All right. Good afternoon, everyone, and thank you for joining the presentation of our financial report for the third quarter and an update from the company.

My name is Hilde Steineger and, as you probably are aware, newly appointed as CEO of Cantargia. Next slide.

Patrick, may I ask you to change the slides? All right.

Slide two: Safe Harbor. Slide three.

Patrick? Let me just finish.

With me today, we have our newly appointed Medical Officer, Dr. Wolfram Dempke, and our CFO, Patrik Renblad.

Slide four. We reported this morning our interim report for the third quarter and the first 9 months of the year.

It has indeed been a transformational period for the company, with the Otsuka transaction as the main event. At about the same period, we communicated on the primary endpoint from our TRIFOUR Phase 2 study on the objective response rate, ORR, and the results show no difference in ORR between the control group treated with chemotherapy and the patients treated with nadunolimab in combination with chemo.

We are awaiting the mature overall survival data, which is expected around year-end 2025. I joined Cantargia as CEO on September 1st, and I have extensive experience from leadership roles in the pharmaceutical R&D and business development, as well as background in the financial sector as an analyst and venture capitalist.

I'm also very happy to introduce Dr. Dempke, who's joined Cantargia as Chief Medical Officer, and I would like to hand it over to Dr.

Dempke for a brief introduction of himself.

Thank you, Hilde, and thank you very much for inviting me here. It's a pleasure for me attending this meeting.

My name is Wolfram Dempke. Just a brief overview about my career: I'm born and raised in Germany, holding a German passport.

I studied medicine in Germany in Essen, and I'm a fully qualified and board-certified hematologist and oncologist. I'm also holding an MBA in International Financing.

I worked in the industry for quite a while, and I'm still seeing patients at Munich University and from time to time at Cambridge University, as I'm a full professor at Munich University, hematology-oncology, and in Cambridge I'm a senior lecturer. I'm also holding a passport in the UK.

I worked at several pharmaceutical companies, and I have an extensive experience in clinical drug development. Just to give you a few examples, I was responsible for bringing dasatinib, Sprycel, to the market while working at Bristol Myers Squibb for the CML indication.

I was the mastermind behind ipilimumab for malignant melanoma. I was responsible for the relaunch of gefitinib, Iressa, in 2014 while working for AstraZeneca, and at least in part, let's say 50%, for the launch of Tagrisso, which is osimertinib.

I was the European representative for mogamulizumab while working at KHK. I was responsible for the launch of capmatinib from Novartis.

At that time I was working at Incyte, and Novartis had hired me to get capmatinib, which is a c-Met inhibitor, to the market. Lastly, I'm, in a way, responsible at the moment, as I'm a board member at Moleculin, I was responsible for bringing Moleculin from phase nought, if you like, to the currently active Phase 3.

My last role was at Otsuka, especially at Taiho, and therefore, I was responsible for the development of zipalertinib, which is EGFR mutant TKI, and the drug is currently in Phase 3, and the filing will be at some stage next year. My research focus is, as you can see, mainly on GI tumors, especially on pancreatic carcinomas.

I did my PhD on RAS in England quite some time ago, and for the last two decades, I worked on non-small cell lung cancers and acute leukemias. From my clinical perspective, I'm seeing pancreatic carcinoma patients on a regular basis, I'm actually treating them.

I do know how these patients are suffering from their disease as pancreatic carcinomas are a very tough disease. I'm now overlooking 35 years in medical oncology and hematology, and during that time, I've seen everything, every trend on the market, including CAR-T cells—I'm treating patients with CAR-T cells—autologous and allogeneic transplantations.

It is a matter dear of my heart to point out that nadu is definitely the best drug I've ever seen for patients with pancreatic carcinomas. Therefore, I was really keen joining Cantargia and to bring that drug to the market as soon as possible.

That is my driver, and that is something that thrives me, and it is very important for the sake of the critical ill patients. Thank you.

Thank you, Wolfram. Let me then go into detail a bit into the Otsuka transaction that we now announced in July and closed in September.

As I said, it was in many ways transformational for Cantargia because it provided us with the financial flexibility that has enabled us to reinvest into the next generation of anti-IL1RAP antibodies. Equally important, the company sees it the deal as a validation of both the target and the technological and commercial value of Cantargia's antibody platform.

When the deal closed, Cantargia received $33 million, and we are eligible for receiving up to $613 [million?] US dollars in upfront and milestones, in addition to up to double-digit royalties.

Now, let me review our pipeline and our strategic priorities. Bringing nadunolimab to forward in pancreatic ductal adenocarcinoma, or PDAC, remains our key strategic focus based on our very compelling Phase 2 data, which I will elaborate a little bit later on in this presentation.

We have observed promising results in non-small cell lung cancer, particularly in a subgroup of patients receiving second-line treatment following immunotherapy, more specifically in those with non-squamous tumor types. While these findings are encouraging, they are derived from a limited sample size of only 11 patients.

At present, there are no plans to pursue further development based on these preliminary data. Regarding triple-negative breast cancer, as mentioned, we have previously shared the results from our primary endpoint ORR this summer.

We are now anticipating more mature overall survival data and expect to provide an initial readout before the end of the year. As mentioned, the Otsuka deal provided means to invest in our very promising pipeline.

With CAN14, we intend to develop an anti-IL1RAP bispecific antibody for inflammatory and/or autoimmune disease. We are, in parallel, exploring the options related to anti-IL1RAP antibody-drug conjugates, or ADCs, also as a next next step in oncology under our CANxx umbrella and platform project.

Last but not least, CAN10 remains a very important asset in our portfolio. Even though it's in very capable hands of Otsuka Pharmaceutical, we will continue to follow and report on the assets as it progresses through development and hopefully, later on, for in approval and commercialization.

If successful in all of these steps, the product will provide important non-diluting funding for Cantargia in the future. Let's dive into nadunolimab in PDAC, and once again, I want to emphasize that nadunolimab in PDAC remains our primary strategic focus.

A crucial link between our target, IL1RAP, and patient is is analyzed both with us and several other groups. Several studies have shown that high tumor expression levels of IL1RAP serve as a marker of poor prognosis, as demonstrated here in the three graphs.

On the left, the data from Cancer Genome Atlas mRNA database shows a connection between high IL1RAP levels and poor survival. In addition, the middle middle figure from PanCan shows the same, and our own study together with Herlev University on on biopsies, we could also show the results from protein expression that will showed the same pattern.

Interestingly, also, we were approached by an AI company who has access to a large RNA database. They had identified IL1RAP as an interesting marker of disease and saw that two genes in two subnetworks enriched for IL1 high IL1RAP correlated with worse overall survival.

To us, these studies confirm that elevated levels of our target molecule, IL1RAP, in PDAC form the basis for our convictions and are strongly linked to poor patient survival outcomes. PDAC is a devastating disease, often diagnosed at an advanced stage when treatment options beyond chemotherapy are extremely limited.

The prognosis remained poor, with median survival between 9 and 12 months. Current chemotherapy regimens have been standard of care for decades, and unfortunately, there has been little progress in improving these outcomes.

That said, the field is seeing promising new agents in development, and there has been significant recent investments driving innovation in PDAC, and these emerging therapies provide hope and for meaningful advances and improved survival for patients in the coming years. In our Phase 1b/2a CANFOUR study, we enrolled 73 patients with first-line metastatic PDAC who received a combination of nadunolimab and gemcitabine/nab-paclitaxel, or GN.

We observed deep and durable tumor responses, as shown in the figure to the right, which translated into a median overall survival of 13.2 months. Although this was a single-arm study, comparison with historical controls, marked here in gray line, indicate that expected median overall survival with chemotherapy alone is approximately 8 to 9 months.

These findings suggest a meaningful improvement in outcomes with the addition of nadunolimab. Then our scientific team analyzed tumor biopsies from 49 patients to assess the expression levels of IL1RAP.

These analyses revealed two distinct groups: 29 patients with high IL1RAP expression, while 20 was deemed as low expressors. When we then correlated these expression levels with overall survival, the findings were remarkable.

Patients in the high IL1RAP group demonstrated statistically significant median overall survival of 14.2 months, compared to 10.6 in the low expression group. As shown in the previous slide, high IL1RAP expression in PDAC tumor is clearly associated with poor patient survival, reinforcing the significance of targeting this molecule and the overall survival in patient population.

In this study, the data suggest that IL1RAP expression is associated with better clinical outcomes, underscoring the therapeutic promise of targeting IL1RAP with nadunolimab. By selecting patients with elevated IL1RAP levels who are most likely to benefit from nadunolimab treatment, we hypothesize that we will be able to maximize the potential on with clinical impact.

In conclusion, nadunolimab has now been investigated in over 300 patients, and the accumulated data continue to demonstrate promising safety and efficacy profiles. Clinical results strongly point to a potential unique first-in-class opportunity for nadunolimab in PDAC, and also in non-small cell lung cancer.

Notably, PDAC patients with high IL1RAP expression, who traditionally have a poor prognosis, respond best to nadunolimab in combination with GN. Over the last year and a half, our team has developed a robust assay to test IL1RAP in tumor biopsies, which we intend to use in our in the next pivotal study to test and select patients that are expected to respond the best.

Importantly, we shared our results and discussed our next steps with the FDA this summer, which led to the Fast Track designation for nadunolimab in patients in PDAC patients with high IL1RAP. Building on these foundations, we plan to advance nadunolimab into a pivotal trial, which, pending funding and regulatory approval, is anticipated to commence mid-'26.

Now, let me spend a few more moments outlining our existing early pipeline, which we are further investing in. As previously discussed, our CANxx platform continues to offer robust opportunities for antibody innovation.

CAN14 is the next initiative emerging from this platform, and we intend to build on the preclinical and clinical experience gained gained through our CAN10 program, and we are advancing an anti-IL1RAP bispecific antibody for CAN14. For intellectual property and competitive reasons, the second target remains undisclosed, but we anticipate it will address inflammation or autoimmune disease mechanisms.

We expect to select a formal drug candidate of CAN14 around year-end 2026. Earlier this year, our scientists shared also promising preclinical data on antibody-drug conjugates, or ADCs, and this approach combines cytotoxic payload with targeted IL1RAP binding, which may offer higher efficacy with reduced side effects.

We continue to evaluate this ADC concept in within our CANxx project, and we will assess to move forward with this dedicated progress after evaluated the preclinical results. With this overview, I'm pleased then to hand over to our financial update to Patrik.

Thank you, Hilde. Our Quarter 3 was indeed transformational.

For the first time ever, Cantargia reported revenues and profits. When the Otsuka payment had been duly recognized and converted into Swedish kronor, our revenues amounted to 308.6 million SEK.

With operating expenses of 41.7 million in the quarter, our operating profit amounted to 267 million. From that, we deducted 1.5 million in net financial items to reach a profit for the quarter of 265.5 million.

It is worth noting that despite reporting a profit, no tax will be triggered due to our accrued tax losses. Our reported earnings per share were 1.07 Swedish per share.

For the full reporting period, or year-to-date, our revenues were obviously the same. With operating expenses amounting to 126.2 million, we reported operating profit of 182.5 million, net financial items at 3.2, leading to a net profit of 179.3 million, corresponding to earnings per share of 72 0.72 SEK.

Looking at our operating expenses, both quarter and year-to-date overall costs were similar to the respective comparison periods, with the comment that our R&D costs were significantly lower, both in the quarter and in year-to-date, due to a ramp-down both for nadunolimab and CAN10. This was then obviously offset by increased spend in general and administration, driven by our transformation, both in regards to transaction-related costs, but also the leadership transformation that we have reported earlier in the year.

Our end of September available funds amounted to 339 million Swedish, and we estimate a cash runway into 2028 with our current and ongoing commitments on nadunolimab and the investments that Hilde mentioned for CAN14 and CANxx, but excluding a pivotal program for nadunolimab and also excluding any potential milestone payments payable to Cantargia from Otsuka in that timeframe. With that, I hand the word back to Hilde for closing remarks.

Thank you, Patrik. As closing remark, we have a significant potential to become both first-in-class with an anti-IL1RAP antibody in treatment of metastatic PDAC.

The development is bolstered by clear biomarker strategy that guides patient selection. We anticipate being ready to initiate a pivotal study by mid-2026, contingent upon secure necessary funding and regulatory approvals.

In addition, strategic partnership with Otsuka has provided crucial external validation as well as financial flexibility, enabling us to reinvest the development of the promising next generation of anti-IL1RAP antibodies. With these initiatives, we expect to achieve and report several key milestones in the near future.

Thank you for your attention, and I now welcome any questions that you might have.

Hello, and good afternoon. I'll start with a question about nadunolimab.

How long would the proposed pivotal study take, and could you tell us something about what funding options you foresee?

We have yet to land on the design of the study and also the number of patients, it's a bit difficult to commit to any timelines. This has also to be cleared with FDA and EMA, of course, the design.

If you look at our competitors, they spend around 3 years from 2.5 to 3 years in their pivotal trial. With regards to funding, we will, of course, continuously explore all opportunities to support and accelerate our programs.

While partnerships can play an important role in this funding strategy, we do not have any specific commitments for the moment. We remain flexible on financial resources.

Okay. I noticed there's an increased, to me it seems, you are focusing even more on the autoimmune space with CAN14, and okay, maybe if someone could confirm that From what I've seen, there are no approved bispecific antibodies in that space.

Is that correct? Would you say that this is a more attractive area for investment compared with oncology right now?

Maybe, Wolfram, do you want to comment on the oncology part, and I can take the bispecific afterwards?

I'm not sure whether I got the question right. Was that the role of bispecifics in this indication?

Yeah. I haven't seen any approved bispecifics for autoimmune diseases.

Is that

This is right. There are some early trials ongoing, but you are right, currently no bispecifics are approved for autoimmune diseases.

You are right. That is new and that is, in a way, a land of opportunity for the company.

Great.

That's just my thought. It seemed like an open space with not so much competition as in oncology.

Mm-hmm. Yeah.

My last question was about the significant increase in administrative costs compared with previous quarters. Could you expand on why that is?

Patrik, do you want

It's costs related to the transaction itself, it's one-off costs to advisors and consultants and lawyers.

Very well. Thanks for taking my questions.

Hello, team, and thank you for taking the question. I just had one regarding the TRIFOUR study in that triple-negative breast cancer.

I know, as you stated, it didn't show difference in ORR versus chemo alone, and as we're awaiting more mature survival data, I was wondering if you could walk us through maybe how you interpret that data in context to pursuing your strategy in pancreatic and non-small cell lung cancer, and maybe specifically if there are any key biological or clinical learnings, and how those are shaping your development strategy going forward. Thank you.

Thanks, Sara. I'll leave that question to Wolfram.

I'm afraid. Yes.

There is no one-fits-it-all. You can't lump all the tumors together.

You can't say this is the drug and this drug is the panacea for everything. We have a very good signal in non-small lung cancers and we do have an excellent signal in pancreatic carcinomas.

The biology of breast cancer is totally different. Breast cancer is normally a multicentric disease, as we call it, and systemic disease of the breast is a totally different biology.

We cannot expect that the drug is equally effective in all of these cancers tested. In addition, breast cancer is, in a way, a endocrine-dependent cancer, and that might alter the effect of interleukin-1RAP inhibitors as well.

We do see a signal, certainly not strong enough to move on, but this is not our target cancer, and therefore, we are focusing on the other twos. We do not expect that we see a negative result in all the other cancers and vice versa.

Does that

Just to clarify, although the primary endpoint was ORR, we are still awaiting the mature overall survival data, and the biology of this that we can learn from this study will, of course, help us to make a final decision.

Okay. Thank you.

That's very helpful.

Again, if there are other logistic aspects here as well, this was a study in a single country, in a single or more or less single institution, a few institutions, oligocentric. That will explain some discrepancies in the result as well.

It is not a standard Phase 3 trial with well-defined criteria.

Okay. Thank you for the extra color as well.

Appreciate it.

Thank you for taking my questions. Could you provide any color or an estimate on how much the Phase 3 trial in PDAC is expected to cost?

Thank you.

Yes. Hi.

Again, I think we, as I alluded to with Richard's question, we have not formally decided on the design, and we're not ready to share our design right now. We need to run this through our regulatory interactions, both with FDA and EMA, stay tuned.

Thank you.

The first question from the web is related to the triple-negative breast cancer study: Do you expect any negative results from that trial on OS, and why do you think that CAN04 will work in PDAC if it doesn't work in triple-negative breast cancer?

I think we touched on that. I think we can reiterate that even though ORR is the primary endpoint and showed no difference between the two treatment arms, we still would like to see the mature overall survival data before we conclude.

I think also Wolfram did sort of run through with the previous question why we expect a difference or why we expect an effect when we enter into development of PDAC.

Let me chime in here. Obviously, this is something that is in the mind of all participants.

Let me make it perfectly clear: there is no panacea for all cancers. All cancers are different, and therefore, we need to treat them in a different way.

This is the first thing we have to learn. The second thing is mammary carcinoma, breast cancer, is a very difficult thing and a very heterogeneous tumor.

I give you a striking example: pembrolizumab plus nab-paclitaxel resulted in a triple-negative breast cancer in a huge overall survival benefit. Pembrolizumab plus paclitaxel did not show anything.

Why is that? We don't know.

It is the same indication, it is obviously the same drug, and it is the same tumor, and there are different results. That is something that we know for breast cancer, which is very tricky, but this does not apply to non-small lung cancers, and I'm overseeing 25 years research in non-small lung cancers and even pancreatic carcinomas.

This is a totally different type of cancer with a well-defined and a very distinct molecular biology behind, and therefore, this is, in a way, not very unexpected for us. Hope this clarifies.

Thank you, Wolfram. I think I just want to add that we do have overall survival data connected to high IL1RAP in PDAC, while we are still awaiting that analysis in triple-negative.

Thank you. This second question is related to the CAN10 project.

As there are other companies advancing their own programs within that area, could you comment on your patent position and your competitive standing relative the other programs being active in that area?

We first need to know which indication Otsuka will want to target, it's a bit difficult to be precise on the competitive landscape. I also would like to say that the product is in excellent hands with Otsuka Pharmaceutical, and we are not for the time being able to disclose any specific details of where they want to go.

We'll keep you posted as soon as we know more.

Yeah. Another question related to the CAN10 program: is the handover to Otsuka fully finalized and are all responsibilities on their hand now going forward?

Yes. All the responsibility of the product is in Otsuka's hand.

They acquired the product, they have full freedom to operate in their future clinical development. However, of course, the program is important for Cantargia, we will monitor the progress tightly.

Yeah. Going over to the PDAC study, how confident are you that you will manage to acquire the funds needed to start this study mid next year?

We will look at all different combination of financing this study, but as I'm sure everyone is aware, a pivotal study in PDAC requires quite a substantially large amounts, we will come back to our strategy with regards to financing when we have a bit more insight in where we want to go.

Thank you. Also related to that study, will that study be a combination with other drugs like gem/nab or what's the thinking on the combination strategy for that study?

We'll have a study in combination with standard of care. Now, how standard of care will look like at the time of when we conduct the study, we don't really know yet because Revolution Medicines is approaching the market when we are in our study.

However, it will be a randomized two-arm study on top of standard of care.

Thank you. To finish

Let me chime in here. I know what you are driving at and what you're alluding to.

Revolution Medicine is conducting or has conducted a second-line trial, which will have a readout and has already the database lock, and that will come to be filed in a due course. This is second-line.

We are talking about first-line, and the RASmute study, which might have the potential to change the control arm, is not even enrolling one patient. That is 300 3, and that will take quite a few time.

At the end of the day, both first-line studies will run in parallel, so that will actually minimize the risk of changing the control arm during the trial.

Thank you. Two questions related to the financial aspects: What are you expecting in rolling cost per quarter in the coming next 18 months, excluding the new studies?

Could you elaborate a bit on the upcoming milestone payments that you see in the future?

Patrik, do you want to take both of them?

Yeah. We have approximately 340 million by the end of September, and we have said in our cash runway estimate that it will suffice a bit into 2028.

We can assume that that's 10 quarters. You don't need a calculator to calculate what the quarterly burn rate would be then, I think.

That is sort of a linear and things in this business seldom happen linear, but that's the best answer I can give right now.

Thank you. If possible, could you elaborate around the potential correlation between high KRAS expression and high IL1RAP expression, where high IL1RAP expression indicate high responses to CAN04, and further elaborate around your thinking and the strategy around targeting hard-to-treat KRAS-driven cancers through the IL1RAP pathway?

I'm not 100% sure I understood the question, but which indications we can target, Jonas, do you think that was the question?

No, it's more about the correlation between high KRAS expression and high IL1RAP expression, and how that sort of affect your strategy.

Okay. We are targeting indications that we see a good correlation of where high IL1RAP is a prognostic marker for poor prognosis.

There are at least four or five indications where this is the case, but for now, our focus is on PDAC. I think you can understand that a small company, we need to focus, and right now, PDAC is our sole focus.

Thank you. The final question is related to whether you will be organizing any presentation together with Otsuka in the near future around the CAN10 project.

We don't know, but we don't expect to do that. If we do, we'll, of course, keep you updated.

Thank you. There's no more questions coming in from the web.

Okay. Thank you, everyone, and thank you for listening, and all of your good questions.