Good morning. My name is Martin Olin, and with me today I have Cristina Oliva, the Chief Medical Officer of BerGenBio. Today, we will provide you with an update on our business and our Q3 financial report. And we will provide you with some insight into what we consider to be a very novel approach to address a significant unmet medical need in non-small cell lung cancer. I'll just remind the audience about the formalities on forward-looking statements. So, to recap, BerGenBio, what we're doing, it is known that AXL, a cell surface protein, plays a key role in the progression of cancer, including non-small cell lung cancer. And we are focused entirely on developing our lead compound bemcentinib, for selective inhibition of AXL, to delay chemo resistance and also potentiate immunotherapy in non-small cell lung cancer. Two of the known poor prognostic factors in a large subset of non-small cell lung cancer patients that today doesn't respond very well to standard of care, which consists of chemotherapy and immune checkpoint inhibition. We have shown and seen some very encouraging, both preclinical, but also clinical data when we combine bemcentinib with the checkpoint inhibitor pembrolizumab or KEYTRUDA. And what we saw was actually a very meaningful improved survival versus what you would expect in second line non-small cell lung cancer. In particular, we saw an extended benefit in those patients that have a high expression of AXL, the target that we are inhibiting, which is very encouraging. But we also saw some very interesting data in patients that have a low expression of PD-L1, which is the target for our checkpoint inhibition or pembrolizumab. And this is very encouraging. We also saw some very encouraging early data in patients that have so-called hard-to-treat mutations. Those are patients that have a mutational driver that doesn't respond to standard of care. Our data that we have generated in totality guide us to focus on the first line setting in non-small cell lung cancer, which is a significant market opportunity, and we have received a Fast Track designation from the FDA, recognizing the unmet medical need in this setting. We have recently and over time, right sized our burn significantly and extended the runway, so we can support the future value inflection points that we believe inherently lies in the program that we are pursuing. We also see potential upside from additional programs, earlier programs, and also from out-license, out-license programs. Let me remind you about the devastating outlook for lung cancer patients. More than two million people, so kind of twice the size of Oslo, gets diagnosed with lung cancer each year. 85% of that is non-small cell lung cancer, and unfortunately, only 25% of these patients are alive after five years. That's a pretty devastating outlook, and it continues to be the largest cause for cancer-related death worldwide, with an increasing incidence due to the rise of smoking in developing countries. Unfortunately, patients are diagnosed too late, so the disease has become metastatic. And also, over the last few years, it has become known that there is a number of mutational drivers that leads to the patient not responding to today's standard of care therapy. If we look at how non-small cell lung cancer patients are treated today, it's basically a molecular-driven disease therapy. So first of all, patients will be tested for their PD-L1 expression, which will reasonably suggest how likely it is that you are going to respond to checkpoint inhibition or KEYTRUDA, which is standard of care in first line today. And while 30% of the patients have a high expression of PD-L1, the majority of the patients are either low or negative in terms of PD-L1 expression, i.e., they don't respond particularly well to the therapy. In addition to this, there are a number of mutational drivers, some of which can be addressed with targeted therapies. But again, the majority of mutational drivers are not being addressed by available therapies today. And amongst that, there is a significant portion, STK11-mutated patients, which accounts for 20% of first line non-small cell lung cancer patients that, in particular, have a significant unmet medical need. There is a vast majority of real-world data showing that these patients do not respond well. And as a patient with an STK11m in frontline therapy, you could expect to be on treatment for less than four months and have a median overall survival of around 10 months, which is significantly worse than if you do not have the STK11m. And very interestingly, these patients actually have a number of characteristics that we believe fits very well in terms of applying bemcentinib or treating them bemcentinib. First of all, there are no targeted therapies for the patients today. They universally have a high expression of AXL, and as I said before, that is what we have seen, that these patients with a high AXL expression actually are those patients that respond particularly well to bemcentinib. We also have shown, together with UT Southwestern in the U.S., that AXL inhibition improves the response to checkpoint inhibition in preclinical models, and we've seen some very encouraging early signs of efficacy in our second line study or the BGBC008 study. If we look at this significant unmet medical need, it actually translates into a very large market opportunity, which today is characterized by being a wide space, i.e., there is no targeted or available therapies for these patients. We believe that we are one of the frontiers in addressing this significant unmet medical need by our BGBC16 study, our Phase 1b/2a study in frontline therapy for STK11-mutated patients. I'll now hand over to Cristina to walk you through the data and where we are going. Thank you, Martin. Good morning, everyone. I'm Cristina Oliva. I'm the Chief Medical Officer at BerGenBio. Over the next few slides, I would like actually to show you the recent data that have been recently presented at some major scientific conferences, and also an update on how we are proceeding with our focus strategy in first line non-small cell lung cancer. We really believe that bemcentinib, as a small molecule and oral, orally available, can actually represent a very attractive opportunity that would allow us to address some significant unmet medical need, as you have heard just now from Martin. So what are the interesting characteristic of our lead compound, which is bemcentinib? First of all, is a highly differentiated AXL inhibitor. It has actually an improved potency, which means that there are less off-target adverse events, so a better tolerability. Interestingly enough, it concentrate a lot and very highly in lung, and it's able to cross the blood-brain barrier, which is particularly relevant in non-small cell lung cancer patient that unfortunately very often have brain lesion at initial diagnosis. We have demonstrated across multiple indications that bemcentinib has monotherapy effect, and this actually corroborate our structure to combine bemcentinib with chemoimmunotherapy. In the next few slide, I will also show you actually what has been already proven, which is that bemcentinib can be combined either with immunotherapy, namely pembrolizumab or targeted therapies. We have several evidences that have been published in combination with targeted therapies and the standard chemo, but also with checkpoint inhibitor. The FDA has granted bemcentinib for the STK11-mutated non-small cell lung cancer patient population, a Fast Track designation. What does it mean? That we will actually have access to very quickly and frequent interactions with the regulators. This is a designation that is only given to indications where there is a very high unmet medical need, and where the current therapies are not bringing benefit to patients. And then I want to remind you that we have an extensive IP through 2042. So what is actually the role of AXL, and why we believe that the inhibition of AXL could be relevant? AXL is overexpressed in many cancer types, and its overexpression actually is correlated with the aggressiveness of the disease, but it is also correlated to the occurrence of treatment resistance. AXL definitely plays a multifaceted role in cancer therapy resistance, and in particular, it has been shown that an AXL receptor is also associated with a very peculiar characteristic of cells, which is called epithelial cell plasticity, which actually gives the cells the ability to invade and metastasize. AXL is expressed not just in the tumor cells, but also in the tumor microenvironment. And its inhibition actually is able to reduce this aggressiveness of cancer, to also reduce the DNA damage and cell death, and at the same time, and we have shown it in clinical, is able to reactivate the innate immunity. So being actually AXL clearly defined now as a pro-tumoral, pro-metastatic, and with a very clear resistance role, there have been several investigations about how to target it. In this cartoon, we have tried actually to summarize the very active field of try and identify the best inhibitor of AXL. As you see, there is a wide variety of compounds. One is an antibody drug conjugate, for instance, but we go actually into the naked antibodies as well, or for instance, the inhibition of the Gas6, which is actually the main ligand for AXL inhibition. And then we move actually into a very selective field, which is actually the bemcentinib selectivity and inhibition. Not many of the completed studies with AXL inhibitors have been published. But sometimes actually there have been the data reported that the off target, the toxicity actually was requiring a modification of the study design. So going back to actually AXL inhibition and the STK11 patient population. Bemcentinib, as of today, is the only AXL inhibitor that is in clinical development for a very specific patient population, which is actually the STK11 mutated patient population. You've heard how dire the prognosis is for these patients, and just our study, Phase 1b/2a, is targeting specifically the STK11 population. All the others that I have reported here that you can read at your leisure, actually have a more variegated patient selection. Over the months, the recent months, there has been a constant increase of the role of STK11 as poor prognostic factor in non-small cell lung cancer. And at the very recent medical international conference I had the pleasure to attend, there is now clearly an awareness across the medical community of the role of STK11 in non-small cell lung cancer. Because of this, bemcentinib actually has grown interest, and we have several papers and publications accepted, specifically trying actually to define the role of bemcentinib in poor prognostic patients. What is actually the foundation for moving forward? Over the next few slides, I would like actually to summarize with you what's been the foundation for BerGenBio to move from a second line indication into a frontline indication. We have extensive data that really substantiate our move into first line. Namely, two Phase 2 studies that have tested bemcentinib in second line non-small cell lung cancer. Over 100 patients have been exposed to this, and the outcome of this study has been, in the combination with pembrolizumab, a meaningful progression-free survival and overall survival. We have then observed that patients, actually, they have a high expression of AXL, indeed can live longer when treated with bemcentinib and pembro. We have also interestingly observed a clinical response in patients that usually do not respond well to immunotherapy, who are those with low PD-L1 status. There is also initial benefit of the role of bemcentinib, not just in STK11, but also in additional very hard-to-treat mutations, and I will give you a few insights. We have just presented the data just few days ago at the SITC Conference. What is the compelling rationale beyond the Phase 1b/2a study that is an international study actively enrolling? Number one is to try and target a very high unmet medical need in this patient population. The ability to potentially actually move the response of a mutated driver into the wild type outcomes, which usually is much better for patients. So as we studied bemcentinib and the role of AXL specifically, we have noticed that most patients, roughly 88%, are actually indeed AXL positive, and as you can see from this slide, have a significantly longer. Moreover, if we actually take a look at the patients with negative or low PD-L1 status that are a group of patient that cannot or has not yet benefit properly from the use of checkpoint inhibitors, you actually see that they respond to bemcentinib and pembrolizumab, and that's actually a kind of a reassuring clinical demonstration that bemcentinib might be able actually to remodulate the immune system in these patients. Our analysis actually are expanding into better understanding the role of bemcentinib also in other mutations. As you have heard from Martin, the non-small cell lung cancer field is really based on biomarker-driven solution. So the effort actually of identifying prognostic or predictive biomarkers is a constant evolution. We have recently reported, actually at SITC, as I said, just few days ago, the analysis that we performed on the samples from the second line study, so the BGBC008 study, and we compared our results to the kind of a data set, the MSK-IMPACT data set, just to have an understanding of the mutation frequency of some of these hard mutation, namely STK11, KEAP1, and KRAS, and PD-L1. Also to try and identify what's the impact of our treatment intervention, bemcentinib and pembro, on this patient population. If you wanted to actually take a look at the poster, you will see that actually there has been a kind of a consistent message that pembro and bemcentinib seems actually to have an equal impact on wild type and mutated patients. So in other words, the intervention of bem and pembro seems actually to reverse the mutated status into the wild type status, hence enhancing the clinical outcome. We have also reported, it was just the end of October, if I'm not mistaken, the very final results of the BGBC008 study, the pembro and bemcentinib study. Out of this, I just wanted to put in a comparison, in a kind of a modern and contemporary comparison, what we have observed in 008 in patients who had been treated with I-O chemo, or chemo and I-O. You see that actually in ESMO there was a lot of debate about the results, sorry, of the SAPPHIRE study in second line I-O in patients pre-treated with I-O. You see that actually our all-comer results, but also our actual selective results, well compared to the most recent approach in second line. Safety is very important. Safety is really, really important in any combinatorial regimens, but also in monotherapy. And we are actually pleased to report that, the combination of bemcentinib and pembrolizumab has a favorably comparable, profile to what's been observed with pembrolizumab alone. No new safety signals have been identified. The majority of adverse events were mild or moderate, so grade one or two, and reversible and manageable. I also want to remind the audience that zero zero eight used a different treatment regimen, where bemcentinib was applied with a loading dose of 100 mg, then followed by a maintenance of 200. In the future, actually, studies, we will have a significantly lower dose, which is really based on the simulation and the target engagement that we have observed. So we really expect an even better tolerability of bemcentinib. So let's move now to the past and into the present and the future of BerGenBio, which is really the delivery of the BGBC016 study. This is an ongoing, multicenter, international, open-label study in first line non-small cell lung cancer. It's made actually of two parts. The Phase 1b will actually test the safety and tolerability of pemetrexed, carboplatin, and pembrolizumab in association with three different doses of bemcentinib. For now, they are 75 mg, 100 mg, and 100 mg. Once actually the two best doses are identified, we will move into the Phase IIa. What's the main difference between these two parts? The 1b is gonna be in all comers, so regardless of the PD-L1 status, regardless of the STK11 status, patients are only required not to have actionable mutation that should be treated with some currently targeted therapies approved. When we move into the 2a, we will enroll only STK11 mutated patients. I just want to remind the audience also that in many countries and most of the sites, STK11 is part of the normal panels that are used at the site to identify if a patient can be treated with the targeted therapies. So there are also additional complications, let's say, in this patient population, which is that actually there are co-mutational status that could impact significantly the clinical outcomes of these patients. There are actually several data that are coming out of the real-world ability to gather clinical outcome information, where actually we know the STK11 gives a poor prognostic condition to patients. But if STK11m is also co-associated with other hard-to-treat mutations, the prognosis is even worse. So this these differential outcomes, of course, would require a kind of a study control that take into consideration all the different permutation, but it's not really very easily implemented. And why? Because first of all, we are in a very early stage of the development of this combinatorial drug. Regardless of this, we have decided to include in the 2a study an approach that is called a synthetic control arm. What is a synthetic control arm? Synthetic control arm actually enables from real-world databases that are fully validated, the extraction of digital twins. So, every patient in the 2a study, the 40 patients that we will actually enroll in the interventional phase, will be matched with the same patient that will be treated in the real-world setting, same patient's characteristic, disease status, same therapy, and we will actually try and extrapolate the added value of bemcentinib through this. Why are we going to do this? Because we really want to strengthen our observation and really try and compare as quickly as possible, the benefit of the quadruple combinations versus the current therapy. So all in all, I think I have, I hope I have actually walked you through the observations that this year has brought us, really strengthening our understanding of the mechanism of action of bemcentinib, also of the understanding of the mechanism of action of bemcentinib in combination with different treatment agents. We are trying really to target a very significant unmet medical need. You see, the PFS is really dismal, and the OS doesn't never reach the 12 months mark. We know now that there is actually a highly immunocompromised and toxic tumor microenvironment. There have been a lot of effort in understanding the role of tumor microenvironment in creating immune resistance. We know that AXL is nearly universally expressed in non-small cell lung cancer, and that by inhibiting this pro-tumoral and pro-metastatic axis, we should be able, we will be able to reactivate the anti-tumor immune response, but also to delay chemoresistance as long as possible. So we really believe that actually we'll be able to move the 016 study with speed and quality, and the medical community has been really thoroughly engaged with us. Martin? Thank you, Cristina, and thank you for a very encouraging review of the data we have generated and where we're going. This slide summarizes the news flow that we have delivered in the first half of this year. As we previously announced, we have enrolled the first patient, and we are enrolling more patients into the 1b study, which is in the U.S., but also now in Europe. We have presented the very encouraging data on STK11 loss at AACR. We've also shown some very promising early indicative data in the first line setting. Going forward, the singular focus we have on the BGBC016 study will allow us to hopefully generate some very encouraging data in the first line, non-small cell lung cancer STK11 patient population that really deserves a treatment option that they don't have today. I think all the data, or pretty much all the data we have generated so far, points to the same direction, is that AXL inhibition actually activates or reactivates or remodulates the innate immune system, and therefore allows both chemotherapy, but also checkpoint inhibition to work better in a setting where it's not really benefiting the patients. We are going to continue to present our data, but most importantly, we're going to continue to progress our BGBC016 study, which is the completion of the 1b part, and taking two doses into the Phase 2a part, which is for the STK11 mutated patient populations. We have also announced other news. These indications are not part of the priority for the company in the present situation, but they all point to the same evidence, which is that inhibition of AXL bemcentinib actually makes a difference for the patients. We have seen monotherapy activity. We have seen some less encouraging activity, one might ask in melanoma, but if you analyze the data, maybe the patient enrollment was a little bit skewed and, you know, we had some bad patients in this, in the, in that study. Overall, we did not expect to see a huge benefit. That's, of course, easy to say in hindsight, but I think that was the notion when the study was recruited. The impact of the restructuring and the focus of the company really comes out now in the Q3 financials. The burn in the third quarter operational loss was less than NOK 30 million, compared to an average of around NOK 60 million in the previous quarters, which is a significant reduction. We expect that the current level is going to be at about or so the level that the company will have going forward. Of course, there are some quarterly variations that will, by all means, mainly be related to the enrollment activity, and the purchase of KEYTRUDA in those countries where it's not reimbursed as standard of care therapy. The cash flow for the quarter was somewhat higher than the operational loss, but it also reflects a reduction, a significant reduction over the last year in short-term liabilities. So short-term liabilities now is at a much lower level, and therefore, we'd expect that the operational loss and the cash flow is gonna be closer to each other going forward. We ended the quarter with NOK 169 million. With a burn at the current level, we expect the current financials to take us through the end of 2024. Of course, we have the warrant element, which is that for every two shares that was subscribed for in the rights issue, there was a warrant which can be exercised. That warrant window actually opens tomorrow. It's the first warrant window. I should mention that the warrants are actually tradable, with a ticker of BGBIS, and the first window opens tomorrow at 9:00 A.M. and closes on the November 28th at 4:30 P.M. CET. The exercise price for the warrants will be set on the weighted volume average price in the days from the 10th to the 14th of November and will less 30%. However, not less than NOK 0.10 and not more than NOK 0.13, and the exercise price will be announced tomorrow morning before the market opens. Here is a timeline for the exercise period of the warrants. I think it's relevant to inform the market that all the primary insiders of BerGenBio are going to, and have committed to, exercise all their warrants in the first window, which is opening tomorrow. Here are some alternative procedures on how to exercise your warrants. You can either follow the link here, or you can complete and return an exercise form before the end of the exercise period. And if you have any questions, don't hesitate to reach out to the company or Carnegie or Arctic. They will be more than willing to assist you in the exercise of the warrants. So in summary, BerGenBio, a very focused approach in non-small cell lung cancer, a significant unmet medical need. We have a strong IP protection, but we also have a differentiated approach compared to what we see other companies are doing. We expect to have the 2b readout early next year, and therefore we will be able to initiate the Phase 2a also in the first half of next year. Our cash position takes us into the end of 2024, but the warrant element that was issued in connection with the rights issue, if fully exercised, may actually finance the company into the second half of 2025 and enable the company to have a mature data set in the first line STK11 non-small cell lung cancer setting, which we hope would showcase the opportunity that bemcentinib represents in this setting. Thank you very much for listening, and I think we will now go to the Q&A session. Yes. We have some question related to the first line lung study. So how do you identify the STK11 mutated patient, and how will they be enrolled into the trial? Thank you. Very good question. So as I mentioned in my presentation, in most of the sites, we have actually identified and selected, and some of them already activated. STK11 is part of a panel, it's called a panel, where actually multiple mutations need to be identified or potentially excluded. So the patients receive these actually biopsy. Over this biopsy, which could be liquid or solid biopsy, actually, there is a panel that develop and identify which mutation the patient has. Most of them are non-actionable, some of them are actionable, and this will influence the enrollment into our study or to receive other treatments. Next question is, how confident are you in the possibility to enroll the trial, and what makes you excited about it? So I have actually been really lucky to visit all the sites so far that have been activated, and the interest and the interest on the scientific, actually, rationale, but also the engagement has been really, really, really encouraging. Sites actually are very keen to evaluate the value of bemcentinib, this unmet medical need. The medical community, as I said, has identified this as a very poor prognostic marker with nothing available, no therapies. I think we have the right sites, the right support, and the right investigators with us, actually, pushing for this enrollment to move as fast as we can. What defines success, of the trial, in your opinion? What defines success of the trial in my, in my eyes? So for me, success of the 2b would be actually to be able to identify two doses according to the Project Optimus, that the FDA is really moving forward. So safety should be not only acceptable, but safety actually should be promising, and early signs of activities that we will actually be able to observe. What's success for me in the second part is clearly to identify a significant clinical outcome that actually will compare to what this patient can receive now. And actually to have this synthetic control arm built in, so that we will really be able to try and dissect the role of bemcentinib in this patient population. Then it's a question about the warrants and funding. Will you be able to get the final readout from the trial if all the warrants are exercised, or do you need additional capital? It's a very good question. Of course, we hope that the patients will live very long, but we will be able to deliver a mature data set based on a full exercise of the warrants. If the patients live really long, we might be in a situation where we would need a little bit extra funding to take us into 2026, but that's a dream scenario, Cristina, if the patients would live that long. It is. Yeah. Yes. I think the answer is, with the warrant exercise being exercised, the company is funded to complete the study and have a decent assessment of a mature data set. Yes. Then, there have been a few questions on partnering discussions. Why don't you have a partner at this point, and what are partners looking for? I can take. Let's say the first part of it. There have been a lot of discussions about this, and I want actually to take us back to where we are now, which is we are actually exploring a completely new treatment regimen. We haven't established the treatment yet. We are in a phase of doing it, and we are trying to do it as quickly and as safely as we can. A partner in a first line indication is looking for an established treatment, as established as it will be, with some initial insight on the clinical outcomes. So I would say at this stage, it's not particularly surprising to actually be left in independence, I would say, to develop these this treatment. I don't know what you think, Martin. No, I fully agree with that. I also think that we have to realize that oncology, over the last year, has been crowded with a number of combination trials. I still think there is over 1,000 trials ongoing with KEYTRUDA, different combinations, and the bar has been raised because there's been a number of significant disappointments For these combination studies. Although we have monotherapy activity, we've not really shown it in non-small cell lung cancer. So I think that's also the evidence, in addition to the safety profile and the established regimen, that a partner would look for. But personally, I also think that it may not be the best time for the company to partner the asset at this time. I think there is a significant value incremental to be delivered by the company, keeping its independence and executing the study and showing that the role of bemcentinib actually does matter in this setting. A follow-up question on out-licensing. Is there any update on the process of outlicensing tilvestamab? There is an update, and the update is that we have ongoing discussions, but we have no conclusion at this point. Then it's a question about some preclinical work. So, Cancer Research UK has given the first preclinical package award in fighting pancreatic cancer, combining chemo and bemcentinib. Can you comment on the reality of bem being chosen by authorities both in the U.K. and the U.S.? That's a good question. We had some... Among our investigator-led studies, we had actually conducted a clinical trial in pancreatic cancer, PDAC. Unfortunately, that's a disease that is very hard to treat, and there is a huge effort of the medical community to try and identify any therapy that actually could prolong the survival of these patients. Having said that, we know preclinically that actually AXL is overexpressed in pancreatic cancer cells, so there is a rationale, actually, for this combination. We have decided not to pursue the pancreatic indication because we just want to be focused on the first line non-small cell lung cancer. It's a question about the cost reduction, and can you discuss if you have the right organization to move forward? We do believe we have the right organization. That was part of the right-sizing exercise we did in connection with the rights offering this summer. So, the answer is yes, we do have the adequate organization to execute on the BGBC016 study. A question about if you have control about the cost, the currently cost bar? I think the third quarter really shows that we have adequate control over our burn. Yeah. A quick question about the status of drawing facility from Meteva to BerGenBio. So, back in 2022, Meteva, and BerGenBio entered into a loan facility agreement of up to NOK 100 million as a loan facility, and that loan facility, that was part of the terms, would disappear in the event of a significant offering, which was by definition, achieved with the rights issue this summer. So, the company does not have any loan agreement facility with Meteva as of that date. A question about the variance between the operational loss on 28 and the cash flow, which is significantly higher. That's primarily driven by the payment of short-term liabilities, which is actually really linked to the closure of previous conducted studies. So going forward, as I said, we expect the operational loss to be much closer tied to the cash burn on a quarterly basis going forward. Thank you, Martin and Cristina. That finalized the Q&A. Thank you. Thanks for listening. Thank you. Bye.