Good day, ladies and gentlemen, and welcome to Farron Pharmaceuticals Full Year Results 2020. I will now hand over to CEO and Founder, Markku Jelkanen, to open the presentation. Please go ahead, sir.
Good afternoon and good morning for those in U. S. And many thanks for joining us today for Farron's full year results update for 2020. We are very happy at taking you through the company's performance over the last year, but obviously would like to, of course, to have I'd like to call this meeting in person. As ever, we appreciate everyone joining us here today and hope to meet all of you in person soon.
Again, joining me here today is our CFO, Tony Hanninen. And he will explain the Results, financial part later. And then let's move on to the moving Slide number 2. Before we begin the proceedings, I would like to bring your attention the standard disclaimer slide, which is included in the presentation for completeness. So could I have Slide number 3?
So we have 3 target assets, Clever one, CD73 and AUC3, they all deal with our immune system. And obviously, we believe that Harnessing the power immune system is the best way to tackle some of those medical condition where the unmet need is very huge. And this hopefully becomes really clear also in our presentation. The first one is targeting a cancer growth and spread. We believe that converting Klev1a positive macrophages into a negative ones, we can actually shut off their immunosuppressive activities.
And that is a key thing really to reactivate the immune system. And I'm happy to share some of the recent data also with you today. And with the CD73, it's a long term project where we have really seen a lot of evidence that controlling CD73 on the surface So, endothelial cells, you can also regulate and control the organ function. And obviously, if you lose this molecule, you have Put your lungs or kidneys in a dangerous situation because they may lose their function due to the leakage of the capillaries It's those issues. And we talk about that as well.
And then few words about this Hematokine project, which is now at the preclinical stage, but hope to Really get to move it on the clinics as well. Next slide, please. Out of these three assets, this is the pipeline. Starting with the clevesen, pexmarilimab, it's the name of the humanized antibody we are using to block the CLEV1 function. We started with the solid tumors.
These patients had no options anymore when they entered the Matins trial. Out of those ten Tumor types, we already have signal in 6 of them for the clinical benefit. And I will show some of the data that as well. And obviously, this METEANS trial can be expanded all the way to the pivotal part. And those would be really interesting times once we have data collected From the Part 2 patients, which is still ongoing.
We would like to expand also this trial or treatment to one of the standard combination Treatment with the PD L1 inhibitors and that is lung and that's about the beginning this spring as well. And then the third one is the acute myeloid leukemia, which is a very interesting target for us because these myeloid leukemia cells actually have Rather significant expression of Klev1. And obviously, if you could knock that out, it would be interesting to see How much we can actually suppress the replication of these cells and that data we have seen in ex vivo settings already. Then with the trauma kind at the end from PRAB project, we are involved in the relap gap, the global study. We don't exactly know when we get the readout from that.
But more importantly, we are starting the hibiscus trial in the U. S. It's now going at the final ethical round and hopefully get the 1st patient in very soon. But as we have said for years, this treatment of interferontera protecting the central organs can be applied widely in other Organs as well. And one interesting one and large volume 1 is the acute kidney injury, which is a significant patient number today on this planet Due to number of reasons.
So obviously that is a moving on as well. Could I get the next slide? Now we are moving really look at the key events on 2020. So we have made a significant Progress with recruiting the patients to the trial. We have seen a survival benefit among those Patients who responded to the treatment and I saw that data.
We have also learned that we need to Increased the dosing frequency of these patients, and that's largely due to the discovery a soluble Klev1 in the circulation. And that finding is much more important that maybe people have not realized because Klev1 is a direct inhibitor of T cell activation. And obviously, if you would have a soluble Kleva 1 around, you can actually suppress T cell activation in all the locations in those patients. And maybe this is the way how Cancer actually could influence on the immune system on the remote locations. And obviously, that would be a great advantage for those metastasis cells who actually try to comb into those tissues and start to grow distally.
And if you can prevent that one, that would be a Significant benefit to the patients. With the interferon beta, we are involved in the COVID-nineteen treatments, both the remap Yeah. And Hippiscus are really focusing on those ones. But as said earlier, we really would like to also expand this. And we have a very interesting collaboration With the U.
S. Army unit and partially funded also by the Department of Defense as we have announced. And that Of course, related more to the trauma treated patients. And obviously, there the risk is that they may have a lung injury as well and Develop ARDS. And we believe that interferontera treatment is really proper treatment for those patients.
So that in line, I ask Toni to explain the next slide, which is the final. So
Thank you, Marco, and warm welcome from my side also for everybody online. We closed the year with €4,100,000 in the bank and The loss for the financial year of 2020 was 16,900,000 which was 3,600,000 higher than the year before and this was mainly driven by 1 third To our additional headcounts, we increased our headcount by 25% last year and the 2 thirds is by clinical trial expenditure and the CMC Build up. Our net assets at the end of the year were minus 1,800,000 And we did during the period in April of last year, a $14,000,000 fundraise very successfully virtually for the first time. And additionally to that, we received SEK 7,900,000 of grants, loans and guarantees from Business Finland, The European Innovation Council and FIN VERA. Out of this, SEK 7,900,000, SEK 2,200,000 was disbursed to the company last year, Remaining, €5,700,000 will come post period as we're speaking now.
Then additionally, post period, in February of this year, we did additional fundraise of €15,000,000 by issuing 3,500,000 shares.
Thank you, Donnie. Thank you. Let's move on to the next slide. Now we focus on macrophage guided immune therapy, our lead asset. Next slide, please.
So what we have learned in the past is that when we knock out Klev1 function on these tumor associated macrophages, We can convert them back to the immune system activating a phenotype, then now secreting many of the Chemokines and Factor, which are known to be involved in immune activation. And obviously, this is a key thing if you really would like to Get the antigen from the tumor to be presented to our immune system and you get 10 T cells to respond to that. The surprise was really When we started to look at the treatment cycle and look at the soluble Klev1, and you can notice that on the right hand side, a lower panel, That within a week after dosing, we actually reached back the original baseline, meaning that the 1 week interval, 3 week interval is not Really high enough to treat these patients properly. And I'm glad to say that we are now in the middle Of increasing this frequency and also dosing with these patients. So in general, the about level 1 amounts are increased.
You can see that on the upper panel, compared to normal control. And obviously, this could be a key thing for us also maybe to predict which of the patients actually are the best responders in our future activities. So, and that assay development and measurements are ongoing while we speak. So, not only we target anymore a tumor So, with macrophages, we also would like to remove the soluble, Klev1 from the plasma blood and tissues in order to get maximal T cell activation. And maybe this molecule also could be the one that actually can prevent immune checkpoint inhibitors to work Because at the same time, you have an inhibitor that actually prevents the T cell activation when we are giving treatments to activate the T cells.
So obviously, giving significant evidence that the combinations of these checkpoint inhibitors actually could be really important part of our development work in the future. Next slide, please. This monotherapy, what we are doing at the moment is really with the patients who have a progressive disease. They are difficult 3 of the other ones have been failed previously. They may have seen 3, 4, 6, 7 lines of treatments previously.
And as I said earlier, this provides us a really a significant combination potential. And as the Product itself, pexmarilimab seems to be extremely safe, well tolerated. The combinations would be then really possible to And a number of other checkpoint inhibitors. And obviously, this would then provide us an opportunity really to challenge the current treatments. So let's look at what's going on.
Next slide, please. Mattin's Part 2 is ongoing. I will explain the Part 1 data in a minute. But we already have 6 cohort groups out of these 10 different cancer types Who have shown early clinical benefit. This is a stabilization of the disease or then even seeing a partial response.
And obviously, these 6, ovarian, hepatocellular, cutaneous melanoma, colorectal, cholangiocarcinoma and gastric cancer, They all are candidates to move on to the pivotal part. We are waiting the data to be completed somewhere later this spring in order to make the right Analysis of all of these individual cohorts before we can make the decision, which of them actually will be taken further to the pivotal part first to expand that to 30 patients and then later on really to the size that actually would allow us to go to the regulators and ask marketing approval. But let's look the Part 1 data for a minute. Next slide, please. Top line safety data on left hand side.
And as you can see, there was really no Grade 3 and 4 adverse events. The one infected is Serona. I don't believe it's really caused by the drug itself, But it was listed in those and it's here. But then also the grade 1 and 2 very rare. These are something you can see With the patients when you infuse antibody like we do.
So again, not necessarily related to the antibody, but yes, They are there, but very low number. Then the preliminary efficacy from this Part 1, 30 patients. We had 2 partial 7 stable disease or mixed responses in those target lesions. And when I talk about these, these are always image analysis of those target These are not opinions. They are really hard core data.
And if you drop out the lowest concentration, 0.1 mix per kilo, We have roughly 1 third of the disease control already at this stage of these patients. And obviously, this is a very exciting Outcome, we also learned that when we give pexemarrelimab to these patients, we increase the peripheral natural killer cell count. And obviously, that is really important if you believe that you can activate the innate immunity. The reason why innate immunity is so important is that, That is the only way you can actually generate additional T cell response, T cell repertoire. And if that happens against the cancer antigens, then you know that We've become kind of a vaccinated against those antisense and that would be a significant benefit because then you could assume that you are treated for good really against that cancer type.
So let's move on and look at some examples. Next slide, please. These are Part 1 patients. We have MSI negative colorectal cancer. Harrow is pointing the shrinking a lung metastasis in this patient.
The second is a refractory melanoma patient. And again, you can see the ratamassive metastasis going away From the lung and at the same time all the interstitial tissue was removed and the patient really felt much better after this one. These are now Part 1 patients. Then we started to look the Part 2. Next slide.
And we Wanted to show that they are all progressive diseases and that's on the left side. And as you can see, this is A83 patients And all of them have a progressive disease before they enter the trial. Then if you look at the overall survival of the patients who had a clinical benefit, That's on the right hand side. Out of those 100 patient follow-up, which is the 4 cycles, we only lost one of them. But the ones who had no response, roughly 85% of them died.
So obviously, this is an important information for us for two reasons. First, this is an additional efficacy signal, which we can see. But secondly, now we start to identify the patients and can analyze them further who are the potential responders to this Sweet. And obviously we are happy to tell more about this later this spring, once we have completed the analysis with the full cohort sizes. So Be patient, stay with us, we will do it.
Just few more months and hopefully we have the answer to all of these. We have the next slide please. And this is also supported from number of other reasons. This is a genetic analysis looking to data banks. And here we have a total tumor pools.
Red one high expression for KLEV-one, that's a stapylin gene that is analyzed here and that's And coding for Klev1 and the blue one is the low expression, significant difference in the mortality. If you then move on and look at the immune therapy response. If you have a high expression of Klev1, you have a really low survival prediction. So significant difference to the blue line where we have a low expression of a Kleber 1. And the same is also shown in this bold way, where you can see the individual levels of transcript analysis.
And high expressions of Clever 1 have really a much, much higher mortality tendency because already with these patient numbers which are not that many, You have a p value very low. So very promising support as well. And then the next slide please. This is my favorite slide. This is a looking a negative checkpoint molecules post treatment.
You have a pre dose and then 7 days later. And the red one shows again, T cell activation Immune system activation by increased CD25 expression that is ILN Interlocking 2 receptor, some chemokines. Good, very good. Especially the naive cells are responding, which is really nice. Then look at the blue ones, that is a decline in expression.
Very familiar molecule, CTL-four, PDL-one, even PD-one. So one pexmarilimumab treatment can Regulate the expression of these negative checkpoint molecules to the point where actually the current other treatments are trying to do at the moment. And obviously, this is extremely important finding. We know today that this will last also for 1 week. So we really need To increase the dosing frequency.
And as said earlier, that's ongoing at the moment. On the right hand side, you can also look at the increased number of the effector cells In those patients who responded, which is really good result and explains why we actually have a clinical benefit in those patients. Next slide. If you look at the revolution of the checkpoint inhibitors, what has happened in the past, these Inhibitors is expected to sell SEK 50,000,000,000 in SEK 25. And if you look at the efficacy between the placebo And in this case, a Benprolimat that is a KEYTRUDA from Merck.
You can see, yes, it is beneficial to the patients, but it's not that dramatic. If you think if we can now combine this treatment with our treatment shown in the next slide, We may have a significant step up. And now we may have a possibility to treat maybe half of these patients. So and that is our aim directly with the combining the PD-onePDL treatments with pex And obviously, if we can really demonstrate this increase in the efficacy and outcome of the patients, this It's a very significant commercial opportunity as well. And that is already predicted and so on by other examples.
So we are very confident that this will move on a really successful in the future. Next slide, please. And obviously, the pipeline is here to demonstrate first that the Matins trial cohorts, not all of them, For example, uvea melanoma was a disappointing to us because we didn't see any response there. But some of the cohorts will move on all the way to pivotal part Because regulators believe that if you have these patients with no options, already 2 out of 10 Would look be will be looked and analyzed favorably by the regulators. And obviously, that data is coming on later this spring.
But then moving on to lung cancer model or lung cancer patients with the combination with PD-one and the acute mitral leukemia is really Exciting one. But my own opinion is that we really need to get orally on the first line treatments. And those are the black blue Indications, ovarian cancer, combination with the standard of treatment, that's a platinum globally used. So there you actually could have a rather impressive results as well. And obviously, that is something that we plan to do We have learned dosing and having probably demonstrated efficacy earlier.
All right. Then moving on. Next slide please. There will be a significant news flow later this first half and then later on once we move And obviously, we are really looking forward really to let the market know about the additional information. But as time is flying, let's move on to trauma kind, the interferon beta.
Next slide, please. Use for the up regulation of CD73. Could I have the next slide please? Here the aim is what we have been saying for years. We would like to re Gain CD73 to the surface of the endothelial cells so that they can maintain the endothelial integrity.
The reason we are using interferontera is very simple. They have interferontera response element. So it is our natural defense system and we do have endogenous That is doing it normally. And especially in the viral infections, this is one of the first reactions our system, Our immune system actually put up against the viral infections. They want to protect the cells and that's the reason why they are using this adenosine activation locally to protect the cells.
So we did earlier, next slide please, a trial in U. K. Where we demonstrated that using From Pira intravenously, I repeat that intravenously, we can reduce the mortality of these lung Injury patients, they are called ARDS because they already have been ventilated. But obviously, you may be considering already Earlier treatments in order to reduce the risk of getting to the point where the ventilation is needed. In our next Trial, you may remember this.
Next slide, please. That's the INTEREST trial. We didn't get the similar efficacy, The placebo and the treatment group gave identical mortalities, but we were able to explain this. If you look at the ones Who have a biomarker response, that's the blue line here on the right hand side and those who didn't. You've noticed that the one who responded showed the biomarker activity is up.
They had a Strongly reduced mortality, getting close to the original finding. But then the orange line where the biomarkers are not Great. Up, up, up regulated. You can see the mortality is almost 50%. So we made a very simple question, what's the difference between these Groups and we learn it's the greater significant use of corticosteroids at the same time with interferontera.
And today, we know and have shown and published That corticosteroids can block interferontera action. And I'm a little bit worried about this that if people use a corticosteroids too early on these COVID-nineteen patients because it's not shutting off our trauma kind. It's also closing the endogenous pathways To protect those cells in those conditions. Next slide. And that is the reason why we are waiting really to start this Ipisco study in U.
S. We have 7 sites now waiting the final ethical approval ready to go. And here, we just make a placebo controlled randomized study first interim analysis With the 70 patients then to estimate the final size and then moving on to the pivotal part Phase 3. And this is now controlled that there is no Steroid interference with the interferontera. It can be used post trauma kind treatment, but not The same time.
So we are really waiting. And the next slide just shows you why we have been in here. We already have a fast track designation From FDA, we have a promising innovative medicine status from MHRA. And we already have orphan drug from European regulators. And obviously, this is an ongoing condition now related mostly to the COVID.
But when COVID is over, I believe that then we may have a serious Influenza season, maybe there are some additional COVID variants coming on, which is now indicated in number of articles and this is a condition will stay with us for a long time and that's reason we need to get any treatments really to rescue those lost lungs. Next slide, please. Looking again at the information coming from these trials starting to Hibiscus. We Still do not know when we get the remap gap readout, but hopefully that is progressing well. And then moving also to other indications.
And on the right hand side, you can see the numbers, which these conditions and treatments are targeting. And it is a very significant upside as well. And finally the news flow for this part. Next slide please. We have again Steady news flow coming in.
And obviously, very key one is the interim analysis of the hibiscus. And we predict that we would get that on the 3rd quarter this year, but if everything goes well, it can even be earlier. And then finally, a few words about the hematokine. Next Slide, this one and one more. Next slide, please.
Here we have a Very interesting target. It's AOC enzyme. It has several other names as well. But what it can do, it can oxidize a Primary AMAs. Those are normally, arginineolysine residues of the proteins.
And when it does, it Produce is local, converts the amine into a corresponding aldehyde and that change will release Hydrogen Peroxide. And that hydrogen peroxide is a control element for hematopoietic stem cells. Next slide, please. These reactive oxygen species on the left side, when you lower their concentration around These cells you make them to proliferate and colonize. And obviously this is now the aim for us.
We could use these in Vivo settings making the cells to proliferate either from the donor or from the blood bank and then give them back or then try to do that in Vivo settings. And obviously, this is not that huge number of the patients, but they are very much needed when, for example, they have a failure in the graft, For example, but there are some other conditions and obviously really would like to get this project to the clinic as well. So All three projects really targeting the immune system and we believe very strongly that all of these treatments We'll find the way to the market because they are really targeting the huge unmet medical need And COVID-nineteen is just giving us an example where that need is rather practical today among us. And with this word, I would like to then have the final slide to look at the News bits we believe are coming in. So additional Matins cohort data from trial part 2, Selection the 1st pivotal cohort to be expanded.
And obviously, that is possible to do once we have The final dosing frequency and level. And then initiation of those other trials. And when we have a first patient in all of those, we obviously will inform the market. With the trauma kind, Hippis could start, Hopefully get some information from recap. And then also really continue to further develop of these indications what we had in that pipeline chart in order to really be ready to move on.
For both of these, pexmarilimab and trauma care, we are now establishing the brand new Manufacturing Facilities and that is in collaboration with AGC, Contract Manufacturing And I can just report that pretty much they are in time line what we have anticipated. And obviously, that is really important once we expand The use of them also in the marketed situations. So that's what we are at the moment. And then finally, just thanking you And have the final slide, next slide. And then that brings me to the end Our presentation today and I would now like to hand back to the operator for any possible questions you may have.
Thank you very much.
All questions will be answered in the order received and you'll be advised when to ask your 20. Okay. Our first question comes from Myles Dickson from Peel Hunt. Please go ahead. You're live in the call.
Many thanks. Hi there, Mark and Tony. Two questions from me. I think firstly on the bexmarinumab. You've shown some impressive data on the Not only now the messenger RNA expression and the correlation, but also the soluble Clever 1.
You alluded to us You're being able to hear about some data later on in the year. Do you actually expect there to be a difference between the responding patients and the non responding patients? And has it changed how you're collecting data from current patients? Thank you.
That is a very attractive possibility. And obviously, We have to now carefully look at and we have a lab based assay to do it, but we are also building a sophisticated assay that actually could be validated and Brought in whenever, especially if it becomes a part of the companion diagnostic system. It also could be that it's not only the soluble clever one, it The combination with some other parameters. And obviously, that's the reason why we have to very look carefully at the data for the individual cohorts. And it could turn out that in some of the cancer types, these signals are better than the other ones.
And we need to understand that because obviously, if If you want to move to the pivotal part, we would like to optimize the patient population we want to treat. This is a very exciting time for us and Definitely, we'll have a lot of activities really to be reported later in the year.
Thanks, Marco. And similarly on the well, really interest versus Hibiscus. I think I mean it's a fascinating difference that you've got when you extract the Steroid impact out of that interest trial group. Do you expect so I know that for instance the corticosteroid is a reason for Inhibiscus, but what is the is there a dedicated time period between when interferon may be administered and then Steroids in the Hibiscus trial. Thank you.
Thank you. It's again very good questions. And We have indicated many times that corticosteroids may be at the best service in the final stage of this Kind of a injury in the lungs when the fibrotic process has already taken place. And there are some information deleterious, yes, that really helps. But to be too early with the corticosteroids to shut off the interferon pathways, that could be a very significant Problem.
And we have solved that by letting the doctors use them post trauma kind treatment. So Now the patients come to the hospital and they're hospitalized and for 6 days they get the trauma kind treatment. And if that is not helping them, then the doctors are allowed use corticosteroids post that 6 day treatment. So that is the structure what we have within the hibiscus. Would 3 days be enough or some other period?
I don't know, but they should not use them at the same time and that is now controlled In-depth trial structure.
Thank you very much.
Okay. Our next question comes from Julie Simmons from Panmure Gordon. Please go ahead, Julie. You're live in the call.
Thank you. Hi, Marky. A couple of questions. Firstly, just following on from one from Miles. With the map cap, Is this sort of is there likely to be a problem with steroid use in that?
And I know it wasn't how it was designed originally, but then COVID was sort of Stronium as an extra bit into that trial. Do you have any ideas how they're are they separating the use of steroids and formokine in
They are separated. So they are individual arms. So they should not overlap. Do the doctors really follow that? Yes, they should when they commit themselves to use a trauma kind as a single agent for the treatment.
And I know a few of the sites, 1, for example, being here in Finland, they follow that advice. So that would be a single treatment of interferon beta only.
Excellent. So we might actually get some useful data out of what is ultimately quite a large trial the way they're recruiting into that at the moment.
Do you
have any idea how much trauma kind has been used or you don't have access to that?
The only information I have is that they have not reached the 1st interim readout. There is an independent data monitoring committee who is looking at the data all the time. So we are really dependent on that readout.
Okay. Fine. And then on bexorilumab, with the dosing, clearly, when you did part 1 of Matins, you looked So different doses and you didn't actually choose the top one when you sort of moved on to Part 2. I was just wondering now you're looking Sort of moving up the dosing, I mean, is it the fact that in Part 1, I suppose it's really a question, is it dosing frequency or concentration that needs to be increased because and how is the trial set up to identify which is The sort of the factor there, because clearly, if you're giving a higher amount on a less frequent basis, you might not be seeing the same profile you're seeing currently. That
is again a very good point. In the Part 1, we had 5 patients in each of those dosing cohorts. And obviously, if you had some patients, cancer types, which were not Best candidates and good kind of have a peculiar behavior. They may have fooled us. We started to see some Suppression of some markets that actually started to indicate a suppression of the treatment at the highest concentrations.
And we got worried if that is The case, but that may be more related to those patients more than dosing. Now, Gus, that is really important now to look at what happens to those patients when you increase the frequency. My own opinion is If you have a circulating T cell inhibitor around, you don't want to have that. You need to remove it. Even for the benefit of the other checkpoint inhibitors, because remember, these are immunological synapses Activators or inhibitors.
So they need to deal with the T cells and that's the reason why they are used. So obviously, we would benefit The use of those as well as we benefit the activation of the immune system in other locations as well, not only around the tumor, which is probably critical.
Absolutely. So the data you've got reading out next on this is going to be what, A more frequent dosing within colorectal cancer patients. Is that right? And then a higher dose will come out at a later point. Is that have I got that the right
That's pretty much the development at the moment. But then also we get Part 2 cohorts analyzed in full size. No, that was not in this release we did earlier this week. It was really related to that number and the data that was Presented to the data monitoring committee and they were extremely happy and almost thrilled and maybe that explains why the recruitments Have been rather successful along these months and year. So that I believe That data sometime in quarter 2 should become available.
And obviously, that is very exciting to report to the markets as well.
Our next Question comes from Jon Bergren from Kepler Cheuvreux. Please go ahead. You're live in a call. Yes.
Hi, Marco and Toni. So I have four questions. I can just we can take them 1 by 1, if that's okay with you. So the first one regarding the Press release you sent out on Monday. So you said that the analysis was based on 6 to 7 patients that you have 10 responders that are either Paltrow responders or that have stable disease.
So and then you said that you couldn't provide data on overall response rate because you haven't followed All these patients long enough, but for those 10 responders that you have, how long have you followed them? And How many of them should departure response to that time of assessment?
That data came after 4 cycles of the treatment and one cycle is a 3 week, so 21 days. So, and as you if you look at the slide in my presentation, it's roughly 100 days. So obviously, we are as excited as you are really to look at The data post 7 cycles when the protocol based imaging is done again. They may do imigings more often than just on those request But that is really the data points what we are mainly looking. So the whole cohort, not only those 67, but The other ones, which were not included yet in that one, they are all moving every day.
So that is the reason that I believe that we have additional information to provide To the
market. Okay. So it was to do dosing schedule. That makes sense then. Okay.
Thank you. And second one, so in terms of the survivor benefit that you also communicated in the same press release, so how did you do that analysis? Did you compare responders to non responders for each On this for each indication or did you just compare responders to non responders across all indications?
Yes, all indications because Again, the cohorts are not full in all of the cases. The only one that was full, which was a bit surprising, was UBL melanoma. And unfortunately, there were no responders in that group. And that may also explain why the overall benefit Was less than in the Part 1, where we have 1 third maybe responding. Here we have maybe around 15%.
But keep in mind that some of the cohorts had no Wondering that's diluting out obviously the previous finding or the numbers.
Yes, got it. Okay. So how many patients do you have in total today in the maintenance trial? And how many of these are in the 6 indications that you have Where you have seen early signs of efficacy?
So the plan is in part to have 10 patients for all of those cohorts. And in February 21, if I recall correctly, we had 83 out of 100 already on the trial. And I know that Progressing well. So I believe that we are almost full now with those 100 patients. So it means that we have 30 patients from Part 1 and then 100 patients from a part 2.
And then we would should have a full 10 patient cohorts for all of those cancer types. And that is why it becomes so important really to make the thorough analysis of all of those cohorts and then look at And make the decision which will then continue with the Werther expansion and all the way to the pivotal part. I cannot say yet the exact numbers for each of the cohort.
Got it. And the last question is maybe more for Tony, but can you give us some flavor on what the run rate will look like for this year? So I think it's mostly related to the R and D costs for the new trials that started and then to start. So now also you said that you increased headcount 25% For last year, do you expect this trend to continue in this year as well?
Thanks. That's a great question. In terms of The headcount, yes, we did increase the headcount by 25% last year. So the average was 30. And at the moment, we are still in a hiring mode.
So we are Going to have soon roughly 35, 36 people on board and we have added 4 people already this year. So the trend is absolutely continuing. In terms of the run rate, as Marco showed on the trials, we have the DoD grant, which is then With the hibiscus trial and then on the margins is really depending on the recruiting of the patients. What we do see the cost is relatively upfront. So that's why we had a very steep increase last year as these cohorts were they have opening costs and different milestones with our CRO.
So they're a little bit front loaded. So that gives us then a pretty good control for this year.
I also wanted to add here that we do have a plan to set up a U. S. Unit, because now there's an increase in number It is on the U. S. Side and obviously the communication with FDA is really important.
So that is part of that expansion of the personnel headcount.
Okay. Thank you. Okay. We have a question from Myles Dickson from Peel Hunt. Please go ahead Myles.
You're live in the call.
Yes. Just following up from a question that Geely had earlier on. You were asked about how often How often you use them to the trauma kind in remap cap? I was just wondering if you do you expect any data to come out of the SOLIDARITY trial in terms of how much it was
Thank you. Thank you. We have really tried to push So to get that data to us and as we said in the release, they have not yet provided. It's kind of a pity because Based on the agreement we have with them, they actually should do it. And FDA already has asked that data to really to be provided To them as a package when they are going through the approval process.
So we are reminding them all the time And I hope the Fund, David, will have it. I just believe that in the SOLIDARITY trial, they didn't really use intravenous interferon. It was also good, because of theaneous. And maybe that is the reason why they may have difficulties providing any data if they don't have any patients treated with the intravenous one.
Okay. There are no further questions on the conference line. I will now hand over the presentation to the management team.
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