tumor. And if they have good neoantigens, they will — this will be included in the vaccine. And then it will be complemented by strong ERVs at the same time. So, we try to pick the best from both worlds. Hopefully, we can also expand the target group quite significantly.
Swayampakula Ramakanth: Thank you. Thanks for taking all my questions.
Per Norlen: Thank you so much, RK.
Operator: Thank you. [Operator Instructions] There are no further questions at this time. I would like to hand back over to Per for final remarks.
Per Norlen: Okay. Thank you, everyone, for joining, and thank you for all the questions, and we look forward to stay in touch. Thank you. Bye.
Jesper Nyegaard Nissen: Bye.
Operator: That does conclude our conference for today. Thank you for participating. You may now disconnect.
