Good morning, and welcome to BerGenBio's Fourth Quarter Financial Report and Business update. I'm Martin Olin, the CEO of BerGenBio. Today I will, together with Cristina Oliva, our Chief Medical Officer, take you through a business update centered around our strategic focus in lung cancer and severe respiratory infections. Just remind everyone about the formalities. Yesterday, BerGenBio announced the top-line data from our second-line non-small cell lung cancer study, in which we have enrolled patients who have received at least one prior line of therapy, and the patients were treated in a combination of bemcentinib, our selective AXL inhibitor, in combination with pembrolizumab. It's with great confidence that I can say that it actually does matter to inhibit AXL specifically in non-small cell lung cancer. The top-line data we announced yesterday very clearly show that AXL inhibition makes a difference, and we saw that in terms of very significant clinical benefit for the patients who received the combination of bemcentinib in combination with pembrolizumab, in particular for patients who had an AXL score higher than five, where the overall survival and median progression-free survival benefits were significant. We believe that this data set actually is a strong justification for our strategy in the frontline setting, in first-line non-small cell lung cancer patients who harbor a mutation in the STK11 gene. First of all, it's a significant market opportunity. There's more than 30,000 patients today in the U.S. and the five big European countries that have STK11 mutations. This is associated with poor prognosis. There are no available therapies for these patients. The STK11 mutation, actually creates a phenotypic environment in which AXL is expressed and activated, which is particular the setting where the inhibition of AXL by bemcentinib have shown to work, as I just told you, in the 008 study. We believe that almost universally these patients, the STK11 patients, harbor or create an immunosuppressive environment that leads to AXL expression, roughly in around 80% of the cases, compared to around 50%, as we have seen in the second-line setting. There is very little competition for these patients. We have a very strong proprietary position, and we also have gotten a Fast Track designation by the FDA. If we go back a little bit, we believe that the data we have seen in the RAD-18-008 study, but also in the RAD-18-005 study, which is now finally reported, shows that the scientific rationale of why it makes a difference to inhibit AXL, leads also to clinical benefit. This is a picture showing on the left-hand side, what happens when you treat patients with chemotherapy. The treatment with chemotherapy, create an oxidative stress, inflammation, hypoxia, which leads the cancer cells to activate AXL to escape the effect of chemotherapy. It leads to EMT and metastasis. It drives resistance to DNA damage, which is one of the core elements of chemotherapy. By that activation, the cancer cells are surviving the effects of chemotherapy and potentially also create resistance to it. On the right-hand side, in the STK11 mutation creates an AXL activation that leads to immunosuppressive environment or a so-called cold tumor environment where checkpoint inhibition is no longer effective because the immune system has been deactivated or dampened and can therefore not respond to checkpoint inhibition. The second line data validates the clinical relevance of AXL inhibition. In particular, the RAD-18-008 data, where we announced the top-line data yesterday, shows extended median overall survival versus all relevant historical comparators. We saw a particular strong benefit in patients who have AXL TPS score higher than five versus AXL TPS score lower than five. We saw a survival benefit regardless of PD-L1 status, which is particularly interesting when we combine this with checkpoint inhibition. The RAD-18-005 study, we have reported data from earlier, but now we have the final data. The final data, I think in conclusion, shows an impressive overall response and also a significant median overall survival benefit, in combination with docetaxel or chemotherapy, compared to historical controls as well. In summary, these data are highly encouraging, and it confirms AXL as a relevant target. We believe that AXL inhibition in combination with both chemotherapy but also immune checkpoint inhibition provides clinical meaningful benefit and strongly support our strategy to go in the frontline setting for the STK11 mutated patient that has a specific characteristics, which is AXL activation. That's basically what we believe the data strongly indicate from both the 008 study but also from the 005 study. I will hand over to Cristina, to take you through the eight and five data but also to give you an update on our strategy within severe respiratory diseases. Thank you, Martin. Good morning everyone. In the next few slides, I would like to present you the results of two studies that we have conducted in pretreated non-small cell lung cancer patients. One study was conducted with bemcentinib in combination with immunotherapy, and the second one with bemcentinib in combination with chemotherapy. The treatment of non-small cell lung cancer in second line and beyond remain today unsatisfactory. As you can see, there is a variety of therapies and approaches that have been utilized. The outcomes still, unfortunately, remain disappointing with the median overall survival that it's approximately 10 months, and a median progression-free survival of only three to four months. We are here reporting the top line results of one of these studies conducted in second line and beyond non-small cell lung cancer patient. Further analysis will be presented at an upcoming scientific conference. I want to remind you the study design. This is a phase II, multicenter, international, multi-cohort, phase II study with the patients either pretreated with chemotherapy, with immunotherapy, or the combination of the two. Primary endpoint was objective response rate, secondary endpoints, a lot of other efficacy outcomes, including duration of response, disease control rate, progression-free survival, overall survival, and safety and PK analysis. The study enrolled 90 evaluable patients. A clinically meaningful survival benefit and disease control was demonstrated with the combination of bemcentinib and pembrolizumab in this RAD-18-008 study. This is regardless of prior therapies and regardless of the PD-L1 status. As you can see here, this combination provides a median overall survival of 13 months and a median progression-free survival of 6.2 months with a disease control rate in over 50% of the patient population, specifically in 51.1% of patients, and an objective response rate of 11.1%. What's is even more encouraging actually are the results of PFS and OS when they have been stratified according to the AXL status. That was a preplanned exploratory analysis. A statistically significant and clinically meaningful improvement in median overall survival based on the AXL TPS score greater than five was observed. As you can see on the left-hand side, patients with an AXL TPS score greater than five, which represents 46% of the evaluable patients, achieved a median overall survival of nearly 15 months, specifically 14.8 months, compared to the patients with an AXL less or equal to five, who had a median overall survival of 9.9 months. A longer median progression-free survival was observed again in patients with a TPS score greater than five, 8.7 months versus 4.6 months, where the TPS score were equal or less than five. The overall response rate, interestingly enough, in AXL TPS score greater than five was 21.1%. The treatment combination was well-tolerated, with no new significant safety signal. The majority of the adverse events were either mild or moderate. There were very rare instances of treatment discontinuation due to any treatment-related adverse event, and toxicities were overall manageable and reversible. I want also to remind you the dose regimen that was selected for this patient population, which was bemcentinib with a loading dose of 400 mg, followed by a maintenance of 200 mg per day. While actually for further study, the dosing regimen is going to be with a lower dose of ben. Let's put now in the previously described context our results. It's always difficult to make a cross-studies comparison. Overall, the results in all comers actually support a clinical benefit in median PFS and median OS that is even higher when the patient population is selected for the expression of AXL, with a median PFS of 8.7 months and a very long median OS of, again, as I said, nearly 15 months. The other study that I would like to report to you is an update on an investigator-led study. It's called RAD-18-005. The initial data on the MTD, DLTs, and overall response rate were reported at ASCO last year. Here, I'm glad to report the final analysis on the progression-free survival and overall survival. This was a phase I study, dose escalation, single institution, with bemcentinib in combination with docetaxel. The results were actually an impressive overall response rate of 35%. Let's put this one in the context of what's achievable with docetaxel, which is usually in the single digit. A PFS that is in the range of what's expected, and the median overall survival that actually goes above the mark of one year, which is actually longer than what's currently achievable. Most common adverse events are expected with the bemcentinib base combination, namely diarrhea, fatigue, and nausea, and also as expected in a combinatorial treatment with docetaxel neutropenia that was controlled with the addition of growth G-CSF in the treatment regimen. Overall, this data from 08 and 05 definitely validate the importance of the AXL inhibition in combination with chemo or immunotherapy in non-small cell lung cancer patient. We believe that this data support our ongoing Phase I-B/II-A study in first-line non-squamous non-small cell lung cancer in a STK11-mutated subgroup of patients. This is a large underserved patient population. We are talking here of over 30,000 patients in the non-small cell lung cancer group, and these are data from the five major EU countries and the U.S. These patients have actually a poor prognosis, unfortunately, with the currently available treatment regimens. By poor prognosis, we mean lower response rate, a shorter overall survival, and PFS. They definitely represent a high unmet medical need. STK11 mutation actually creates a severely immune-suppressed tumor microenvironment, which is actually associated with AXL expression in the vast majority of patients, over 80% of them. This activation results in several aspects that are important for the tumor progression. One is the development of drug resistance, but also immune evasion and metastasis. AXL inhibition actually targets key survival and resistance mechanisms within the tumor macro environment. The AXL inhibitions reduces the EMT-driven immune resistance evasion and drug resistance. It also reduces the DNA damage repair, but also reactivates the innate immunity, the proliferation of the CD8 T cells, so to reengage actually with the checkpoint inhibition. This is actually the study design that is based on the current promising and encouraging data from the 05 and the 08 study, where bemcentinib in combination with the standard of care of pembrolizumab and a doublet chemo will be tested in a Phase I-B/II-A study. This is an international study with a traditional 3+3 study design in the I-B. The phase I-B study will be conducted only in the U.S. It will be targeting a first-line non-squamous non-small cell lung cancer with no actionable mutation, no stratification for STK11-mutated patients. Once the dosing regimen has been identified out of the three cohorts that we plan to enroll, we will move into a selected patient population in the dose expansion phase of the study, which is going to be an international effort with the EU countries and U.S. countries aiming at enrolling around 40 patients, again, selected for STK11-mutated disease. You see the primary endpoint of the phase 1b is going to be most related to safety and the tolerability of this combination. We will also assess the preliminary antitumor activities of this combination. For the phase II-A, we will aim at identifying the objective response rate and all the traditional efficacy and safety outcome of this study. As Martin referred to, there are few competitors within the STK11-mutated setting. They are namely targeting a subgroup of the STK11-mutated patients that are patients with the co-mutation of KRAS G12C. A smaller definitely patient population. We can say today that the selective inhibition of AXL represents an important new treatment option for first-line STK11-mutated non-small cell lung cancer. We aim at targeting a significant patient population with a high unmet medical need where no available targeted therapies actually can improve their prognosis. We know that there is a high incidence of AXL expression that can be targeted by bemcentinib, and AXL is indeed expressed in the vast majority of these patients. Inhibition of AXL, especially from the data just reported, may indeed delay chemoresistance and rescue an antitumor immune response. We have also, as mentioned, a strong proprietary position in STK11 mutated non-small cell lung cancer within the competitive environment. Let's switch gear for a second and assess our strategy in severe respiratory infection. The severe respiratory infection has always been part of the strategy for the development of bemcentinib, and this is really based on the multiple mechanism that bem can have in managing a viral infection. Let me list here a few of them that are particularly relevant across many infective pathogens. Number one is actually the impact on the viral entry and the viral replication, but also the control of the antiviral immune response, and last but not least, the ability to reduce the damage to the lung tissue and to facilitate its healing. This is for us the foundation of our ongoing strategy for the development of bemcentinib in severe respiratory infection. We are aiming at maximizing our understanding of bemcentinib activity on the successfully conducted COVID-19 studies, but we are also exploring other severe respiratory infections with studies in preclinical model in collaboration with leading academic institutions. As we've done with COVID, we aim at leveraging on ongoing and existing platforms really to optimize the efficiency of these studies. I want to remind you that the COVID study is conducted in collaboration with the EU-SolidAct platform in hospitalized COVID-19 patients. For the future, SRI studies, we are aiming and doing something similar to really leverage existing platforms to test relevant pathogens like influenza or RSV. Overall, the strategy will be really to activate and initiate a pathogen-agnostic trial for the treatment of Acute Respiratory Distress Syndrome. Now I would like to hand it over to Martin for his financial remarks and update on the news flow. Thank you, Cristina. This is a snapshot of the financial performance of the fourth quarter but also in totality for the financial year of 2022. The net cash flow for the period in the fourth quarter was NOK 75 million, and we ended the period with NOK 151 million almost in cash. Our burn rate of around NOK 65 million on a quarterly basis is impacted in the fourth quarter by payment of a manufacturing of bemcentinib to support our clinical studies. As we are expensing those costs immediately and not carrying them on the balance sheet, this shows as a rather material deviation compared to the third quarter. If we neutralize for that, the trending burn rate of the company is definitely going down and around NOK 60 million on a quarterly basis. This is showing the summary of the development in our cash position and the cash flow. As I said, we had a quarterly cash burn in Q4 affected by the CMC payment or manufacturing payment at NOK 71.6 million. We ended the period with NOK 151 million or NOK 150.8 million to be exact in cash. In addition to that, as we also announced in the fourth quarter, we secured a NOK 100 million shareholder facility from our largest shareholder. In combination with the cash position at the end of the year, this will fund the company's activities throughout 2023. We expect to have a very interesting 2023 with a number of very significant news flow during the year. In relation to STK11, as Cristina said, we are going to provide further analysis of the RAD-18-008 study at an upcoming conference. We also expect to provide additional updated information around STK11. At major conferences, we will provide additional preclinical data to further understand the relevance of co-mutations, where we now have clinical data from the 008 study. Of course, we expect to get the enrollment going in the first-line setting. In the second half of this year, we will be able to initiate the phase II part based on the three cohorts that we have selected for the I-B. For the severe respiratory infections, we will provide an update on the EU-SolidAct. I think it's obvious to everyone that the pandemic has evolved, and we are monitoring the development in collaboration with the sponsor of the study, the EU-SolidAct platform, and we'll update the market during the first half of 2023 on the conduct of the trial. We also expect to provide additional preclinical information for severe respiratory infections, which will further guide us into the clinical development in, as Cristina said, a pathogen-agnostic approach relevant for a number of severe diseases. We will also report the second line AML data or the 003 data in the first half of 2023 as previously guided, and we expect to present the data from that study and also some other studies that we are finalizing at major conferences in the first but also in the second half of 2023. Quite a number of significant news flow to support the encouraging data we have seen from 008 but also five. We will also provide an update on the status on the partnering effort on tilvestamab, which was initiated in the fourth quarter of 2022. That's the end of the presentation, so I think we can hand over to a Q&A session. Yeah. We have a question about the 008 data. The question is, can you detail the patient outcomes by prior treatment regime, meaning the different cohorts on the 008 trial? That will be part of the analysis that we will provide an update at a conference, going forward, as Cristina said. The analysis by cohort will be part of the total data analysis that will be reported later on. It's a question about recruitment status. What is the recruitment status in the STIC-11 and the COVID study, and can you estimate when these studies will be fully recruited? In the STIC‑11 study, the first-line non-small cell lung cancer sites are activated and actively screening. We don't have a patient being treated at this point, but we expect it to be any day. Depending on the safety profile, we expect that the phase I-B will be fully enrolled in the second half of this year, and we will be able to initiate the phase II-A part also in the second half. It's too early but also outside the guidance we're giving as to estimate when we can complete the enrollment of the phase II-A part. With respect to the EU-SolidAct, I believe that there's also a newsletter that is provided by the EU-SolidAct as a sponsor. There's currently two patients enrolled in the study. The protocol has been amended to allow for the involvement in the disease and hopefully increase the enrollment of eligible patients. It's too early to make judgments on the impact as the amendment has just recently been or being approved as we speak. We want to see the winter wave through before we are making any consideration as to the execution of the study. Again, I remind the audience that it's not our study. It's a sponsored study by the EU-SolidAct platform. You just recently guided on when we can expect the AML data, but it's a question about why we haven't communicated the AML data yet. There is absolutely nothing to hide. It's simply a question of priorities. We have prioritized the RAD-18-008 data, which we believe are instrumental and was instrumental and vital to support our strategy that we guided on in May of last year. We are finalizing the RAD-18-003 data analysis, and we will report the top-line data in the first half of 2023, as we have previously guided. There's no change in the guidance as to when we will report the data on RAD-18-003, and there'll also be data published at major conferences on the RAD-18-003 study itself. Next question is about the cash runway. What is the cash runway, and which milestone can we expect during the current runway? I think I've already addressed the question in my financial overview. To reiterate it, the cash position at the end of the year together with the Seattle loan facility funds, the planned activities for 2023. The milestones, I think I've also walked through. In particular, the milestones that we believe are important are the milestones related to our strategy. The first line non-small cell lung cancer study. In that respect also the 008 full data analysis. For severe respiratory infections, of course, further guidance on the EU-SolidAct and other severe respiratory infections, preclinical data, but hopefully also the ability to announce the clinical program going forward in the second half of this year. It's a question about potential license agreement with tilvestamab. Can you share any details, which type of agreement we can expect for a potential out licensing for the tilvestamab? It's a good question, and the basis for our partnering efforts here is that we want to find a partner who can fully take over the development of tilvestamab. Not in any specific indication, but of course, supported by the data we have already generated in ovarian cancer. We have ongoing discussions, but it's too early to provide any guidance. It spans from small biotech companies to large pharmaceutical companies. Thank you, Martin. That's, completes the Q&A session. Thank you. Thanks for listening, and have a nice day.