Circio Holding ASA (CRNA) Earnings Call Transcript & Summary

And welcome to this ad hoc webcast and presentation. My name is Øystein Soug, and I am the CEO of Targovax. So most of you who listen in now will know that we sent out the press release last night on the melanoma, so that is our trial with ONCOS-102 in combination with KEYTRUDA in checkpoint inhibitor refractory melanoma. And just to be clear upfront, we are very proud about this data. We're very happy, and we think it is very impressive. And to explain why to you and show you the data, we also have Magnus Jäderberg with us today on Video Link from London. Hi, Magnus.

Hello. Good morning.

If you have questions, you can submit them during the presentation, and we will answer them towards the end. But before we get to Magnus and the data, I will give a few words of introduction and background. So moving on to Page 4. As you know, we don't develop checkpoint inhibitors in Targovax. But checkpoint inhibitors are what we combine with in this trial, and they're also important to the story. They have revolutionized the treatment of cancer over the last 10 years. So they are very important. They sell for more than $20 billion per year. KEYTRUDA is the second highest grossing drug globally at the moment. And they work very well in a subset of patients. But even in the best indications like melanoma in lung, they don't work in all patients. They're working from 10% to 40% in those indications. And the reason for that is manifold. But one important reason is that the patient does not have the right T cells in his tumor microenvironment because checkpoint inhibitors don't kill cancers. T cells kill cancers. And this is where ONCOS-102 comes in as a combination product with checkpoint inhibitors because whereas the checkpoint inhibitors enable the T cells to get access to the tumor and kill them, ONCOS-102 actually tricks the immune system into producing the right T cells that will then do the killing. Our pipeline, most of you is familiar with this one. What we're going to talk about today is the melanoma trial, which is the second from the top here, where we presented data in the press release yesterday. But 8 days ago, we also sent a press release on mesothelioma. We had more or less the -- almost final results from that trial as well. So we'll say a few words about the mesothelioma data in this presentation as well. Now to melanoma. So the patients we're talking about here, they are very sick. This is advanced unresectable melanoma. They have disease progression despite prior treatment with a PD-1, like KEYTRUDA or Opdivo. What happens with these patients is that there is no standard of care for them. So they will be sent home on palliative care or, in some cases, sent on to a clinical trial like ours, but to be sure, they are very sick. In this trial, we had 20 patients, and they were all Stage III and Stage IV. The trial was run in -- at 4 sites. Memorial Sloan Kettering in New York was the coordinating site for this trial. And there were 2 more sites on the U.S. East Coast as well as Oslo here in Norway. And the trial was divided into 2 parts. So there's a part 1 where the patient has got few injections of ONCOS-102. And then part 2, where they got more injections of ONCOS-102. And as you can see on Slide 8, the trial design, just showing you that in part 1, ONCOS-102 was given 3x during 8 days, and then KEYTRUDA treatment starts after week 3. And the idea here is that during this period, between ONCOS-102 treatment and KEYTRUDA treatment, the patient's immune system has been reactivated so that KEYTRUDA can do his job. In part 2, we simply added more ONCOS-102 treatment. So we dosed the patient for the entire 24-week period. So that's the background. Magnus, over to you and the data, please.

Thank you, Øystein. Hello, everyone. So if we look at Slide 9, this is a slide that explains some of the background information for the 2 populations. You just heard Øystein talking about 2 parts. And what we found when we compared these 2 cohorts was that patients in the second cohort had more advanced disease. Maybe before we go into look at some of the details, just to mention, some of you will remember that last summer, June-July 2019, we presented preliminary data for Part 1, and we then have 9 patients. Well, as we now have finalized the data, gone through all the quality checks, we found that indeed 1 of those 9 patients didn't actually qualify for going into an efficacy analysis. This was a patient that had actually responded to checkpoint inhibition previously. And as Øystein mentioned earlier on, the criteria, the key criteria for going into the trial is that patients had not responded to a checkpoint inhibitor. So we ended up with 8 patients in part 1 and 12 patients in part 2, making a total of 20 patients. And what one can see on this page are some of the key features when we look at these 2 cohorts, so median time for -- from diagnoses. To start, there's some difference there. A slightly longer time in part 1. On average, number of checkpoint inhibitor treatments prior study was 2. Some of the patients have had several. Some of the patients had only had 1 course of checkpoint inhibition. And the average number of lesions, targeted lesions, you can see that there is somewhat more lesions in part 2. And when they looked at the average tumor burden less targeted lesions, there's also a greater size if you measure the total size of those targeted lesions of 66 millimeters compared to 50 millimeters. But maybe the most striking difference between the 2 cohorts is when we look at staging of patients. Øystein mentioned to you that we only included Stage III and IV. And you can see here, when you look at the relative number of patients with Stage IV to Stage III, there were -- the majority of the patients in the part 2 had Stage IV, while actually, in part 1, the minority of the patients had Stage IV. And that's an important finding when we looked at some of the outcomes. So let's go to the core of the data that, as Øystein said, I'm very excited personally about this, having worked on this project for some 5 years by now. And designed the study with Professor Jedd Wolchok back in 215 (sic) [ 2015 ], and got the trial started in 216 (sic) [ 2016 ]. So what you see here is what we call it waterfall plot. And you can see that 7 out of those 20 patients that went into the analysis had either a partial or a complete response. And by that, we mean that we have 6 patients with partial response represented by the light blue color, and 1 complete response represented by the dark blue color. And that makes a best overall response rate of 35%. You can also see what happened to the other patients. We had a couple of patients with stable disease and a couple of patients with progressive disease. So going to Slide #11. We are excited about the fact that we've seen response in non-injected lesions. That can also be called abscopal effect. And we saw it in several patients, and we saw it in both Part 1 and Part 2. So what am I talking about? Well, what this little picture is trying to illustrate is that we will inject the virus into 1 melanoma lesion. And then we are also interested in looking to see if the systemic effect from the virus is able to impact positively on lesions that were spread around the patient and not injected by the virus. And that's what we call abscopal effect or effect in non-injected lesions. And so these are very early days, have been very exciting for us, let's say, something we haven't seen much at all with oncolytic viruses. And what we did here was, in collaboration with Professor Wolchok, we did set a limit for how to count or classify a non-injected lesion as an abscopal lesion. And we said that we're willing to go for those non-injected lesions who had shrunk by at least 30%. And thus, if you are familiar with the RECIST criteria, the criteria for response. And we saw when we looked at these non-injected lesion response, there's actually 2 non-injected lesions that had completely disappeared. So exciting data, early data, and we will continue to analyze these data but, of course, publish later on. So if you go to Slide 12. Now how do a data that I just presented you stack up to the competition? Well, if you see here on this slide on the ONCOS, 35% Over Response Rate. You can see Replimune, a compound not that dissimilar to ONCOS-102. They presented some data, more or less in the same ballpark. And we have a company called CheckMate that have a Toll-like receptor 9 agonist coming in around 25%. And then we have a couple of other compounds, including a stack inhibitor at 17% and 19% in total ORR for that compound. So when you look at this, we are competitive and suggesting that we are sort of at the very top end of what's been produced in checkpoint refractory melanoma, which makes me very excited. If we go to Slide 13, I'm going to hand over back to Øystein.

Thank you, Magnus. Just to sum up, on the safety side, there are no concerns. We have not seen any major things to worry about in this trial or in previous trials with ONCOS-102, so that's consistent. As Magnus said, 35% ORR, we're very happy with this. We think this is top of the league. This is really leading data. And the systemic effect that we see with the treatment of ONCOS-102 here is really encouraging. This is data we need to dig further into, but we think this is very exciting. Now when it comes to the next steps, we are, of course, looking at this data and seeing that it warrants a follow-up trial. So we are, at the moment, planning how to follow this up with a confirmatory trial in melanoma. In the shorter term, we will also get some more immune markers. As you will notice today, we did not present any immune markers. We have some from the first part of the trial. There will be more coming for the whole patient population later, and we'll evaluate those data as well before we finally decide on which steps to take further. So that's melanoma. Mesothelioma, as I said last week, we sent out a press release. We have data from that trial as well with overall survival, and Magnus is ready to present that data. As you know, mesothelioma is a disease with very few opportunities for the patients. It's hard to operate on these patients. It's hard to do radiotherapy because of where the lesions are in the body of the patient. Chemotherapy standard of care has been around since 2003. There hasn't been much new things for these patients over the last few years, apart from checkpoint inhibitors that are starting to come in, into this indication. There have been mixed results. But in October, ipi/nivo showed results and got an approval for mesothelioma. They actually had good results in a subset of patients, not for the whole patient population. So we think there is still enough space for us in mesothelioma. About the trial and the data, I'll give the word back to Magnus on Page 16.

Thank you, Øystein. So yes, we have presented this to you earlier on, but let's just recap. So what we did in the mesothelioma trial is that we included patients who were first and second line, meaning they were either just diagnosed and needed to have their first chemotherapy cycles or they had already been treated with chemotherapy and had relapsed and were retreated as part of study. And we used pemetrexed/cisplatin. That's the only standard of care, actually, in this disease. And we injected the patient's tumors with 6 intratumoral injections. And the layout of the trial was one where we started with a safety lead-in of 6 patients. You always want to make sure when you have a new combination, in this case, the virus plus chemotherapy, that patients can tolerate that combination therapy. And we had no problems with tolerance, which meant that we could open up into the randomized phase. And you can see that there were 14 patients in the experimental group in the randomized phase and 11 patients in the control group. So what about the data if we go to Slide 17? Well, we're very excited about this date. Øystein mentioned we issued a press release a couple of weeks ago with very promising median Overall Survival in first-line patients. What we've done here is we've also included a safety lead-in group of patients because previously we have reported all the experimental patients, meaning we have grouped the safety lead-in patients or 6 patients with the experimental patients in the randomized phase 14. So we have looked at those 20 patients. What we want to do now is just to show the separation of the 3 cohorts because, of course, the important thing when we talk about comparison with the control group is to just look at the randomized patients. So in first-line disease, you can see the number of patients. Median progression-free survival look pretty good. So we're hovering around just under 10 months for the experimental group in first-line disease randomized group. We're looking at 18-month survival rate, is looking positive for the first-line group. And when we look at median Overall Survival, we can here say that we haven't reached the median Overall Survival. We have put a red box around 18.2. That means that, that's a very minimum length of time that we will get for median Overall Survival, but we haven't reached it yet. So it will either be 18.2 or better, meaning longer. While in the control group, at the very right, the 14.2 months is the very most that the control group's median Overall Survival will reach, and it could be shorter than that. And we've also, for complete list included here, second-line patients, we'll discuss this further on, and you can see here that for median Overall Survival and for progression-free survival, the standard of care only patients performed a little bit better, and this is something we also discussed earlier on, one of those chance findings that you sometimes see when you have very small number of patients. So let's go to Slide 18. And again, like I did before for melanoma, how do we stack up with this data? Well, they're looking good. Small numbers of patients. But if you look at the comparison of the Targovax' experimental arm in first-line disease compared to other data, and what are the other data? Well, the gray dots here are represented by various trials, small and large, with pemetrexed/cisplatin, the control arm that we had in our study, and the chemotherapy that we combine the virus with. And you can see here how we plotted median progression-free survival on one axis and median Overall Survival on the other. And the dark blue here is, as I said earlier on, where we are at the moment with the experimental group of 18.2, but could become better. And that's what we try to represent with a shaded line towards the right. While the control arm, you can see that's further down in gray, maximum 14.2, but could become lower. So that's the reason why we are, of course, following patients further on in 2021 to see when we reach a definitive median Overall Survival for both arms in this trial. So our data are maturing, but as we're suggesting, already looking very interesting actually. Slide 19. What we are excited about is that we can see an association between immune activation and outcome. And of course, when you are operating in the immuno-oncology area, that's exactly what you want to see. That's what makes people interested. That's what makes big companies interested in talking to small companies. If you can explain the mechanism of action, it's not just a chance finding, but there's actually a story, a scientific story and explanation behind it. And what we've done here is that we have plotted some of the key immune markets on what's called a spider plot. And just to go through some of those, so cytotoxic CD8+ T cells, those are the kind of T cells that are able to kill cancer cells. And another one is important, which is PD-L1 expression. I think a lot of you would be aware that PD-L1 expression is one of those underlying biomarkers that are associated with a response if you add a checkpoint inhibitor. So it's important to see what happens with PD-L1 expression when you're planning to combine it with a checkpoint inhibiter, which we are. And the M1, M2 ratios is another important one. So macrophages are peculiar immune cells, and some are good and some are bad. The good macrophages are called M1. They help the immune system to fight the cancer. While M2 macrophages are the bad ones. They actually hinder the new system to fight the cancer. So the ratio of M1 and 2 is very important. Now let's go back and see what we've done here. You will notice there's a little bit of a red line in the middle of the spider plot. And that's represented, as you can see on the right-hand side, top corner, by patients who received the control arms and had only chemotherapy and who had died by 18 months. Yellow are those who were alive at 18 months in the controlled group. Light blue, ONCOS patients who have died by 18 months; and dark blue are patients who were alive at 18 months. And what one can see here from this first part of what's becoming a buildup slide, you're going to see in a moment, is that when you have no immune activation, that's associated with a poor outcome. Now let's just continue here. If we go to Slide 20. Here, we've plotted those ONCOS-102 in chemotherapy patients who had died at 18 months. And we can see here that they are clearly immune activated, but not quite sufficiently to have an impact on survival. So it does sort of talk to the importance of sufficient, meaning a broad and relevant immune activation to impact survival. Now here is Slide 21, which has a yellow line. And this yellow line, as I said, is represented by standard of care patients who are alive at 18 months. And you can see here that there is some immune activation. And so it sort of, again, speaks to my earlier point that immune activation is actually correlated with clinical outcome. And what we know today, what -- which we didn't know 10 and 20 years ago, when I started in the '90s with oncology, is that chemotherapeutic agents are also impacting the immuno system and sometimes positively. So that's all we can see here. There is a correlation or an association between the degree of immune activation in the chemotherapy-only group and survival. And then if we go finally to Slide 22, that's the slide that shows the ONCOS-102 patients who are alive after 18 months. You can see here a completely different picture where we have, for example, excellent ratio of cytotoxic T cells. These are T cells, I mentioned to you earlier on, that we need to have in the patient's immune circulation to kill cancer cells. We have a healthy ratio of M1, M2 macrophages, and we have a good PD-L1 expression level, which means that not just whether these patients are alive at 18 months with a good mechanistic action reason behind them, but we also can see here that we're actually on the right path when we're now talking to Merck and combining with a checkpoint inhibitor, which is where we are at the moment with this program. So to summarize the mesothelioma data, we find that the combination of ONCOS and chemotherapy is well tolerated. Median Overall Survival haven't yet reached a definitive point for at least 18.2 months, so that's stacking up very nicely. And by the way, that is the figure that ipi and nivolumab presented a couple of months ago from the large Phase III trial. And we can stay at that figure or we can possibly also have an even better figure in the future we'll see next year. Median progression-free survival at 9.8 months also looking good. As I've just talked a little bit just before this slide, we see a very important correlation between immune activation as broad and powerful and clinical benefit. So what are we doing? Well, we have told the market early on that we are continuing in the first line. We're talking to Merck. I just mentioned that. And it makes a lot of sense immunologically and clinically to combine ONCOS-102 with the PD-L1 or PD-L1 checkpoint inhibitor standard of care chemotherapy. So exciting times for the company. And back to you, Øystein.

Thank you very much, Magnus. So now it's the time to look at the questions we have got from the web, and we have CFO, Torbjørn Furuseth, with us in the room to read those questions for us.

Yes. Hello, everyone. Thanks for all the questions. There has been quite a few. So I have tried to group them in first, some more questions on the melanoma data and then a question on mesothelioma. And then lastly, the plans and financing. So first on the melanoma data. Magnus, it's great to see effects on non-injected lesions. Can you say what the responses were in the 2 patients with non-injected lesions that completely regressed? And why they were not a complete response on their RECIST score?

Okay. So the 2 patients who had non-injected lesions that completely disappeared were part 2 patients. And they had partial response in both cases. Obviously, we would love to see even more complete responses, but the fact that they were non-injected lesions that completely disappeared, as I said earlier on, is really interesting and encouraging because it does show that when you inject the virus in one place of the patient, you get an effect in a different place. So it's the demonstration of systemic effect on the virus.

Yes. Very good. And then there's a question on sort of the patient population. What was the refractory status of the patients assessed? Was disease or progressive disease confirmed by 2 consecutive scans? And was anti-PD-1 -- PD-L1 the last prior line of treatment? And also a question if -- how many patients were previously exposed to anti-CTLA-4?

Right. So let's see if I can -- so the first thing I can say is that all of the patients have failed on an anti-PD-1, okay? So they all had, had progressive disease on anti-PD-1. And a number of those had also have had CTLA-4 in combination, I can't remember the exact figure. Your question was then -- what was the first question? Can you remind me? You asked me 3 questions.

Whether the refractory status was confirmed with 2 consecutive scans?

So we followed the RECIST 1.1 guideline. And when you run a trial where efficacy is the secondary end point, you only do 1 scan. So you don't do follow-up scans. And that's what we did. So we just followed RECIST 1.1.

Yes. And I think it was the inclusion of the patient. So prior to inclusion, whether it was confirmed, I think, we don't know that for sure if the patient was confirmed to be a progressive patient before it was included in the trial. But it was the decision of the physician that this patient is now progressing, and we should move on with something -- a different treatment.

Yes. Yes. Right.

And then on the dosing, when you inject ONCOS-102, do you always inject in the same lesion? Or do you inject in different lesions over time?

So you can move around. What the investigators do is that they number the lesions, so they keep track of the lesions. And as those of you who are familiar with RECIST, which is the international system for measuring tumor response when you use anticancer agents, you pick from the beginning what we call targeted lesions. So those are the lesions that you follow throughout the trial, and those are the lesions that you measure, and those are the lesions on which you base your RECIST determination, progressive disease, stable disease, partial response or complete response.

Yes. And then a question on the Part 1 versus Part 2. It doesn't seem the number of injections played much on ORR. Could you comment on that? And what is your view on optimal dosing?

Okay. I mean, I'd make 3 comments on the first question. Firstly, if you remember, Part 2 patients had more advanced disease. So we need to remember that. That's one of the drawbacks with a smallish trial. You just have to accept that sometimes the 2 cohorts aren't exactly matched. So had we had 200 patients or 100 patients instead of 20 patients, we probably wouldn't have seen that. But we do see now very clearly that patients in Part 2 had more advance disease. So the immune therapy had a little bit more to do to achieve the same level of response. Having said that, when we look at the non-injected responses, so most of those were in Part 2, actually. And in fact, the 2 complete regressions that we had with non-injected lesions, as I mentioned early on, they were both in Part 2. So I think it's difficult to say based on 8 versus 12 patients, whether there's a difference between the 2. What's very clear though is that the abscopal or the non-injected lesion effect is an important one. Another one -- another point is very important for the future, of course, is durability and that's something we're going to build into the next program as we move forward. I think you also asked where we're going with our future administrations? Well, it's clear to us that we will continue to give ONCOS-102 over a longer period of time. If you look at the latest guidelines on treatment of melanoma, there is a clear recommendation that one should treat for at least 1 year. And if we look at what other trials are doing or other companies are doing with trials, they often treat with oncolytic virus for at least up to a year. so I guess that we will be doing something similar in our next program.

Yes. And that also probably touches upon the next question regarding the duration of response, if we can? Do we have any preliminary views on the duration of response?

So we didn't measure duration of response simply because it's a short trial of 5.5 months. But what we do know is that there are patients who, at the end of the trial, had responded and then could potentially be followed to see how their response state with them, so to speak, but we haven't built that into this trial. And as I said, that's something we're going to do in the next program. It's an important thing to look at for the future.

Yes. And we will, of course, analyze the data more in detail going forward. But so far, do we see any difference on the safety versus competition, the other compounds being developed?

No difference. No. I mean this is one of the good things about working with oncolytic viruses, they're very well tolerated in general. Not just ONCOS-102, which is an adenovirus, but other oncolytic viruses are generally very well tolerated. And we certainly haven't seen any difference between our safety data and other company's safety data on oncolytic viruses.

Yes. And when do you think the evaluation of the rest of the data will be complete? Will we see more data this year? And also a question, what type of immunological data will be presented?

Yes. The immune market data is going to be very important. I mean I sort of talked a little bit about that before that without understanding the immune markets and the correlation with the clinical effect, you only see part of the picture. So early part of next year, we're going to get all the immune markets in. We're going to do what we call a correlation analysis of immune markets and clinical outcome. And of course, we're going to share that with everyone.

Yes. And there are also a few questions on -- a bit more detail on patient information. I think I will note them down, and we will come back to them individually. I think it's detailed to go into all those details now. But it's another comment or question. It's great to see that Jedd Wolchok has been involved in the trial. Could you explain more how he has been involved?

Yes. So Jedd and I worked together. When I was Chief Medical Officer of Bristol-Myers Squibb Europe, Jedd was one of the key players running the YERVOY registration program, which I supported. And Jedd, as some of you probably will know, he is one of the biggest names in the world in melanoma research, I'll say, probably top 3 names in the world. So I had got to know him. And when I then joined Targovax, I started to talk to him about the possibility of looking at a melanoma trial where we specifically focus on all those patients that don't respond to checkpoint inhibitors. And he liked the idea and we basically sat down in his office in late 2015 and designed the trial. So he is very much behind the design of the trial, followed the trial very closely and very interested in all the data now getting out, so people can see what we've done.

Thank you, Magnus. So a couple of questions to Øystein. So you had some comparisons on the slide. How do you believe this data will compare to Replimune? And why would that be an important reference?

Now Replimune is one of the more valuable companies in the oncolytic virus space. They are now in a Phase III or registrational trial with their virus. What we've seen in this particular indication is that the data are fairly similar. I would say our data is a little bit better. We have a few more responses, a little bit bigger trial versus small trials. But I would say we are on par with Replimune.

Yes. And according to DNB analyst Ling, he expect Targovax to out-license its products and not take any of your products or indications to the market by your own. What are your aims for further progress in melanoma?

So I think it's a bit early to talk about the end game here. But for us, we now have data that supports continued development in melanoma. I would say also in mesothelioma. But talking about melanoma, we think that it's possible to contemplate a registrational program without too many patients here. As I said, today, there is no established standard of care for these patients, which means that you probably can -- with good data, you can get to the market without a very, very big trial. Whether we are going to do that alone or with a partner, time will tell, of course. But we're not going to guide on that today.

So yes, and then there was a question. Do you think the next trial in melanoma can be a single arm trial?

From discussions we've had with potential partners and KOLs, that is certainly a viable route, as we see it right now.

Yes. Maybe I'll just add a comment to that, just to remind everyone that it's a very good question because when we look back in time at the approval of KEYTRUDA and Opdivo, both of those compounds were actually conditionally approved on about 100 patients single-arm trials. So I guess, from my perspective, the regulator, sorry to say, have already shown that if you are addressing an important medical need area, they can accept a smaller number of patients, a single-arm design for a conditional license.

Yes. Good. So one question on mesothelioma. Why can you say that median overall survival is 18.2 months or more when this was an 18-month readout?

So that's because when we performed the follow-up assessments of patients, we look to see if the patients are alive or if they had passed away. And if they're alive, they are what we call censored patients. So they are still plotted on if the audience is familiar with the Kaplan-Meier diagram. So you can still see that those patients are alive. But before they've actually passed away, you cannot determine what the final median Overall Survival is. So we still have more patients in the experimental arm that are alive, which means that the median Overall Survival has not been determined yet. But what we can tell from the point in time where they were last followed up and alive is that the median Overall Survival of 18.2 months can only be the same or better. I hope it makes sense what I've tried to say.

I can also comment on that. And I understand the question is why can't we have a data showing 18.2 months when the trial is an 18-months follow-up? And that's because 18 months, that's from the last patient. So most of the patients, they have, of course, been in the trial for much longer than 18 months. So that's where we can come up with a result like this. But as Magnus says, it's very important to understand that the median Overall Survival is not 18.2 months. It is probably going to be better because more patients have to die for us to see the median Overall Survival in that patient group. And when we checked the last time, that hadn't happened. So when we check the next, next time, it will be exciting to see whether we then have a median Overall Survival or whether we have to wait even further before we see it. But this is, for us, is very encouraging. The fact that you haven't seen a median Overall Survival yet is the most positive outcome that we can have.

Yes. So I mean we've already touched a bit on plans going forward. But moving on to that now. Also, do you see other indications that can be relevant for this combination with ONCOS and KEYTRUDA or anti-PD-1?

Magnus?

So what we've said from the very beginning of this trial is that it's not just -- I'm here to talk about the melanoma trial with Jedd Wolchok Group and some other sites in U.S. and Oslo here. What we said from the very beginning is that it's not just a trial of melanoma, but it's also a proof-of-concept study for other indications where checkpoint inhibitors don't work particularly well. So we are already looking at other opportunities. One example of that is head and neck cancer. So head and neck cancer is a highly malignant type of cancer where the checkpoint inhibitors have not had a great impact and where it's relatively easy to administer the virus. As you know, we inject the virus with a syringe and needle. And where we -- based on the data that we had today shown in melanoma, we could potentially also address head and neck cancers. So yes, it's a good question. And there are, in summary, lots of opportunities actually for us to look at additional indications with ONCOS-102 in a checkpoint inhibitor.

Yes. And then a bit on financing. What are you thinking about -- on financing going forward, how will you finance a new trial in melanoma? Are potential partners interested moving forward?

As always, we won't give any concrete guidance on finance. We'll keep all options open. But I'd like to remind the audience that we raised money already in October, just 1.5 months ago. So at the moment, at least, we are in good shape.

And in terms of potential partners, is there any interest in pharma companies to collaborate on further trials?

Yes, we're in discussion with pharma companies to partner up on these future trials specifically.

Good. So then a bit on deals. How do you see Targovax results from the ONCOS-102 platform compared to data and peer transactions, deals done in the market? And to me -- it seems to me that comparative deals have been done in earlier clinical phases than you are now. Is that correctly understood? And what do you think is the way forward to get similar valuation on Targovax?

That's a big question. It's correct that there are quite a few deals that have happened over the last couple of years with oncolytic viruses. And the race in oncolytic viruses you can divide in 2. So there's a group of viruses that have clinical data. They usually have GM-CSF as a transgene. They have been around for a while. And ONCOS-102 is one of them. There's also a parallel race going on with preclinical viruses, with novel modes of action, maybe different "more exciting" transgenes, multiple transgenes. And they haven't come as far yet as the first generation of oncolytic viruses. And you see deals happening in both groups. Now we are also in the second group with our ONCOS-200 series and our collaborations, our various collaborations within this area. We're also starting to position ourselves to do deals in the earlier phase. So I think that's my answer to that question. We know that there are many early deals. You can make very good deals on exciting constructs, not only exciting data, and we will try to do both.

Yes. And I think we'll wrap it up now with the last question. Are these good data going to affect the 2021 plans or much later?

Well, it takes a few months to plan and set up new trials. But within a 1-year horizon, we will certainly have progressed our plans in one or both of these indications significantly. Whether it's going to be patient recruitment in a new trial during 2021? I cannot say that today, I doubt it. It will take time to actually get the trials up and running. But certainly, this is -- this data has major impact on Targovax and for our plans going forward. That was the last question?

Yes.

Good. Then thank you, Magnus.

Thank you.

And thank you for everyone listening in, and thank you for the good questions.