Good morning, and welcome to the third quarter 2022 update from BerGenBio. I'm Martin Olin, the CEO of the company. I just remind everyone about the formalities for forward-looking statements. BerGenBio, in summary, we are entirely focused on the development of selective AXL inhibitors for the treatment of aggressive diseases. Our lead compound, bemcentinib, has already been studied in more than 600 patients, as of today and is currently being advanced in two significant opportunities. First one, first-line non-small cell lung cancer in a particular subset of patients that carry a mutation in the STK11 gene, and we are moving forward with phase I-B/II-A study. I'll come back to that. We're also advancing bemcentinib within hospitalized COVID-19 patients through phase II-B study. We are laser-focused to deliver clear value drivers in the next 12- 18 months. This is the recent highlights. We announced in the third quarter that we had dosed the first patient in phase II-B study under the EU-SolidAct platform, enrolling up to 500 patients across Europe. We also initiated phase I-B/II-A study in evaluating bemcentinib in combination with standard of care, which is checkpoint inhibition and chemotherapy in first-line non-small cell lung cancer patients that harbor the STK11 mutation. We know that STK11 mutations occur in up to about 20% of this population and result in inferior survival outcomes on current standard of care. We ended the period with NOK 225 million in cash, and we announced post-period the closing of a NOK 100 million loan facility from our largest shareholder, Meteva, enabling the execution of the focus strategy that we announced earlier this year in May, particularly focusing on the two opportunities that I just mentioned. We're also pleased to report that we had the last patient, last visit in the 003 study, so that's the relapsed, refractory AML second-line patients. We also recently had the last patient, last visit in our 008 study, which will allow us to lock the database and analyze the data, and we will report those studies in the beginning of next year. In line with the focused strategy, we've also announced that tilvestamab is not within the focus strategy, and we have therefore initiated partnering outreach for the tilvestamab, which is our monoclonal antibody that has completed a phase I study in ovarian cancer. Not specifically for ovarian cancer, but we believe that the ovarian cancer setting was the right setting for us to acquire the tissue biopsies under which we could evaluate the fibrotic impact of tilvestamab. The whole rationale behind BerGenBio's focus on why AXL inhibition. Well, it's known that AXL activation results in several deleterious effects in cancer and severe respiratory infections. Potentially others, but we are focusing on these two indications. In cancer, we know that AXL activation leads to invasion, migration, drug resistance, proliferation, survival, increased survival of cancer cells, but also immune suppression. In respiratory diseases, we see that it involved in viral entry, migration, immune suppression, ECM production, basal cell proliferation, but also reduced cytokine signaling. This is a snapshot of our clinical pipeline, that shows bemcentinib, has or is being studied across a number of oncology indications. The first-line is one first-line non-small cell lung cancer STK11 patients, which we are initiating or have initiated. The two studies that I just mentioned have now been completed. That's the second-line non-small cell lung cancer study, where we have combined bemcentinib, with pembrolizumab and also, docetaxel. We've also completed the 003 study, relapsed and refractory AML second-line patients and in MDS and solid tumors as well, which is an out licensed program with ADC, so we don't have any control over that. Finally, with bemcentinib, the phase II-B study. As I mentioned, tilvestamab is. We have initiated the partnering effort for that. The focus of today's presentation will be the priorities or the focus for the company, which is first-line non-small cell lung cancer STK11 mutated patients and COVID-19 hospitalized patients. I'll walk you through the first indication, which we believe represents a unique opportunity for bemcentinib to address a significant unmet medical need. Why do we believe that? Well, our data from our completed second-line studies in non-small cell lung cancer supports, in our mind, why it makes sense to inhibit AXL with bemcentinib. First of all, in the 005 study, to remind everyone, that's bemcentinib in combination with docetaxel in second-line NSCLC patients, demonstrated improved efficacy and therefore also demonstrate the potential for the delay of chemo resistance that we see patients are acquiring. In the 008 study, which is a study where we combined bemcentinib with pembrolizumab, we have seen a very interesting and encouraging efficacy in patients that has overexpressed or activated AXL, showing median PFS and median overall survival outcomes that are actually pretty similar to what you see in first line, which we believe is demonstrating the importance of AXL as a driver of disease progression. In addition, we have supporting data that identify this as significant opportunity. First of all, we know that these patients have inferior outcomes on standard of care therapy today. We also have seen with our own data, but also data that we have collaborated with others on, that these STK11 patients almost universally overexpress or have AXL-activated AXL. We know that the STK11 patients are characterized by a severely immunosuppressed tumor environment with high levels of ROS, EMT, oxidative stress. That is actually, in our opinion, a result in the poor prognosis. The early retrospective data that we have mentioned before, it's a small data set, but they also support that there is benefit for these patients of inhibiting AXL with bemcentinib. The studies that I'm mentioning, the 005, in essence, we believe that that data justify that there is an opportunity to delay the chemo resistance by reversal of the cancer cell survival and escape mechanism. The 008 data justifies the combination with tremelimumab. The two elements that are standard of care today, we believe fits very well with bemcentinib. This is the 005 data that we have shown before, with an overall response rate in second line and beyond of 35%. One should reckon that what you normally see with docetaxel here is 6%-9%. Almost a four-fold increase in the response. 47% of the patients had stable disease at the best response. The most common side effects we believe are not detrimental and are manageable in this setting. There were very few non-hematological grade three events. They were rare. In the 008 study, when we specifically look at those patients who are AXL positive or have an activated AXL, that's about 50% of the patients, and they actually show benefit that are pretty close to what you see in first line non-small cell lung cancer patients, as also referenced here on the two tables. Both on the median progression-free survival and on the overall survival, these are very, very meaningful benefits in second-line cancer patients. AXL, when it's activated, actually reduces the apoptosis, so the ability to kill the cells, but also promotes the immune response microenvironment. On the left-hand side, we know that AXL activation leads to an improved cancer cell survival and escape mechanism for the treatment. On the right-hand side, we also know that in the microenvironment around the tumor, the AXL activation leads to immune-suppressed environment, causing the tumors not to respond to today's therapies. When we look at the STK11 patients, we can see that it causes high oxidative stress hypoxia inflammation, which results in an almost universal AXL expression in this population, which is quite interesting. The cancer cells are using the AXL pathway to sense the stress, and therefore, they are to trigger a molecular mechanism to actually enable the cancer cell to survive the toxic environment that they are being exposed to. They have a phenotypic characteristics that are known to drive the AXL expression and the activation. What we see is a pretty significant increase in the AXL expression in these STK11 mutated patients, why we believe it's particularly relevant to consider that population. We know this is just a summary to remind you about the size of this opportunity. On the pie chart on the left-hand side, it's about 20% of first-line non-small cell lung cancer patients in U.S., and the four big European countries is actually more than 30,000 patients on an annual basis. We know that they have low response rate, we know that they have shorter survival and median progression-free survival, and we also know that they have a reduced response to both chemo but also immunotherapy, and there is no targeted therapies available for these patients today. Indeed, this is a significant unmet medical need, which we believe can actually be targeted by bemcentinib to potentiate the current standard of care. In combination with today's standard of care, which is a checkpoint inhibition and chemotherapy, on the left-hand side, we are showing the cellular impact of bemcentinib inhibition of AXL by reducing or it causes reducing of EMT driven immune evasion and drug resistance. It enhances the antigen presentation, and it also reduces the DNA damage repair and enhance cell death. On the tumor microenvironment, also very important, it reactivates or resensitizes the tumor to checkpoint inhibition therapy, through the proliferation of the TCF1 and CD8+ T cells. From a safety perspective, the educated listener will know that we have dosed bemcentinib previously in the oncology trials with a loading dose of 400 mg and daily doses of 200 or maintenance dose of 200. This is a snapshot of the safety data that we have seen when we combine bemcentinib with pembrolizumab at that dose level, which in reality tells you or shows you that there are no significant safety issues of that combination compared to other relevant therapies. The important thing is here that we are moving forward with phase I-B/II-A study at a significant lower dose. No loading dose, and a daily dose of less than, probably potentially less than 50% of the previous dose. We do expect that we're not going to see any additional safety issue, even in the triplet combination. From a competitive perspective, we consider the opportunity to be a significant wide space in the broader STK11 mutated population. Yes, there are competition in the KRAS G12C area, but that is only 12% of the STK11 mutated population. Indeed, we believe that bemcentinib is well-positioned from a competitive point of view. Indeed, we are, to our knowledge, the only one that is moving forward with a broad approach for the first line STK11 mutated patient population. With that, we are moving forward and have initiated the phase I-B study, which is the dose escalation part in the U.S. The doses that we will test is 75, 100, and 150 mg in all-comers patients. Why all-comers? Well, we want to get the safety done as quickly as possible. The II-A part, which will be the dose expansion part, potentially involving two doses, will be in the STK11 mutated population particularly. So we believe that we will be able to report the data from the 1b in the second half of next year and be able to initiate the phase II expansion study also in the second half of next year. Now move on to the hospitalized COVID-19 opportunity. We believe, and we have said that many times, that we believe bemcentinib offers a novel approach to an effective treatment for hospitalized COVID-19 patients. We have a strong package of preclinical but also clinical evidence that supports the unique mechanism of action, which is three. The prevention of the viral entry, the increased immune response to the virus, but also importantly, the ability to repair the lung tissue damage that is important for the recovery phase. Our preclinical data points to an almost universal efficacy, regardless of the variant, but also in other diseases, respiratory diseases, I should say. The two prior COVID-19 studies that we have conducted shows clear trend to improve survival and a delay of disease progression. We also believe that the recent events, including the Veru outcome meeting, shows that our approach of doing a significant and robust study, phase II-B study with up to 500 patients, is the right approach to seek an approval in this indication. This is just a little bit of repetition, but to remind everyone, this is the unique and also the competitive advantage, in our opinion, of bemcentinib by the three mechanisms of action or the modalities by impacting the viral entry, increase the immune response, but also repair the lung tissue damage. We don't see any change. This is the current guidelines from the NIH in treatment of hospitalized COVID-19 patients. There is, in our mind, no change in that landscape, so there is still a significant medical need for those patients who are hospitalized and require oxygen. The ACCORD-2 data, in our mind, justifies why bemcentinib in combination with standard of care is a relevant treatment modality. Already at day 29, we saw a survival benefit, which is retained throughout at day 60. Also, very importantly, the clinical benefit that the patients are seeing is at 90% in the active arm versus 69% in the control arm or standard of care alone. These are some of the recent data that we have generated, which clearly points to the fact that on the relevant markers that are relevant for this particular setting, potentially also other respiratory diseases, clearly points to the fact that the mechanism of action that we're talking to is reflected in the outcome of the relevant clinical biomarkers. With that, we are moving forward. We are enrolling patients through the EU-SolidAct study. We are still activating sites, and hopefully very soon, most of the sites will be up and running. We are really looking forward to report the data as we have guided previously in the second half of next year. Our third quarter 2022 financials show a decrease in the operating expenses, which is actually also what we implicitly guided on when we announced the focus strategy. We are seeing a reduction in our burn, right-sizing the organization and focusing on the two indications. We expect to see a lower burn going forward compared to the historical burn. If we look at our cash burn in specifically the third quarter, NOK 65.8 million, or $6.6 million, which is somewhat lower than the quarterly average from the last year. We ended the period, as I said, with 225.1, it says here, million NOK, which is about $20.7 million. Importantly, we also secured the shareholder facility from Meteva of NOK 9.5 million, providing cash resources of more than $30 million. Then again, at a projected lower cash burn going forward than previously. If we look at the key catalyst relevant for the two indications, we are going to report the 008 final data in the first part of next year, which is certainly relevant in terms of the argument and the clinical efficacy of bem in this indication. We hope to be able to report the phase I-B data in the second half of next year. We will initiate as planned, hopefully, the phase II-A study also in the second half, and we will have additional preclinical data in the STK11 mutated population also in the first half of next year. For the hospitalized COVID-19 patients, we expect to report the data in the second half of next year. We're also going to provide additional preclinical data on other respiratory infections. With that, I would like to say thank you for the attendance, and we will open up for questions. Thank you. First of all, are there any question in the audience here? If not, we can go to the online questions. The first one is about the STK11-1B study. Will the data from the STK11-1B include focus on efficacy? And if yes, do you expect that it could trigger interest from large players in the business? Do you want to answer that question, Cristina? Yes. The primary endpoint of the phase I-B study is going to be safety and tolerability. We will have a secondary endpoint, preliminary antitumor activity. The reason for these two endpoints is actually to give us enough confidence from a feasibility and safety perspective to move into a biomarker-driven patient population. We will have only very preliminary antitumor activity, keeping in mind that the sample size is going to be pretty limited. Thank you. The next one is about the EU-SolidAct study. Could you say something about how the recruitment for the EU-SolidAct is progressing? Do you have some guidance on when we can have the first data from that study? I think we have already provided the guidance, which is the second half of next year. That's when we expect the outcome of the study. It's really too early to provide any guidance as to the enrollment. I don't think that we would provide any specific guidance on the enrollment as such, but we will, of course, update the market when relevant in terms of the finalization of the enrollment. It's really too early at this point actually to say anything other than what we have already guided. It's a question about respiratory infection collaboration. You guided in the second quarter presentation on additional data from respiratory infection throughout the collaboration that you would soon announce. What is the status of that matter? We will soon announce the collaboration. It's a question about the loan facility. It's more related to why we haven't offered that to all shareholders. I think maybe the answer to this question is to remind about the terms for the loan. This is a non-secure loan from the largest shareholder. Mm-hmm. It's an intention to convert to equity. It's no fixed term on the conversion to equity, so it's just an intention. I think that addresses the question why we haven't offered it. It's favorable terms for the loan. It's given from the largest shareholder. It's nothing else to disclose. The announcement we did when it was completed included all the terms. Yeah. I think that's conclude the Q&A. Okay. Any questions in relation to what has been said here? No? Okay. Thank you.