Good morning, and thank you for joining episode 22 of Baird's Biotech Discovery Series. I'm Mike Perrone, Baird's Biotech Specialist, and I'm pleased to be joined by Immutep CEO Marc Voigt, as well as Dr. Martin Forster of the University College London. Also joining us on the call is my colleague, Baird Senior Biotech Analyst Joel Beatty, who will be moderating the discussion. As a reminder, Baird's Biotech Discovery Series is an opportunity for investors to hear directly from interesting and innovative public and private biotech companies in a fireside chat format. A few quick logistics: if you would like to submit a question, you can do so via the webcast portal, or you can email Joel at jbeatty@rwbaird.com. Finally, before we begin, I'm required to remind attendees to please refer to the event calendar, published research, or Baird's website for important disclosures regarding the companies discussed during this event. I'll now hand it over to Joel to kick off the discussion. Thanks. Yeah, so let's jump in. First to begin, Dr. Forster, could you provide an overview of your clinical experience with eftilagimod alpha? Hi, Joel. Thank you very much, and thanks for the opportunity to speak with you this afternoon, here in England at least. So yeah, so I've been involved. I'm a medical oncologist based in London. I've been involved in a number of different drug development programs from phase I mostly. And I've been involved in the sort of collaborating to co-develop the efti, so really very novel immunotherapeutic since it went into the TACTI-002 study. I predominantly manage patients with lung and head and neck cancer, although I also do some phase I or early phase type studies. And so I've had the real pleasure of being involved in this study when it was in the sort of phase II combination and then into the TACTI-003 study as well in head and neck cancer. So let's begin by jumping into head and neck cancer more. Could you provide an overview of the results that were recently presented at ESMO I/O, and how those results from the efti Keytruda combo compare to historical results from Keytruda alone? Yeah, sure. So it was a pleasure for me, actually. I presented these data at ESMO I/O, so it's sort of a really highlight because I think the data are really, really, really good. They're really promising. So the study was looking at two different cohorts, and this was particularly focusing on the cohort of patients with PD-L1 expression of less than one by the CPS route. So that's a specific scoring that's used in certain types of cancer, which is linked to pembrolizumab in head and neck cancer particularly, amongst others. And in this patient population, single agent checkpoint, whether that's nivolumab or pembrolizumab Keytruda, is actually pretty disappointing, the activity. So although this was a non-comparative study, it was a single-arm study in this population with a huge unmet need because the current options are really quite limited, and the immunotherapy activity is really disappointing. The data were really exciting, so we saw a higher response rate, certainly, than I was expecting, and what was particularly interesting is the durability of that response was really quite outstanding, I think, and that led to, so we saw good responses. We saw complete responses, which is pretty much unheard of in this patient population with checkpoint alone, and we saw durability of the responses, and all of that happened without really much added toxicity as to what we would have expected with single agent checkpoint, so really, for me, it was a real pleasure to be presenting the data because I think it's what you want to see: more activity without toxicity, durable activity. Very good. Great. So for patients with first-line head and neck cancer with PD-1 expression below one, what's the standard of care for those patients now, and then how do the efti plus Keytruda combo results compare? Yeah, so here there's a difference between the U.S. approvals and the rest of the world as far as I'm aware, certainly Europe. And in the U.K. and Europe, for those patients where the PD-L1 is less than one, we have no option of first-line immunotherapy. So the patients can either be treated with chemotherapy, platinum doublet chemotherapy, or what I call biochemotherapy, so chemotherapy with cetuximab. So we are unable to use immunotherapy in that setting because the data were not that compelling from the big phase III trial with Keytruda. In the U.S., actually, the combination of chemotherapy and Keytruda is approved in this population. So there's a difference there across the Atlantic. Relative to these data, though, as I was alluding to, in that study, either single agent Keytruda or chemo plus Keytruda, actually, these data in this particular subpopulation of less than 1% expresses PD-L1, these efti data are dramatically better, so it's obviously not directly compared within this study, but I think it's a real step forward in activity, independent of the fact that this is also avoiding chemotherapy, which is a different story, but actually, just from a point of view of activity, I think these are really exciting. Yeah, and when you say dramatically better, could you help me frame that a little bit more? Sure. So I think it's predominantly the durability of the response, which is exciting. So when we use chemotherapy and immunotherapy in that combination, as I say, not something we do here in Europe for this population, or when we give chemotherapy with or without cetuximab, the overall initial response rate is not unreasonable, but the durability of that response is quite disappointing. It's only a few months long. Whereas what we saw in this study was the durability of response was around about nine months, and with a really quite good sort of overall survival, albeit provisional at the moment, rates a year, and we haven't even reached the median overall survival yet. So I think the likelihood of response is not dissimilar. We do get good responses for chemotherapy in that setting, but the durability of the response is really what stands these data out. Got it. Maybe thinking about the use of chemotherapy in this setting more, is there a percentage of your patients that either can't take chemo or perhaps could but refuse to take chemo? And could you frame how common that is? That's quite tricky because in the U.K., as I say, outside of the U.S., well, in fact, even in the U.S., for PD-L1 negative patients, there is no alternative to chemotherapy. So this is the only treatment. I think in the U.S., there is approval for cetuximab as a single agent. I'm not sure about the subtleties of that opportunity. But everywhere else in the world, we only have chemotherapy as an option for this population. So if patients are either not particularly fit, then we might have to dose-modify chemotherapy or give them a single drug rather than a combination. And for those patients who don't want to have chemotherapy, there really is no alternative. So actually, it's a really tough situation. We do have patients who've had, obviously, one of the things about head and neck cancer we haven't touched upon is most patients who have recurrent metastatic disease like this population have already had. The majority of patients present with local regional disease for this particular type of cancer. Most of them will have had really intensive treatment for that with either surgery or intensive radiotherapy. They come to this situation, sadly, with quite a lot of sort of baggage, if you like, toxicities, not only from their current cancer, but from the legacies of the treatment they've had before. They've taken a lot of punishment already. It's a really kind of unfortunate situation. It's a very nasty cancer. There was quite a lot of people who've had experience with radiotherapy and/or chemotherapy before in that curative setting, and despite that, have had recurrent disease. So I think it's a very small proportion of people in my practice. There's some people definitely who are not fit for any further treatment where only supportive management is possible. But to be fair, I think those patients who are unfit are not really represented by this trial because we're also looking at patients who are reasonably fit for immunotherapy as well. But for those patients who don't want to have chemotherapy, who've had a tough time with it before, there is really no other option. Yeah, yeah, the subtle context, and I mean, maybe taking that further in the context of where efti could fit, if there was an effective chemo-free option in the first-line setting for these patients, how could that? What would be the important factors in that split between the current approach or a chemotherapy-free approach? So I think to some degree, that depends a bit on more data. Always, we say that as clinicians because I think for patients who are, at the moment, chemotherapy is not very attractive. We're always looking for opportunities to use immunotherapy, which we know has that possibility of really durable effect. And the data that we've seen from this study suggests that that's really potentiated by this very novel approach of improving the presentation of these cancer antigens to the tumor. So it's a very novel strategy, different from other checkpoint immune combinations, which, where there were lots of studies of, particularly in lung cancer, we'll probably come to. But so I think there's a high proportion of people who would be happy to be. And you have to remember, this is not for the vast majority of people, unfortunately, none of these treatments are curative. So it's not a question of not giving chemotherapy, but it's hopefully by delaying it by a long time and using it as a second option rather than as a first option. So I always talk to my patients about the fact that we're trying to select the most effective treatment first. And then it doesn't mean to say we can't use alternatives as and when we need to, but we're just selecting the best treatment. So I think that from the data we've seen, albeit in a single-arm set of sort of relatively small number circumstance, I think the many, many patients, if not the vast majority of them, would be better served going down this route and would prefer to do so. Great. Can you help us think through the size of the different populations in first-line head and neck cancer by CPS status and how many are above one versus less than one? Yeah, so I think that in my mind, from the very early studies, which were in the second-line setting, there was roughly around 80%-85% of patients would express PD-L1. So it's around 15%-20%. I think as we've got now, obviously, from the clinical trials, a bit more breakdown, we've got a little bit more sort of real-world information about PD-L1 expression now that we're testing it routinely for this patient population. It's probably closer to around the 20% mark, I think, rather than the 15%, which was originally sort of presented. So yeah, it's around about 20% of patients. Got it. All right. So a question for Marc now. It seems that most companies that combine with anti-PD-1 therapy are focused on patients with any PD-L1 expression or CPS greater than one. Does that kind of fit with your perspective on things? And what would you say is the competitive landscape for the patient population with PD-L1 below one? Yeah, thank you, Joel. And besides listening here to a terrible German accent, in addition, on top of that, I have also a strong cold. So apologies for that if it's a little bit rougher. But to answer your question, first of all, all the existing therapies contain chemotherapy. So in the U.S., as Martin mapped out, you have on the one hand side pembro plus chemo, in Europe, cetuximab plus chemo, doublet chemo typically. And if you look at the late-stage development and the activity in the biotech field, then predominantly, we do see activity in CPS greater equal one in terms of development. We can look at the Merck, Bristol Myers Squibb and other companies, PDS Biotech, and so on and so forth. So predominantly, the competition or the focus in combination with anti-PD-1 is CPS positive simply because CPS below 1 has not been identified as a very promising target, as pembro and also nivo didn't really deliver there. And I believe it's important to keep in mind also the different approaches you are seeing there. We are working not on the T cell, but on the antigen-presenting cells. So our mode of action maybe comes here stronger into play as we create more CD8 T cells and help with the tumor-specific antigen presentation. So from a competitive point of view, CPS below 1 seems to be very attractive. And I personally believe we see the highest unmet medical need there. Great. And I guess with that said, what are the next steps for development? Yeah, on the one hand side, of course, as always, collecting more data, following up the patients. That's number one, but definitely, we are going to discuss with the FDA and potentially other regulators regarding the path forward. We have fast-track designation in first-line head and neck cancer, and we certainly will discuss the results we saw to date, and this is definitely on the agenda for possibly the first half of 2025. Got it. Let's switch to lung cancer and you've recently been announcing the phase III trial, including the collaboration with Merck. Could you tell us more details about how that collaboration with Merck works and the meaningfulness for Immutep? Yeah, first of all, it has been a very intense process to get to this stage. We know Merck quite well. We have two other collaboration agreements, so clinical trial collaboration drug supply agreements, to be more precise for TACTI-002 and TACTI-003. And it was when you looked at that prior to us announcing this collaboration, it seemed maybe a little bit more unlikely that we are going to pull it off because it's indeed the first time since more than two and a half years that Merck entered into such a collaboration. Before us, it has been at the beginning of 2022, if I recall correctly, it has been Gilead. So it is intense, has been intense, but it's, of course, very good to see the drug supply. If you look at the commercial value, if we would need to buy it, it is certainly between $100 million-$120 million. And of course, also the expertise from the guys at Merck. And we have a year-long relationship. So it was a good logical consequence, also given the strategic position of eftilagimod alpha. But of course, if you look there at the collaboration behavior and how restricted it is these days, it was by no means guaranteed. So I see it as a strong vote of confidence, actually, from our collaboration partner. Great. What are the key aspects of the phase III trial design, including the primary endpoints and any interim analyses? And then also was Merck involved in the trial design? Yeah, it's a, if you like, classical phase III clinical trial, one-to-one randomized, looking at the best available standard of care in first-line non-small cell lung cancer, which is Keytruda plus chemotherapy in the two arms, plus minus efti and placebo. So it's obviously double-blind, multinational, so high-quality standards and also from the statistical plan, I believe, robust, about 750 patients. So no, let's say, biotech way to cut corners, but really pharma-standard clinical trial. We have here a dual primary endpoint, progression-free survival and overall survival. And it's also a clinical trial which has a futility analysis. It's, of course, event-driven, but could be in about a year from now, give or take. And of course, also an interim analysis, which could be by a back end of 2026, potentially, on which, if sufficiently positive, you always need to look at the data, of course, we could maybe even file. So it's a robust clinical trial. It's a large clinical trial. It has been carefully checked. And I believe one can be very confident if a collaboration partner like Merck agrees to such a study that it has been very robustly designed. And of course, there's also a joint development committee for such a clinical trial. Great. Anything else on Merck, on kind of the total collaboration beyond supplying their drug? So on the one hand side, I would just like to highlight the drug supply. Again, it is an important aspect. It has high commercial value. But of course, you have access in numerous working groups to the expertise of the other side. I can't be too precise that this is touching the confidential sphere. And of course, this is a clinical trial which will be followed by numerous analysts around the globe because it could send an improved standard of care in one of the most important indications in oncology, first-line non-small cell lung cancer. So there are, of course, also reputational elements which are coming to the table. And for us as a company, it's very important. We move into the phase III stage, so another part of the value chain. We don't do this alone, but hand in hand with Merck based on the collaboration agreement and also together with the top-selling brand in the industry, which is Keytruda. It's for us very, very important, actually. For the patient population in this phase III trial, it seems to be one of the broadest in terms of capturing almost all first-line metastatic non-small cell lung cancer patients who are eligible for anti-PD-1 therapy. Is that accurate? Yeah, that's an accurate statement. It's a TPS score of 0-100. So all three segments are being addressed. And it's a squamous non-squamous cell as well. So it's one of the largest settings you can think of if you go into first-line non-small cell lung cancer. Are you aware of any other phase III trials out there that are targeting this broad of a patient population that would include Keytruda? There might be in total, including ours, two to three, so it's a very limited number. I think one is performed by Novocure. They have an electric field approach, practically, so quite different compared to what we do, but it's one of the very few clinical trials looking so broadly at this, and of course, this is important if you look at the market, at the patent cliffs, at the strategic setting of this clinical trial, which could really address the entire first-line non-small cell lung cancer population eligible to anti-PD-1 treatment. Got it. Can you tell us more about the competitive landscape in the IO field and first-line non-small cell lung cancer and how eftilagimod alpha could fit in if this trial is successful? Yeah. So the competitive landscape in terms of IO in first-line non-small cell lung cancer has been way more intense two, three years ago, even one year ago. We all know concepts like anti-TIGIT, anti-LAG-3, for instance. Unfortunately, for the patients, these concepts don't seem to be very successful, at least in non-small cell lung cancer. BMS will kick off a clinical trial of phase III in the 1L to 4L, so in a specific subsegment. They have been criticized for that. So the competition, the IO competition, is going down. We certainly have a unique approach in terms of the mode of action. We do not work on the T cell directly, but we work on the dendritic cells, monocytes, on the antigen-presenting cells. And we create more CD8, more CD4, more NK cells. We help with boosting the dendritic cell network and with the tumor-specific antigen presentation. Actually, a few days ago, Merck announced that they will drop anti-TIGIT and anti-LAG-3, I believe, for good reasons. While this is very sad for the patients, it's, of course, good for us because the relative importance of eftil agimod in the field, and we entered into the agreement with them mid of this year. It's not ages ago, and one saw it, I believe, coming based on the Roche Skyscraper trials that anti-TIGIT has problems. It's also focused on a certain segment, predominantly on TPS high, that things are not going so well. Also the earlier data in terms of non-small cell lung cancer was anti-LAG-3. Different story. Anti-LAG-3 is, of course, registered in first-line melanoma, but it has not been very effective, I believe, in first-line non-small cell lung cancer. There is still activity ongoing, also in other indications. So if you compare TIGIT with anti-LAG-3, it's a different story. But for first-line non-small cell lung cancer, the relative importance of eftilagimod alpha has just been increasing. Got it. For the phase III trial, I think Immutep announced about a week ago or so that it's initiated. Could you tell us more about the current status of enrollment and how you see that changing over time? So all strategies are nice and fine, but of course, the execution is everything. So we need to move forward with the recruitment of the patients. We have been press releasing that we have been getting first regulatory approval in Australia, that the U.K. is quite close to it. A number of other European countries and North American countries will follow. So we have here a clinical trial which will certainly be tested or rolled out in more than 25 countries, certainly in about 150 hospitals or more around the globe. And we are very well on track. We are publicly guided for first patient in quarter one next year. We are perfectly on track for that. And we are working very hard with our different collaboration partners to kick this off and to have this recruiting very well. And I believe this trial has a chance to recruit very well. Why? Because the patients get simply best available standard of care, what is anyway predominantly given, Keytruda plus chemotherapy. This applies to both squamous non-squamous and then plus minus eftilagimod alpha. And also in light of the previous question, the IO field, when you give two ICIs, immune checkpoint inhibitors, you see also an increase of autoimmune diseases, induced autoimmune diseases. We do not have a safety problem to date. We are relatively safe. We have injection site reactions, but this is very manageable. So you provide the patients with best available standard of care plus a relatively safe option, eftilagimod alpha or placebo. So it's very hard for me to think of a stronger option for the patients and, of course, principal investigators to participate in the study and hopefully to have a swift and good recruitment. Great. And so I think here I'll bring in Dr. Forster on non-small cell lung cancer. And first, can you describe the current standard of care? Yeah. So thank you. Yeah. So in the U.K., there's quite a few different options globally, mostly based around Keytruda on its own or with chemotherapy. That's certainly the treatment that we use predominantly here in the U.K. There are a few other licensed approved combinations looking with, again, based around PD-1 and chemotherapy, but with or without CTLA4, for example. So there are a few other options. But I think that by far the dominant, and certainly in the U.K., the almost unique treatment that we use is with this combination of either chemotherapy with the Keytruda or Keytruda alone. Got it. So how is that performing? I guess, where does that leave the unmet need for a new therapy? I mean, I think it's almost certainly the case to say that it's the most exciting time to be looking after patients with lung cancer. I mean, there's so much going on at the moment. It's really exciting. Obviously, separate from today's discussion, we're really leading the field, I think, around precision thoracic oncology, and there's lots of drugs coming in there. I think that it's very exciting how they're being able to translate some of these drugs into early-stage disease, so there's loads of really exciting things happening, so it's really promising. Having said that, sadly, when we look at our five, 10-year survivals for our patients with lung cancer, particularly those without oncogenic drivers, they're still really poor. I think there's an unmet need about improving the activity of the regimens that we do use or finding new regimens, particularly improving the durability of the effects of those treatments and increasing the proportion of people who get really durable benefits. Because we've certainly seen the, even in the time I've been in practice, we've seen the median overall survival for patients with sort of non-oncogenic-driven lung cancers move from around 10-11 months to maybe closer to two years. But that's still nowhere near where we want to be. There's loads of unmet need really throughout that. A lot of that is about getting treatments that are tolerable, that derive durable benefit. That's really how you improve quality of life by not adding too much toxicity, but adding durable response. Got it. That's helpful context. Even though there's been improvements in the efficacy and survival and responses over the years, still a lot of opportunity there. But then you also kind of threw in at the end that there's room for better tolerability too. And could you maybe elaborate on that aspect and kind of where there's an opportunity to add on tolerability? Sure. So there's different strategies being explored always to try and improve cancer treatments. And being somewhat involved in early-phase trials, we're looking at the whole range, including very intensive treatments requiring hospitalization and very close monitoring with significant risk of toxicity. And there's probably roles for all of these things going forwards. But at the end of the day, we're not treating the scans and treating responses. We're treating the patients and trying to improve their quality of life and their sort of life expectancy. And always having to, as a clinician, you're always having to balance sort of cancer control with not too much toxicity and therefore actually improving how the patient feels. So there's always a trade-off because any treatment can have toxicity. But if you're able to improve those efficacy endpoints and those long-term outcome benefits without compromising too much on the toxicity side, that's obviously a win-win. And we've seen examples of that where even relatively low-level toxicity over a long period of time is quite intolerable for patients. So things which we are in our trials score quite lowly can be quite challenging if they're going on for many, many months. So I think we have to, we're always looking, obviously the Holy Grail is to find treatment that works with very, very little tox because that gives the best chance to have the biggest impact for the patient outcomes in how they feel as well as in their life expectancy. Got it. That's helpful. So kind of narrowing down specifically on efti for non-small cell lung cancer, how do you kind of feel about this trial that's underway and the probability of success as well as kind of how it could fit in future use? Yeah. So I think, well, again, without wanting to sound too positive, I think it's got a good opportunity there. Because I think we've got one of the things which we've seen, which I don't think we're necessarily expecting when the first wave of first-line immunotherapy trials came through, was because when those drugs first became licensed, particularly Keytruda as a monotherapy, the data were really quite outstanding. And we felt that that was probably going to be the way many of those patients with high levels of PDL expression were going to be treated. But actually, now we see in the real-world data sets and in clinical practice that actually the majority of people are getting chemo IO as their first-line treatment as a standard at the moment, and more so than I would have predicted, really, even in those patients with high levels of PDL1 expression. Interestingly, that, I think, as a backbone to this trial design, I think is a good option because I think that actually it's less than you would think who would be given single-agent checkpoint. I think that element of it, I think, is a good starting point. I think that the data that we've seen so far around the added toxicity of efti to that backbone, or indeed with a bigger patient number to immunotherapy in general with pembrolizumab, shows that this is hopeful, but I think very optimistic that this is going to be something which is going to be very well tolerated with little added burden of toxicity compared to what we currently use. I think that I certainly view ourselves as being quite lucky in lung cancer. The platinum, particularly the platinum with pemetrexed, but the platinum doublet immunotherapy first-line treatment is actually very well tolerated by most people. So when people think of chemotherapy, there's a whole load of different drugs that people use. And actually, this is generally speaking on the good end of the spectrum for tolerability. And in this data so far, at least, adding efti to that doesn't add too much burden. So I think there's an opportunity. And as we've talked about already, the activity that we've seen in the combination with Keytruda in particular, but also in lung cancer, there's been a safety study which has shown good tolerability and promising activity in the combination with the chemo and Keytruda. So I think there's a good robust evidence base to try this. I think there's definitely an unmet need to improve from what we currently have. Adding a drug which is relatively minimal extra toxicity, but seems to show promising activity to the population is obviously first-line lung cancer, which is quite a big population. I think it would be great for us if we could have a go-to improvement, a step-change improvement for our patients who we would otherwise be offering chemo immunotherapy combination at the moment. I think there's a big opportunity there. Great. That's really helpful. And so, Dr. Forster, I know we're getting close to our time. So I just want to ask, anything I didn't ask about on eftilagimod alpha that you think would be helpful for the audience to hear that we haven't really talked about yet or any kind of closing comments? Nothing specifically. I think that, as Marc alluded to, I think this is, and I think I said as well, it's a novel drug. So the mechanism of action of this is really quite different to other drugs out there. I think that there's a lot of activity in lung cancer. There's obviously, it's a big patient population. There is a huge amount of need. So there's lots of stuff going on. We've been quite disappointed. The sort of Keytruda and then subsequently Keytruda with chemo was a total change in our whole strategy for treating lung cancer. And since then, we've had a series of studies that have failed to add value to that, which is quite disappointing. And so I think the fact that this is taking that approach, not with a subtly different checkpoint combination, but with a totally different strategy, I think is really exciting. Hopefully, that will bear fruit to being a more promising way forward. I don't think there's anything specific around efti for me to add from what we've discussed already. It's terrific. Thank you, Dr. Forster. And Marc, we have a question from the audience, and I'll paraphrase here. And you mentioned earlier how just a few days ago, Merck discontinued their LAG-3 program. Where does that leave the opportunity for Immutep to strengthen or expand its relationship with Merck? Oh, I believe there are lots of opportunities to do that. Definitely, we have a unique asset. It's technically an MHC class II agonist. We use LAG-3 as a tool to activate the patient's immune system. So it's not the target. So it should not be mistaken for another version of an anti-LAG-3. It's entirely different. That's really a key point, and of course, in a data-driven mode, and we have been showing, I believe, quite good data. Maybe the other side steps up eventually to deepen the relationship, however that could look like at the end of the day. But we have a number of different discussions of that nature. And time will tell. We are here to execute, to move forward. And it's, of course, right that we can't do everything. That's completely right. We need to focus. The key value driver of the company, certainly non-small cell lung cancer, the phase III. And then we have to see what the other development options are and with whom, actually. Terrific. Another question that's just come in on dosing. Recently, you've been conducting the trial on breast cancer, looking at either the 30 milligram or 90 milligram dose. Could you tell us about where you're at in deciding on what dose is the go-ahead dose, including for the phase III lung cancer study? Yeah, indeed. That's the so-called Project Optimus from the FDA. In Europe, it didn't play a role, to be honest, or at least not the predominant role. We have been finishing the last patient in for the so-called AIPAC-003 study. You refer to breast cancer. That's exactly the study, and based on this study, looking at 30 milligram plus paclitaxel versus 90 milligram plus paclitaxel will identify the optimal biological dose. We do not work with the DLT or MTD concept, so we don't give drug, drug, drug to the maximum practically, but we work with the optimal biological dose, especially in immunotherapies. You need to be careful not to come to the danger zone and see cytokine release syndromes practically. We are very calm in terms of the outcome, so we are currently collecting the data, and this will be analyzed in due course. Then there will be the outcome practically, but we can live with every outcome. At the end of the day, it's about the risk-benefit ratio. Either it's a well-established 30 milligram dose where we know it's very well tolerated, safe, has been delivering great results, or if the risk-benefit ratio is better with 90 milligram, then it will be 90 milligram, so there we are very calm. In relatively due course, we will see the results. Then we can also identify with which dose we will move forward, actually, for the entire program. The dose coming out of this exercise will be relevant for the entire program. We have for agonists, if you allow me to make that statement, also a larger therapeutic window, which starts already at a much lower dose, for instance, 6 milligrams of eftilagimod alpha, where we saw also some very nice results. With agonists, you have broader therapeutic windows. Let's see where we land. If it is 30, if it is 90, we take whatever comes. Terrific. And I guess with that, Marc, anything else you'd like to cover before we go? No, it has been increasingly active here, quite busy, all hands on deck. We will be determined to execute predominantly the phase III clinical trials. So you will see us very busy. I would like to thank you all for your support and also, of course, Dr. Martin Forster for joining here to this call, and thank you, Mike and Joel, for setting it up. Yeah, thank you, Dr. Forster. Thank you, Marc. I'll turn it over to Mike to wrap up the call. Yeah. Thanks again, Marc and Dr. Forster, and for the investors on the line, if you'd like to connect with Immutep, we'd be happy to do so, so just please reach out to your Baird representative, but that wraps us up for today, so thank you all and happy holidays to everyone, and get well soon, Marc. Thank you so much. Bye. Thanks, all. Thank you.