Good day. Welcome to the half-y ear report for six-month period ended thirtieth of June 2018 conference call. Today's conference is being recorded. At this time, I'd like to turn the call conference over to Rolf Sorensen. Please go ahead, sir.
Yes, good afternoon. My name is Rolf Sass Sørensen, and with me, I have our President and CEO, Paul Chaplin. Before we begin, I would like to read the following. This presentation includes forward-looking statements that involve risks, uncertainties, and other factors, many of which are outside of our control, that could cause actual results to differ materially from the results discussed in the forward-looking statements. Forward-looking statements include statements regarding our short-term objectives and opportunities, financial expectations for the full year, and financial preparedness as of year-end, as well as statements concerning our plans, objectives, goals, future events, et cetera. All such forward-looking statements are expressly qualified by these cautionary statements. We undertake no obligation to publicly update or revise forward-looking statements to reflect subsequent events or circumstances after the date made, except as required by law. With this, I will hand it back to Paul.
Thanks, Rolf, welcome everyone to our half- year update. We've had a very strong first six months of 2018, particularly with regard to our growth strategy to expand our pipeline. As I'll get to later in the presentation, we've reported strong clinical data from our RSV program, we've initiated new studies, and today, as I'll go into more detail, we're highlighting new approaches that we'll be bringing to the clinic in terms of immunotherapy. On the finances, we will remain completely on track to meet our guidance by year-end. The production of IMVAMUNE, which amounts to the bulk of our revenues, is on track. Production is going well, and, you know, they will be seen in those revenues will be seen in the second half of this year.
If we go to slide 3 and talk about some of the recent highlights. One of the big highlights was the reporting very successful results for our RSV phase II. We're essentially the only company now that has reported a vaccine candidate generating broad immunity against the virus, and with these new data, we're the only company that has demonstrated that the vaccine candidate will be an annual booster, generating these broad and hopefully protective responses. We're broadening our immunotherapy strategy based on some exceptionally exciting results that we've seen out of our research labs in Munich.
I'll get more to that but w e've found that if we apply our vaccine platform either directly into the tumor or intravenously, it's much more potent way of stimulating T-cells or other arms of the immune response and has a great efficacy, greater efficacy in animal models. For CV301, we have or will be, later this year, initiating 3 phase II studies. The first in colorectal has been initiated, and the next 2 will be initiated in the coming weeks and months. In line with that strategy to only look at the efficacy in combination with checkpoint inhibition in 3 indications, we will no longer be proceeding with the phase II study in lung cancer.
For brachyury, we received orphan drug designation from the FDA. Later this year, we'll be initiating a pivotal phase II study in a rare indication, called chordoma. We've strengthened our cash position with the recently announced loan facility from the European Investment Bank. This not only strengthens the cash, it gives us much greater flexibility to continue our investments in the infrastructure in terms of manufacturing, but also to take opportunities in the pipeline. Moving to slide 4. Our RSV vaccine, just to remind everyone, is completely differentiated from the competition and those who've gone before us. We are not targeting only generating antibodies, as most of the competition. From our work, it's clear that you need a much broader immune response, kind of mimicking what a natural RSV infection induces.
We're looking to induce broad T-cells, antibodies, and importantly, mucosal immunity. For this, our vaccine encodes five separate proteins from RSV. The data we've already presented supports the preclinical concept in that in the clinic, a single booster vaccination does boost these responses, and we see these broad antibodies, T-cells, which have remained durable actually now for longer than an RSV season. Moving forward, we are preparing to engage with the FDA to have discussions on the next steps for licensure. In parallel, we continue to look at the feasibility of developing a more efficacious human challenge model, where we could evaluate the efficacy of a vaccine candidate before we go into phase III. Slide 5, we just reported booster data, and Slide 5 shows you the study design.
The middle box is the design of the phase II, where we had 5 groups evaluating 1 or 2 vaccinations of a higher or low dose compared to placebo. What we did last year was to re-enroll essentially half the subjects from 2 groups which received either a single vaccination of the low or the high dose. This allowed us to have the 12-month follow-up to see how durable the immune responses were, and after which we gave a second booster, mimicking the annual booster regime, which we believe will be required. On Slide 6, to sum up the data that we've reported, surprisingly, actually, the immune responses were durable out to 12 months.
More than at least 60% of the subjects still had elevated antibody responses, whether we're talking about IgG, IgA in the blood or mucosal IgA from nasal swabs. We were able to rapidly boost these responses so to total antibodies against both RSV subtypes, including neutralizing antibodies, but also mucosal IgA from nasal swabs, which has, from other publications, been associated as a correlate of protection. Regarding T cells, we also saw boost responses to all 5 RSV proteins. As I'll show you in the coming slides, these boost responses were strongest than those that had the weakest immune responses after a year, which is exactly what you want to achieve in an annual booster regime. Of course, these findings fully support the fact that our MVA-BN-RSV candidate will be an annual booster vaccine.
As I said in the introduction, I believe we're the only company that has actually generated any clinical data supporting that concept. If we go to Slide 7, this shows you the kinetics of one of the parameters, which is the serum antibodies against RSV. The main study, which is highlighted in red, was the main phase II study, where the subjects received either a low or a high dose of the booster vaccine at week 0, and these are the data that we've previously reported.
If you look at the booster study highlighted in green, at week 56, prior to the annual booster, you can see that these responses, these antibody responses in both groups remain elevated, and yet after the booster at week 56, these responses were rapidly boosted again, really supporting, as I said, the annual booster concept. This obviously is one parameter, but it is illustrative of all the other antibody parameters that we measured, which whether it's neutralizing antibodies against both of the subtypes, A and B, it's serum IgA or even mucosal IgA. If we go to the next slide, Slide 8, what we're trying to show here is that the boost responses that we saw, were strongest in those that had a weaker immune response.
On the left-hand side, these are the fold increases in the various antibodies that we measured against RSV, and they range from 1.3 to 2-fold increases. The reason these fold increases are lower than what we previously reported for the phase II, is that the antibody responses were higher prior to the boost after a year. This can be seen if you look at the right-hand side of the graph, because here we're now comparing the boost responses after a year to the pre-vaccination levels at week 0 the year before. This is prior to them receiving any booster with our MVA-BN-RSV candidate.
Here you can see that now we see the boost responses are 1.5- to 3-fold higher to the boost levels prior to any vaccination. This is clearly in line with the fold increases that we'd previously reported for the phase II. If you go to Slide 9, Slide 9 is showing the mucosal IgA responses. Here we're looking at a median analysis. We're looking at those subjects who had a weak immune response, so those who were lower than the median starting titer prior to the annual booster, which is the green. Here you can see that we see a boost effect, whereas those who had a strong starting immunity after 1 year, which is the red, those who were higher than the median value at the beginning, there really isn't a boost effect.
That's because these subjects already have a strong immune response, and you can't boost it further. Whereas those who had a waning immunity after a year, we can further increase that immunity back to what we presume are protective levels. Go to Slide 10. Now we're looking at the T cell responses, and again, we're looking at the entire course of the study from week zero, where they received an initial booster. Whereas we've already reported, we saw strong boost to all five proteins encoded in the protein in the vaccine, including to the whole virus. These responses, for the majority of the proteins encoded in the vaccine, remain durable up to week 56, and again, you can see that we can boost them.
If you look at the blue or the red line, which is the protein M2 or the G from the glycoprotein from subtype G, these actually drop to the same levels as we saw at week zero. You'll note that the boost effect in these two is higher than in the others, where the responses remain durable. To sum up in terms of the RSV data, we're very excited. We couldn't have asked for more than what we're seeing. We see good boost responses following the initial vaccination. One year later, these responses in the majority of the subjects remain durable. Those where the responses have waned, we are able to boost them significantly, both in terms of antibodies, broad antibody responses, and these broad T cell responses a year later.
Now we are preparing to discuss the results, our clinical results, with the FDA and our thoughts regarding the phase III design, which will happen later this year. In parallel, we continue to look at the feasibility of developing a human RSV challenge model. If you go to slide 11, our immunotherapy strategy using our platform is based on our ability to use the platform to stimulate killer T cells, recognizing tumor-associated antigens in the view that those T cells will kill the tumor, prolonging survival or causing tumor shrinkage. We continue to follow this strategy. I'll come to in the future slides, particularly in combination with checkpoint inhibition with CV301.
In parallel to our clinical activities, we've been working long and hard in research to try and find ways of making our platform more immunogenic and more efficacious in terms of our ability to use it to stimulate responses to kill tumors. Two findings that we have now found, and some of which we've already published, is if we vaccinate or inject the vaccine directly into the tumor, or we deliver the vaccine intravenously, we find that both of these are much more potent at stimulating T cells and/or changing the inhibitory environment within the tumor, allowing a much better environment for allowing T cell killing. Based on these findings, we now believe we're at the stage where we want to enter the clinic and evaluate these two different approaches starting next year.
CV301 will be going into a phase I study, looking at the direct intratumoral vaccination, and brachyury vaccine will be going into a phase I study beginning of next year, looking at the intravenous administration. If you go to slide 12, this is just a snapshot of a small part of the data that we've generated supporting these two concepts. On the left, you're looking at a mouse tumor model that if we treat with placebo or PBS, the green line, the tumors grow, and they kill the mice.
If we inject an MVA-based vaccine directly into the tumor three times, as depicted by the dot-dash lines, you can see that we get a good control of tumor growth, and I don't have that data today, but if we combine it with other things, such as checkpoint inhibition, we can actually see a curing of these animals. On the right-hand side, you're looking at an intravenous model, where again, you're looking at a tumor model in mice. If they remain untreated, the blue, the solid blue line, the tumors grow and kill the animals. If we just apply an MVA-based vaccine, given IV, the green, there is some control, good control initially, of the tumor growth.
After about 30 days, the inhibitory mechanisms that we keep talking about with the tumor take over, and the tumors begin to grow. If you add an anti-PD-1, a checkpoint inhibition, it's similar to the vaccine alone. If you combine the two, the red, if you vaccinate IV and you combine it with an anti-PD-1, we get good control of tumor growth, and the majority of the animals actually survive. We're particularly excited about these data, and we are eagerly awaiting the initiation of the clinical studies next year. If you go to slide 13, as I said, we still believe there is strong scientific merit in looking at the application of cancer vaccines in combination with checkpoint inhibition.
Our strategy for CV301 has always been to look at 3 different indications with potentially 3 different checkpoint inhibitors, and that we will now achieve as we initiate all of the phase II studies that are listed on this slide. The first study in red, the colorectal cancer indication, has already been initiated, which is a combination of CV301 with Nivo from BMS. Two other studies will be initiated in the coming weeks and months. The second will be a colorectal and pancreatic indication, using AstraZeneca's durva antibody, which will be sponsored by Georgetown University. The third and last study is a bladder cancer study that we'll be sponsoring in collaboration with Roche's Tecentriq.
This will be a two-stage design, initially enrolling 26 patients, looking for initial responses, which, if we see, we'll enroll more subjects. In line with this strategy, we have decided not to proceed into the phase II lung trial, as we now have 3 trials that will be initiated, which will allow rapid proof of concept of whether CV301 in combination with checkpoint inhibition is efficacious in one or more of these indications. Slide 14, brachyury, another cancer vaccine, which is currently in phase I. As we round up that phase I study, we are preparing to initiate a phase II study, in a orphan drug indication called chordoma, which is a rare cancer of the bones at the base of the skull, and spine....
This study potentially could lead to registration, as currently there is no real treatment that is effective for chordoma patients. We'll initially enroll 10 patients starting later this year. If we see an objective response in at least 1 subject, we'll go on to enroll another 19 with a view that we actually want to see up to 4 patients responding, which we believe would be very compelling evidence of efficacy of a combination of our BN-Brachyury vaccine together with radiation. Slide 15 outlines another brachyury study that's sponsored by the National Cancer Institute, called QUEST, or a Quick Efficacy Seeking Trial. The good thing about this is it's a multi-company collaboration that's sponsored by the NCI, where a number of different companies have agreed to combine their investigative drugs in combination with brachyury.
The base combination is always our vaccine, and then it will be used in combination with a PDL-1, anti-TGF beta, a fusion protein, and/or an IL-15 superagonist or an IDO inhibitor. This should actually generate a lot of exciting and new data on the combination of our vaccine with a number of other investigative products in men with castration-resistant prostate cancer. Slide 16. Janssen, we have a broad collaboration with Janssen on four different indications. Our Ebola collaboration is in phase III, and we have three other indications which we've licensed to Janssen, and their HPV and HIV vaccine concepts, which are both therapeutic concepts, will be entering phase one later this year.
We're making good clinical progress moving forward, and obviously, with this collaboration, there is still more than $1 billion worth of future milestones and payments, in addition to royalties, should we be successful with these approaches. Slide 17. Our IMVAMUNE contract, as I said, our current manufacturing is on track. To just, again, remind you all of the recent award from last year, which is the single largest IMVAMUNE order that we have in the history. It was more than a $500 million contract, which was initially to produce more bulk, in addition to the bulk we've already produced under past contracts. There was an initial $100 million bulk order, which, as we said, we would manufacture in 2018 and 2019.
We would be revenue recognizing $50 million in each of those two years. In parallel to producing the bulk, we are investing $75 million, expanding our manufacturing facility to include our own fill finish line, capable of producing freeze-dried IMVAMUNE as well as other products. This line will come on board in 2020, whereby $300 million, or $299 million of the award, will be used to convert all the bulk from this contract and previous contracts into freeze-dried doses, which is approximately 13 million doses. In parallel to that, there's $140 million that's already been awarded, which is supporting the phase III study, which we'll be initiating later this year.
Some manufacturing activities in transferring the process from our CMO in Germany to our new facility, which we will be seeing over the coming years. This is a 10-year contract. Just as our previous contract started at half a billion and ended up being a billion, this is starting at half a billion US dollars, and we have agreed future pricing for bulk orders, for liquid frozen doses, and also freeze-dried doses. We believe the new contract that is in place will provide future revenue streams, moving forward way beyond this initial order. In addition to our manufacturing activities, of course, we're also moving towards filing a BLA for our liquid frozen indication.
We're still on track to file later this year, which we hope will have a 6-month review, meaning that we should see approval in the first half of 2019. As I'm sure you're all aware, we are eligible for a priority review voucher, which we could either keep to accelerate the approval of another product or sell in the open market. Slide 18 talks about the financials. As I said, we remain firmly on track to meet our guidance. DKK 350 million of the revenues that we're guiding are associated with the production of our initial bulk order under the freeze-dried contract. As I've said, I think twice now, production remains firmly on track, and we're on line to invoice in the second half of this year.
The other revenues are all associated with existing R&D contracts. There are no risks in terms of waiting for new orders or new contracts. We're only guiding on the money that we know that we'll be receiving. As I said at the beginning, we have improved our cash preparedness with the new EUR 30 million loan facility from EIB, which gives us added flexibility, not only to pursue investments in our infrastructure, but also to take up opportunities, new and exciting opportunities in our pipeline. Slide 19, the news to come. Well, as I said, we will be filing a BLA in the coming months for liquid frozen.
We'll be initiating the phase III, fully funded by the U.S. government, first half of 2019. We do anticipate the approval of IMVAMUNE with actually the award of a priority review voucher in 2019. Based on the reporting of our exciting RSV results, we'll be meeting with the FDA to talk about the future phase III design, while in parallel, continue to look at the feasibility of developing this improved human challenge model. Our Janssen collaboration continues to progress with 2 new vaccines entering phase I, both for HPV and HIV, which are both therapeutic approaches. On CV301, we'll be initiating the 2 other phase II studies I outlined.
We will be reporting phase I data from our lung trial later this year. Obviously next year, we'll be starting one of the new approaches, looking at the intratumoral administration of CV301 in a phase I study. Brachyury, we'll be reporting phase I results later this year. We'll be initiating our chordoma pivotal phase II study later this year. Next year, we'll be starting an intravenous phase I. Again, another exciting new approach that we're introducing into the pipeline. With that, I conclude the presentation. Operator, I will open now to Q&A, please.
Thank you. If you would like to ask a question, please signal by pressing star one on your telephone keypad. If you're using a speakerphone, please make sure your mute function is switched off to allow your signal to reach our equipment. Again, please press star one to ask a question. We will now take our first question from Boris Peaker from Cowen. Please go ahead. Your line is open.
Good morning, or I guess good afternoon, where you are. My first question is on RSV. I'm just curious, how far do you plan to take this asset on your own?
Hi, Boris. We've said all along, we need a commercial partner for RSV. It's far too big a product, global product, to imagine that we would have the capability to launch and market that ourselves. Right now, without having concluded any discussions with the FDA, it's a little unclear how large the phase III study will be. I have never really commented on how large it would be. It really does depend on some of the endpoints and some of the statistical parameters that we need to agree with the FDA. We don't know how large the phase III is. I know there is a growing concern in the investor community about how would we fund the phase III, and would we go alone?
What I would say is, you know, I'm never gonna expose, overexpose the company to one asset. However, I don't know what the phase III design is, and whether we can initially take that on board, increasing the value of any partnership deal. If the phase III is large, which I think a lot of people, maybe not myself, but a lot of other people are anticipating, clearly, I think we would need a partner prior to phase III. I'm afraid the answer is, it depends.
Gotcha. Let me ask some of my last questions on the chordoma. You mentioned that nothing is approved, I'm just curious, what is the current standard of care, and how long do these patients live from diagnosis? Just to kind of use it as a basis of what your potential endpoints would be to get something approved.
Yeah. Chordoma is a very slow-growing tumor. I don't have the number off the top of my head, exactly how long.
Less than five.
Less than five, it is?
5% less than.
Yeah. At the moment, the standard of care really is radiation therapy, where less than 5% really respond in terms of objective responses. Currently, there's no real other treatment that is that effective. What we're really looking for is objective responses. You know, we're looking at 4 objective responses out of 29, we believe would be extremely compelling in this setting. As it's ultra- rare orphan application, you know, large studies are not practical or likely to be required.
Gotcha. Just the last question, I just want to squeeze one in. As you mentioned, there's over $1 billion of milestones from J&J. How much do you anticipate to receive that in the next 12 to 18 months?
You know, we received upfront payments, and what we have said is that the next milestone payments are associated with initiation of phase II. You know, they're not our programs, so I need to be very careful on announcing timelines of Janssen's own programs. We haven't guided on when we anticipate the timing of those, but the next milestones are associated with phase III. Two programs are going into phase I now. You know, that's all I can really say on that.
Great. Thank you very much for taking my questions.
No problem.
We will now take our next question from Peter Welford from Jefferies. Please go ahead. Your line is open.
Hi. Yeah, thanks for taking my questions. I've got 3. Firstly, on RSV, just we're curious here as to what you're continuing to look at with the feasibility of the human challenge trial. That seems to have, I guess, been a lengthy discussion now. What exactly is it that's the potential hurdle there to get that trial started? Secondly, then, some of the charts you showed on the booster study seem to suggest that the serum IgG actually increased week 30 until the start of the booster study. I wonder whether that was replicated in any of the other parameters you looked at and what the rationale for that is. Is this exposure to natural, I guess, RSV beginning again in the next season, or, you know, what potentially is it?
I think, is it just variability potentially, given the relatively small sample sizes? Just a financials one, were there any U.S. government IMVAMUNE revenues in 2Q? I presume there were. Could you perhaps just give us the magnitude and the amount that was actually sold to the U.S. government during 2Q? Thank you.
Yeah, thanks, Peter. Your first question was on RSV and the feasibility and what are we still doing. It's not just discussions. We're working on the hypothesis that if we take a primary isolate of the RSV, currently most people grow up RSV in Vero cells. What happens when you do that is that virus becomes attenuated and the mechanism which are in the literature and the like. We believe, together with our CRO, that we may have found a way that we could grow up RSV and retain its virulence.
What we're currently doing, we have grown up the RSV, and what we're currently doing is trying to characterize that RSV to determine whether we have retained the original virulence, and if we've overcome the issue of growing it in Vero cells, where you lose virulence. While we keep saying we're looking at the feasibility to make a decision, if we haven't retained the virulence of the isolate, we won't be going into a human challenge study because it won't be any better than the existing human challenge study, which we've evaluated not to be useful to evaluate vaccine efficacy. That decision should be made in the coming months. Your other question related to the potential increases in the RSV IgG from, you know, in between from week 30.
We see that, but actual fact, I think that's probably the variation that we're seeing with the assay, and as you say, the sample size, where we've gone from half the number of subjects in the booster compared to the main study. We don't believe that is a natural exposure or anything. We probably think it's most likely related to the variation of the assay. Your last question was on the revenues. I don't actually have that breakdown in front of me, but it's minimal revenues, actually, for IMVAMUNE in Q2.
That's great. Thank you.
As a reminder, to ask a question, please press star one. The next question comes from Suzanne Voorthuizen from Kempen. Please go ahead. Your line is open.
Hi, good afternoon. I have a question regarding RSV. Can you give more color on the roughly 2- to 3-fold increases that you see in the IgG titers, and how this ties into the often-used rule of thumb to look at the 4-fold increases? Have you gotten already some views on this from the outside, from regulatory agencies, or maybe from KOLs? What are the current thoughts or options that you see as potential next steps, and what would your considerations be?
Yeah. Fourfold increases that, you know, the way you look at whether an increase is significant or not, isn't based on a particular numeric fold increase. It's based on the variability of the assay, and you're looking for normally twice the lower limit increase. For ELISAs, a fourfold increase would be a very large increase. For more variable assays, you often see fourfold. In our assays, and as supported by KOLs that have looked at the data and other partners, potential partners that are looking at the data, these are significant increases in serum antibodies. When you start looking at the mucosal responses, again, that's why we always stratify it to show the weaker and the stronger immunity.
We are seeing, more marginal fold increases, but you do see those increases in those with a weaker immunity, which is lending to, more convincing data that the increases we're seeing are real and significant in terms of, what we're allowed, what we can actually boost. In terms of future considerations, as I said, we haven't openly talked about what we believe phase III requirements will be, because we have our view and opinion, but until we actually discuss them with the FDA, you know, I don't see the point in doing that. We have a number of different options that we wish to discuss with the FDA.
Hopefully, during the second half of this year, we should get much greater clarity on what the phase III requirements will be.
Cool. We'll stay put on that. I also have a few questions on CV301. Can you give some more color on the discontinuation in lung cancer? You mentioned the competitive landscape, but have you seen any data so far that could also have tied into this decision? For the readout, what kind of data do you expect to report on? Will it be responses or also PFS and OS? Yeah, what kind of data from this study would you see reading through to other indications?
Well, first of all, let's answer the middle question: Have we seen any data that has driven the decision not to continue? No, is the answer to that. At the moment, we're in phase I. We have, I believe, somewhere in the region of almost 10 subjects enrolled, so it's very few subjects that are actually enrolled, and it's primarily looking at the safety of either CV301 alone or in combination with Nivo, which was our initial start of the study or with Keytruda. It's primarily a safety study. The sort of data that we will be reporting on is obviously safety, immunogenicity. In that CV301, as you know, we changed the platform from Prostvac. We reengineered the priming dose to be an MVA-based, which we give at very high dose levels to each limb.
There are 4 vaccinations, one in 2 arms and the other in the 2 legs. We do that 4 weeks apart. We're giving a lot more MVA or pox virus than we did with Prostvac, then we follow up with Fowlpox boosters. There will be immunogenicity data, which will be important for CV301 as a platform. Then potentially, there are objective responses from the patients at the turn of the year. Those are the real main drivers, and I think the real read-through will be the immune responses. Are we actually stimulating good T-cells to CEA and MUC-1?
All right.
The main reason for not continuing into phase II, we said all along from 2014 that our strategy for CV301 was to look at 3 indications with checkpoint blockade. We are able to do that with the 3 phase II studies, 1 which is initiated and the 2 that will be initiated in the coming weeks and months. There was no real need to go into lung. The other issue with lung is the standard of care has changed essentially every 3-6 months since we tried to start the trial. We've moved already from second line, where the initial approval was for Nivo, to first line, and it's clear Keytruda is probably now the drug of choice. Also, it's a highly competitive indication with a lot of competition for patients.
We just saw that it would take a long time for the readout, and then we believe we can get the proof of concept data we're seeking from the three other studies. That's the main reason and driver for the decision, and it's in line, as I keep saying, with the initial CV301 strategy.
All right. Thanks a lot.
Our next question comes from Michael Novod from Nordea. Please go ahead. Your line is open.
Thank you. It's Michael from Nordea. A few questions. To the human challenge trial on RSV. You're going into the end of phase II meeting with the FDA, but you don't have these data. How crucial are they to the final design? When you are able to finally initiate this trial, How fast will you actually get some sort of indication and readout from this, supporting the plans for phase III? Secondly, on the chordoma trial with BN-Brachyury. When is it possible to get the first signs of, say, impact or effect in stage 1?
To that, since you now move on with a intravenous formulation of BN-Brachyury, how will that potentially impact the plans for the chordoma trial? Would it make more sense than also doing IV BN-Brachyury in chordoma?
Yep. Thanks, Michael. I would say, regarding RSV, there are two tracks basically. One is we will have the discussion with the FDA on the assumption that we're going to go into phase III with no additional data than what we already have. Those are discussions about what the endpoint could be, statistical assumptions, which will affect, obviously, the total number of subjects and the like. In parallel, potentially, we'll be doing a human challenge. We could have some initial human efficacy data for our vaccine at the turn of the year.
If those things all turn out positive, i.e., we do develop this model, we do generate some efficacy data, you're right, that would have an impact on the study design, but that would allow us to go back to the FDA at that point, not only to talk about revising the study design based on new input and new potential efficacy data, but also to discuss the feasibility of potentially using a human challenge model as the main way of generating efficacy for the vaccine. There are multiple things that are potentially possible, but right now, our primary focus with the FDA is only to talk about the existing clinical data, and based on that, what would the design be? Hopefully, that answered your question.
Yeah.
You were asking about chordoma and when could we get some initial data readout? You know, you know, we're looking for 1 patient to have an objective response, and of course, if it's the 10th patient we enroll...
If it's first or second patient we enroll, will have an impact. You know, I would say next year, most likely, is our ambition, that we would have a readout from that first round of 10 patients. Regarding looking at the IV and will that impact? Of course, every new concept, as exciting as it may be, has to go through the stages. We need to generate safety data in a phase I before we move forward. As we've indicated in the announcement today, we are moving forward with CV301 and BN-Brachyury, looking at those two new approaches. It's a way of generating some initial clinical data while actually we continue to work on what we believe could be better candidates coming through for those two approaches.
Having said all that, of course, if we get amazing data with IV, we may adapt the design of ongoing or future studies.
Just one follow-up on the RSV, if I may. It's just from, you know, from the outside, looking at this market, you are saying that you definitely still need a commercial partner. It seems like, at least from the outside, the clinical plans, they are perhaps taking a bit longer, also now with, say, all the feasibility around the human challenge trial and all that. I'm fully aware that you're not, say, necessarily willing to give this up to a big partner, for, say, for all amounts that you could be offered.
On the other hand, wouldn't it be a significant advantage for a company your size, doing clinical trials in this area, and you still want a commercial partner, to get someone on board that has all the infrastructure to do this in a, say, perhaps a bit faster fashion than you're doing it? How do you just to get a grasp on how you actually say, judging the different scenarios in terms of not giving away too much value, but also you need to get to the market, speed it up? It is still a competitive market. I know there's nothing approved, but it still could be competitive. Just to get a sense of how you put these different parameters up against each other?
Well, they're all important parameters. You know, you've highlighted it. They're all important parameters when you're considering your various options. I would say, in terms of speed, in terms of where we are right now, if I was to license this program next week, even a big pharma would struggle to initiate phase III for next year's season. There are, you know, there's a lot of things that need to be done. There's production. You know, your phase III normally includes 3 lots, so there's a lot of production activities. There's a lot of discussions with the FDA. You want to make sure your endpoint and your trial design is right.
That even a big pharma would be struggling to get into the 2019 RSV season, which means that you probably, at this stage, are in the 2020 RSV season. I think it's a very valid point that, obviously there will be more financial clout to move things. They may not do a 2-season study. They may do one big season. As I said, I think until I really know what that phase III design is, it's a big unknown right now, and it's also a big unknown for partners that we're actually in discussions with, in terms of what is their risk and what is their future investment, when everyone has a different opinion on what a phase III looks like. That's why I really want to get that, those discussions over with this year.
I think that would put us in a much better position to decide what to do, but also help us in our partnering discussions.
Thank you.
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Thanks, everyone, for joining the call and for the great questions, and thank you very much. Have a great day.
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