Cantargia AB (publ)

Thank you. It's a pleasure to present Kantariga's half-year report of what I think has been a very exciting period in the company. So to take you into the highlights, we've had a very good news flow regarding both our clinical programs. But what I really like to point out here is that Kantariga has taken a major step forward that we now have two clinical programmes of significance. So the CanTen programme passed a number of important milestones during the period. We are almost completed with the initial SAD part of the phase one trial. And SAD means then single dosing. And we've had the independent safety review on unblinded data that has not picked up any safety concerns. So the safety is obviously very good on CAM-10. But we also start to generate biomarker data, which shows that we have a very potent drug. So for instance, we've documented receptor binding on to the target I1 wrap on immune cells at a relatively early and predictive dose level. And we also generated strong biomarker data. So we'll present more about that when we go through the slides later on. And there's also been several scientific publications with new data. So obviously, that's also creating additional interest. In the oncology program, nadinilumab, we have presented data at several conferences. So we presented new data in pancreatic cancer, showing additional features on antifibrotic effects. We have new clinical results on prevention of neuropathy. And we also looked into that there is actually a link between K-RAS mutations, which are a major problem of pancreatic cancer, and how it fits very nicely with our mechanism of action. And finally, we are making progress in the upcoming leukemia trial, and we're also starting to see the end of recruitment in our triple negative breast cancer trial. And finally, we also have a much cleaner sheet now when it comes to our patents where the latest appeal against one-hour granted patents were withdrawn ahead of proceedings. So a good period for sure. So then just to remind you then on our pipeline, so to basically make it simple, we have two clinical programs. where we have most data in pancreatic cancer, triple negative breast cancer, non-small cell lung cancer. And then we have our second program, CAN10, which is in phase one. Plan is to enter phase two, second half of next year, once we're through the MAD part. And the lead indications, and here we have a small update, is that we're generating more and more support to go into a serious dermatological disease called hydrodinitis suppurativa. So that's clearly on our radar. And the second indication we're targeting is systemic sclerosis, which is also a very serious fibrotic disease affecting skin and lungs and internal organs. So very excited about these opportunities. And we also have the potential to broaden our pipeline as we have our CanXX program with new opportunities, both as ADCs as well as by specific antibodies. So very quickly then, we have had a good 24. We have high expectations for the rest of the year and next year as well. So obviously to continue to generate data in our two clinical programs, we have several milestones ahead of us. And I think as an investor, you should also expect that we are visible when it comes to publications and conference presentations of new data. Starting out with Canten, and Canten is really where we have made significant progress lately. So to just take you through biology first, Canten is targeting what's called the I1 family of cytokines. And the VIL-1 family of cytokines are driving several inflammatory diseases. So the potential in CAN-10 is enormous. And we're really having much more opportunities in front of us than we can handle. And as I said, we've decided to look into HS and systemic sclerosis lead indications. But the really key feature here is that, if you look at the bottom of the slide, is that CANTEN is, through its interaction with IL-1 RAP, is blocking the activity of three different cytokine systems. So you have IL-1 system consisting of IL-1-alpha and IL-1-beta. You have the IL-33 system as well as the IL-36 system. And they are all responsible to drive several diseases, but very often they work together. And that's been very clear when you try to block them individually, but in most cases, it's been very difficult to get strong, meaningful clinical signals. And it's just because you're just blocking one out of several compounds driving the disease. And if you look to the bottom and to the right, we're trying to illustrate this in a in vitro experiment where we are basically looking at the signal induced by a mix of IL-1, IL-33, and IL-36. And if you then try to block them individually, like all these black lines, you can see that there is very little potency in blocking IL-1, IL-33, or IL-36 individually. But if you use CANTEN like the blue line here, suddenly you have a super potent molecule which is active at the sub-nanomolar levels. So clearly a major step forward here. So going then into the next slide, the phase one has progressed very well and very timely. So if you, the trial is designed as in intravenous administration in the first part in healthy volunteers so that's the sad part we have really seen a very good safety we've seen receptor occupancy and that's illustrated on the top here to the right where we where we can look at The binding of or content to either monocytes or neutrophils, the two different types of immune cells in the blood. And if you look at what's called SAD1 and SAD2 to the left, that's the very low dose levels of contents. Obviously, the dose levels are too low to document anything. We increase the dose levels in SAD3 and upwards. You can start to see that we are saturating IL-1 rep on these immune cells. So, and this is very much in line with our predictions. But the next step, which has made increased enthusiasm even more, is that we have collected blood from these individuals, and you can see it in the bottom here. And we stimulated the blood with IL-36 before and after CAN-10, a single shot. And then we analyzed the ability for IL-36 to stimulate the cells eight days after they got CAN-10. And you can see that there is a nice dose response here as well. So at SAD-5, it's clearly that already here. we have a very potent inhibitory effect, which is then getting stronger and stronger. And at SADD7, we blocked the IL-46 signal. So it shows that CANTEN is doing its work, and it gives extended effect at least during a week afterwards. So we are very excited about this, and we are now very excited as we are starting the MAD part, which is carried out in participants with the plaque psoriasis, mild or moderate plaque psoriasis. And so it gives us another opportunity to learn even more as we can get skin biopsies from these patients in addition to what we already can measure in the blood. And we expect the first individual to start treatment any day now. So very good progress in this phase one trial. And as I said, we are already planning for phase two to make sure that it can start as quickly as possible once the phase one has finished and sometime during H2. So then just a comment on hydrogenated suppuritiva, because I'm sure everyone are not extremely familiar with it. But it is a very complex disease which starts out as inflammation, which is then getting worse and worse on the inside of the skin. And what's interesting is that there is documentation that all the components were addressing. So IL-1, IL-43, and IL-46 are all upregulated in the skin from these patients. And recently, there was clinical data being presented on IL-1 blockade using ludicizumab from AbbVie that reached a primary endpoint in a controlled phase two trial. And the results were strong enough for AbbVisa to start phase three, which started earlier this summer. And in parallel, Boehringer Ingenheim is developing an antibody against IL-36, which also showed positive results in a phase two randomized trial. Boehringer Ingenheim is also continuing the development. So our anticipation here is that the very positive data from the tachysomab especially on some parts of a disease combined with what you're burning in our soul with specialimab can be added together and that can can combine all these features into one product so we are super excited about this and also hs it is a very common disease It's estimated that around one percent of the European and the US population suffers from it right now and it's increasing. So so if we summarize a little bit, It has been shown that the IL-1 blockade can counteract the inflammation. And it's also been shown that the IL-36 blockade from Bering-Ingelheim is affecting something called the draining tunnels, which is an important part of the disease development. And more speculatively, IL-33 is involved. We know that from other diseases that it's contributing to serious itch. Even though there is no data, we have a strong belief that blocking IL-33 through CANTEN will also have an effect on that, which means that CANTEN actually can attack three different parts of this serious disease. So then moving over to nadunilumab, we have previously presented data in pancreatic cancer, which shows that what clearly indicates a treatment effect and with nice survival data in first-line patients where we combine with chemocytopenia braxen, which is part of the standard therapy. And we've also shown that the more IL-1 rep the patients have in their tumor, the stronger efficacy we can observe from this combination. And this is exciting as the high IL-1 RAP is associated with the worst prognosis from KRAS mutations. So if you look to the left here, you can see that the survival is about 14.2 months in the high IL-1 RAP group versus 10.6 months in the low IL-1 RAP group. And also, if you look at these spider plots to the right, you can see that here in the middle where you have IL-1 wrapped high patients. that they respond to the therapy in a stronger way, but also that the responses are much more durable. So you can see that you have patients that have been in response for almost one and a half or two years, while the high IL-1 RAP group, they typically deteriorate after six months. very positive results in pancreatic cancer, which is obviously very, very difficult to treat disease. And we are planning to take these findings forward into phase 2B trial. But another interesting observation from this trial, which was presented during the period, is that not only do we have an interesting anti-tumor effect, but we also seem to alleviate a serious side effect from the chemotherapy combination partner, which is neuropathy. So if you look to the left, that's data from the clinical trial. You can see that the patients that were treated with 1 mg of nadonidumab, which is the gray bar here, developed much more neuropathy. also got the onset of neuropathy earlier than patients that received all the higher dose levels of 2.5 or above. And to remember, 2.5 is the dose level we are targeting in future clinical trials. And to the right, we also have a collaboration with a group in Brisbane, Australia. who have been investigating mouse models of chemotherapy-induced neuropathy. And again, we can see that nadonimumab seem to counteract this neuropathy. It could be sensitivity to mechanical pressure, or it could be grip strength. Nadonimumab seem to do a very good job here to counteract this very unpleasant side effect. And then to remind everyone that besides pancreatic cancer, we're also working in triple negative breast cancer. The initial part of the trial has been presented as it was non-controlled. It was more dose finding. And here we can see a 60% response rate, which is about twice as high as expected from chemotherapy alone. And again, this is chemotherapy combination of first and second line patients. And the survival was also longer, and the progression-free survival was longer than expected from historical controls. So we're very excited to start to deliver those results, and we're looking to do that first half next year. So to quickly summarize the biology here, and I apologize because this is a slide which It may be a bit difficult to read, but the point is here that if you look to the left and into this biological mass, which illustrates what's happening in the tumor, nadunarumab can block signals at all these different red crosses here, which is leading to different type of tumor-promoting signals. Then if you look very carefully, you can see that there are some yellow parts here, which indicates IL-1 rep overexpression. And here, this antibody has been designed to stimulate immune cells to attack these tumor-promoting cells. So the drug is active at a large number of different places to really block the tumor progression. And at the same time, it's interesting that the same signals can then be used to counteract the neuropathy as illustrated down here at the lower part of the leg, where you can see red crosses blocking some inflammatory mechanisms that will lead to this unbearable pain of neuropathy. So that, I think, reflects the progress, but also reflects a little bit of what's going to come here during the next part of the year. So for that, I would like to hand over to Patrick, who can go through the finance part.

Yes, thank you very much, Joran. And I'm going to take you quickly through the highlights of finance. And we do not mirror the same successes or progress with increases in cost. As you can see, it's quite the opposite. We have a 30% reduction in our operating expenses in the second quarter, where we went from 63 million in 2023 to 44 this year. And it's driven, as you can see, by R&D. So we dropped 17 million to 40 million SEK in the quarter. And our cost for administration, so we report in this graph, we combine it with other operating expenses, but our main administration costs were unchanged, but we had less other operating expenses, which then reduced the total by 2 million from six to four in the quarter. And then if you look at the results for the first half year, we had a 39% reduction in OPEX from 140 to 85. Again, obviously driven by R&D. And if I just take two seconds to explain what's behind that, and it's the fact that we are now running two clinical trials. As Joran has mentioned, we are running the triple negative breast cancer study with Nadenolimab Tri4, and we are actively recruiting the CAN10 first in human study. Whereas in the same period last year, we had a full program for Nadenolimab with studies that are still active. They are still active, but from a financial point of view, we are about to reconcile and eventually close them down. So the spend is much lower. We have been able to reduce our administration cost by one million in the first six months. So that's included in the reduction there that you see from 11 to 7. The rest is operating expenses that were lower. All in all we reported a Operating expenses of 85 as you can see there and all in all the net loss was 80 million because we have 5 million in financial Gains so net financial items were positive 5 million. So, um, We also report on the development of our available funds, which, of course, is important. And our available funds are important because that's what's funding all the activities that we do. And available funds, repeat, is the sum of what we report as cash and bank balances, as well as short-term investments. And those are mainly fixed-term interest rate funds. We ended the six months or end of June we had 105 million in available funds which represents a decrease of 38 million which was lower than the 52 that we saw in between the fourth and the first quarter of 2023 to the first quarter of this year. We expect that the 105 million that we have available now will suffice through to the first quarter next year or if we make prioritizations we can extend that to the first half of next year. With that I hand over back to you Joran.

Thank you. So I would just like to finish off here with showing some of the upcoming milestones. So the Venadunilumab program, there are lots of activities ongoing right now. So we have a pancreatic cancer trial, which is still pending financing, but we have a number of interesting discussions ongoing regarding our pipeline here. But the plan is to start a phase 2b trial, which will be a big trial in 150 to 200 patients as quickly as we can. We have a triple negative breast cancer data where recruitment is ongoing, but we expect randomized data to be released in June first half next year. And we're also very excited about the grant from the US Department of Defense to sponsor the upcoming trial in leukemia, AML and MDS. And as you may have seen from the communication, the IND was approved We expect the ethics approval to be done in the near future, which then means that the site can start to initiate for recruitment of patients during Q4. So exciting progress and much more to come. And the CanTen program obviously has generated lots of interesting data from the SAD part during 2024. And our intention is to continue to be transparent when we reach material progress. And what we now have in front of us is the start of the multiple dosing, the MAD part, where we believe that we will put another level of excitement around the data as we now can collect tissue from participants with psoriasis. And the plan is then to go ahead and file a USID and start phase two next year. And we also have a number of clinical trials where, as we continue, we will get long-term follow-up of patients. And in the near future, we're presenting new data in lung cancer, as well as on the Keytruda combination at the ESMA conference. And I'm sure it's going to be more data at upcoming conferences, both in 24 and 25 from this program. So by that, I'd like to thank you for your attention, and Patrick and I are extremely happy to make additional clarifications or take questions afterwards.

If you wish to ask a question, please dial pound key five on your telephone keypad to enter the queue. If you wish to withdraw your question, please dial pound key six on your telephone keypad. The next question comes from Victor Sundberg from Nordia. Please go ahead.

Yes, hello, and thanks for taking some questions. I'll ask a couple here all at once. So first off, I just wanted to understand a bit more on the delay on the Triforce study. I just wanted to understand a bit more why recruitment slowed down a bit during the summer. Was it due to competition in triple negative trials, lack of interest, vacations, et cetera? Any detail here would be really helpful. Secondly, on CAN10 and your ambition to go after Hidrogenitis superativa, I just wanted to understand a bit more what could differentiate you against the up and coming IL-36 drugs such as Pevigo and Imcidolimab and what unmet needs you want to address with currently approved drugs such as Cosentix on IL-17 and the TNF-alpha inhibitors, etc. Is it mainly improved efficacy or do you also see any safety concerns with the currently up-and-coming drugs? And maybe a quick comment on the pros and cons of hitting several interlockings versus specific inhibition. And finally, on cost for the full year, Your R&D has come down, as you showed, by a lot year over year. But just looking at the second half here of the year, any one-time payments to CROs that you know today that we should factor in that could increase R&D here in the second half? And also given your runway, maybe, is it still feasible we try for results before you need to raise cash? A lot of questions, but I appreciate the time I get there. Thanks.

Yeah, thank you, Victor. Yes, I agree. Lots of questions and hopefully I got it all now. But you have to remind me if I forget something. It's not on purpose. So try for delay. So we are working with the GACAM, who is our partner in Spain, to understand more about why recruitment slowed down during summer. But we noted the same thing last summer that as clinics take holiday it has an effect on recruitment. But it was let's say more pronounced this year. So I don't have a good answer on all parts of the background here and how much competition is behind. But we are following up and it's probably several factors behind this. But we also believe that guiding for H1 gives us let's say good room to maneuver and make sure that we deliver on this milestone. Then for CAM10 in HS, so I think, as you rightly point out, patients with HS have treatment options today, so they have anti-IL-17s, there is also anti-TNF, which has been used for a while, but reality is that It's a ballpark number. It's somewhere in 50% or slightly higher numbers that respond to these therapies. So you have a huge unmet need here in patients who are not responding to these therapies. And we clearly believe that we can do this better. And again, if you look at IL-1 like lutecizumab or IL-36, it's not that they individually has provided much stronger efficacy than anti-TNFs and anti-IL-17, but the interesting part of anti-IL-1 is that it has shown efficacy in patients that are no longer responding to anti-TNFs. But with a very complex biology, we believe that we can beat those two when it comes to efficacy and long-term effects by attacking both the draining tunnels, potentially itch, as well as the general inflammation. And then you asked about pros and cons of taking several versus the individual cytokines. I clearly believe that as long as the safety is good and we have not picked up any major safety concerns and we're not expecting major safety concerns by blocking IL-1, IL-33 and IL-36 at the same time. And again, IL-1 blockade is safe, IL-36 blockade is safe. So we believe it's going to be an efficacy argument in the end of the day, which we hope to beat the rest. But it's a complex disease and there is room for several treatments for sure. And so hopefully I answered those two. And then I said, yes, that Patrick takes the cost question.

Yeah. So are there any significant payments to CROs or suppliers scheduled for the second half of the year? I think that was the question. And it's nothing that is out of the ordinary. We are running the two trials that we have communicated or I've mentioned and you're an also. And that there's no normal business there and nothing extraordinary planned. And then the cost for driver, I think we should perhaps take that as a question of our financing. I'm not sure if you want to just take that.

no but clearly we understand that we're in the biotech business and you there's always a constant need for financing and the situation we're in right now is that we have several different ongoing discussions and it's very tough to to be concrete about what they are until until they have let's say reached the goal so but So I cannot comment any further, but we have several options, and I think that's what's important right now.

Thank you very much. Thank you.

The next question comes from Richard Romanious from Red Eye. Please go ahead.

Hello, guys. Good afternoon. could you tell us more or less where you are, at what stage you are in the triple negative breast cancer, could you say how many patients you've recruited us for, and in relation to the same study, what data can we expect to see in H1 2025? How many patients, from how many patients, for example?

Yeah, so... Sure, so the majority of patients have been recruited today. And we believe that the trial will be fully recruited sometime during Q1 as it looks right now in the prognosis. And the intention is to communicate early stage efficacy data as well as safety data. So that would be response rates as quickly as possible once we have the data on patients in the trial. So it will not be the complete data set, but it will certainly be a very material data set based on all patients in the trial. But it will not contain the long-term follow-up.

Okay, and the second and last question. Could you discuss how your plans look like when you have these full data, placebo-controlled and triple-negative breast cancer, what you're going to do with them? Because I assume that would help you in partnering discussions, for example.

No, but I think they are... a very important part of, let's say, a more complex picture here. So clearly, getting randomized data will give us the necessary and important signals to prove that the drug is is active in such a setting. And then obviously where we see a very huge commercial opportunity is in pancreatic cancer. where the competition is much, much lower. So it is a combination of getting randomized data in one cancer disease and then obviously use that as a trigger to build a completer story and understanding mechanism of action and clearly increasing the chances of a partnership.

My last question, but I've got a quick follow-up. Do you think the pancreatic cancer will start before the first readout in triple negative breast cancer or afterwards, considering this could be a signal that it should work in pancreatic cancer as well?

No, but my desire is to start the pancreatic cancer trial ahead of getting results in triple negative breast cancer. I believe that we have a very interesting case in pancreatic cancer, and I'm always a little bit impatient, so I'd like to start this as quickly as we possibly can.

Okay, very well. Thank you.

The next question comes from Louisa Morgado from Van Lanshot Kempen. Please go ahead.

Hi, team. Thank you for taking our questions. From our side, two questions. The first one regarding the current cash runway. How far along does this take you in all the different programs, and are you willing or are you trying to prioritize here not only mob and content development equally? And secondly, could you elaborate a bit more on the results that you will present at ESMO in September? And is this the only conference in 2024 that you will be presenting new data? Thank you.

Patrick, will you start with the cash questions?

So the pure prioritization between our two clinical programs, if you ask me, and I think Jaron will agree, we have two wonderful children and we don't prioritize between them. We look at the most value-adding activities regardless of whether it's NADU or CAN-10 when we decide where to invest but I think right now we have the ongoing clinical studies those are the two most important activities that we have and we make sure that we put our money there and then we reprioritize other activities that can wait if we are constrained for cash. We're always constrained for cash but that's my answer to the prioritization question. Sorry, did I miss a question there, Luisa? Or was it only one?

No, indeed. Just in terms of these two programs, which activities are currently, well, englobed in this cash runway?

No, no. So it's the ongoing Trifor and CanTen First in Human that we are prioritizing and we're not investing in new activities until we have secured financing for sure.

The next question comes from Sten Westerberg from Analyseguiden. Please go ahead.

Good afternoon to all of you and a question regarding If you could share some more of your thoughts on a potential PDAC study, for example, you've been historically alluding to the possibility of some risk sharing or the fact that you may carry out the study all along yourself. And find a second question on PAN10. if you could share some of the criteria when you're picking the MAD dosing. For example, will you run through the same doses as in the sad part, or will you try to cap the first doses in the MAD part? And how confident are you that you will end up with a maximum tolerated dosing in this study? That would be all my question.

Thank you. Yeah, so so if we start with the PDX studies, then so I think we are currently looking into several opportunities here, like. Which could could involve some kind of risk sharing code development. or partnership versus doing it ourselves. There are ongoing discussions, but nothing concrete here. So I will not... It's impossible to guide which way we will go. The only thing I can say is that we strongly believe in our data. When we show data to experts, they are also excited about the signals. So let's see where we are getting. Then the second one on the CANT-10. So the way it's done is that the SATA doses are quite straightforward. There is a fixed scheme where the dose group 9, which we're looking into right now, is 400 mgs of antibody. Then for the MAD dosing, That takes into account the pharmacokinetics measured in the sad part. But typically, we're dosing slightly above 100 right now in the first cohort. And if we will reach a maximum tolerated dose, I think we will reach a dose where we have good evidence that this will be a highly active and efficient dose level, and if it will be the maximum tolerated, or let's say the highest studied, which is of relevance, difficult to say. So, yeah, just follow up.

No short follow up. Are you in any way surprised that you haven't seen any safety signals so far in the SAD dosing?

No, I would have been surprised. We have not picked up anything in our TOCS studies that could be of relevance here and we also have significant information from nadunilumab which in a way could be regarded as probably if anything a slightly more toxic variant of can 10 but we we have no major safety signals here either so no we didn't expect to to see any safety concerns at those levels we're right now okay thank you but then to underline it's much better to have data to show that you don't see any safety signals when guessing Fair enough.

Thank you.

The next question comes from Arvid Nikanda from Carnegie. Please go ahead.

Good afternoon, and thanks for taking my questions, a couple if I may. First off, on adunale mabs, you've put forward some data suggesting a correlation between KRAS mutations and an activated IL-1 system in pancreatic cancers. KRAS inhibitors are now making some strides, perhaps most notably with revolution medicines moving into phase three, albeit in the second line setting, as I understand it. Has this in any way influenced your development strategy? And given the high prevalence of KRAS mutations in pancreatic cancer, Where do you see the main opportunity for differentiation, assuming that their data holds up? And then secondly, if just there's anything you can share on your partnering strategy for Can10, how actively are you pursuing partnerships at this stage? Or is this something you see ramping up significantly once the phase one is concluded next year? Thanks.

Yeah, so thank you, Arvid, great questions. So it's absolutely right that revolution medicine has generated some interesting data targeting KRAS mutations. It has not affected our development strategies right now, but Clearly, I think, if anything, it strengthens the whole case. And in the future, you could probably argue that a combination here could be a very potent way forward, where you, let's say, both attack the mutation, but you also attack, let's say, some downstream effects of the KRAS mutations and one issue with KRAS when you're attacking them is that very often the responses are relatively short-lasting because once you attack one mutation there are new mutations coming up but so having a second mechanism which is that they were blocking the consequences of all of these K-RAS mutations. I think it's super interesting and an exciting way forward. But right now, I think There is a need for several different new medications in pancreatic cancer, so I think we're really focusing on advancing our own program as a first-time combination. And the second question related to a partnering strategy for CanTen. As Kantarga is evolving right now, we have programs in or entering phase two in both oncology and inflammation. And it makes lots of sense to partner one of these programs and focus our attention on the second leg. And hopefully, the partnering will also add program and at this point in time I'm pragmatic of if can tennis or program to partner first or if it's not due to the map okay great thank you there are no more questions at this time so I hand the conference back to the speakers for any written questions or closing comments

There are a couple of questions coming in from the web. And the first one is partially answered, I guess. But the questioner wonders why it seems like you have shifted focus from having to start up the PAMFOR study this summer to evading results from the triple negative breast cancer and the CAN-10 study before deciding to proceed. Is that correct?

No, we have not changed strategy, but I think once you get into these mid to late stage clinical trials, obviously the financial need gets higher and higher. And for us, it's really important that we do this trial that they are not only financed, but also financed in a way which makes sense to the shareholders. So therefore, we try to be patient to find the best possible solutions for forward.

Yeah, and in connection to that, the questionnaires also wonder whether it's correct that you need to secure an additional 250 million in funds before starting the PAMFOR study. Is that correct?

So if it's 250 or whatever, it remains to be seen. But if you go ahead and start this type of trial where you have to assume that the cost for each patient is one million SEK or above, that clearly you need to have substantial financing in place, and you obviously also need a way to either continue to full recruitment with additional financing or a way to step out of the trial and still generating meaningful results. So again, I think it's very much a question of being responsible in how you finance these trials.

Thanks. And getting back to the readouts that you're expecting, could you elaborate a bit more on what you're expecting from them and also maybe define what you mean by near term in that respect? When will you be getting these readouts?

I'm not sure if it's a question more specific about readouts. Otherwise, I can be more general. So I think The way Kantarga has been operating when it comes to clinical trials is that we're trying to secure robust data sets, and then we communicate it. And then obviously, there is always long-term follow-ups along the way. So if you take, for instance, a triple negative breast cancer as a major readout in the near future, We will always communicate the safety at that given time point. And the plan is now that since not all patients have long-term efficacy data, we will focus on the short-term efficacy where we can feel that we have robust data. And then we will present the long-term efficacy data, I don't know, half a year later or whatever, once we become more robust.

Thanks. That was all coming in from the web.

Thanks. And I realized that I have one question which was asked earlier about guidance for what are we planning to present at ESMO and if there are more conferences during the year. So at ESMO, it would be data on the Keytruda combination. So we have presented An earlier dataset which showed the safety and short-term effects of the combination. We now have much more robust survival data. We have much more robust progression-free survival data. And we can link all this to the extensive biomarker analysis that has been done. And that will be presented in one poster. The second poster relates to non-small cell lung cancer. And as you may recall, we have presented data on 30 patients, first and second line patients getting combinations with gemcitabine cisplatin. The trial then added another 10 patients getting Pemetrexed plus carboplatin. So, that data set will be incorporated, and we will present more on biomarkers and subgroup analysis at conference. And the plan is to present more data from other trials or around the NADEMMA program later on this year. By that, I'd like to thank everyone for your attention and I'd like to thank you for your interest with lots of very, very good and relevant questions. And I hope you're just as excited as I am about the autumn and upcoming milestones. So really look forward to continue working here and to deliver results and look forward to the Q3 call in a few months time. So thanks a lot.