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Edited Transcript of TRVX.OL earnings conference call or presentation 7-Nov-19 9:00am GMT

Q3 2019 Targovax ASA Earnings Call

Oslo Nov 15, 2019 (Thomson StreetEvents) -- Edited Transcript of Targovax ASA earnings conference call or presentation Thursday, November 7, 2019 at 9:00:00am GMT

TEXT version of Transcript

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Corporate Participants

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* Øystein Soug

Targovax ASA - CEO

* Torbjørn Furuseth

Targovax ASA - CFO

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Presentation

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Torbjørn Furuseth, Targovax ASA - CFO [1]

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Good morning, everyone, and welcome to the third quarter presentation of Targovax. I am Torbjørn Furuseth, the CFO of the company. And together with me today also have Øystein Soug, our CEO.

There will be forward-looking statements today. The agenda. First, we will start with a short introduction of the company and the financials and the highlights of the quarter. And then Øystein will take you through melanoma. We will present preclinical data on our next-generation viruses, short touch-up on the mesothelioma trial and then the upcoming news flow.

Cancer therapy has gone through a paradigm shift with the introduction of immunotherapy, and this shift has been led by the checkpoint inhibitors that have cured thousands of patients and is now a $20 billion market.

Despite this success, it's actually only 10% to 40% of the patients that are responding to their checkpoint inhibitors. And for some indications, the response rates are even lower. You could be -- you could combine some other checkpoint inhibitors, but that typically leads to unacceptable toxicity.

So this has led to a very strong interest and a high medical need of immune activators. And this is where Targovax can play a central role in immunotherapy going forward. So we are developing our ONCOS oncolytic virus platform with adenoviruses, targeting tumors that are hard to treat, solid tumors.

Our lead asset is the ONCOS-102. And it's actually one of the furthest developed oncolytic viruses in the field. We now have treated more than 180 patients. And the trial -- and the compound is now being tested in 4 ongoing clinical trials. So the coming period of 3 to 12 months will be very interesting with a strong news flow coming out.

Already to date, we have encouraging data. We have strong data in -- with a single agent, and that is very difficult to get these days. We have the biggest event of the quarter, we published the overall response rate from our melanoma trial, with a 30% -- 33% ORR, which is really strong in this population, and we will talk more about it also later. And lastly, also, we have promising data in the ongoing mesothelioma trial. This is a trial we are running in combination with standard of care chemo. So in the context, in this background, we have set out our development strategy.

First of all, we have defined our path to market. And we have defined a niche where we have orphan drug indication, very high medical need, which is mesothelioma. So all existing therapy today is not really giving patients a good response. So here we have an opportunity to become a front-line therapy. Secondly, we also want to expand and to activate the checkpoint inhibitor refractory tumors -- some noise outside there. And this is really hard-to-treat tumors. They are not responding. They're refractory to the checkpoint inhibitors and they're progressing. And this is really a benchmarking arena for all the immune activators now.

And if you can show that you are in top of class here, then you also can open up for new indications going forward. So this is also a very interesting field for us. And then thirdly, we also want to expand the checkpoint inhibitor indications. As I mentioned initially, there are several cancer indications where checkpoints do not respond or their response rates are very low. And if you're able to increase the response rate by the activation of our virus, this can open up also a large potential for patients.

Finally, we also want to expand our platform with building upon our virus backbone with the next generation of viruses. So here, we have now developed new viruses with double transgenes and they have utilized all the recent knowledge in immuno-oncology, so that we can develop new distinct mode of actions. Øystein will tell more about the new viruses later today.

So based on this strategy, we are now running this clinical development program. The light blue boxes are completed trials. The dark blue boxes are ongoing trials sponsored by us. And the gray is sponsored by someone else and a partner. So the mesothelioma trial is the randomized trial. It's fully recruited. We will release data, we've said, around new year. Now we see it's going to be January before we have everything ready. So that will be a major event from us -- for us in the near future. Secondly, to activate the checkpoint refractory tumors, we are running a trial in the very hard-to-treat melanomas. Patients are progressing although they are on revolutionizing checkpoint inhibitors. And as we published earlier in third quarter, we were able to turn around 3 out of 9 patients to responders. So these data are very strong. We will also talk more about them. Thirdly, to expand the checkpoint indications, it's the peritoneal malignancies. So these are tumors originating from ovarian and colorectal cancers. This is a very strong collaboration where we are invited to participate together with AstraZeneca and the Cancer Research Institute. So we're really glad that we were invited.

In addition to those 3, we're also -- ONCOS-102 is also being tested in prostate cancer, in combination with our dendritic cell vaccine. This is led by SOTIO, and it's not really a part of our strategy, but can still provide some additional data on the virus.

So to the highlights of the quarter. As I mentioned, the melanoma data we published in July. This is a very challenging patient population, but still, we were able to achieve a 33% ORR. So that's very strong data we are proud of. And we were also selected for an oral presentation at the SITC conference that is now taking place. The presentation is on Saturday. Also what happened in this -- in the third quarter was we completed the safety lead-in in the peritoneal malignancies trial, that's an important milestone as well, and we are now in the expansion phase recruiting patients, both in the ovarian and colorectal indications. And finally, also, we actually opened Oslo University Hospital as a center to recruit patients in the melanoma trial, and that's also good for us to also come to the home turf and offer this treatment to patients.

So over to the financials and the P&L. Third quarter numbers to the right. Drawing attention to the total OpEx in the quarter, which was NOK 18 million lower than the previous quarter. And that is mainly due to the downsizing that we said -- we announced in the last quarterly presentation. We had to downsize and train the organization, so that led to additional costs in the second quarter. And now we are down to the cost level that we will go forward.

We said we reduced FTEs with 1/3. And if you compare with the third quarter in '18, you'll see that the costs in this quarter was 1/3 -- no, 2/3, so down 1/3. It will go up a bit in the next quarter due to the periodization of the holiday pay and so on. Also, the external R&D expenses were a bit lower. That is due to the high levels in the previous quarters from the mesothelioma trial. Also, we reversed some of the provisions we had on the melanoma trial. And also the CMC costs were a bit lower, that's also linked to the periodization when we produce the batches and so on.

So all in all, reduced OpEx, we expect it to go up a bit again in the next quarter, but not to the levels seen in the previous quarters. Going to the cash side. Net change in cash was down NOK 31 million, and that leads us to a cash position of NOK 104 million at the end of the period. So to sum up, as I mentioned, the cash in the end of the third quarter. When it comes to the share at the price per share of around NOK 5, where we've been trading lately, the market cap is NOK 340 million -- NOK 320 million. And the daily turnover is also a bit down in the quarter compared to previous quarters.

So with that, I'll leave the word to Øystein that will take you through the rest of the presentation.

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Øystein Soug, Targovax ASA - CEO [2]

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Good. So as Torbjørn mentioned, the definite highlight of this quarter are the melanoma data that we released in July. Just to remind you, this is a very sick patient population. These are patients that when they are on the checkpoint inhibitor and start progressing, there's really nothing for these patients.

You can get on the clinical trial, but normally, patients are being sent home on palliative care.

So at least in Europe, you will get on my clinical trial. And as you can see, the patients that we had, mostly treated in the U.S. East Coast, they have been through 2 or 3 previous immunotherapies. So they were heavily pretreated. They were old and they were sick. What we did was to give them ONCOS for 1 week. Then we gave them -- put them back on the checkpoint inhibitor. And of course, the hope is that we have immune activated the patients in the meantime. We produce the T-cells that the patients need in order to respond to a checkpoint inhibitor, again, which, in our case, was KEYTRUDA. And the results were good. Safety, as always, has never been a problem with ONCOS-102. And also in this trial, as we've seen in other trials, the immune activation is very strong, it's very robust, both on a lesion level and on a systemic level. But of course, the highlight here is the 33% ORR, meaning that 3 out of 9 patients, they actually had a reduction of their tumor burden by more than 30%.

But what does that mean compared to other treatments? Well, as I mentioned, there's nothing there for the patients which is registered. So we have to compare with other clinical trials. And you see 3 sections here. All the patients on this slide, they are PD-1 refractory, so they have progressed on a PD-1 checkpoint inhibitor. And the top section, we are giving -- [we will see] ourselves, together with other drugs in combination with a PD-1. So these are patients that are refractory to the checkpoint inhibitor they are given. And we stack up well against these. Two of them are TLR9 agonists. And I think it's quite logical that ONCOS-102 is better than a TLR9 agonist because ONCOS-102 is also a TLR9 agonist. But in addition, we immune activated patients through antigen release, so there's an additional mode of action here compared to the TLR9.

Second section, these patients are also PD-1 refractory, but they get CTLA-4 combined with something. So they're not refractory to CTLA-4, so they get a checkpoint inhibitor they're not refractory to, which means that there probably is some effect out of the checkpoint inhibitor in these case, maybe 10% to 20%. So it's not a direct comparison. I think we stack up well compared to those 2 as well. CAVATAK is, as we mentioned before, a virus that was bought by Merck for $400 million last year. And on the bottom, you have T-cell therapy. So this is the therapy where you take T-cells out of the patient, you grow it up in the lab and put it back again, which is obviously not an off-the-shelf treatment. It is highly individualized, and it involves fairly complex and expensive logistics. So it's not really a comparator from a commercial point of view.

The data that we have presented so far is in the Part 1. So in the Part 1, we see that we only gave ONCOS 3 times during 1 week. We are now in the middle of Part 2. In Part 2, we keep giving ONCOS for 1 week, but we dose also for almost half a year after that, concomitantly with KEYTRUDA. The hope is, of course, that we will get even better responses in the second part. That trial is not fully recruited. But we are guiding that data will come before summer next year. It has been mentioned by Torbjørn, we're very proud that the data from the Part 1 is being given an oral presentation at SITC, now on Saturday. The week after, the same data and more will be presented at a KOL event in New York.

Now we're going to show you something that we haven't showed you before, which is the first data from our new viruses. So we have ONCOS-102 with a GM-CSF Transgene, but we have been experimenting with some new modalities, new viruses, with double transgenes. I showed you this one before. It's the overview of the viruses that we have in preclinical development at the moment. It's ONCOS-102 and ONCOS-210 and -212. They have the same transgenes. It's pretty much the same virus. It's just built in a different way. And then we have 210 (sic) [211] and 214. And what we're going to talk about today is 210 and 212, this is the one we have data from. But the modality here, what we're trying to achieve is to use the transgenes to, in a way, strangulate the tumor. Tumors when they're growing, they have a tendency to break down and consume surrounding tissue and also to build a network of blood vessels around and in the tumor, and the modality of these 2 transgenes is to inhibit that, to stop this tumor from growing by giving itself nutrition. The 2 other ones have a modality of inhibiting immune suppression and crossfire in the oncolysis itself. But we don't have data on that now, that will be at another session.

So what you see here is the results in a mouse model, where the mice does not have an immune system. So the effects you see here is purely a local effect. There's no immune effect on these mice. On the Y-axis, you see the volume; X-axis, you see time. And we have several groups of mice that have gotten different types of treatment. ONCOS-210 and 212, you see these are then the new viruses with double transgenes. But we also have viruses with single transgenes. So we have each of the transgene in their own virus. And there's also an arm here with the combination of the 2 single-transgene viruses. And what we see here is that there is a slight effect from the single-agent viruses, but we only get the true effect when you add the 2 transgenes together, either in 1 virus or in 2 different viruses. And looking at this graph also, you can see that is suggesting that the 3 viruses on the bottom here has more than an additive effect compared to the 2 single viruses. So there seems to be some sort of synergy here. Using the calculator on that, you will see that compared to the expected additive effect, it's almost double. So what that tells us is that we've chosen 2 good transgenes to put in one virus that gives us a synergy.

Also, we tried these constructs in mice that has a human immune system. So here, you will see an effect which is not only local, but also potentially an immune system activation and an immune effect. And the conclusion here is the same. The double transgenes perform better than the other ones. And we also have put in survival curves here that are a bit interesting. So we have the number of -- or the share of the mice still alive on the Y-axis, over time on the X-axis, and you see that in most of the groups, the mice, they die over time, unless they get a double transgene. So the mice that get the double transgene, they seem to perform the best, and they live the longest.

What does this mean? Well, it means that we are able to construct double transgenes in our backbone -- on our backbone, and that it has an effect. We see that 2 transgenes are better than one transgene, and at least in the case of 210 and 212, there is a synergistic effect, which we're happy to see. That means that we'll keep on working on this virus. We'll keep on working on the other viruses as well, and data will be presented on conferences in 2020. So we'll start submitting this data to various conferences. And the aim of all of this is, of course, that we will get a second-generation virus into the clinic. So we expect to be able to select a clinical candidate maybe sometime in 2020 or 2021.

Now our more immediate future is going to pivot around mesothelioma. Just to remind you, mesothelioma is an interesting indication to us because we have some good data in our Phase I. We have a mesothelioma trial ongoing. We have orphan drug designation, both in Europe and the U.S., which gives us 10, respectively, 7 years market exclusivity, and probably also an opportunity to get favorable treatment by regulatory authorities. The competition that we face in this indication is not strong. We seem to be maybe not the only virus, but the only virus with any data at this point. So we don't -- there doesn't seem to be any competition from any other viruses.

Today, this is not a checkpoint inhibitor indication. But as Torbjørn mentioned, the big promise of oncolytic viruses and ONCOS-102 is in combination with checkpoint inhibitors. And checkpoint inhibitors are starting to come in now. In the U.S., it's being used in second line. So we see that if this data is good that we have on our current ongoing mesothelioma trial, the next trial will be in combination with the checkpoint inhibitor. So we welcome checkpoint inhibitors in. We think that's goods for it -- we think that's good for us.

The trial, which is fully enrolled at the moment, it looks like this. It has 20 patients in the experimental arm. They are on, I guess, both ONCOS-102 and the standard of care, which is chemotherapy, and there are 11 patients in a controlled arm that only get chemotherapy.

As I said, it's fully enrolled, which means that we are just waiting for the data to take in. As Torbjørn mentioned also, we see that, that data will be in our hands in January, and we will report that data in January. And that's going to be very exciting for us. It's a big trial. It's the biggest trial we've ever reported on, and it's randomized. Melanoma trial is also interesting, of course. As I mentioned, it's not fully recruited, but we expect to be able to report data by the summer next year. The peritoneal trial is also ticking along nicely. We don't talk too much about this trial because we're not running it ourself. But of course, it is a very important trial. We're very proud to be part of that trial. We were asked to participate with our virus in that trial. And it has -- it can have up to 75 patients. So it's potentially a very important set of data coming out of that trial for us. Not any formal guidance on when data is coming, but potentially something in 2020 there as well. And as we said on the new viruses, there will be data produced regularly on an ongoing basis from that program, and we will release data whenever we're ready, and this is probably going to be something before the summer there as well.

Good. In the more immediate near term, you will see an overview of what the company is participating in. SITC again, very proud to be there. Then we will also be presenting at the Oncolytic Virotherapy Summit in Boston in December. We will have a TG poster at ESMO-IO in Geneva also in December. And we will see most of you or some of you at the DNB seminar in December, I hope.

Good. That concludes our presentation, and we are ready to take questions.

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Questions and Answers

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Torbjørn Furuseth, Targovax ASA - CFO [1]

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Are there any questions in the room? I can start with the questions from the website. So there's a question here about the melanoma trial. And if we can elaborate on our plans for the melanoma study, if the readout in the Part 2 is replicating the previous results.

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Øystein Soug, Targovax ASA - CEO [2]

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That would obviously be very good. As we've shown you, 33% ORR in this indication, in this patient population is very good. When we talk to KOLs and potential pharma partners, they are very curious about this data. But of course, what they're waiting for is for this to be confirmed. This data, I think, will be good, as you saw in the comparison. It's going to be considered good if it's somewhere between -- it's somewhere above 25%. If we can confirm that it actually works well in melanoma as we think today, the next step will be a trial. We haven't settled on what type of trial that is going to be, but the current thinking, which, of course, may change, would be that it is possible to get further in this indication with a single-arm trial. So we don't -- probably don't need a controlled trial in this indication in order to show efficacy to the regulators.

Our hope is if -- as the question was, if the efficacy is the same is that you don't really need a whole lot of patients in a single-arm trial in order to get this approved.

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Torbjørn Furuseth, Targovax ASA - CFO [3]

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Good. And then there was also a question on TG. If we -- if you can say or elaborate a bit more on TG. What's happening in terms of partnerships and Parker?

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Øystein Soug, Targovax ASA - CEO [4]

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So on TG, we're working in 3 directions. One is to work with collaborators on developing the technology platform per se, and maybe not necessarily as we do within peptide vaccines, but in other ways of using our vast know-how. So that's one way we're working. Another direction is to do collaborative trials with academics. The decision that we made before the summer was to stop investing a lot of money into this platform. That does not mean that we'll keep on developing it. But we are relying on partners, usually academic partners, to do the trials for us and also get some funding from the outside to complete it. So we're working in that direction. And we're also looking at global and regional out-licensing. Obviously, if we have something to report, we would report it, and we will as soon as we can.

Yes, also on the Parker, of course, is a question that -- the Parker is just the question that we should mention. We've told Parker that we're not going to finance our share of the trial. So they are considering how to include us into that trial without us contributing financially. What the answer or the end of that process is going to be, we don't know yet. But I think before too long, we will be able to conclude what it means for us.

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Torbjørn Furuseth, Targovax ASA - CFO [5]

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Then to the mesothelioma trial. How do you see -- in case of positive results, how do you see the development in this indication going further? Given the unmet need, is there a possibility for an accelerated approval, i.e., a well-controlled trial?

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Øystein Soug, Targovax ASA - CEO [6]

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Yes. So in mesothelioma, we are -- we have been running a quite elaborate process with KOLs throughout the world, also talking with potential partners. And we have now sort of sketched out the plans to move forward given positive results. We believe we can have a trial -- the next step would be a controlled trial, randomized trial. And we will probably sort of make a protocol that can be expanded into our registrational trial. So to say exactly sort of when it is, that's -- it's too early, but absolutely an opportunity to have an accelerated approval path for this indication and building on one trial going forward.

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Torbjørn Furuseth, Targovax ASA - CFO [7]

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May be too early, but what are the indications of interest for the new viruses?

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Øystein Soug, Targovax ASA - CEO [8]

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So if you look at the deals that are being done in the virus space in general, it seems to be a lot of deals, a lot of interest in early-stage viruses. For us, that is also true, and we're talking to several potential collaborators on developing that platform. And there also are some potential in-licensing discussions on the new viruses. Obviously, that does not mean that I'm guiding that it's going to be an out-licensing on the viruses, but there is interest, and we're working in that direction as well. But, of course, it will be very interesting for us to have a solid partner to help us developing this part of the platform. We will welcome that.

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Torbjørn Furuseth, Targovax ASA - CFO [9]

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Yes. And I think we indicated a bit on the slide, what type of tumors that could be natural to pursue and to target for each of the trial -- each of the viruses, but it's too early to say exactly what type of indications we will be targeting.

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Øystein Soug, Targovax ASA - CEO [10]

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But also going back to what Torbjørn said about checkpoint inhibitors and the need to reactivate patients that are refractory to checkpoint inhibitors, and in order to expand the checkpoint inhibitors into other indications, is that people are seeing that viruses can actually play this role, and there's data supporting that viruses can play this role. And when the big pharma start thinking about ways to attack this possibility or this problem, many of them look at early-stage viruses because they can, of course, in-license something late. But many of them, they also want to get hold of something earlier, so they can do the development themselves. So it is actually a strong interest in early-stage viruses.

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Torbjørn Furuseth, Targovax ASA - CFO [11]

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That was the questions on the web. Any last questions in the audience? It doesn't look like.

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Øystein Soug, Targovax ASA - CEO [12]

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Good. Then thank you very much.

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Torbjørn Furuseth, Targovax ASA - CFO [13]

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Thank you.