Cantargia AB

STO:CANTA

Earnings Call Analysis

Earnings Call Transcript 2024-Q2

[Operator]

Welcome to the Conference call. [Operator Instructions] Now I will hand the conference over to CEO, Goran Forsberg and CFO, Patrik Renblad. Please go ahead.

[Goran Forsberg, executive]

Thank you. It's a pleasure to present Cantargia'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 Cantargia has taken a major step forward that we now have 2 clinical programs of significance. So the CAN10 program past a number of important milestones during the period. So we are almost completed with the initial SAD part of the Phase I trial and SAD means 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 CAN10. But we also start to generate the biomarker data, which shows that we have a very potent drug. So for instance, we've documented receptor binding on to the target IL1RAP 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 in -- 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, nadunolimab, we have presented data at several conferences.

So we presented new data in pancreatic cancer, showing additional features on anti-fibrotic effects. We have new clinical results on prevention of neuropathy. And we also looked into -- that there is actually a link between KRAS-mutations, which are a major problem of pancreatic cancer and how it fits very nicely with our mechanism of action.

And finally, we have made -- we are making progress in the upcoming leukemia trial, and we are 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a much cleaner sheet now when it comes to our patents, where the latest appeal against one of our granted patents were withdrawn ahead of the proceedings.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 2 clinical programs nadunolimab 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 I, plan is to enter Phase II 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 hidradenitis suppurativa. So that's clearly on our radar. And the second indication we're targeting is systemic sclerosis, which is also very serious fibrotic disease affecting skin and lungs and internal organs.

So very excited about these 2 opportunities. And we also have the potential to broaden our pipeline with the time as we have our CANxx Program with new opportunities, both as ADCs as well as biospecific 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, as we continue to generate data in our 2 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.

So starting out with CAN10 and CAN10 is really where we have made significant progress lately. So to just take you through biology first, CAN10 is targeting what's called the IL-1 family of cytokines. And the IL-1 family of cytokines are driving several inflammatory diseases. So the potential in CAN10 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 slide is that CAN10 is through its interaction with IL1RAP is blocking the activity of 3 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 talking 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 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 always 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 CAN10 like the blue line here, certainly, you have a super potent molecule, which is active at the subnanomolar levels.

So clearly, a major step forward here. So going then into the next slide, the Phase 1 has progressed very well and very timely. So if you -- the trial is consigned as 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 can look at the binding of CAN -- or CAN10 to either monocytes or neutrophils are 2 different types of immune cells in the blood.

And if you look at what's called SAD1 or SAD2 to the left, that's a very low dose levels of CAN10. So obviously, the dose levels are too low to document anything. But as we increase the dose levels in SAD-3 and upwards, you can start to see that we are saturating IL1RAP 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 in the videos, and you can see it in the bottom here. And we stimulated the blood with IL-36 and before and after CAN10 a single shot.

And when we analyze the ability of IL-36 to stimulate the cells 8 days after we got -- CAN10 -- and you can see that there is a nice dose response here as well. So at SAD5, it's clearly that already here, we have a very potent inhibitory effect, which has been getting stronger and stronger. And at SAD7 we've blocked the IL-36 signal. So it shows that CAN10 is doing its work. And this -- it gives extended effect at least during a week afterwards.

So we are very excited about this, and we're now very excited as we are starting the MAD part, which is carried out in participants with plaque psoriasis, mild to 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 first individuals to start treatment any day now.

So very good progress in this Phase I trial. And as I said, we are already planning for Phase II to make sure that it can start as quickly as possible once the Phase I has finished and sometime during H2. So then just a comment on hidradenitis suppurativa because I'm sure everyone does not -- are not -- extremely familiar with it. But it is a very complex disease, which is -- starts out as inflammation, which is then getting worse and worse on the inside of skin.

And what's interesting is that there is documentation that all the components were addressing, so IL-1, IL-33 and all, IL-36 are all up-regulated in the skin from these patients. And recently, there was clinical data being presented on IL-1 blockade using Lutikizumab from AbbVie that reached a primary endpoint in a controlled Phase II trial.

And the results were strong enough for AbbVie to start Phase III, which started earlier this summer. And in parallel, Boehringer Ingelheim is developing an antibody against IL-36, which also showed positive results in the Phase III randomized trial.

Boehringer Ingelheim is also continuing the development. So our anticipation here is that the very positive data from Lutikizumab, especially on some parts of the disease combined with what you're -- Boehringer Ingelheim saw with Spesolimab can be added together and that CAN10 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 1% of the European U.S. population suffers from it right now and it's increasing. So if we summarize a little bit, it has been shown that IL-1 blockade can counteract the inflammation. And it's also been shown that IL-36 blockade from Boehringer Ingelheim is affecting something called the draining tunnels, which is an important part of the disease development and more speculative, the IL-33 is involved.

We know that some other diseases is that contributing to serious itch. And [indiscernible] data, we have a strong belief that blocking IL-33 through CAN10 will also have an effect on that, which means that CAN10 actually can attack 3 different parts of this serious disease.

So then moving over to nadunolimab, we have previously presented data in pancreatic cancer, which shows that what we -- clearly indicates a treatment effect and with nice survival data in first-line patients where we combine with gemcitabine abraxane, which is part of a standard therapy.

And we've also shown that the more IL1RAP to the patients have in the tumor, the stronger efficacy we can observe from this combination. And this is exciting as high IL1RAP is associated with adverse 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 IL1RAP group versus 10.6 months in the low IL1RAP group. And also, if you look at the spider plots to the right, you can see that here in the middle, where you have a IL1RAP high patients, but 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 1.5 or 2 years while the high IL1RAP group, they typically deteriorate after 6 months. So again, 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 a Phase IIb trial.

But another interesting observation from this trial, which was presented during the period is that not only do we have an interesting antitumor effects, 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 data from the clinical trial, you can see that the patients that were treated with 1 mg/kg of nadunolimab, which is the gray bar here, developed much more neuropathy and also got the answer to the neuropathy earlier than patients that received all by higher dose levels of 2.5 mg/kg or above. And to remember 2.5 mg/kg is the dose level we are targeting in future clinical trials.

And to the right, we also have a collaboration with the group in Brisbane, Australia who have been investigating mouse models of chemotherapy induced neuropathy. And again, we can see that nadunolimab seem to counteract with neuropathy, could be sensitivity to mechanical pressure or it could be grip strength. Nadunolimab 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. We -- the initial part of the trial has been presented as it was noncontrolled. It was more dose finding. And here, we can see a 60% response rate and -- 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 this -- I apologize because this is a slide which may be a bit difficult to read. But the point is here that if you look to the left, its biological mess, which illustrates what's happening in the tumor, nadunolimab can block signals at all these different red crosses here, which is leading to different type of tumor-promoting signals.

And then if you look very carefully, you can see that there are some yellow parts here, which indicates IL1RAP overexpression and here this antibody has been designed to stimulate immune cells to attack with tumor promoting cells.

So the drug is active at large number of different places to really look the tumor progression. And at the same time, it's interesting that the same signals can then be used to counteract with neuropathy that's illustrated down here at 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 quarter of the year. So I guess I would like to hand over to Patrik who can go through the finance part.

[Patrik Renblad, executive]

Yes. Thank you very much, Goran, 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 costs. 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 SEK 63 million in 2023 to SEK 44 million this year.

And it's driven, as you can see, by R&D. So we dropped SEK 17 million to SEK 40 million in the 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 SEK 2 million from SEK 6 million to SEK 4 million in the quarter.

And then if we look at the results for the first half year, we had a 39% reduction in OpEx from SEK 140 million to SEK 85 million, again, obviously driven by R&D. And if I just take 2 seconds to explain what's behind that, and it's the fact that we are now running 2 clinical trials.

As Goran has mentioned, we are running the triple-negative breast cancer study with nadunolimab TRIFOUR, and we are actively recruiting the CAN10 first-in-human study, whereas in the same period last year, we had a full program for nadunolimab 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 costs by SEK 1 million in the first 6 months. So that's included in the reduction there that you see from SEK 11 million to SEK 7 million, the rest is operating expenses that were lower. All in all, we reported a operating expenses of SEK 85 million, as you can see there. And all in all, the net loss was SEK 80 million because we have SEK 5 million in financial gains.

So net financial items were positive SEK 5 million. So we also report on the development of our available funds, which, of course, are -- is important and our available funds are important because that's what's funding all the activities that we do.

And we -- 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 6 months or the end of June, we had SEK 105 million in available funds, which represents a decrease of SEK 38 million, which was lower than the [ SEK 52 million ] that we saw in between the fourth and the first -- fourth quarter of 2023 to the first quarter of this year.

So we expect that the SEK 105 million that we have available now will suffice to through to the first quarter next year or if we make prioritizations, we can extend that to the first half of next year. And with that, I hand over back to you, Goran.

[Goran Forsberg, executive]

Thank you. So I would just like to finish off here with showing some of the upcoming milestones. So the nadunolimab program, there are lots of activities ongoing right now. So we have a pancreatic cancer trial, which it's 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 150-200 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 during first half next year.

And we also are very excited about the grant from the U.S. Department of Defense to sponsor the upcoming trial in leukemia, AML and MDS. And the -- as you may have seen from the communication, the IND was approved recently. We expect Ethics approval to be done in the near future, which then means that the site can [indiscernible] to initiate for recruitment of patients during Q4. So exciting progress and much more to come. And the CAN10 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 of the MAD part where we believe that we will put another level of excitement around the data as we now can collect the tissue from participants with psoriasis.

And the plan is then to go ahead and file the US IND and start with Phase 2 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 ESMO Conference.

And I'm sure it's going to be more data at the upcoming conferences both in '24 and '25 from this program. So by that, I'd like to thank you for your attention. And Patrik and I are extremely happy to make additional clarifications or take questions afterwards.

[Operator]

[Operator Instructions] The next question comes from Viktor Sundberg from Nordea.

[Viktor Sundberg, analyst]

I'll ask a couple here at once. So first off, I just wanted to understand a bit more on the delay on the TRIFOUR 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 like of interest, vacations, et cetera? Any detail there would be really helpful.

Secondly, on CAN10 and your ambition to go after hidradenitis suppurativa. I just wanted to understand a bit more what could differentiate you against the up-and-coming IL-36 drugs such as Spevigo and imsidolimab and what unmet needs you want to address with currently approved drugs Cosentyx on IL-17 and the TNF-alpha inhibitors, et cetera. 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 also hitting several interleukin 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 year of the year, any onetime 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 with drive for results before you need to raise cash? A lot of questions, but I appreciate the time I may get there.

[Goran Forsberg, executive]

Yes. Thank you, Viktor. Yes, I agree lots of questions, and hopefully, I got it all now, but you have to remind me if I get something, it's not on purpose. So try for delay. So we are working with [indiscernible] who is our partners trying to understand more about why recruitment slowed down during summer. But we noted the same thing last summer. But as CANxx takes 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.

And for -- then for CAN10 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 as a ballpark number, it's somewhere 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 lutikizumab and/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 have are no longer responding to anti-TNFs. But with a very complex biology, we believe that we can beat those to when it comes to efficacy and long-term effects by attacking both the draining tunnels, itch, 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 I said, it is good, and we have not picked up any major safety concerns, and we are 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 very strong for several treatments for sure.

And so hopefully, I answered those 2. And then I suggest that Patrik takes the cost question?

[Patrik Renblad, executive]

Yes. So the -- 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 2 trials that we have communicated or I've mentioned and Goran also and that there's no normal business there, nothing extraordinary planned.

And then the cost for TRIFOUR, I think we should perhaps take that as a question of our financing. Goran, I'm not sure if you want to just take that.

[Goran Forsberg, executive]

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 be concrete about what they are 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.

[Operator]

The next question comes from Richard Ramanius from Red Eye.

[Richard Ramanius, analyst]

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 thus far? And in relation to the same study, what data can we expect to see in H1 2025, how many patients -- how many patients, for example?

[Goran Forsberg, executive]

Yes. So sure. So we -- the majority of patients have been recruited today. And we -- so 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, let's say, 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 -- 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 a long-term follow-up.

[Richard Ramanius, analyst]

Okay. And second -- last question, could you discuss how your plans look like when you have this full data [indiscernible] and triple-negative breast cancer, what's your -- what you're going to do with them as I assume that would help you in the partnering discussions, for example.

[Goran Forsberg, executive]

No. But I think they are very important part of, let's say, a more complex picture here. So clearly, getting randomized state will give us the necessary an important signals to prove that the drug is active in such a setting. And then obviously, the where we see a very huge commercial opportunity is in pancreatic cancer, where -- so 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 complete story and understanding the mechanism of action and clearly increasing the chances of a partnership.

[Richard Ramanius, analyst]

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

[Goran Forsberg, executive]

No, but my desire is to start with 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 in patients. So I'd like to start with as quickly as we possibly can.

[Operator]

The next question comes from Luisa Morgado from Van Lanschot Kempen.

[Luisa Morgado, analyst]

From our side 2 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 nadunolimab and CAN10 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?

[Goran Forsberg, executive]

Patrik, will you start with the cash question?

[Patrik Renblad, executive]

So the -- as the prioritization between our 2 clinical programs. If you ask me, and I think Goran will agree, we have 2 wonderful children, and we don't prioritize between them. We look at the most value-adding activities regardless of whether it's Nadu or CAN10 when we decide where to invest. But I think right now, we have the ongoing clinical studies. Those are the 2 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 the only one?

[Luisa Morgado, analyst]

No, indeed, just in terms of these 2 programs, which activities are currently well included in this cash runway?

[Patrik Renblad, executive]

No, no. So it's the ongoing TRIFOUR and CAN10 first-in-human that we are prioritizing and we're not investing in new activities until we have secured financing for sure.

[Operator]

The next question comes from Sten Westerberg from Analysguiden.

[Sten Westerberg, analyst]

And a question regarding, if you could share some more of your thoughts on 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 a second question on CAN10. If you could share some of the criterias when you're picking the MAD dosing. Will you -- for example, will you run through the same doses as in the SAD part or will you try to cut 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 questions.

[Goran Forsberg, executive]

Yes. So if we start with the PDAC studies then, so I think we are currently looking into several opportunities here like -- which could involve some kind of risk-sharing, co-development our partnership versus doing it ourselves, where our ongoing discussions, but nothing concrete here.

So I will not -- it's impossible to guide what -- 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 CAN10. So the way it's done is that the SAD doses are quite straightforward and 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. So -- but typically, we're dosing is slightly above 100 mg right now in the first MAD cohort. So -- 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 highly active and efficient dose level.

And if it will be the maximum tolerated or let's say, the highest study, which is of relevance difficult to say. So...

[Sten Westerberg, analyst]

Yes, follow up -- no, short follow-up. Are you in any way surprised that you haven't seen any safety signal so far in the SAD dosing?

[Goran Forsberg, executive]

No, I would have been surprised if we -- we have not picked up anything in our tox studies that could be relevance here. And we also have significant information from nadunolimab, which in a way could regard us probably if anything, slightly more toxic variant of CAN10, but we have no major safety signals here either.

So no, we didn't expect to see any safety concerns at the dose levels we're right now. But then to underline, it's much better to have data to show that you don't see any safety signals than guessing.

[Operator]

The next question comes from Arvid Necander from Carnegie.

[Arvid Necander, analyst]

A couple, if I may. First off, on nadunolimab. 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 III, albeit in the second line setting, if I understand it.

Has this in anyway influence 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 1 is concluded next year?

[Goran Forsberg, executive]

Yes. So thank you, Arvid, great questions. So it's absolutely right that Revolution Medicines has generated some interesting data targeting KRAS-mutations. I -- 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 only issue with KRAS when you're attacking them is that very often, the responses are relatively short lasting because once you attack one mutation or new mutations coming up. But -- so having a second mechanism, which is let's say, the blocking the consequences of all of this KRAS mutations.

So 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-line combination. And the second question related to the partnering strategy for CAN10.

So as Cantargia is evolving right now, we have programs in or entering Phase 2 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 valuable financing to the development program. And at this point in time, I'm pragmatic if CAN10 is probably going to partner first or if it's nadunolimab.

[Operator]

There are no more questions at this time. So I hand the conference back to the speakers for any written questions for closing comments.

[Patrik Renblad, executive]

There are a couple of questions coming in from the web. And the first one is partly answered, I guess. But the questionnaire wonders why it seems like you have shifted focus from having to start up the CANFOUR study disrupt [indiscernible] awaiting results from the triple-negative breast cancer and the CAN10 study before deciding to proceed. Is that correct?

[Goran Forsberg, executive]

No, we have not changed strategy. But the CANFOUR, I think once you get into this 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 finance, but also financed in a way which makes sense to the shareholders. So therefore, we try to be patient to find best possible solutions go forward.

[Patrik Renblad, executive]

Yes. In connection to that, the question here is also wondering whether it's correct that your -- that you need to secure an additional SEK 250 million in funds before starting the CANFOUR study. Is that correct?

[Goran Forsberg, executive]

So if it's SEK 250 million over there -- 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 SEK 1 million or above. But clearly, you need to have a substantial financing in place and you obviously also need a way to either continue to full recruitment with additional financing all the 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.

[Patrik Renblad, executive]

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 results?

[Goran Forsberg, executive]

I'm not sure if it's a question more specific about readout. Otherwise, I can be more general. So I think the way Cantargia has been operating when it comes to clinical trials is that we're trying to secure robust and data sets. And when we communicate it and then obviously, there is always long-term follow-ups along the way.

So if you take, for instance, triple-negative breast cancer, there's a major readout in the near future. We will always communicate the safety as that given time point. And the plan is now that since not all patients have long-term efficacy data or 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.

[Patrik Renblad, executive]

Thanks. That was all coming in from the web.

[Goran Forsberg, executive]

And I realize 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 will be data on the KEYTRUDA combination. So we have presented an earlier data set, which share safety and short-term effects of the combination. We now have much more robust survival data, we have a much more robust progression-free survival data, and we can link all this to be 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 getting combinate first-line, second-line patients getting combinations on with gemcitabine/cisplatin, the trial when 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 the conference.

And the plan is to present more data on from other trials or around the nadunolimab program later on this year. So 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 we 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.