Please go ahead. Thank you, Simon, and thank you all for attending this webcast. I know that many of you are shareholders and have been looking forward to this, for SynAct, important day. Publication of our top-line data in RA, and we thank you very much for your support, attendance, and interest. On the call today, I'm joined by our chairman, Dr. Torbjørn Bjerke, and our CSO and founder, Dr. Thomas Jonassen. The program for today is that I will cover a few points on what impact the results mean for SynAct, seen from a strategic point of view, followed by Thomas and Thorbjørn, who will discuss the key results from the RA study in more details. At the end of the session, we look forward to answer your questions and discuss the situation. Please move to slide number two. Just a short disclaimer in relation to forward-looking statements. If you will move on to slide number three. Just a few highlights and background on SynAct Pharma. SynAct is focused on the development of novel and first-in-class agonists that target the melanocortin system. We are a team of three people that have worked together since 2000, and we have been working with this technology for a long time, creating a couple of other companies. 2021 has been an important year for SynAct. We have advanced our three programs into phase II, and in the second quarter of 2021, we have got positive data on the COVID study, including ARDS. Now we are able to present you our RA top-line data. We have just recently completed the development of our tablet and also received further data on our toxicology program, enabling us to develop further and redesign a bit on the nephrotic syndrome. That is a study that we expect we will be able to come with data in the coming year. On the right side of the slide, just a few facts and figures on the company. The company was founded in 2013. We managed to list the company on the Spotlight Stock Market in 2016. We have had a good journey on the stock exchange with a market cap of EUR 350 million at this point in time. We're in a situation where we in the management are top motivated. We hold more than 20% of the shares, and we have more than 11,000 shareholders. We also have a plan for an up-listing to Nasdaq main market during the first half of next year. As I think you all know, today's results have been an important milestone for SynAct, and we are very pleased that we, for the second time, are able to show efficacy in a phase II study. Earlier this year in our COVID virus-induced RDS study, and now in our main study, RA, based on our compound AP1189. This data brings us into a very favorable position and enable us to drive multiple strategies going forward. One strategy is that the data strongly supports further development of AP1189 and enable us to seek scientific advice and open an IND with the FDA to prepare for phase II-B studies. This activity is very important for us, and will bring us into a position where we'll be able to drive the company further and create value during 2022 towards hopefully another round of positive data. In parallel with this, we will advance our other programs in clinical development. The second dimension in our strategic position is that with today's data, we become even more attractive for potential partners. These partners are big pharma companies or big biotech companies, and we have for some time seen a clear interest in different discussions. These discussions will be intensified with today's results, and we hold all options open, ranging from potential licensing deal to full acquisitions. We are now in a position where we will be able to negotiate our strengths and at the same time take advantage of our program internally, maximizing our strategical position. In addition to this, we also see that some of our competitors established in the market with JAK inhibitors have safety issues, and in all honesty, creates many of those improved opportunities for positioning and later commercialization of AP1189. I will now hand over the word to Thomas and Torbjørn, who in greater detail will discuss the key finding of the results. Thomas. Yes thank you very much. Thomas Jonassen here, Chief Scientific Officer in SynAct Pharma. Next slide, please. In rheumatoid arthritis, as most of you know, it is a common autoimmune disease, affecting joints but also with systemic affection. Untreated, it can induce devastating and irreversible loss of function. It affects somewhere between 0.5%-1% of adults in the developed world at one time point in life. Onset of disease is typically what you see in middle age, and it's more pronounced in women than in men. Despite a continued development of new treatments for rheumatoid arthritis, we still think there is an unmet medical need for an oral available agent with the ability to control disease activity without inducing immune suppression and other potential dose-limiting effects. Here, immune suppression means that the effect of a given compound is mediated through inhibition of the immune system to such a level that there is an increased risk for infections. That is one of the things with our technology here exemplified by our lead compound AP1189, which is a novel compound developed for oral once daily development. AP1189 is a biased melanocortin type 1/3 agonist inducing anti-inflammatory and pro-resolving effects. Importantly, the mode of action of stimulating these receptors expressed on the surface of immune active cells including neutrophils, macrophages, and dendritic cells or some subtypes of T cells is that it do not suppress the immune system, but more you consider it as balancing the response. We have never shown that we can inhibit a specific pathway to or rather block it. We can inhibit it up to 50%-60%, meaning that we can reduce influx of neutrophils in a given inflammatory system, but we can never block it. Importantly, we can boost endogenous pathway that helps in clearing the inflammation. Among those we know that we change the phenotype of macrophages, thereby giving them the ability to clear up inflammation. That is what we call promotion of resolution, and that is really a novel way of addressing autoimmune to inflammatory and autoimmune diseases. That is what we currently are evaluating in an autoimmune common disease as rheumatoid arthritis, where we today will present the data from our first clinical study in the patient population, the BEGIN study, which is a phase II-A study. We also address the potential in idiopathic membranous nephropathy, which is an autoimmune disease that causing nephrotic syndrome, meaning that it induce a disease where you have severe loss of protein in urine. In addition to that, and also highlighted by Torbjørn Bjerke and Jeppe Øvlesen, we have tested the concept in COVID-19 patients in a collaboration we called RESOVIR, together with some of our collaborators, Mauro Perretti in London and Mauro Teixeira in Belo Horizonte in Brazil, where we have shown that going in patients with the compound to patients who have an activated hyperinflammatory state with a respiratory insufficiency. We were able to show recovery from the disease, defined as need for oxygen, with almost four days compared to placebo. That's to say again that the concept of this treatment is not to block inflammation, but to go in and modulate an overactive immune system. The aim of the BEGIN study was to compare efficacy and safety of the compound versus placebo in patients with moderate to severe rheumatoid arthritis. Actually, it was defined as severe rheumatoid arthritis based on the inclusion criteria as where the clinical disease activity should be higher than 22. The study design, that's on the next slide, please. Slide five. The study design was that we set up the study in two parts. In part one, where we tested two doses of the compound versus placebo in two consecutive cohorts. First we tested 50 mg versus placebo in two to one randomization, meaning that two patients were treated with compound for every patient treated with placebo. Then we went to 100 that we tested against placebo again. The patient population that we have tested this compound in and was patients with high disease activity, meaning that they had significant clinical symptoms defined as severe rheumatoid arthritis based on a scoring scale called Clinical Disease Activity Index, meaning that higher than 22. These patients were referred to hospital and if they were found eligible for first-line treatment, methotrexate, which is the disease-modifying agent methotrexate, they were offered the opportunity to participate in our study. Then they were in parallel with starting treatment with methotrexate. They received treatment with our compound or placebo for four weeks. The first part of that study that was patients previously treatment-naive, who in combination with our compound or placebo, also started up on methotrexate. We had an interim analysis where we had an independent data management board who reported safety and recommendation for which doses to bring to the second part of the study. The second part of the study was then continued last year, almost just about a year ago, with the recommendation to take those 50 and 100 and test it against placebo. We had a three-arm second part of the study. The data set we are going to present today is data from the full study, meaning both part one and part B, as we did not unblind the part one, but we had for the company or for the investigators. It's the full data set I'm going to present today. As it is a phase II-A study, safety and tolerability is of course very important. We have had specific interest in or a focus on safety profile in this study. In addition to that, we also had a primary efficacy endpoint defined on the CDAI score. In other words, the clinical disease activity index, the scoring system used to characterize the patient's degree of disease has been used to characterize potential efficacy of our compound. There we have the primary readout is, was then defined as mean change in CDAI within the group, and the proportion of patients who went from high disease activity to moderate disease or lower, meaning that we could change the disease from a scoring higher than 22 to 22 or lower. The study was then conducted at sites in the Nordic country, and from the spring, we also included Moldova and Bulgaria. In total, we screened 157 patients, of which 105 were randomized. The reason for the high screening number is that we had built-in to the system measurements of a number of analyses that took data from the screening, and that was analyses relating to whether the patient had or had tuberculosis or hepatitis, which, in those cases, would be exclusion criteria, not only to participate in our study, but also to receive methotrexate. In addition to that, there was also a question of we defined the patient to be patients who had what is called a positive rheumatoid factor, meaning that if it was not positive, then they were also excluded from the study. Then there were patients who at screening were eligible for treatment based on the activity of disease. But at the time of randomization, meaning starting up dosing, the CDAI was too low, so we had to exclude them from the study. Finally, we had a few patients who during the screening period developed uncontrolled concomitant disease that we had to exclude. All in all, we came out to a screening number of 157 with 105 patients randomized. These patients were then randomized in three groups, in placebo where we ended up having 34 patients, in the 50-mg group where we ended up at 35, and in the 100-mg group where we ended up at 36. We had in each group two patients who discontinued treatment, and I come back to that on a later slide. In addition to that, we also had patients who were excluded from the efficacy evaluation due to violation to the protocol. It was in all cases a question of receiving glucocorticoid treatment at one or more occasions, typically by injection into a joint. It was so that we had a total of seven, whereas only one was on the 100 mg group. Simply not to bias the results from any effects of glucocorticoids, they have been according to protocol excluded for the efficacy analysis. Next slide, please. Excuse me, could I have next slide, please? Oh, sorry. Sorry. Here is the baseline results. As in the background population, we had. The number of females were in this case almost 80%. In the background population of rheumatoid arthritis patients is somewhere between 70%-75%. Age, middle age. All, you could say there is no difference in with regard to age, race, weight, or height in these patients. From that perspective, the three groups were very similar. Please, next slide, please. Baseline characteristics with regard to disease. I will today keep it on a very, very high level, focusing on baseline level of characteristics of the patients, high level on efficacy readouts relevant for the compound developed for rheumatoid arthritis, and then also a high level on safety profile. We have not; we do not report any data today on vital signs, but there have been no reports on any signs that in any way could induce that it would be an issue, which was also supported by what we saw in phase I. That's simply because we keep it here to a high level and also in terms of the primary readouts as well as the secondary readouts, we keep it exploratory on a high level. If we look at the baseline level of these patients, and here we have placebo, we have CDAI scoring, which were comparable in placebo and 50 milligrams, but slightly higher in the 100 milligram group. In total, for those of you who have looked into our interim data, this baseline around 37 was slightly higher than what we saw in the first part of the study, where the average level was 34. When you go through the numbers, you can see there is a significant number of tender joint. There is a significant number of swollen joints. If you then look at an alternative scoring for disease activity, the DAS28 scoring, which in many ways is comparable to CDAI, but where you have measurement of, in our case, of C-reactive protein, CRP, as part of the scoring. You also can see that they are slightly comparable, these patients, even though that as for the CDAI, the 100 mg groups numerically were slightly higher. Global disease assessment is scored by the VAS score as well as physician global assessment also by VAS score, also comparable between groups. Finally, you can see CRP here, where numerically is higher in the 100 mg group, but also with quite large variation, which is absolutely what you would expect in such patients as the one that we have included. As I said, there were exclusions. Some of the patients were excluded from the efficacy readouts simply because there was a violation to the protocol. From here, I think we should go to the data. Before that, before we go to efficacy, here is an adverse event profile, where we have, here on slide number nine, we have the adverse event profile. Importantly, we did not see any serious adverse events in this study, meaning we had no serious adverse events in the placebo group or in any of the two active arms. When it comes to adverse events, here, from baseline and on in the study, we had a total number of 21 in placebo group, 38, and 27 in the two active arms. On the next line, you can see the severity of the adverse events from mild, moderate, and severe. You can see that the vast majority of the adverse events were all mild and self-limiting character. Discontinued due to IMP-related adverse events were absent, and we had one discontinuation due to methotrexate treatment in the placebo group. That was what we saw. In total, two in each group were discontinued during discontinued treatment, two due to, or actually three patients decided to do them because they did not want to continue dosing. We had two who very early showed up that in one patient, we had a miscalculation of CDAI, so it was actually not fulfill the inclusion criteria. Another turned up with a very high level of aminotransferase as baseline and were therefore excluded. That was the kind of exclusion we had in the study. With regard to adverse events, the most common adverse event was nausea, but it was divided through the three groups. We believe that it's most likely associated. We know that methotrexate can give nausea, but we also know that a suspension as the one we had used in this study, which will in future development be changed to a tablet that we just recently have developed and reported data on last week, is associated with the risk for developing nausea. That's typically also what we have seen and the experience we had with phase I is that the nausea comes very fast after intake of the medicine, and then typically stays for two to three hours and actually disappears while we reach a Cmax for the compound. It's most likely associated to the formulation. From the ongoing study with our new tablet in healthy volunteers, it seems to confirm that. We also saw increases in aminotransferases. We know that methotrexate can induce increases in aminotransferases. We saw three patients who were reported in the placebo group, six in the 50-mg group, but none on the high dose with our compound. With regard to the level of increases, two in both the placebo and the 50 mg groups were reported as clinically significant, meaning that it increased at least 2.5 time from baseline. In all cases, perhaps one in the placebo group, it was self-limiting, whereas one continued with increased levels after our follow-up visits. I've since then forgotten the confirmation that it continued for a few weeks, and then gradually it returned back to normal. One of the patients in the 50 mg group was an Asian woman in general. Asian population in general do not tolerate high doses of methotrexate, and she was titrated up to 20 mg methotrexate, and when changed to subcutaneous, these increases disappeared. In addition to that, the most common side effects were gastrointestinal adverse events of all kinds including nausea, including constipation, discomfort in the stomach, and so on. That was slightly higher. That was higher on the 100 mg group than in the two other groups. That was our finding. In general, few adverse events, and most of them were mild to moderate in intensity and were self-limiting. Next slide, please. The conclusion for the adverse event profile here is that the compound seems very well tolerated. I will go to the efficacy readout. The primary readout was changes in disease activity. As I said, the patient were included based on clinical disease activity index, which is a way to calculate the patient's disease. What you do is that you measure the number of tender joints, swollen joints, and then using this VAS, visual analogue scale, both for the investigator and patient to give a number of the severity of disease at a given time point. You simply add these numbers, and then you end up with the baseline level, which were 60, 36, and 39 in the three groups respective. This slide here shows the treatment effect. How much had the CDAI changed from start of treatment to end of treatment. You can see here that we had 9.3 point reduction on average in the placebo group. We had 12 points reduction in the 50 mg group, and we had 15.5 points reduction in the 100 mg groups. That reduction in disease activity were clinically significantly different from the placebo effect. The placebo effect is, of course, an effect combined of placebo and initial effects of methotrexate, which in general rule works in initiation of efficacy starts quite slow. Four weeks treatment with methotrexate placebo, 9 points reduction. 100 milligram combined with our compound combined with methotrexate, 15.5 points or it was also expressed the other way around that we had a more than 60% increases in activity that showed to be statistically significant. Before going on to the next slide, I would like to just comment on this effect and then compare that to what we saw in the first part of the study. In the interim data, as I mentioned, the baseline was slightly lower than we see now here in the full study. I've been into now and looked into the interim data, 15.2 in the 100 milligram group in the part one of the study reported in interim analysis were 15.2 points, meaning that it seems to be quite a consistent response on this compound. Next slide, please. On the next slide here, we show the fraction of patients who go from high to moderate disease. What we see here is that we have 40% responders in the placebo group, meaning that 40% of the patients in the placebo group went from high disease activities to moderate or lower disease activities. On the 50 mg, where the response in actual numbers were numerically higher than the placebo group, we also saw a higher response rate with regard to go from high to moderate disease, as it was as high as 62%, which were comparable to what we reported in the interim analysis in this dose. On the highest dose, where the baseline level were somewhat higher in the full data material, and the response and the change in disease activity in the group were higher, then we had a response rate of 52%. On this specific readouts, we were not able to show statistical significance, which would have meant that we should have had an average of the two active groups around 70%, which were the case in the interim analysis. Still, we have a statistically significant reduction in disease activity on 100 mg. But as there were more disease than the other group, it most likely explain why the response rate were 52, which is still quite attractive. When we then go to the next slide, here is another scoring system. In this case, we use the DAS28, which again also is based on swollen and tender joint, as well as disease activity by the investigator and the patient. In addition to that, you also build in changes in C-reactive protein, indicating that you have a modulation of the inflammatory response in the body. In here, you see that at the end of the four weeks treatment, then 23.3% of the placebo-treated had moderate disease activity overall. We had 37.8% in the 50 mg groups, and we have as high as the 51.5% in the 100 mg group. Here we have, as we had for the reduction in CDAI, a very nice dose response from the two active, showing the treatment potential of the compound. As this study was not dimensioned to show changes in DAS significantly, changes in this score, it did not reach the statistical significance, but very clear trend. Next slide, please. This slide here shows the ACR score. That is the American College of Rheumatology's classical scoring system for treatment effects in rheumatoid arthritis. Like the other scoring systems, it's built on both clinical activity as well as measures of inflammation. Here we show that 25% of the placebo-treated had a 20% or higher, a minimum of 20% improvement in disease activity following the four weeks treatment. We had 31% in the 50 mg groups, and the 100 mg group, we were as high as 48%. We are still looking more into the ACR scoring, which is for sure more suited for phase III development than dose finding, where both the U.S. FDA and EMA recommend that you use the scoring system as DAS or CDAI, as that gives a direct number of patients who go from one level of disease to another. Like for the DAS score and for the changes in CDAI, we here see a very nice dose response indicating that 100 mg is effective as a suitable compound or dose to go forward in further development of the compound. If we go to the next slide. Fatigue is a significant issue for rheumatoid arthritis patients. A way to score the level of fatigue is to use the FACIT-Fatigue score, which is a questionnaire combined with evaluation of fatigue and in total, a compound with the ability to reduce fatigue is of significant interest for patients with rheumatoid arthritis. Here, it is the higher number the better treatment effect on fatigue. As you can see here, we had an almost doubling up of the level of improvement on the 100 milligram group compared to placebo, and again, a clear dose response. If we then go to the next slide, there is the patient's evaluation of pain based on VAS score. What you can see from this data is that you have a 0.9% reduction in the placebo group, where we have all the way up to 1.8% reduction in the 100 milligram group, and again, a very nice dose response. We think that this actually is significant for the patient as pain is an issue. To have a reduction like this for a four-week treatment is not bad. We look very much forward to dig into this moving forward with the compound in later clinical development. Next slide, please. In summary, we have much more data that we are looking into subgroup analysis and also more severe cases and trying to get more understanding on that in subgroup analysis. From high-level data, we can conclude that in a four-week study, patients treated with once daily 100 mg AP1189 achieved a significantly greater reduction in mean clinical disease activity score as compared to placebo. We also evaluated the changes in disease activity in the ability to move the patient from high to moderate disease. There were numerically higher numbers in the two active treatment groups, but it did not reach the statistical significance. It could most likely be explained by a higher baseline level in the CDAI group and also potentially a higher level of inflammation at the starting point. In any case, we had consistent dose-dependent result effects seen on secondary readouts, including disease activity score, the DAS28, ACR20 score, and the fatigue, FACIT-Fatigue Score, as well as on pain that I also showed data from. Importantly, from a safety perspective, the compound was well-tolerated and presented with a favorable safety profile. We saw no serious adverse events reported in the study. Based on this, on these positive results, we intend to continue or at least plan for continuing development of this compound. The first next step will be to go to FDA, open an IND, and during that process, discuss the development program and thereby preparing the compound for phase II-B development. With that, I will give the word to Torbjørn Bjerke, the company's Chairman. Thank you very much, Thomas. Let us go to slide 17, please. This is quite a busy slide. Sorry for that. I will make some take-home messages on that. One of them is that despite the vast opportunity we have for the treatment of rheumatoid arthritis today, there are still a large percentage of the patients that do not achieve remission, meaning that they do not get rid of their symptoms. In addition to that, we have several treatments that do have severe side effects. I guess that quite a few of you have read about the JAK inhibitors that emerges on the treatment of rheumatoid arthritis these days. However, they are linked to severe side effects, which actually also FDA has noticed quite severely and made black box warnings. Despite the fact that we have both antibodies, we have small molecules like the JAK inhibitors, there's still a big medical need, and there's a big medical need for a new treatment concept, we believe, that are linked to a good efficacy, however, with a very good safety profile. Why do we believe that AP1189 has multiple opportunities in the management of RA? Why do we believe that the compound could have an attractive treatment in RA? When you look at the drug development, I've been in this industry for quite some years. What is important when you get results like we did in this current study, it's important to say, "Okay, do these results justify further development? And how is the emerging profile of AP1189, how does it fit into this treatment paradigm of rheumatoid arthritis, as well as, I would say, other inflammatory diseases, severe inflammatory diseases?" As both Jeppe and Thomas alluded to, this is our second proof of concept in severe inflammatory diseases. Going back to the emerging profile, what we can see today with these results in BEGIN is quite a fast onset of action, and this is very important for the patients in order to get rid of the symptoms as soon as possible. We must remember that this first study is a four week study. Next study will be longer, and we believe that could potentially also increase the efficacy of the compound that we see from the BEGIN study. Fast onset of action is important. Very good safety profile. This is important in several aspects. One, this is a chronic treatment, so it is extremely important that the compound is safe. What we have seen so far with 1189 is a very clean safety profile, as Thomas alluded to. This is also important when we look at normal treatment concepts today, combination treatments, and this is actually what we did in the study. We combined with methotrexate, and despite that, we get a good safety profile. The third one, which obviously is extremely important, is a good efficacy. What we see today, and what we have presented for you today, is a consistency in results, and this is also very important in drug development, that you see consistent dose response in an early study like the BEGIN study. This gives quite some opportunities in order to see and plan for the next study with AP1189. This could really fit very well into this $28 billion market that we have in RA today. If we can continue to show a profile like I just went through, we do believe that AP1189 could have an important place in the treatment of RA. Let me also say that the last year we have actually prepared for success, meaning that we have developed the tablet formulation. This study was done with a liquid formulation. A commercial formulation is a tablet and once daily. This is a good profile of a treatment in RA. We got some astonishing, fantastic results comparing the tablets with the suspension, and this is important. Next study will definitely be done with the tablet formulation. We have done toxicology in order to do longer studies, and this toxicology was very clean, and that means that we are now ready to go into the next phase, being phase II-B. In addition to that, we have also strengthened the intellectual property, the patents, around AP1189, which obviously is important in order to be a commercial attractive opportunity in the marketplace. What we will do now is really to think about what will the next study be. As Thomas alluded to, we need to digest all the many data we have. We need to do sub-analysis in order to really learn about the data. We need to talk to the FDA and other regulatory authorities. In addition to that, we will also do market research in order for us to learn how the key opinion leaders out there treating all these patients, how they look upon the profile or the emerging profile of AP1189. These are all these puzzles that needs to go into a good next clinical trial. As Jeppe also said, in parallel we will be talking to interested parties from both big pharma as well as big bio in order to get their feedback on our plans and their potential interest. With the data today, we have made a big step towards a potential new treatment in rheumatoid arthritis, but in addition to that, also other inflammatory diseases which could impact the life of many patients around the world. With that, I think we should leave the word over to Simon and open up for questions. Please, operator. Thank you. If you do wish to ask a question, please press zero, one on your telephone keypad. If you wish to withdraw your question, you may do so by pressing zero, two to cancel. We will take a brief pause while questions are being registered. Our first question comes from Sebastiaan van der Schoot with Kempen. Please go ahead. Hi, good afternoon, everyone. Hi, team. Congrats on the data, and thank you for taking my questions. First one, does the current data stack up against the standard of care, seeing your trial design uses a four week treatment period in treatment-naive patients, while most studies that are now approved use a 12-week design, and in patients that have an inadequate response to MTX? Should I take that? Yeah, Thomas. For sure. I mean, in order to a phase II-B study, which would be the next natural step for this compound, should also be a 12-week study. We have, as we have alluded here during both this call and during the autumn by communication with Mauro, we have now developed the preclinical development as well as our new tablet formulation brings us in a position to set up a phase II-B study with 12 weeks treatment will be a natural next step. We fully agree with you. Nevertheless, we do have here a compound that shows following four weeks treatment, a very good safety profile and also with efficacy of this reduction in 15.5% is clinically relevant and comparable to what we have seen with other drugs. Sorry. I think that the answer is yes, we have the next step would be to conduct a three-month study as you would do according to regulatory guidelines. Okay. Great. Thank you. Sebastiaan, it's Torbjørn here. It's of course difficult to compare apples to oranges or whatever. When we look at the four week results we have with the BEGIN study and compare that to, for example, JAKs at the same time, there are some data showing JAKs after four weeks. We find it quite comparable, and JAKs are known to be quite effective. However, we do believe that so far we do differentiate on the side effect profile being quite clear. Okay, great. Thank you for that, clarification. To follow up on that last point that you made, would you say that the four-week treatment period is long enough to make meaningful conclusions regarding the safety of the compound? Do you also see safety issues already at four weeks for JAK inhibitors, for example? We do see with regard to let me start with JAK inhibitors. Yes, you do see side effects after four-week treatment. Is four week treatment enough to give us a full impression of adverse events and the safety profile of compound? No. But four weeks with a very clean safety profile is a very good start. From an efficacy point of view, we hardly have reached that in this four-week study. We have a substantial effect already here, and most likely, we haven't reached the full efficacy. Okay. Thank you. Yes, yeah, very clear. Thank you very much. Regarding the gastrointestinal effects, can you maybe comment on whether those effects are also related to the formulation or- We believe it is. Likely. But, but- Okay. I mean, it is well known that oral formulation as the one we have used is not something that you would use for continued dosing simply because it gives nausea and also gives other gastrointestinal symptoms including pain and discomfort. That is the obvious. The patients have also reported. That is that kind of side effects we see. Importantly, we now have the tablet and what we have seen there for the healthy volunteers is really that these side effects, that means that we can induce with the suspension is absent when we go to the tablet. Okay, very clear. Would you be able to go straight into the phase II-B study with a tablet formulation, or would you first need to perform a similar four-week study? No, we could go directly into phase II-B. The beauty about this study that we have in here, that we have ongoing, is that the first part we re-reported, we had 12 healthy volunteers where we had them in, each individual got three doses, two different tablets, as well as the suspension. That means as we have a fantastic PK profile, we can make calculations to equivalent doses and then go directly into phase II-B. Okay. Clear. What do you feel would be the next logical study design for AP1189 in rheumatoid arthritis? I know that you already alluded to it a little bit, but maybe you can also give some guidance on timelines. I think that a next logical step would be to make what you alluded to previously would be an industry standard 12-month study, 12-week study in patients in methotrexate treatment with inappropriate response. Meaning that so compared to what we have done here, now we have shown you could say treatment naive as a co-treatment with methotrexate. An attractive way of doing especially if we can control side effects in such a dose regimen. From an industry approach and what we know would be something that potential partner would look into and would like to see is three months data in this DMARD non-responders or inappropriate responder. Patients who have been treated with methotrexate for two to three months and still have significant symptoms, meaning that the compound do not work. The alternative would be second-line treatment. That would mean biologics until recently, and also potentially JAK inhibitors. That would be a natural next step to test the compound in such a setting. Okay, great. My final question is regarding the AP1189 program in COVID-19 and membranous nephropathy. Can you maybe expand a little bit on what your plans are now for those programs? Let's start with the COVID-19. There the plan is to continue development. We find it natural to. A next step would be using the tablet in patient and confirm the data that we generated in the RESOVIR-1 study, which were conducted in Brazil. We are in the planning phase for continuing development. As we alluded in a press release a few weeks ago, we will on, as soon as we have the results here from the rheumatoid arthritis study, the BEGIN study, we will come back with more detailed plans of what next to do. Virus-induced inflammation, hyperinflammation, including respiratory insufficiency, as we see in COVID-19, is a priority area for us. I think it will. We all believe and intend to continue development in that area. You also asked about the nephrology study. Yes, we have generated data in four weeks treatment in idiopathic membranous nephropathy, and we were limited to dose for four weeks simply because it was a question of having the preclinical documentation for longer treatment periods available. Now we have that with a very nice safety profile in the animals. We also have the tablets. Instead of continuing the study and then it would simply for our. Would be a logical consequence of that to redesign and go for longer treatment periods, as that would be much more relevant for the patients as the onset of action is present early with stimulating immunoglobulin receptors in nephrotic syndrome patients, especially in idiopathic membranous nephropathy. The full efficacy is not reached within a four-week period. It would simply be logical to go out and then make a full proof-of-concept instead of a proof-of-principle PK study as a start. We have decided to redesign the study, and we will also come back with details about that in the near future. Okay, great. Thank you so much, and congrats on the data again. Thank you very much. Our next question comes from Adam Karlsson with ABG. Please go ahead. Hi guys. Thank you for taking my questions. Just a few if I could. A first question on the methotrexate dosing. Was there any difference in the doses used across different treatment groups in terms of up or down titration during the treatment period? The answer is in the Nordic country up titration on methotrexate follows the current guideline where the ambition is to go for approximately 10 mg up to 20-24 mg, 25 mg and even up to 30 mg within four, six weeks. In Nordic country here we have quite an aggressive increases in methotrexate, whereas in the Eastern European sites they tend to but not restricted to the more traditional approach where you increase doses every four weeks. Potentially, yes, there is a difference, but without having the full overview at this time point, it seems not to be so that we have marked changes in responses, but that is for the future to decide. I'll find out. Okay. Gotcha. Thank you. I know you're going to do an analysis based on polymorphism, but based on the top line data that you have so far, have you seen any kind of interesting trends in terms of responders and non-responders and if there's any kind of baseline characteristics that predicts response or so? We know that we have, as we also reported previously in the phase I for the part one of the study on the blinded data, we have a subset of patients who respond really well. We have and that means that they go within four weeks treatment, they reduce clinical disease activity for up to 30 points or more. If we go into that analysis, it's very clear that looking at the picture of the different groups, there is a higher number of placebo-treated patients who do not have a reduction in CDAI at all. Whereas we have on 100 mg better than 50 mg, we have some patients who respond really significantly. We are generating a picture where we can see that there is like a cutoff of around 15 points. If we come up there, then it's almost only on the high dose. It's still too early to say whether that has anything to do with specific phenotypes or polymorphism on the receptor, but that is for sure. We know it's part of the overall study to make correlations to efficacy versus polymorphism on the receptor. Okay, great. Maybe just a final question. We've seen that the 100 mg group had more severe disease at baseline, higher inflammatory markers, which would be, you know, a plausible explanation for that group not showing the same kind of improvements as it relates to the CDAI 22 cutoffs that we saw in the Part 1 data. Conversely, could the fact that they had more severe baseline disease and higher inflammatory markers also mean that they would be more likely to be able to show a high means for reduction in CDAI? Could that have kind of skewed the data in favor of the 100 mg group, if you see my question? Yeah, I do understand the question and I think it's kind of the same way that Sebastiaan from Kempen in his update on the results here this morning interpreted the data that could be a potential way or explanation. What I can say is that we are digging into that. We know that we do have. The first way to look into it would be to look at the data in the interim analysis for the part one of the study, because there the data, the baseline were somewhat lower. I think we have reported it was 34 on average. I have just been able to look into and make that sub-analysis and see that the 100 mg response, the delta value in the 100 mg group, that it was only eight patients, but it was 15.3, and that was from a lower level. That talks against that hypothesis. I cannot say whether that's right or it's wrong, but it logically, or at least from the data we have right now, it seems not to support that notion that the higher disease you have, the easier it is to induce an effect. Okay, great. Thank you very much. That's all for me. There are no further questions. I hand back over to our speakers. Jeppe? Yes. Okay. Thank you very much for all of you listening in. I think we will conclude the presentation here. It is 4:00 P.M., and I think the time's up. Thank you very much, all of you, for listening in. Thank you.