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Edited Transcript of TRVX.OL earnings conference call or presentation 22-Aug-19 8:00am GMT

Q2 2019 Targovax ASA Earnings Call

OSLO Sep 9, 2019 (Thomson StreetEvents) -- Edited Transcript of Targovax ASA earnings conference call or presentation Thursday, August 22, 2019 at 8:00:00am GMT

TEXT version of Transcript

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Corporate Participants

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* Magnus Jäderberg

Targovax ASA - Chief Medical Officer

* Øystein Soug

Targovax ASA - CEO

* Torbjørn Furuseth

Targovax ASA - CFO

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Presentation

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Øystein Soug, Targovax ASA - CEO [1]

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Ladies and gentlemen, welcome to Targovax's quarterly presentation. My name is Øystein Soug. I'm the CEO. And together with me today, we have Magnus Jäderberg, who's the Chief Medical Officer; and Torbjørn Furuseth, who is the CFO of the company. There will be possibilities to ask questions from the room after the presentation. But during the presentation, everyone can file your questions on the web, and we will answer them as we finish.

Now in Targovax, we develop oncolytic viruses. And our lead product is called ONCOS-102. It's an oncolytic adenovirus that we use to make cultured mesoth, which means, in essence, to produce T-cells to kill cancers. We are one of the furthest-developed oncolytic viruses on the market today. We have compelling Phase I data, and currently, ONCOS-102 is in 4 different combination trials. We're combining both with chemotherapy and with checkpoint inhibitors.

Since 2016/2017, we have started and recruited patients into 4 trials that are currently maturing, to the extent that we are now seeing those trials being completed and data coming out of them. And clearly, the highlight over the last few months is the last -- or the first bullet on the post-period box here, namely our data in checkpoint inhibitor refractory melanoma. I'm not going to say too much about that because most of this session is going to be devoted to that data, and Magnus is going to present it to you. But I would like to mention that we are particularly encouraged by this data because it has happened under a treatment regime which we consider to be suboptimal.

And another highlight of the last quarter is that we have started a second cohort with -- in that trial with a more optimal treatment regime. So instead of treating the patients with 3 injections over 1 week, we will now treat the patients with 12 injections up to 34 weeks. So it's a completely different treatment regime, but Magnus will talk more about that. But that's clearly 2 of the highlights over the last few months.

We're also conducting a trial in mesothelioma, and that trial completed enrollment during the quarter. So we're now sitting and waiting for the 6 months data to read out approximately around New Year's Eve. And there's a third trial that we're running together with Imfinzi of AstraZeneca, which successfully passed through dose escalation and safety and is now into the expansion phase of that trial. So very good development on the clinical trial front.

We also have 3 new viruses that we talked extensively about the last time we were standing here. They have gone into in vivo testing and also to the extent that we'd be able to file patents on those viruses. In addition to that, we published a paper in the Journal of Medical Virology, and we raised NOK 74 million in the capital markets. So these were the operational highlights of the last few months.

Now the last bullet on this slide regards strategy. In May, we decided to fully focus on the ONCOS platform, which means that we will not continue to invest actively in the TG platform in its current form. And that, of course, is a complex decision that we have been going through. But essentially, there are 2 main components to that decision -- that led us to make this decision, and one has to do with TG -- or TG01 itself. So we are taking TG01 through Phase II in a non-randomized trial, and we have a good signal efficacy, which requires as a next step to do a larger trial -- a larger randomized trial, which is going to be costly. And the decision implies that we will only take that step together with a partner who can pay for it. The second component of the decision has to do with the alternative, namely ONCOS-102. And there's been a development in the ONCOS -- or in the virus field over the last few years, which has made it more natural for us to focus on that.

Now on this slide, you see an overview of the various viruses that are in development today. This is a list ranked according to maturity, and you will see to the left the name of the companies, the name of the virus -- or the type of the virus and then the name of the virus, then mode of action and the highest phase. Now you also see here that ONCOS-102 is positioned fairly high up. And I'm not going to go through all of these viruses. I only want to point out a couple of them.

And the most important here clearly is IMLYGIC, which is the only one which is on the market. It has been on the market since 2015 as monotherapy. And now they're conducting a Phase III in combination with checkpoint inhibitor, and some data has come out of that trial which is really compelling. So that's an interesting compound to follow and an interesting trial to wait for readout.

The second I would like to mention is Merck's CAVATAK. That was developed by a company called Viralytics in Australia and then sold to Merck in 2018 for $400 million. They also have good data, particularly in combination with the checkpoint inhibitors.

And then we have us. And we are a leader in this field of oncolytic viruses, not only because we have a Phase II asset and not only because ONCOS-102 has been tested in more than 180 patients, not only because we have compelling Phase I data, but now also because we have compelling data in combination with checkpoint inhibitors as do CAVATAK and IMLYGIC.

Now if we take a look at the virus landscape. We still believe that over the next years, surgery and chemo, and in some instances, also radiotherapy is going to play an important role. But we know that the new therapies, immunotherapies and particularly checkpoint inhibitors, they have come to revolutionize the field. And checkpoint inhibitors, as we know, they're selling for approximately $20 billion per year already, but there is mounting body of evidence that in order for these checkpoint inhibitors to have a deeper effect and an effect in more patients, they should be combined with oncolytic viruses.

Our virus is an adenovirus. We think adenoviruses are particularly well suited, and particularly our adenovirus is well suited to do this job. One reason is that it's highly immunogenic. It means that it creates a strong, innate immune system jolt when the patient is being treated, which we have shown to be important for the clinical benefit of the patient. It's well characterized. There are no known safety issues or no major safety concerns with this virus. And ONCOS-102 also has a backbone that allows it to be used as a platform for other viruses. So we can put in all the transgenes and create a whole platform based on it.

The industry is also starting to recognize that viruses are an emerging interesting class of drugs. And in 2018 and 2019, we picked out a few interesting deals that have happened. I already mentioned Viralytics and Merck, which happened in 2018 for $400 million. But I would also like to point your attention to AstraZeneca's preclinical R&D partnership with transgene that yielded an upfront of $10 million for transgene. So this is something that is happening as we speak, and more and more pharma companies are seeing the promise of using oncolytic viruses, particularly then in combination with checkpoint inhibitors.

This is our entire program as it stands today. The 2 light blue boxes are the completed trials. The rest of other trials, we're running at the moment. Usually, Magnus goes through all of these trials and gives an update on what has happened. Today, Magnus will focus on the melanoma data on the RECIST trial.

So with that, thank you, and I give the word to Magnus.

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Magnus Jäderberg, Targovax ASA - Chief Medical Officer [2]

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Thank you very much, Øystein, and good morning, everyone. Nice to see you all again. So I'm going to talk to you a little bit about this trial that you've heard me talking about before, which is a study in a very specific subpopulation of patients with advanced melanoma. So we're talking here about patients who have not responded to checkpoint inhibitors. Some of you may be aware of my own background helping Bristol-Myers Squibb to develop ipilimumab or YERVOY as a first checkpoint inhibitor in melanoma. And what we now know with the subsequent checkpoint inhibitors is there are only about 40% to 50% of patients who will actually respond to a checkpoint inhibitor. And as Øystein alluded to, what we now know is that it's important to make sure that in the immune therapy setting, the right kind of T-cells are being generated in order for checkpoint inhibitors to work, and I'll come back to that point later on.

What you can see here are some of the features of those patients. And you can see that these are patients who had several lines of therapy beforehand, often 2 or even 3 immunotherapies, sometimes even 2 checkpoint inhibitors before they went into the trial. It's a pretty elderly population if you look at the median age of 73 years. And of course, this is indeed a group of patients that are very difficult to treat today, and we don't have any good treatments. Again, Øystein alluded to some earlier data, looking at IMLYGIC in combination with PD-1 antagonist. And yes, there are some good data coming through, but too early for clinicians to be able to know really how to handle these patients. And we feel that with this trial, we're really right at the front to address this important area of medical need.

So what did we do when we gave patients 3 ONCOS-102 injections in 1 week? We left them for 2 weeks, and then we followed it 5 months of KEYTRUDA. So that's 8 cycles of KEYTRUDA during the subsequent 5 months. In total, it's a 6-month trial.

What did we see? At the bottom of the slide, very good safety profile. So no concerns whatsoever. We found an overall response rate of 33%. So of those 9 patients that went into this Part 1 of the trial, 3 actually responded. And I'm going to come back to you about that point later on to put that figure in context with other modalities addressing a similar kind of patient population. So we had 1 complete response and 2 partial responses measured by RECIST. And just briefly, to mention, we were also very encouraged to see robust and relevant immunoactivation, not just of patients' immune cells that are circulating, but also immune cells that managed to reach the tumors. I'm going to come back to you with some information about that in a moment.

Now there's a complementary way of looking at overall response rate, which is a look at the target lesions. And for many of you who are used to this area of oncology, you will be familiar with this whole concept of change in tumor burden of target lesions. And what you can see on the slide here is that we have presented 7 patients. And you may ask why. Well, the reason is because 2 of the patients actually progressed before we did the 9-week CT scan. So that's why we ended up with 7 patients. You find here also indication of the stage of the patient. You can see here Stage 3 to 4, so very late-stage melanoma patients, nonresectables. In other words, surgeons can't help these patients.

What you can see here then on the left-hand side of the x-axis is 3 patients progressed, and that's what we have discussed before. And then further down the line, you can see that 4 patients actually responded. So we have 1 complete response at the very right-hand side of the slide, and then we have 3 partial responses.

I wish to highlight 1 patient that -- which you see sort of next to the last bar. That's a patient where the target lesion nearly disappeared, but the patient had a new lesion coming up later on. And therefore, that patient in the overall response rate, the RECIST calculation, ended up as a progressive disease. So that's just to explain, while you heard about, on the overall, there were 3 improvements or 3 patients out of 9 that responded, and here you can see 4. So it just explained that this is a sort of a complementary way of looking at tumor response in this particular setting.

Now here we have clearly the most interesting patient in the trial, which is this patient that had a complete response, meaning the entire tumor of this patient's melanoma lesion on the knee disappeared. And you can see here the pictures at baseline and week 3 and week 9. And what I think is very interesting is already at week 3, if you look at that middle picture, you'll notice that just after 3 2.5-milliliter virus injections, the lesion has reduced by about 60%, 70%. So with no other treatment apart from 3 virus injections, you have a significant reduction in size. And then after 2 cycles of pembrolizumab, or KEYTRUDA, the lesions actually disappeared. You may ask me, "Why is there some discoloring of the knee?" Well, that's actually hematoma. So it's actually sort of the remnants of injections and scar tissue as the lesion has disappeared.

And what's important then, of course, and that's the whole concept of the trial is to see, well, is there some kind of correlation between clinical outcome and immune activation? And indeed, there is some very clear correlation in this patient. You can see here, we looked at CD8+ T-cells, those important T-cells that are able to kill tumor cells, and to what extent they managed to get into the tumor. And you can see here that it was very low at baseline. And already after week 3, having only had 3 virus injections, we have a sixteenfold increase of those important T-cells.

And there are different ways to look at this activated T-cells. That means that you actually look to see what kind of molecules -- cell-killing molecules are those CD8+ T-cells producing. And there's one -- very important one we measured, which is called granzyme B. And you can see here again that if you look at that subpopulation of the real tough ones, that they were able to really obliterate cancer cells. There was a fivefold increase just after 3 virus injections. We also saw increased PD-1 expression. And importantly, MAGE-A1 is a cancer antigen-specific expression on T-cells, and you could see here that we saw nice and healthy increase during the participation of this trial up to week 9 when we measured. So an interesting case, complete response and with associated immune activation whichever way we look at it. We looked at it systemically. We looked in the tumor with biopsy data, and we find that very neat association, which is exactly what we hoped to see.

So that's 1 patient. If we now look at the entire population of 9 patients. You have a lot of information here. I'm not going to go through all of it, and you have it in front of you and it's been circulated to those who are listening to us over the webcast. But needless to say, we see good increase of pro-inflammatory cytokines. So this is the sort of the rapid response team, if you imagine, sort of the innate immune system as -- the part of the immune system that is able to deal with anything strange or foreign immediately. And then if you look in the lower box, the lower gray box, we have the adaptive immune system, which takes a little bit of time and is a little bit more specific. It targets a specific kind of danger is one way of putting it. And the T-cell infiltration heading is therefore covering the information we got from biopsies, so it would be the biopsies at baseline, week 3 and week 9. And you can see there very good increase in all the relevant immune cells. And I think that the one I want to highlight is the fourth bullet point in that particular section, which is, as you can see, we had T-cells in nontreated lesions on week 3. So that gives us an idea that the virus, we inject the virus in a target lesion, and yet the virus is able to do something notedly in other lesions that were not injected. And of course, that's the beginning of an abscopal effect discussion. We have seen, just to remind you, both in our Phase I study and in previous work we've issued and published that we've seen clinical abscopal effect. This is in local data so I wouldn't call it abscopal, but certainly, this is sort of what is the background to an abscopal effect in patients. And that's, by the way, something we will measure and present to you as we have completed the trial, which will be towards the next spring.

Systemically, you see here also all very relevant changes. And on the right-hand side, on that bottom part of the slide, you can see that we have very important increase of tumor antigen-specific T-cells: a, we saw new ones, that's called de novo; but we also saw in several patients, those who had some relevant tumor antigen-specific T-cells, actually increased during the treatment. So again, a sign of the virus being able to activate all the various parts of the immune system. We also saw PD-L1 expression on tumors. And of course, that is probably the single most important sign of a compound that should be able to work in combination with a PD-L1 antagonist -- or a PD-1 antagonist such as KEYTRUDA or OPDIVO, et cetera. So that's an important finding.

On this slide, we've just highlighted the changes of those important CD8+ T-cells that find the tumor, so talking about TILs, or tumor-infiltrating T-cells. And you can see here on the left-hand side that in those 3 patients where we had a clinical response, we also saw some very healthy increase of that particular cell. I should say that the first dark blue bar is the change from baseline to week 3, and the second one is the change from baseline to week 9. So what you can see here is that -- and it's, by the way, log-ranked, so the first patient had over twentyfold increase just after those 3 virus injections, et cetera. But what you can also see here is that, as we looked at week 9, we saw that several of the patients had a bit of a drop of this important type of immune cell. And that prompted us to add on another cohort to the study, and that's something I'm going to come back to in a moment.

Well, here's sort of a summary of the trial and summary of the first cohort of 9 patients. You can see here very good safety, very reassuring. If you look at the combination with KEYTRUDA, which we never combined with before, we don't see anything that is in any way alarming. If you look at innate immune activation, as I said, good and healthy increase of the important immune cells. Most patient -- and I'm a clinician, as you probably know. My background is medicine. I find it very interesting that pretty well all the patients have a reaction to the virus in the sense of fever or chills. And of course, that's the most obvious sign that whatever we are giving this patient, this patient's immune system is starting to deal with the viral replication. That is a result of the virus injection.

And if you look at the adaptive immune system. This is the most specialized immune system. Again, good increase of the important various aspects. And as I said, the non-injected lesion activation gives us a little bit of an idea what we may see in the future. And finally, the clinical efficacy, the hard figures are really the ones you need to remember, 33% ORR across this first cohort. And that -- as I said, for patient 5 that I looked at in some detail, there is a nice association between the clinical response and immune activation.

Now how do those 33% ORR look in the context of other modalities? And this is an attempt of trying to summarize that. You can see ONCOS-102 at the top. There's CAVATAK, which as I mentioned earlier on is a Coxsackievirus that was purchased by Merck. And you can see here that they ended up with roughly a similar kind of percentage, 36%. However, and that's what I've put in bold here, these patients were ipilimumab-naïve, and they were all given ipilimumab. In other words, they hadn't had a CTLA-4 antagonist such as YERVOY, but they were given that in the trial. And YERVOY was a product I worked on, so I know a little bit about the response rate with YERVOY, and it's about 20%. So you have to see that 36% figure in the context of YERVOY-naïve patients getting YERVOY for the first time.

There's a T-cell therapy here that's produced some quite interesting data, also in the sort of mid-late 30s. What one needs to remember that this is T-cell -- an autologous T-cell therapy. And by autologous, we mean that we take material from the patient, and we take it to a factory, and we modulate the T-cells that we've taken from the tumor of the patient. We expand that population of T-cells, and we have to give it back again to the patient intravenously. So from a logistical manufacturing point of view, it's a pretty expensive and complicated procedure. But nevertheless, some encouraging data here.

Again, I've included 3 toll-like receptor 9 agonists. Toll-like receptor 9 agonism is believed to be probably the most important induction point for activation of the innate immune system. And in fact, just to remind you, you've heard me saying this before, but nevertheless, our virus, adenovirus 5, is actually toll-like receptor 9 antagonist. And you could see here that some companies have decided to focus on that particular aspect of activating the innate immune system and getting some reasonable response rates. But again, if you look at the middle one that came up in sort of our territory of 32%, there is the same caveat again that I mentioned for CAVATAK in the sense that these patients were YERVOY-naïve, CTLA4 antagonist-naïve and yet they were given YERVOY as part of the treatment plus IL-2. And therefore, one has to take that figure with some caution. But still a good figure nevertheless.

And then I've also included an HDAC inhibitor, which is an epigenetic product used at the moment for hematological cancers and where the company just started to look at solid tumors. And they ended up with about 19% ORR. So that hopefully gives you some sense of where we are with our data.

So that's from the first part of the trial. I mentioned to you what we saw immunologically was a little bit of a drop further into the trial in terms of the key immune cells. And so we had a long discussion with Memorial Sloan Kettering, where Jedd Wolchok and Alex Shoushtari who are the key investigators are running the trial with us, and we decided to make a change to the trial by adding a new cohort. So you can see at the top the treatment regimen for the part 1 study that I just presented to you, and at the bottom part of the slide, you can see what change we made. And in fact, Øystein already mentioned this. You can see that we are still giving the 3 ONCOS-102 injections upfront, but then as we start KEYTRUDA on week 2, we're also giving ONCOS all the way through in the trial. And I'm pleased to report that we have pretty quickly recruited 6 patients into that cohort, and the plan is to have completed recruitment for that cohort around Christmas time. So we are certainly on track of -- be able to present to you final data in the first half of '20, which is what we have communicated to you earlier on.

So thank you very much for listening. And I would like to now introduce Torbjørn, our CFO, who's going to take you through some of the figures and some other information that's new.

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Torbjørn Furuseth, Targovax ASA - CFO [3]

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Thank you, Magnus, and hi, everyone. Yes. So to the financials and a bit on the organization. So following the decision to fully focus on ONCOS platform, we have also conducted and concluded a restructuring of the company and set a new organization.

So the first objective of the new organization was to make sure that we have the ideal organization structure and the right people to be able to deliver on the new and focused -- more focused strategy, and we are very glad to present the new management team. We have 4 new members. And Sissel has been with the company previously before this reorganization and responsible for QA, now coming into the management team. Ingunn is new to the company, and we're really glad that we were able to recruit her to Targovax as Head of Regulatory. Anne-Sophie has also been in the company previously and now coming into the management team as Head of the Clinical Science and the pre-clinical work we're doing. And Kristiina has also been with the company quite some time and responsible for the CMC and the virus production. Øystein, Magnus, Erik and myself was part of the management team before and continue on.

And the second objective of the reorganization was certainly also to focus the company and reduce costs. So we have reduced employment base from 28 employees down to 20, and that will result in a NOK 10 million saving on an annual basis.

So going to the P&L and our expenses. We ended up on NOK 45 million total operating expenses. Still, we see high costs on our external R&D, and that's linked to the high clinical activity and the high recruitment of patients, which is certainly good. On the payroll and related expenses, you see a tick up now, and that is due to the booking or the accounting of the restructuring because everything -- the restructuring cost needs to be booked in this quarter. And the other operating expenses, we have also had a focus to reduce unnecessary or less valuable costs, so also a focus there to reduce down. So it's more now -- going forward, we have a more focused organization and a focused cost base.

Yes. In the bottom, you see the net change in cash. So it's a positive in this quarter, and that's due to the private placement and the money that -- the placement happened in March, so first quarter, but the money came to our accounts in April, which is second quarter.

So looking at the overall financial position. This gives us a cash position of NOK 135 million end of the quarter and a positive cash flow, as I said, of NOK 30 million, the total annual run rate of NOK 132 million. So with this cash, we have the resources and cash to execute on our strategy and deliver new data readouts.

I would also like to mention that we -- the analyst coverage. New to this list now is H.C. Wainwright, an American investment bank that took up analysis of us this week. So I encourage you to read that one.

So then going back to the strategy. We're now focused on the oncolytic virus. We believe that's the right thing to do and will enable us to stay ahead in the competition. We have, as we at least believe, a very nice and complementary strategy where we have our path to markets in mesothelioma. We haven't talked about the mesothelioma trial today, but the trial is fully recruited and the patients are being treated, and the data will come around New Year.

And then the melanoma trial, a proof-of-concept showing that we can reactivate the checkpoint inhibitors. Magnus gave you a lot of details on the trial and our plans going forward. We have the trial in peritoneal metastasis or carcinomatosis spread from colorectal and ovarian cancer. As you saw also, we sent a press release that the safety lead-in is concluded and that the expansion phase is now open. So also this trial is recruiting nicely.

And thirdly -- fourth, we have new viruses that we also see create a lot of interest and opportunities going forward.

So to wrap this up in our pipeline: mesothelioma, Phase II, and the data, around New Year; melanoma, we present the data today and we'll also get more data in the first half, as Magnus talked about; peritoneal metastasis is now in the Phase II since the expansion phase is open; prostate trial, still ongoing but recruitment is slow, so we're not expecting a lot of data in the near term at least; and then our 3 new viruses where we will release data end of the year.

So to sum up. Targovax, activating the patient's immune system. We are clinically proven. We have strong single-agent data. We have now also strong combination data, and we are one of the furthest-developed viruses. We have a rich news flow now with our 4 ongoing trials, and over the next 6 to 12 months, there will be more and interesting data readouts coming and an innovative pipeline.

So with that, we conclude our presentation and we are open to take any questions from the audience or from the web. Start with the audience, if there are any questions.

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Questions and Answers

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Unidentified Analyst, [1]

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Just a question regarding the administration of the virus. Of course, you can give it intravenously and have a systemic effect than an intratumor. I saw that the last deals that we made have been focused mostly on the intravenous administration. Can you comment on the advantage, disadvantage about the different way of giving the virus?

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Magnus Jäderberg, Targovax ASA - Chief Medical Officer [2]

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Yes. Well, our -- okay. So yes, I mean, I think you're absolutely right. We all wish to be successful with an IV administration, and just because we haven't started doesn't mean that we don't believe in it. But if you look historically and also what's happening with data being released, there are some significant system challenges when you give a virus intravenously. So the first challenge is that you have in the liver a very effective organ that will metabolize viruses. So what you need to do if you're going to give a virus intravenously, you have to give very high doses of the virus and sort of saturate the liver before you can actually get in the virus out to where you really want the virus to go, which is to find the tumors. There have been several published cases of life-threatening side effects giving viruses intravenously. So that's sort of just -- you can't quite get around that.

Then the other -- there is another challenge which is, depending what kind of virus you use, you have neutralizing antibodies. That can be a problem. So that's the second thing. And then my third comment would probably be to say that if you look at the data that are available, there isn't much convincing data so far that viruses given intravenously will work. But we hope they will because that clearly is going to be the way forward for us as well.

Our -- the Targovax R&D and development strategy is to give the virus first where we know we want it to end up. And that's why we give the virus straight into the tumor to show you and others, the scientific community, that this virus can actually do something when it ends up in the tumor. In other words, the data I showed you earlier on that you get appropriate immune activation. And that immune activation is correlated with an important clinical result.

And then we'll take a step-by-step into different ways of administering the virus. So Øystein and Torbjørn mentioned that we have collaboration with AstraZeneca and Cancer Research Institute. In that trial, we're not giving the virus into a tumor. We're actually giving it intraperitoneally. So we're diluting it with saline and then we give it through an indwelling catheter. So that's sort of our first step in Targovax to test a slightly different way we're administering the virus. So that's sort of where we see things going. We're pursuing intratumoral administration. We think that's quite straightforward. We are starting to look at intraperitoneal cavity administration. We're keeping an eye on the IV administration development and -- to see how that's going to pan out and when it's time for us to get ourselves involved.

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Øystein Soug, Targovax ASA - CEO [3]

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Okay. Let's take a look at the questions from the web. And there's one question here also to Magnus. Can you comment on your plans for mesothelioma if the readout of current data are positive?

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Magnus Jäderberg, Targovax ASA - Chief Medical Officer [4]

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So as you've heard today and previous times, this is the indication that we classify as path to market. And that by definition means that if we produce good data, and we're going to be able to share those data with you around the new year, we will, of course, pursue a subsequent trial. We are not sitting back and waiting for the data. We've already started to make some preparations. So we have, for example, conducted both European and U.S. investigator consultations. We have identified principal investigators both in the U.S. and Europe. In other words, already looking at sites. We're talking to regulatory experts and statistical experts to try to get an idea of which way to go. I should also mention, but I can't mention the name, we are talking to a major corporation who's shown interest in working with us on that trial, which is, of course, very encouraging as a small biotech. What I can say is that it's likely that the trial will be a first-line trial, but please don't hold me to that. But that's the thinking at the moment. That's probably as far as I can go. As we are putting together more plans and as we're getting closer to releasing the data for the ongoing trial, of course, we will share with you how we see this next program develop.

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Øystein Soug, Targovax ASA - CEO [5]

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And then there's a question about TG, which I will answer myself. Regarding the Parker trial, what is happening to that? And what's happening to TG partnering in general?

With regards to Parker, as I mentioned before, we are discussing with Parker the possibilities for doing that trial. As you know, we are in a collaboration with Parker in order to do a trial in late-stage pancreatic cancer. What has changed since we went into that agreement is that we have decided not to actively invest in that trial. So currently, we are in discussion about how to enable that trial without us participating financially, but contributing the drug to the trial. So that's -- it is still not decided how that is going to be.

In terms of partnering in general, we're not going to give detailed updates on exactly what we are doing, obviously, on the partnering front. But on TG, it is challenging and you should not expect major TG deals in the short term. The expectation on TG should be perhaps more in the direction of developing a RAS platform in other developments than resected pancreatic cancer, as we have done before. Of course, larger deals could happen, but the expectation should be more to see developing of RAS.

So there's another question here. When do you expect a readout for the expanded melanoma trial? And Torbjørn, if you go back 1 slide, you will see here, second from the top, is that in the first half of 2020, we expect some data coming from that trial. Magnus already mentioned that this -- that we had 6 patients in that trial already. The protocol dictates between 6 and 12 patients. So at some point, there's going to be either interim data or full data set during 2020 from that trial.

Then there's a question about the new viruses to you, Magnus. The question goes, "Maybe too early, but can you indicate what oncological indications could be more interesting for the new viruses?"

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Magnus Jäderberg, Targovax ASA - Chief Medical Officer [6]

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Yes. It's a little bit early. So let's just go back one step maybe. What we've done, we have cloned the viruses. We have in-vitro tested them, and we're now testing them in various animal models. As you know from previous presentations, we have ourselves developed a couple of pretty interesting models, one in mesothelioma and one in melanoma in combination with checkpoint inhibitors. So we're right in the middle of that with our 3 viruses. They all have double transgenes.

As we've said on this slide, you can see a first preclinical data coming second half of '19 where we are -- I guess you are saying we are now in second half of '19. What we hope to do before the end of the second half, in other words before Christmas, is to give you some more information from those preclinical trials and those data. And that, of course, will direct us into thinking about indications.

Clearly, the next step after the preclinical data would be to do -- to select 1 virus and to go to Phase I. And what we are doing here, as you can imagine, we're also testing these new viruses in -- or rather, against ONCOS-102, our existing virus, to see what benefits we can see by changing the transgenes. So I haven't given you an answer to your question, but just to say that as soon as we have some more information, we'll let you know and we will speculate on indications.

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Torbjørn Furuseth, Targovax ASA - CFO [7]

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Okay. Excellent. So unless there are any questions from the audience in the room, then we conclude the quarterly presentation. Thanks, everyone, for watching us and coming to the presentation.