Afterwards, there will be a question and answer session. Renée, please begin. Thank you very much, and welcome to Calliditas' Q4 2020 report. As you are aware, obviously, there's a disclaimer. During today's call, we'll be making certain forward-looking statements, may include statements among other things about the timing, progress, or results of our ongoing Phase III clinical trial for Nefecon, development plans for setanaxib or any other future product candidates, timing, scope, likelihood of domestic and/or foreign regulatory filings and approvals. Those forward-looking statements are based on current information. Assumptions and expectations are subject to change and involve risks and uncertainties that may cause the actual results to differ materially from those contained in the forward-looking statements. These and other risks are described in our periodic filings made with the Securities and Exchange Commission, including any quarterly and annual reports we file. You're cautioned not to place undue reliance on these forward-looking statements, which are only made as of today's date, and the company disclaims any obligation to update such statements. With that, I would like to take you to page three, just to remind those of you who may not be familiar with the company, that we are a late-stage biopharma company w e're focused on novel treatments in orphan indications. Our lead candidate, Nefecon, is a proprietary novel investigation treatment for IgA, which is intended to be disease-modifying, and this is because we are targeting the origin of the disease, and the disease in question, obviously, is IgA nephropathy. This means that we are not delivering drug to the kidney, but actually to the ileum in the gut, in order to really disrupt or interrupt the very beginning of the disease process. Nefecon, which is our lead candidate, is the most advanced product candidate. We are at position to be the very first approved drug for IgA nephropathy, which is very exciting. We have carried out a Phase III trial t his is obviously what this quarterly report is going to focus on mainly, as we read out very strong and positive data in November of 2020. We are planning to file for regulatory approval both in the U.S. and Europe in Q1 and Q2, respectively. We also believe there's a significant unmet need in this indication, and we believe that there's a very significant commercial opportunity available for Nefecon if it was to be approved. If you turn to page four, this really is a design of the Phase III clinical trial, because as I said, we read out top-line data of this trial in November of 2020. The design of this study was virtually identical to the Phase IIb, which also met both its primary and secondary endpoints, and which was published in The Lancet in 2017. This was a 200 patients in what we would call the Part A, this is the basis for efficacy, safety, and market approval. It's a global trial in 19 countries, across just under 150 sites. The trial is looking at dosing of 16 mg of Nefecon versus placebo on the background of an optimized and stable RAS blockade. Patients were treated once daily for nine months, after which the primary endpoint of proteinuria was read out. If we turn to page five, this is a summary of the clinical trial results of the study NefIgArd. This is obviously randomized, double-blind, placebo-controlled trial. What we saw in terms of the primary endpoint was a 31% reduction in the treatment arm versus baseline. What we also saw in the treatment arm with regards to the secondary endpoint, namely eGFR, was that the treatment with Nefecon stabilized kidney function, which in contrast to the placebo arm, where there was a continuous deterioration of the kidney function in the placebo group, which was about just over 4 mLs per minute at the nine-month endpoint. What we saw, obviously, was a very statistically significant 27% UPCR reduction, Nefecon versus placebo, and also statistically significant eGFR stabilization with Nefecon compared to placebo. These results were obviously w e were very delighted to receive these results. They are obviously completely confirmatory of the Phase IIb data that we had previously shown. Actually in terms of the reduction versus baseline, we actually saw a slightly stronger reduction here of 31% versus 27%, which is what we saw in the Phase IIb. Obviously, the ultimate treatment goal for this disease is obviously to protect the kidney function, and to have this result of being able to see no further deterioration in the treatment group, we were obviously delighted in order to be able to report that out. In terms of some other kind of details around the trial, and if you look at page six, this just really shows you the demographic characteristics of the Phase III versus the Phase II trial. As you can see, and as we have previously been communicating, obviously this patient population was slightly sicker. This was obviously a consequence of the fact that there were some KDIGO guidelines that were introduced between the beginning of the Phase II and the Phase III, which led to a higher kind of inclusion criteria in terms of UPCR for Phase III, as well as the fact that we slightly lowered the cutoff in terms of eGFR from 45 to 35 mils per minute in the Phase III. If you turn to page seven, with regards to the safety profile, there were really no surprises. It's generally well-tolerated, basically in keeping with the Phase IIb results. As we all know, budesonide has very poor bioavailability, and therefore this type of safety profile is what would be expected. The most common adverse events were similar to those which were observed in the NefIgArd. There was a lower frequency in reporting of some of these adverse events, and this we put down to the fact that obviously the Phase IIb design was fairly unusual, in that it had a solicited adverse event reporting, both in terms of potential glucocorticosteroid-related and GI-related adverse events. We also saw similarly, no adverse clinical effects on body weight, on blood pressure, or on HbA1c. Again, this is obviously completely different type of profile compared to that type of profile which we are familiar with regards to high-dose systemic steroids, where there is indeed a significant impact both on the metabolic and cardiovascular system, as well as severe infections, et cetera, which we obviously saw none in the Phase III. Turning to page eight, just again, some general more information about the Phase III. This just lays out the discontinuations, both in terms of the study treatment as well as the study itself. Obviously these numbers are very low. Actually the discontinuation study is about just over 3%, and the total discontinuation study treatment is 9%, which is a very, very significantly different number than what we saw in the Phase IIb, which again, our thesis had been for a long time that the design of the study clearly impacted some of those outcomes. That really is a little bit about the kind of actual data and readouts and numbers, et cetera, of the Phase III. What I now want to do, just to spend a couple of minutes on what kind of implications or what this can be translated into, potentially using a variety of different frameworks and publications. If we turn to page nine, this is something that I'm sure a lot of you will be familiar with t his is the trial level assessment. This is the meta-analysis framework which we collaborated with a variety of universities on and a ctually, the original, version of this was published by Inker et al. in 2016. It was this framework which the FDA then accepted as a basis for kind of looking at proteinuria as a surrogate endpoint. The FDA has since obviously continued to work on this and developed this framework, both in the context of NKF and, again, working with the various universities and other academics. This is an updated version t his is actually another publication from 2019, which also includes additional interventional studies in IgA nephropathy. The head author here is Thompson t his is Aliza Thompson, who's the Deputy Head of the Cardiorenal Division. With this as a background, this obviously framework looks at the correlation between kind of really looking at the treatment effect of proteinuria, which translates into a certain hazard ratio on the left. As you can see, there's a line that runs through this that actually shows the actual kind of line that shows the correlation between a reduction in proteinuria and a reduced risk of ending up in end-stage renal disease. With this framework, which is obviously well-known and published in journals, et cetera, and has been discussed at a variety of workshops, which the FDA and EMA, NKF, et cetera, have organized. If we turn the page, what we can do then t his is a slide which we also showed in our recent R&D day. It's really an illustration of what kind of an impact one could expect if one uses this type of framework that we just talked about in terms of seeing what clinical impact one might expect from a reduction in proteinuria. For those of you who listened in or attended the R&D day, this was actually part of Professor Barratt's presentation at our R&D day. There was a similar presentation that he had made at Travere's R&D day in 2020. What this really just looks at is to say, depending on the kind of reduction in proteinuria that is seen in a clinical trial, and this assumes that is on top of standard of care. One will get a certain hazard ratio when you put that number into the framework that I just reviewed with you, and you read out there from the y-axis what the hazard ratio is. This looks at the different hazard ratios that one would arrive at various kind of treatment effects. As for Professor Barratt's description, obviously, there is some data that comes from the University of Leicester, which actually then provides a kind of a framework in terms of progression without intervention. This would basically be the reflection of a hazard ratio of one. This would show that approximately 50% of the population would progress and have an event, and in this case, an event is described as a composite endpoint of end-stage renal disease or doubling of serum creatinine. This would then result in about 50% of that population ending up in end-stage renal disease or having this doubling of serum creatinine composite endpoint approximately in excess of 12 years. This was actually the slide that was discussed by Professor Barratt at the day. Looking at the difference then with regards to different levels of proteinuria reduction. Obviously, in this framework, one can see what the estimated delay of disease progression then is. As we also mentioned at the R&D day, obviously there is a treatment effect at nine months versus baseline as we have just covered but a lso, obviously, not all patients had reached 12 months at the time of the database lock. Based on the trends of those patients who had reached 12 months, we would estimate that entire cohort would end up somewhere between 42% and 48% at 12 months, which obviously then would translate into a very significant delay in terms of disease progression if one uses the model and the framework on the prior page. This would basically indicate that the treatment effect that we can see and also then in terms of some trend analysis we would expect to see, really would provide somewhere between 15 and 20 years delay with regards to disease progression. Another very important element of this, obviously, of looking at this, if you turn the page, is also obviously the eGFR information from the trial. What we have here is another publication that we also discussed briefly at the R&D day, which again comes out of the work that has been done with ICHOR and also with NKF as well, which is a broader look at kind of CKD, which is also something that the FDA obviously had been part of. These type of publication would say that actually the impact on eGFR at one year is highly predictive of the outcome of eGFR at two years. What we can see here in this kind of ICHOR, this is the ICHOR paper that we’re referring to in terms of broader CKD analysis, shows that this is a one-year slope. If the one-year slope is 1.31 mils per minute- -at one year, then there is an extremely high probability of 97.5% that there will be a delay in the clinical endpoint, and this is the same clinical endpoint that I just discussed on the previous page of ESKD, so end-stage renal disease or End-Stage Kidney Disease, or doubling of serum creatinine. Obviously, we were delighted and very excited in order to see that in the NefIgArd trial at nine months, the difference between Nefecon and placebo obviously was very significant, which represented 3.87 mLs per minute. Again, this is something that adds to the robustness of the data set that we obviously are very excited to be able to enter into discussions with regulatory agencies with regards to. In terms of conclusions on page 12, we believe that there is a robust demonstration of efficacy, both in terms of reduction in proteinuria and very importantly, eGFR stabilization, which obviously in this kidney disease is the ultimate treatment goal i t is to protect the kidney, and thereby delay any further or prevent or delay any further deterioration in kidney function. Tolerability and safety profile was in line in keeping with the Phase IIb, as we've discussed, and very much what would be expected from an active ingredient that has very poor bioavailability. It is also highly consistent between the two trials t here is a broad patient population that shows extremely similar outcomes across the Phase IIb and Phase III. With that, I would like to just spend a couple of minutes talking about the next steps. Obviously, we will submit to the FDA regulatory file for accelerated approval of Nefecon in Q1. If priority review is granted, this would actually position us for potential commercialization in the U.S. in Q4 of this year. We are also on track with regards to the submission to EMA, our regulatory filing, and we will also be requesting accelerated assessment i f that is granted, that could enable us to have an approval as early as Q1 2022. I said we are very much looking forward to our interactions with the regulators based on the robust data package which we have. We're also continuing obviously to build out our organization in the U.S. in line with our communicated plans. We are very excited about the feedback that we are getting from nephrologists through MSLs following the Phase III data readout. With this, we will change tack a little bit and just give you a brief update on the Genkyotex transaction. To remind you, we effected a control transaction of 67.2%, which concluded in 3 November, and that was followed by simplified mandatory tender offer, which closed on 11 December, resulting in a total ownership in Genkyotex by Calliditas just over 86%. We obviously plan to continue to increase our ownership in alignment with originally communicated intentions with regards to this transaction. In terms of operations, the work is continuing with regards to additional compounds from the platform, as well as all the preparatory work with regards to starting our clinical trials in the second half of this year. That work is all on track. The collaboration is working well. If you turn the page, this is really also just a reminder in terms of the mode of action of setanaxib, which is the lead candidate here. There's also been actually a recent forma article of NADPH oxidase inhibition in fibrotic pathologies, which actually provides a very interesting overview of the role of NOX enzymes in a variety of fibrotic diseases. As you can see on this page, in terms of page 15, this covers the NOX enzymes impact across both lung, liver, and kidney diseases and so w e are excited about the continued work on setanaxib that we will be carrying out, as I said, towards the latter half of this year. On the next page, just a very brief summary in terms of the clinical activities. Obviously, we have an ongoing Phase III trial, t hat Phase III trial is fully recruited as of January of this year. All 360 patients have been included and is therefore on track to complete early 2023. We have, as I just mentioned, plans to launch a clinical trial with setanaxib o ne would be it's an adaptive pivotal trial in Phase II/III pivotal trial in PBC, which we would launch second half of this year, as well as a proof of concept trial, which we also plan to launch before the end of the year in oncology m ore specifically in head and neck cancer, in conjunction with immunotherapies. There are obviously two investigational studies which are still ongoing, one in DKD and one in IPF t he IPF study started recruitment, as you may remember, in Q4 of 2020. Obviously, we also have started our open label extension of NefIgArd. We have several patients who've enrolled, and we have dosed the first patient in early February. We would expect a high level of interest from patients based on what we see to roll over into the open label extension after their completion of the Phase III trial. We're also planning to start the NefXtend trial this year, which will be more continuous dosing, longer term dosing using Nefecon. With that, in terms of any post period events, obviously there was the readout of the Genkyotex Phase I study, which provided a pathway really for these trials, which I've just covered. We also, as I mentioned, completed the enrollment as well as the first patient in open label extension. With that, I would like to hand over to Fredrik to take us through the financials. Thank you, Renée, good afternoon, everyone. I will present to you the financial overview for the full year of 2020. All numbers presented to you are in million SEK as usual. To start with, we reported limited revenues in the period of SEK 0.9 million due to the delivery of Nefecon to China for use in the Chinese arm of the NefIgArd study as part of the license agreement with the partner Everest Medicines. Our total operating expenses for the period amounted to SEK 380.6 million compared to SEK 212.8 million for the same period last year. Out of the total operating expenses, the cost for research and development increased by SEK 91.6 million -SEK 241.4 million compared to SEK 149.8 million for the same period previous year. The increase in R&D expenses originates from the increased clinical activities in the NefIgArd trial as we read out Part A and almost fully recruited the remaining 160 patients during 2020, also due to large efforts in the cooperation in the clinical, regulatory, and product development organizations as we are preparing for the regulatory submissions to the FDA in Q1 this year. During the second half of 2020, we also started preparations for the clinical add-on trials, where we dosed the first patients in the open label extension in the beginning of this year, as Renée just mentioned. The sales and administration costs amount to SEK 141.7 million for the period, to be compared with SEK 62.9 million for the same period last year. The increase of SEK 78.8 million between the periods is primarily related to the increased activity and headcount increase in the organization generally, including the increase cost for pre-commercial activities in the U.S. as we grow in all areas and preparing for the potential commercialization in the U.S. Some activities we performed during the year was the [Unintelligible] in the U.S. and acquisition of Genkyotex as the most prominent ones. These have also contributed to the increase in the administration costs. This leaves us with an operating loss of SEK 379.7 million for this period, compared to an operating loss of SEK 28 million for 2019. Remember, we had SEK 184.8 million in revenue included in the P&L from the China deal in 2019. The cash flow used in operating activities for the period amounted to SEK 309.2 million, compared to SEK 71 million for the previous year. The increase in the operating cash flow used for this period is mainly related to the increase in operating expenses. For 2019, as I just said, we had a SEK 15 million upfront payment received from Everest. Our net cash effect from our investment and financing activities combined was SEK 596 million, and this is mainly due to the U.S. IPO on Nasdaq in June, where we raised a gross amount of SEK 891.4 million, less the net cash effect of SEK 254.8 million used in the Genkyotex transaction. Part of our U.S. IPO proceeds have remained in U.S. dollar positions to ensure we control our cash reach, since the buildup of our U.S. operations means cost in U.S. dollar. Having a balance sheet with SEK as accounting currency and with the weakened USD to SEK ratio, we saw in the period financial expenses of SEK 56.4 million due to unrealized foreign currency losses on cash accounts. Our cash position remains very solid, as we had a cash position of SEK 996.3 million at the end of December. This was all from me. Now back to you, Renée. Thank you very much. With this, I would be happy to hand over to the operator to take any questions from anyone on the line. Thank you. Our first question comes from the line of Maury Raycroft from Jefferies. Maury? Okay, we'll try the next question from Annabel Samimy from Stifel please go ahead. Hi. Thanks for taking my questions. Thank you also for laying out the eGFR predictive capacity from the study over there i t was very interesting. I was just curious on that. Did FDA require for you to have met that eGFR secondary to be able to file? or was that a nice to have? I guess, in other words, does that make your filing that much more robust since you had met that eGFR stability in the secondary endpoint? That's my first question, and I have some follow-ups. Okay. There's a couple of answers to this o bviously, the primary endpoint is reduction of proteinuria. This is a supportive secondary endpoint. On the other hand, obviously, this is an orphan disease, and I think the agency has always been very clear about the fact that they would like to look at the totality of the data. Obviously, eGFR is a very important component of what they're looking at as they're trying to assess the data package in its totality. And eGFR, the fact that we've seen such a robust impact on eGFR obviously provides, I guess in my view, certainly adds significantly to the robustness of the data package that we can provide to the regulators. Okay, great. Just on the different types of studies that you're conducting right now y ou obviously have the Part B of the study that's fully enrolled t hen you just started dosing the OLE study. It seems like both of them are enrolling patients from Part A a re we going to see data from the OLE study? Can any of that data potentially derail the Part B or the analysis of Part B? Are they including the same patients? Is it separate patients from Part A? I guess I'm just trying to understand the difference between those two studies and when we might see readout of the OLE study. Sure. In order to qualify for inclusion in the open label extension, you must already have completed two years of treatment in NefIgArd. So basically, all patients are already recruited into Part B. Obviously you wouldn't be qualified to enter into the open label extension until you've completed the NefIgArd study. It is, per definition, the same patients i t's just a timing issue y ou have to go through the treatment first before you go into the open label extension. I see s ince it's open label, are we going to see any data emerging from that before we see the outcome of the Part B study? I guess my view would be most likely not any significant data, because obviously, it is an open trial, so obviously we have different opportunity to report data out on that versus a blinded trial. In order to, obviously, what we're looking at here is also looking at retreatment versus naive patients who've had to been on placebo. I think in order for us to get to a relevant data set, we would need to have a fair amount of patients included in that. Also they would obviously then have to have gone through their nine months of treatment. It wouldn't be my expectation that there would be any kind of significant announcements around the open label extension, until there's a completion or very close to a completion, I guess, of the Part B. Okay. If I may, one more question. I just want to know the difference between the discontinuations that you showed y ou had 5.1% related to AEs, but then you had the full analysis set of 3.5% c an you just explain to me the difference between the 5.1% and the 3.5%? what is the full analysis set? Sure. That you're talking about here? Yeah. I'll ask Richard Philipson and our Chief Medical Officer to take that question. Sure. Part A full analysis set was the analysis set used for the primary analysis t hat's the 199 patients included in Part A. If we look at that population overall, 19 patients withdrew from treatment, but they still remain in the study, or have the potential to remain in the study. They're not completely removed from the study and o f those 19, 10 or 5.1% of the overall full analysis set, 10 discontinued due to AEs. Okay. Okay. Thank you. Great, thank you. I think we'll try Maury Raycroft off the end for Jefferies. Please go ahead. Hi, good morning everyone. Sorry w ait. Sorry, Richard, can you go on mute? Great. Sorry, yeah, go ahead. Congrats on the progress and thanks for taking my questions but, i was going to ask, so with some of the baseline characteristics that you've reported, you've broken out the patients who are less than two grams, greater than 3.5 grams t hen the patients in between there. For your patients at baseline with proteinuria greater than 3.5 grams, can you talk more about the magnitude of proteinuria reduction you're seeing there? I guess, is the 31% mean reduction consistent for the three groups? or can you talk more about the range that you're seeing? I guess that our view is really that we don't provide any additional detail on this simply because we do still have a trial that's blinded and ongoing. I will, for good order, also hand over to Richard, our CMO, just to confirm that. Yeah. I was going to say something similar. That's essentially getting into substantial amounts of detail relating to subgroup analyses. We're not releasing those kind of subgroup analyses in detail, because as Renée has said, this is an ongoing blinded study. Understood. Just as another follow-up on the open label extension data. I think at your R&D day, you talked about potential for repeat dosing and extended dosing. I'm wondering if you're going to include some of the data from those studies in your FDA submission for review and/or for label discussions. Obviously we're filing with the FDA this quarter. The open label extension has obviously just started because the first patient who was eligible to roll over, if you think about our first patient into this study was November 2018. Obviously the first patient who was eligible after a two-year period to roll over into the open label extension was really in November, December timeframe last year. Any kind of data from the open label extension will probably be much further down the line than basically the review period. Got it. That would probably be used for the confirmatory data that expands the label then. Yes. These trials are more just for health economic purposes, and to guide actual clinical practice. Understood. Okay t hank you for taking my questions. The next question comes from the line of Yaron Werber from Citi. Please go ahead. All right. Thank you for taking the questions. To Renée, on the commercial uptake for Nefecon, with regard to feedback from payers, what is your expectation around Nefecon requiring a prior authorization? Is it the expectation that the patient will have to have failed the ACE or ARB or steroids in order for payers to cover Nefecon? Then secondly, what is your expectation with respect to the frequency of therapy? In the commercial setting, are you expecting that physicians will treat beyond the nine-month period, meaning continuous treatment? or will this be sort of an episodic treatment where they're on for nine months and then they're off for a period of time, and then they resume therapy again? Thanks. Okay. IQVIA did a fairly substantial kind of market landscape research work on our behalf. They did, in that kind of research, they did try to address both of these points that you're raising, f rom a payer perspective, there was a large kind of payer research that was conducted. I think it was covering about 225 million lives in the U.S. There, in terms of from a payer perspective, obviously this is an orphan disease that has previously never had anything approved, so the payers are not really used to getting this coming across their desk. They were obviously shown the Phase IIb profile in that market research. On that basis, what we found out was that in that kind of range, the range we've been talking about before, which was a spontaneous range from their perspective, $ 55,000-$ 85,000 per treatment period of nine months. They basically said that they would, in our view, I think, would treat it appropriately. They would expect the prescription to be done by a specialist, and all of these patients really do end up at a nephrologist. They would expect it to have that there would be a diagnosis that was valid in terms of the actual disease. A couple of them did mention that they would look to a step edit in terms of ACEs and ARBs. That's really what came out of that kind of market research that we saw and, o bviously in terms, if you look at guidelines, that is the only kind of recommendation that the guidelines has, is to actually treat these patients with ACEs and ARBs i think that, as in most CKD indications, these patients are already on blood pressure-lowering agents. There's ACEs and ARBs and there's combinations, and they are kind of optimized and titrated with a variety of these ACEs and ARBs to get to as good of a position as they can, o bviously, as we know, that doesn't really address the underlying progression, which we see in a lot of these patients. This is obviously something that we've already done our trial on top of optimized ACEs and ARBs. From our perspective, we would expect that blood pressure-lowering agents will continue to be used in CKD indications, including in IgA nephropathy. We don't really see that as an issue, I must say, because I think pretty much all patients are already on. That's what we found also actually in our Phase II trial. That's really what we found out from that. I think in terms of the treatment paradigm, I would say that the physicians in that market research fell into two buckets really. One group of physicians felt like they actually appreciated the ability to be able to treat patients intermittently. Actually put patients on a nine month treatment period cycle, and then they see these patients three or four times a year anyway, and they would follow them in terms of both eGFR and proteinuria i f they felt that the disease was kind of taking hold again or that progression was starting again, that they would put them on another treatment cycle. There was another group of nephrologists who clearly felt that as long as their patient was seeing a benefit from the medication and could tolerate it, then actually they would just prefer to keep the patient on the medication. I think that there are two different approaches, I guess is what we found from the market research. That's also obviously why we are going to, on the basis of the Part B, we will obviously get a lot of information with regards to the longer-term impact of this treatment and a s we've already indicated, for example, is that there is a continued benefit and significant continued decline in proteinuria, for example, over the first three months. This will give us a much longer time period to be able to know that better than what we do today, and that data is just data that we don't have today. I think that from that perspective, this will also obviously something that we do in both the NefXtend and open label extension, is to provide really more information and background to these treating nephrologists with regards to both of those approaches, both the retreatment as well as the extended dosing. Thank you t hat's very helpful. Just one question on other indications for Nefecon. I think you had mentioned in the past autoimmune hepatitis. What's the status of that planning and are there other indications for Nefecon that you're targeting? Yeah. Last year we did have interactions with the FDA with regards to autoimmune hepatitis. We believe that we've had very good guidance, and I think we're very close to what we believe is a clear regulatory path forward, which would really involve a late-stage clinical trial in AIH. There are a couple more things we'd like to go back and get some further clarity on. We would expect later this year to have final clarity on the way forward in AIH. That obviously would rely on the same type of basis in being able to provide a drug that is more appropriate for chronic treatment than systemic steroids, simply due to the big difference in safety profile, and particularly in something of a chronic treatment like AIH. There are obviously compliance and remission issues, on the basis of what's available today, as there's nothing approved. That's really where we stand in terms of AIH w e have also obviously previously also discussed PBC. We are continuing, actually, we also have dialogues around PBC, and we're continuing those dialogues in parallel but i n terms of a clinical trial, the first clinical trial that we will conduct is with setanaxib in the pivotal Phase II/III trial that we are planning to start this year. Great. Thank you very much. We have one more question from the line of Rami Katkhuda from LifeSci Capital. Please go ahead. Hey, guys. Thanks for taking my question. Just a quick one for me but, b ased on Calliditas' discussions with the FDA, do you still plan to use GGT as a primary endpoint for the upcoming PBC trial? or will you focus on ALP instead? No, since this would be a potential registrational trial, we would seek to use the validated endpoint, if you like, which in PBC is ALP. Got it. Makes sense. Thank you. As there are no further questions, I'll hand it back for closing remarks. Great. Well, thank you very much for taking the time to listen to our Q4 report. We look forward to talking to you again in three months' time, and give you an update as to both our regulatory progress as well as our commercialization efforts in the U.S. Thank you. This concludes the conference call. Thank you