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Galapagos NV (GLPG) Q2 2021 Earnings Call Transcript

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GLPG earnings call for the period ending June 30, 2021.

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Galapagos NV (GLPG 0.95%)
Q2 2021 Earnings Call
Aug 6, 2021, 8:00 a.m. ET

Contents:

  • Prepared Remarks
  • Questions and Answers
  • Call Participants

Prepared Remarks:

Operator

Good day, and thank you for standing by. Welcome to the webcast for the H1 Results of Galapagos. [Operator Instructions] After the speakers' presentation, there will be a question-and-answer session. [Operator Instructions]

I would now like to hand the conference over to Sofie. Please go ahead.

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Sofie Van Gijsel -- Senior Director Investor Relations

Thank you, and welcome all to the audio webcast of Galapagos' H1 2021 results. I am Sofie Van Gijsel, Investor Relations, representing the reporting team at Galapagos. This recorded webcast is accessible via the Galapagos website homepage and will be available for downloads and replay later on today.

We would like to remind everyone that we will be making forward-looking statements during today's webcast. These forward-looking statements include remarks concerning future developments of the pipeline and our Company and possible changes in the industry and competitive environment. Because these forward-looking statements involve risks and uncertainties, Galapagos' actual results may differ materially from the results expressed or implied in these statements.

Today's speakers will be Onno van de Stolpe, CEO, Dr. Walid Abi-Saab, CMO; and Bart Filius, COO and President. Onno will reflect on the operational highlights and Walid will speak to the topline results of our TYK2 and SIK2/3 programs released in July. Then, Bart will go over the financial results and end with expected news flow for the year.

You will see a presentation on screen. We estimate that the prepared remarks will take about 20 minutes, then we'll open it up to Q&A with Onno, Walid and Bart joined by the rest of our management board.

And with that, I'll now turn over to Onno.

Onno van de Stolpe -- Chief Executive Officer

Thank you, Sofie, and thank you all for joining this webcast in the midst of the summer.

I would like to start with the year-to-date review. If we look at Q1, then clearly we had a big disappointment when our ISABELA trial was stopped because of stock signals and lack of efficacy of our ziritaxestat work that didn't meet up to expectations in the IPF trial, a big blow for the Company. The risk of new mode of actions clearly illustrated here.

On the positive side, we had a good data on the MANTA, Manta-Ray study, testicular tox study that we're doing for filgotinib, where we have an interim analysis after 13 weeks. So that was in the positive points. In Q2, Gilead decided to extend the lock-up. We have requested that to answer some request by shareholders and Gilead actually extended the lock-up on the shares that they have in the Company up to 2024. So that is a nice certainty about the -- regarding the commitment of Gilead for the collaboration for Galapagos.

Filgotinib was filed for ulcerative colitis in Japan in the second quarter. For your information in Europe, that was already filed by the end of 2020. And this was a big step forward for us in Japan.

In the third quarter, we had clinical readouts first from the TYK2 in psoriasis, which was the Phase 1b study where we saw very nice data, which made us decide to move forward with our TYK2 in a Phase 2 study. And that will be discussed later on. And we also saw a very promising biological activity of our Toledo program, our SIK2/3 inhibitor both in psoriasis as well as in ulcerative colitis. Also that will be extenuously discussed by Walid in today's presentation. As a consequence of the setbacks that we have seen with filgo, the refusal to get it approved in the U.S. as well as the clinical setbacks in 1972 and ziritaxestat, we decided to do a strategic review, and we are implementing that review outcome as we speak. If you look at R&D, we have refocused the pipeline.

My next slide will discuss that. In BD, we have said that we are looking for substantial opportunity to strengthen our pipeline late stage, and we are in the full process at the moment to see if we can find a product or a company that would fit, but we are looking for and hope to execute on it when that becomes clear. Commercial, we are rolling out Jyseleca throughout Europe as a consequence of the renegotiations around the filgotinib deal we obtained always in -- for Jyseleca in Europe. We've taken over a number of employees from Gilead in the process. And Jyseleca is now rolled out throughout most of Europe and that will be discussed as well by Bart later in this presentation.

And then, we also said that we would save on the financials, on the expenses, as a consequence of the setback that is now implemented and that will show in the savings going forward in the second half and in the years to come. Also to be discussed by Bart.

If we look at the pipeline, then clearly, it's less mature than we had until the late-stage failures. But clearly, still very excited and differentiated pipeline focused on inflammation and fibrosis. The third therapeutic area kidney disease we have added in the first program, in that disease is now in a Phase 2 study. If you look at the pipeline, it's heavily focused on the Toledo program, the SIK2/3 as well as the SIK3 inhibition programs. The other programs moving forward in discovery toward the clinic. So, we hope to see a number of additional molecules reaching the patients in the years to come. We also, as we said earlier, have a very exciting TYK2 program that will go into psoriasis Phase 2 as well as in UC trial Phase 2 in 2022.

Then, I'm not going to discuss the other programs in detail, but clearly, we have still a lot of shots at goal here in these disease areas. These are all exciting new mode of action programs that we're moving forward with the risks associated with it, but we believe that we now have a balanced risk profile in our portfolio in diseases where we think we can make the best difference. And we are very excited with what we have now in development. Add to that what we have in research, I think that we are start -- have started to rebuild the Company after the setbacks in the late-stage programs. And we look forward with confidence.

With that, I would like to hand it over to Bart Filius, our President -- first we go -- we go to Walid. Sorry, Walid.

Walid Abi-Saab -- Chief Medical Officer

No worries, Onno. Good morning, good afternoon everybody. Thank you. I hope you can hear me well. So it's my pleasure to walk you through some excerpts of our data on TYK2 and the salt-inducible kinase inhibitors. Just to put it in context, I will not be doing a full presentation of each of the four study because otherwise it will take a lot of the time today. I'd refer you back to RPRs, which include information on the safety dropout rates and so on so forth because I'm going to concentrate on the specific elements on some of these studies.

So if you can have the next slide, please. So on the TYK2, we're quite excited about this class. As you can imagine, it's also very hot in the field of inflammation right now. TYK2 signals through pSTAT TYK2 pathway and it affects a number of mediators like interferon, IL-12 and IL-23. As a result, blocking TYK2 or inhibiting TYK2 has a number of potential in several autoimmune indications such as psoriasis, such as inflammatory bowel disease, lupus and other types of interferonopathies. So, we're quite excited about this target. Also, based on the fact that it appears that this target also is -- has a promising safety profile. Our own 3667 is a proprietary selective TYK2 inhibitor, which as you know, we've advanced to the end of the Phase 1 program.

So you can go to the next slide. Here, we report on data from our signal detection study. It's a four-week trial, where we randomized 31 patients in a 1 to 1 to 1 ratio, two doses of 3667, low, high dose as well as on placebo. What we found in this trial that 3667 was generally safe and well tolerated. We clearly saw a positive signal as evidenced by the changes in the PASI score. We had four out of 10 patients randomized to be high dose experiencing a PASI 50 or above response compared to 1 on placebo.

But not only that, when we look at the additional endpoints, body surface area and so on so forth that we look at in this indication, we clearly see consistent results across the board. What we also know is based on data from competitors as well as the shape of the curve in our own trial. The plateau is nowhere near -- the efficacy that we see at four weeks is nowhere near the plateau.

Now we had previously planned based on an increase in the safety margin based on longer-term tox studies that were completed sometime early last year -- early this year, I should say, in 2021 that we wanted to explore higher doses. And as a matter of fact, that study is ongoing right now. And this will enable us to evaluate the full dose range in the upcoming dose range finding study in psoriasis as well as in Phase 2 study in ulcerative colitis, as Onno mentioned earlier in 2022.

On the next slide, I'm trying to show here the essentially disposition of subjects based on the change of baseline and what they achieved and the PASI score. So this is at Week 4. You can see at the X axis, the PASI score and on the Y axis, the proportion of subjects who achieved it. So you can imagine on the high dose where we have 10 subjects. Each uptick represents one patient having a response. And the dark green is the low dose of 3667, where we had 11 patients, so each increment is about 9%, so to speak. And you can see very clearly that we achieved -- so one patient clearly has PASI greater than 75. We have another one that had a PASI of 74. You see them barely below the cut-off of 75. And then if you do the cut off at 50, you see that four people are on active high dose and one on placebo achieving that goal. So overall, we're quite pleased in these -- with these results. Clearly, a signal was detected and the overall picture supports further developing -- development of 3667 in psoriasis, but also in other inflammatory indication, ulcerative colitis and potentially other areas that we're evaluating as well.

In the next slide, I will talk a bit about our salt-inducible kinase inhibitors. We're very excited. This is a potential novel mechanism of action inflammation. Salt-invisible kinase is signaled through two different pathways as is depicted on this cartoon here. They affect both pro-inflammatory mediators, as well as regulatory indicators. And that was the reason why we were very excited that with our approach with inhibition of these particular kinases. We can both affect a reduction in the pro-inflammatory cytokines such as TNF-alpha, but at the same time, an increase in some of the regulatory, sorry, mediators such as IL-10. And that's a very promising profile that could potentially have a role in inflammation both by increasing efficacy, but also reducing the long-term consequence of chronic immunosuppression that we observed with some of the treatment of these indications.

Galapagos has played a critical role and pioneering role actually in elucidating what the salt-inducible kinases can do in inflammation. We have a number of compounds with multiple level of selectivity for the Type 2, Type 3 and 2/3 together, as well as different level of potency. And we believe that we have potential for broad application across the board here.

In the next slide, I'm summarizing a bit our experience with our 3970, which is the molecule that we took forward as a SIK2/3 inhibitor in three signal detection studies that were six-week in duration. Overall, we found 3970 to be generally safe and well tolerated, which bodes well for the platform in general. Now, to be perfectly clear, 3970 was not the ideal candidate. We knew that by virtue of some dose limiting toxicity, the margin that we were able to explore in the clinic was not that high. Nonetheless, we felt that it was very important for us to start generating some data that will help inform us and guide the future development of this whole platform, which as you know, we've been investing heavily in.

So in the psoriasis study, CALOSOMA study, which was six-week in duration, we clearly saw evidence of clinical activity as seen by four out of the 13 patients achieving a PASI 50 versus none on placebo. These observations were very solidly observed across a number of secondary endpoints, which we've examined in the trial.

In the case of the SEA TURTLE study in ulcerative colitis, while we have not seen any evidence of efficacy with on the Mayo score and I'll show you that in subsequent slides. When we looked at objective endpoints specifically, when we look at endoscopy and histology and I'll talk about later in more details, we do clearly see signs of biologic activity that are very exciting for us and definitely worthwhile further developing when we look at subsequent molecule.

In the case of rheumatoid arthritis, preclinically, this was actually the toughest indications -- indication for us. We knew that we needed much higher exposures to achieve efficacy based on the animal models. And in fact, actually, that's what translated in the clinic, where we did not see any signal in RA. And I will not talk about it anymore today.

On the next slide, I'm showing the similar graph as I did for 3667 where you see the proportion of subjects at the end of the trial at Week 6. In this case, I remind you the -- we had a 2 to 1 randomization between drug and placebo. So 15 on drug and 11 on placebo. We had a couple of dropouts due to COVID or other reasons between drug and placebo. In the end, we end up with 13 on active and 10 on placebo. So you can imagine, one patient will be about 8% on active compared to 10% on placebo. And you can clearly see how 3970 separates from placebo in this trial.

On the next slide, this is the primary endpoint for the UC trial. This is a trial just to remind you, where we had 2 to 1 randomization, about 20 people on active versus 10 on placebo and the study six-week duration, which is relatively short for ulcerative colitis, but that was the tox coverage that we had at the time. When you look at the change from baseline, actually, they are relatively large on the Mayo score. And that tells you that we had a large placebo response in this patient population, which by the way, were all biologic naive and JAK naive. And as such, we would not see any change between the two.

However, when we -- if you go to the next slide, when we looked at the objective endpoints, specifically, when we looked at on the left hand side graph, when we look at the definition of endoscopic improvement, which is a score of zero or 1 on the endoscopic response sub-score of the Mayo. In the old days, this used to be called mucosal healing. You see that we have one out of nine patients, or about 11% of those who underwent endoscopy at the end of the trial versus seven out of 18, which is close to 40% on active. So, we think this is a clear signal. Again, it should be taken into the context of the fact that we did not see on the primary endpoint, but nonetheless, in small signal detection studies, we have to follow each signal.

And then we look, which I'm showing on the right hand side graph, of those patients who had the endoscopic improvement and tried to look at their histology score, these are the numbers here -- the scores are the robots histology score. And you can see very clearly that those who are on drug have for the majority, the largest drop. As a matter of fact, those who are at the bottom, the four or five patients who have the lowest score on the histology are the ones who actually virtually normalized their fecal calprotectin, which is inflammation marker for ulcerative colitis.

So all in all, when you look at the data from the ulcerative colitis, we are encouraged with these positive signs, despite the fact that we had a large placebo response in this biologic naive population. But I think this bodes well for the platform as a whole.

So in my last slide, I think I'm -- I would like to summarize that we are quite pleased with the biologic activity we've seen with our salt-inducible kinase inhibitors in these short signal detection studies. It's not a given that when you work on novel mechanism of actions, you will be able to translate that to efficacy in the clinic. And it was very clear that we've seen that evidence of clinical activity in psoriasis, which is an important inflammatory indication. We've also seen important signs of biologic activity. I hope you agree with us that there is something there in ulcerative colitis.

We clearly know that 3970 doesn't have the necessary margin that will allow us to fully evaluate the inhibition of SIK2/3 in the clinic, and then we want to go back and work with the compounds that we have now in late-stage discovery to come up with molecules with higher target engagement. And therefore, we conclude that we are very excited with the data that we've seen that these data support further development of our salt-inducible kinase portfolio and point to their potential in inflammatory indications. And our goal is to bring one of our more potent and better pharmacologic profile SIK2/3 inhibitor to the clinic as in healthy volunteer studies in 2022.

And with that, I'll turn that over to Bart Filius. Thank you.

Bart Filius -- President and Chief Operating Officer

Thanks, Walid, and good afternoon, everyone. Good morning for everyone on the U.S. time zones. Let me conclude the presentation. I think I'll take about five to 10 minutes more tackling to other topics, one being the commercial progress that we've made over the last quarter and then the financials for the quarter as well.

And so, first of all, we've made significant progress in the second quarter in terms of reimbursements, in line with expectations, but clearly a big -- big steps forward as you know in Europe, it's not a one shot, you need to basically go from country to country to achieve reimbursement, which is again critical for being able to launch successfully. At the end of last quarter, we had Germany and the Netherlands in the markets. And during the second quarter, we've been able to add France and the U.K. as well as also reimbursement in the whole range of smaller countries, Belgium, Luxembourg and Scandinavian countries Austria and Ireland. So in total, we are now in 11 countries reimbursed in Europe with generally a reimbursement per label. The exception there being France, where reimbursement is female only waiting the review of the MANTA data by the authorities, and then hopefully, being able to implement also -- expansion of the reimbursement label in France thereafter.

And very positively in the U.K., we are the first advanced therapy that is recommended by NICE for the moderate and severe RA population. And that is obviously a big -- big support to our launch there. Both of those countries have launched in the last month of the quarter. So the numbers at stake are still very, very small. But we're happy to see the progress there in terms of achieving market access and still to come for the rest of the year is reimbursement in Spain and Italy. So by the end of the year, in all of the big European countries, we should have the products on the markets.

Just as a reminder, we are not booking sales yet in Germany and the U.K. in the first and the second quarter of this year. It is still booked by Gilead, but as of Q3, we will start to see German sales numbers in our own books. We've started supplying ourselves in July and in the U.K. [Phonetic, and many of the smaller countries will follow by the end of 2021. So that as of 2022, all of Europe will be supplied by Galapagos and sales will be booked by Galapagos as well. So pretty on track on reimbursement there.

Then a quick peek at market performance. Overall signal is that we are in line with our own expectations. With regard to market penetration, it's still very, very early days. The only market where we are now a little bit longer and active is obviously Germany, but maybe also the left worthwhile to highlight how the JAK class as a whole is doing very well in Europe. And over the years, you see now that the class of market share in advanced therapies has increased to 16%, here reflected in the green box in the bar charts and anti-TNFs slowly declining, but other biologics as well. So the JAK class as a whole is doing quite well.

On the right, perspective on how Jyseleca is doing in the German market. And this is an overview of the dynamic markets, so those are all patients that are either switching from other advanced therapies or are yet to be started, only in advanced therapy, be the biologic or JAK. So, this includes also for example patients starting on other biologics on TNF for example. And we see our market share in the dynamic market progressing rapidly to now north of 4%. So, we're pleased with the results in Germany and we're pleased with the results in Europe as a whole with regard to our overall class market share and Michele Manto, our Chief Commercial Officer is available for the Q&A to give further detail on the numbers as well.

Then let me switch over to the financials. First, a few on cash. Our cash balance at the end of the second quarter is a bit north of EUR5 billion. And that's reflected a cash burn of EUR223 million over the first half of the year. As usual, we exclude a couple of extraordinary items from our cash burn in these case in the six months to date. These were positive influences, warrant exercises. The disposal of our fee-for-service business, Fidelta, for EUR29 million of cash impact and then some favorable currency translation effects as well about EUR30 million. Overall, that leads us to a very healthy cash position of EUR5 billion at the end of the first half of 2021.

Then a bit on the P&L. There is definitely a much more detail available in our H1 report, and I invite everyone to take a look there on our website. Our revenues are EUR277 million for the first half, mainly driven by revenue recognition elements for both filgotinib and the platform resulting from our transactions with Gilead. And as of the end of June 2021, there is still approximately EUR2.6 billion of deferred revenue available in our balance sheet that will be recognized over the months and years to come.

Operating costs slightly increasing. On one hand, filgotinib, we've taken over a bigger chunk of the cost from Gilead with our transaction in December of last year. Toledo is higher relative to the comparative quarters in 2020 with the five clinical studies that we had been running in the first six months. And SG&A is up a bit, because of our launch efforts in the various markets in Europe. Our net loss is negative EUR55 million, which includes the effect on currency and the disposal of Fidelta as is reflected on this slide.

A few words maybe on cash burn with a bit of perspective for the future because it's been a topic that we've been discussing with our investors quite intensely over the last couple of months. And I thought it would be useful to give you some perspective on how our cash burn is built up today, as well as where we see it is heading. And this is not formal guidance, because obviously, we are not in a position today to look forward that many years in the future. But it is conceptually what our cash burn is looking like.

So let me start off with 2021. This year, which we anticipate by the way to be our peak cash burn year, so the numbers of cash burn will go down in future years. And out of that takes hundreds [Phonetic], roughly 70% is what we call pure R&D burden and roughly 30% is what we would call Jyseleca burden. Jyseleca burden in this case being not just the commercial field forces and medical affairs activities in the markets, but also the burden for the Phase 3 programs that we're running for diversity, the long-term extension studies that we have for our RA programs, as well as the MANTA study. And it also includes an allocation of our G&A expense that we are making in the Company. But this is the way we look at it ourselves in -- inside the Company. Out of the EUR600 million, which is the midpoint of our guidance for 2021, roughly 30% is connected to Jyseleca and roughly 70% is our R&D burn.

Then going forward, as I announced in the last quarter, we are pushing down our R&D burn expenses. The overall savings program is EUR150 million. We anticipate to materialize another EUR75 million as of full-year 2022. So, we do see R&D burn going down in the next couple of years to a level of, let's say, roughly EUR350 million, which is obviously everything else being equal. As soon as we do, and I don't know something on BD or if we have good successes on some of our -- on some of our pipeline programs, this number can fluctuate. But EUR350 million is sort of your run rate, if you look at it today and that we anticipate as of 2022.

Then we've also announced earlier that Jyseleca should obviously reach breakeven. Actually, we've always said that this would breakeven on a contribution margin basis, but we actually think that we can get pretty close to breakeven with a fully loaded cost view. And so, think about this as you go to 2024 time frame, the net burn for the Company would then also go down to the R&D burn, which is roughly EUR50 million. And then, obviously, what we are doing it for is our -- is the outlook later on in the decade and in the years -- in the next decade because Jyseleca has a very healthy patent life until 2020 -- 2034. And then in those periods of peak year -- peak sales years, we can actually get a healthy contribution from Jyseleca to offset our cash burn.

So if you think about the cash burn in the Company, this is perhaps helpful in looking ahead at how we would be spending our money again caveated by or events that could take place between now and then [Phonetic] these moments becoming -- become a reality.

And then, I'll conclude with an outlook for the rest of the year 2021 and then hand it over to or hand it back to Sofie for the Q&A. So what we've seen so far in the second half of the year is indeed the outcomes from 3667 and our SIK2/3 program and Walid has elaborated on those. Big for us obviously coming up is the decision by the CHMP and the European Commission regarding ulcerative colitis, and we're hopeful to get a positive decision there in the second half of the year. And then trial progress diversity, we anticipate this to be finally fully recruited in Crohn's disease, and also our study with 2737. Our kidney program should be fully recruited by the end of the year.

So with that, I conclude on the presentation and hand it back to Sofie and the operator for the Q&A. Thank you.

Sofie Van Gijsel -- Senior Director Investor Relations

Thank you very much, Bart. That concludes the presentation portion of today's webcast. And I would now like to ask the operator to open the lines for Q&A. Thank you, Christina.

Questions and Answers:

Operator

[Operator Instructions] And your first question comes from the line of Brian Abrahams from RBC Capital Markets. Please go ahead. Your line is open.

Brian Abrahams -- RBC Capital Markets -- Analyst

Hey, good morning, good afternoon and thank you for taking my question. Question on filgotinib, Jyseleca in Europe. I was wondering if you could maybe talk a little bit about the ongoing review there in ulcerative colitis, the role that the MANTA data are playing there? How much you've shared with them and continue to share with them and whether you've had any additional discussion with the regulators in Europe on that dataset? Thanks.

Walid Abi-Saab -- Chief Medical Officer

Thanks, Brian. This is Walid. I'll take your question. Yeah, the review is ongoing. As is the case, we have included the data from the interim analysis that we showed, including all the available data, as you can imagine. When there's an ongoing review, we provide with as much up to date information to the reviewing agency as possible. The review is progressing according to plan. And at this point, I have nothing more to add, except that we share the data with them, and we are in discussions with them. And I'm going to leave it at that. Thank you, Brian.

Brian Abrahams -- RBC Capital Markets -- Analyst

Okay. Fair enough. Thanks.

Operator

Thank you. Your next question comes from the line of Laura Sutcliffe from UBS. Please go ahead. Your line is open.

Laura Sutcliffe -- UBS -- Analyst

Hello. Thank you. Big picture question, please. You've talked about sticking with your core expertise in immuno-inflammation and fibrosis after your strategic review. But is it all about large target populations for Galapagos, or would you consider some of the more niche areas within those therapeutic spaces either with the assets you have or from a BD perspective? Thanks.

Onno van de Stolpe -- Chief Executive Officer

Well, let me start, then maybe Walid can add to that. This is Onno. Thank you for the question. We were clearly interested also in smaller indications and potentially also its first indications for some of our new mode of actions that we not necessarily directly go for the big ticket where we need very large trials with long duration. But if we can identify a disease where we can adjust the trial to, in a shorter period of time, a smaller patient number, I think the -- that is of interest, and then potentially expand on it when we get positive data in that first trial.

Walid, do you want to add to this?

Walid Abi-Saab -- Chief Medical Officer

I think you pretty much covered it, Onno. I think the idea was for us to operate from an area that we know well and a position of strength and know-how, which is the immunology and fibrosis space that we've been working in. But again, Galapagos has always been opportunistic in our quest to look for opportunities from a BD perspective. We will be expanding and evaluating specific maybe niche areas, more specialized disease areas within that space. But I think, Onno covered this point also very well. Thank you.

Laura Sutcliffe -- UBS -- Analyst

Perfect, thanks.

Operator

Thank you. Your next question comes from the line of Dane Leone from Raymond James. Please go ahead. Your line is open.

Dane Leone -- Raymond James -- Analyst

Hi, thank you for taking the questions. I guess, just kind of one for me to focus on the majority of investor conversations we've been having the majority of this year now. Can you just maybe go into how you're thinking about revamping the process of taking research molecules into more development stage? And obviously, there's been a recent your salt-inducible kinase program, TYK2 program. Unfortunately, the investor reaction to that was not positive, evidenced by the stock movement. Is there anything that we should expect in terms of how you select targets move forward to maybe increase confidence within the investor community that what we're spending money on into these Phase I/II studies is going to be, one, a better use of time and also a better use of capital? I guess, I'd put a point on that maybe specifically, when you look at the pipeline that you laid out at beginning of the call, if you're looking at something like GLPG555, a JAK1 inhibitor, we get questions of why you would even start a Phase I study in osteoarthritis, given the increased rate of venous thromboembolism with that group. So just we get a lot of questions obviously across how the selection process is being done. So anything you can help us with there would be appreciated. Thank you.

Walid Abi-Saab -- Chief Medical Officer

[Indecipherable] take that on.

Onno van de Stolpe -- Chief Executive Officer

You can do that, Walid.

Walid Abi-Saab -- Chief Medical Officer

Okay. Well, look, I think it's a fair question. As we have been communicating for the past few months that we've been taking a long and hard look, a critical look at the way we've been doing things. We've also been working with some external experts as well to help us with that. It's premature for us to come up with a finalized theme, but we will be communicating on that. But I can tell you that there are some initial themes that are emerging. I think it's very clear that as we are focusing on novel targets, I think it's going to be important that we spend much more time better understanding the link of these targets to our diseases and invest more time in de-risking these going forward. I think one of the things that maybe we've been a bit guilty of is that we get excited about what we've been working on and putting more valence on speed and want to go quickly to the clinic with some of the molecules that we have. The problem is that when you're working with a novel target, you're already working with a high risk. When you compound that with the fact that maybe you're not spending as much time to much better elucidate the biology and the link to the disease and then later take on molecules that might have a little bit more liability on their own for the molecule itself, now you're compounding your risk and you are increasing -- decreasing your likelihood of success.

So I think we're going to be taking all of these lessons. We're going to take a critical look at the way we do things. I think you will see that we will advance molecules probably with better pharmacologic profile, better margins than what we have done before. And you'll also see that we will be doing studies that probably are more robust maybe representing a patient population that could be more in line with where we are going to be ending up marketing the drug and probably longer, more robust studies. I think you will see that our risk taking is going to decrease a bit so that we can afford to continue working on novel therapies, which is truly what we are interested in doing because that's how we can address the patients' unmet needs and be able to bring something that is meaningful. I'm sorry, I cannot give you a lot more detail because we're in the midst of it and we're not ready yet, but I hope I've given you a flavor a bit as to our thinking and the direction we're taking.

Dane Leone -- Raymond James -- Analyst

Thank you.

Operator

Thank you. Your next question comes from the line of Rosie Turner from Barclays. Please go ahead. Your line is open.

Rosie Turner -- Barclays -- Analyst

Hi, good afternoon. Thank you very much for taking my questions. So, two please. The TYK2, 3667, going into UC, just wondering kind of what the rationale for that was. If there's kind been preclinical studies that give you confidence in that indication? And then, does that mean it's going to overlap with the kind of JAK1/TYK2 program you also have running? And are they basically kind of looking at the same indication?

And then, 4399, I think we've now got confirmation it's SIK3. I'm just wondering if you're able to give us any more detail in terms of what indication [Indecipherable]. Thanks very much.

Walid Abi-Saab -- Chief Medical Officer

Thank you for these questions. So let me start with the last one, 4399, so this is a SIK3 inhibitor. It's currently being developed in Phase I. We still haven't finished our Phase I program, and we should be able to give some more guidance on this toward the end of the year. Preclinically, I think we've talked previously about this molecule that it seems to work more in rheumatologic type of indication as opposed to IBD as we saw with the SIK2/3. But it's a bit premature to go into a bit more details. We will do that once we finish our Phase I with this compound.

Regarding the TYK2, I think the data are preclinically quite robust, suggesting that the role of TYK2 in ulcerative colitis -- we talked about the role of signaling through IL-23 and how IL-23 could be inhibited by TYK2 inhibition. As you guys know, IL-23s do play a role and have been shown to have effects in ulcerative colitis. You also -- deucravacitinib from BMS is being currently evaluated in UC study as well. So I think all of the data, preclinical and also through the IL-23 angle, suggest that TYK2 can play a role in ulcerative colitis.

As to be JAK1/TYK2, 3121, that you referring to, this is a molecule that is -- works on both JAK1 and TYK2, but it's an oral molecule that releases locally in the colon. And here, the key question is, can you with such a molecule produce a significant local effect in the colon, particularly in ulcerative colitis, without having significant systemic exposures, and as a result, reducing significantly the potential risk of systemically inhibiting JAK1 and TYK2. And as a result, you might have a much more beneficial risk-benefit profile in this case. Of course, that concept of releasing locally in the colon and producing better efficacy is one that needs still to be proven in the clinic. But the theory there is very plausible. And I think if the data from Phase I support the release profile that we're looking for, I think the next step will be to do the appropriate Phase II study in ulcerative colitis and look what the risk-benefit of this molecule would be like. Thank you.

Rosie Turner -- Barclays -- Analyst

Thank you. Very helpful. Thanks.

Operator

Thank you. Your next question comes from the line of Matthew Harrison from Morgan Stanley. Please go ahead. Your line is open.

Charlie -- Morgan Stanley -- Analyst

Hi, thanks for taking the question. This is Charlie [Phonetic] on for Matthew. How do you expect the FDA review of JAK safety to potentially impact filgotinib in terms of the EU market from a commercial standpoint of view? And maybe just a quick second question regarding any progress looking at the [asset to] potentially license will buy? Should we -- is there something that we can potentially expect this year? Thank you.

Onno van de Stolpe -- Chief Executive Officer

Michele, would you like to tackle the first question?

Michele Manto -- Chief Commercial Officer

Yeah. So I'll take the first part. So what we have seen in Europe also in the past is that the influences will be related to the reaction of the local European and national authorities. We've seen that with [Indecipherable] which had a very good launch in the past years despite the situation in US. And actually, we're seeing that also in the last month with our launch where actually the debate in the US hasn't really acted [Phonetic] the way that local prescribers and authorities have looked at the market.

Bart Filius -- President and Chief Operating Officer

Let me say a quick word on BD. Always difficult to say a lot on BD when these processes are still ongoing. So I echo the comments from Onno before that this is clearly a priority for the Company to work on BD, which could be licensing. It could be M&A. We are very active on that front. But today, there is nothing to report in terms of any transactions. But clearly, that's a priority for us at the management.

Operator

Thank you. Your next question comes from the line of Jason Gerberry from Bank of America. Please go ahead. Your line is open.

Jason Gerberry -- Bank of America -- Analyst

Hey, guys. Thank you for taking my question. So just on your TYK2, I was wondering if you could talk a little bit about how you differentiate, from a pharmacological perspective, versus the other TYK2s that are a little bit further ahead in terms of TYK2 selectivity. As we start to think about the unmet need that you'd be solving for in psoriasis, just sort of curious if you can frame how you're seeing this molecule as you think about advancing into Phase IIb dose ranging. Thanks.

Walid Abi-Saab -- Chief Medical Officer

Thanks Jason. It's Walid. Look, I think in our hands, our 3667 is selective based on our -- all of our assays that we have conducted in the clinic. We do not see anything that makes us worry about off-target activity. It's very difficult to compare to the others because we don't have all the data that they're basing it on. And if there is something that we've learned from the JAK world with our own filgotinib is that there are many different assays that one can use and in different labs, and unless you do them all at the same way, it's going to be very hard to interpret. And then, in the end, it doesn't matter because what matters is what are the clinical data that you can attribute to activity or off-target activity.

When we look at the data that's available from the most advanced compounds, I would think that deucra is the only one. The others are virtually in the same area where we are in terms of how advanced they are in development. With deucra, the only data we have is what they've been publishing on the Phase IIb in psoriasis. The Phase III study, I don't think we've got a lot of the details of it. This will become much more transparent once the file has been approved and the drug has been approved. You can look at the details of it. But one of the things that caught our eye is that you can see in the Phase IIb study, they've used doses that are higher than what they've used in Phase III. And Phase III, they had apparently a bit less efficacy than what I've seen in -- what they've seen in Phase IIb in psoriasis. So could that be because you go from a smaller Phase IIb to a larger Phase III? Or could it be that the doses that they used in Phase III, which is lower than what used in Phase IIb is the one reason why they have less efficacy? Without knowing all the details and the rationale for why they didn't pick the highest dose to go into Phase III, it's really very difficult to compare, to be honest with you. And at the end of the day, the best way we can do this is to conduct a Phase IIb study that's very similar to the Phase IIb that deucra has conducted. And I think that's going to bring us the closest to being able to see whether we have a competitive profile at the end of that trial. Beyond that, it would be just speculation on our part, to be honest.

Jason Gerberry -- Bank of America -- Analyst

So is it clear -- is it fair to say that you probably don't really know how you stack up until you start to accrue large datasets, I mean, Phase III data sets, and as you kind of proceed, you just have to operate under the hypothesis that you've got good selectivity and you hope that that differentiates your molecule relative to the more advanced players?

Walid Abi-Saab -- Chief Medical Officer

Yeah, that's fair. I think the way you phrase it suggests that we are going blind and we're going to see what's going to happen. That's not true. I think our preclinical data clearly gives us confidence about our selectivity and our clinical data does not raise any concerned about lack of that selectivity. So I think we are pleased with what we have seen. We think so far so good, again, with the caveat that we've just done a four-week study. So our confidence in our potential efficacy and safety are limited by this small number. So we're taking the next step, but I think we're taking the next several confidently based on our preclinical data that we have to date in our clinical data. And then, we think that at the end of that Phase IIb study, that would be truly the right time to look to see whether we have a competitive profile to deucra, but also to other competitors if they've advanced equally around that time.

Jason Gerberry -- Bank of America -- Analyst

Great. Thank you. And didn't mean to suggest operating blind to the activity of the drug.

Walid Abi-Saab -- Chief Medical Officer

Thanks.

Operator

Thank you. Your next question comes from the line of Lenny Van Steenhuyse from KBC Securities. Please go ahead. Your line is open.

Lenny Van Steenhuyse -- KBC Securities -- Analyst

Hi, good afternoon, and thanks for taking my question. As of course there is a lot of focus on the inflammation pipeline, I was wondering if you could provide us with a brief overview on the IPF portfolio and timeline going forward, specifically on 4716, which was expected to head into Phase IIb. What's the status on that one? Is there still some dose finding or still some safety studies ongoing with that compound? And when should we expect another clinical study to commence with this compound? Thank you.

Walid Abi-Saab -- Chief Medical Officer

Thanks Lenny. You're right, we spend a lot of time talking about information. So, IPF, I think that is a -- there were some big learnings that we got and actually a bit of disappointment, as you can imagine, with ziri. What we are doing right now is figuring out how can we de-risk our programs going forward, short of doing a very large Phase II study that's going to cost millions of euros and take a number of years to be able to answer the question, and even there with a lot of uncertainty. As you know, FVC as an endpoint is a bit risky. So to be perfectly honest, we are still gathering actually all the data from ISABELA. We still haven't gotten all the data in. We're trying to better understand whether we can identify certain patient populations that would be maybe rapid progressors or if there are certain signatures that we can use to identify and enrich our population going forward. We're also using this time to increase our confidence in the mechanism of action of 4716 and kinase inhibitors in IPF and other fibrotic diseases of the lung. And we are also doing some necessary drug interaction studies because, again, those were learnings that we obtained from the ziri program, as well as the 1205 program that because of the use of significant concomitant medications, it's important to de-risk the program by doing the necessary drug-drug interactions. So, all of these preparations are happening this year. I'm expecting that in the early part of next year, we will be able to have a better idea about a Phase II study. I'm not sure if it's going to be right off the back going into a Phase IIb study or it's going to be more of a mechanistic Phase II study. This is something that we're still thinking about. And it's part of this rebalancing of how much risk we want to take as we engage, whether we can figure out a way to find biomarkers that increase our confidence in our success before we invest more heavily. But we're committed to the IPF space. This is a space which there's huge unmet medical need. And arguably, we have a lot of knowledge that we've accumulated as a result of the ISABELA program. We're going to put all of those to use and helpful -- hopefully be smarter about the next step that we take with 4716. Thank you.

Lenny Van Steenhuyse -- KBC Securities -- Analyst

Thanks very much, Walid.

Operator

Thank you. Your next question comes from the line of Phil Nadeau from Cowen. Please go ahead. Your line is open.

Phil Nadeau -- Cowen -- Analyst

Good morning, good afternoon, and thanks for taking our questions. Two brief ones for us. First on Jyseleca. Gilead didn't actually break out the revenue recorded in Europe when reported a couple of weeks ago. I was curious if you could let us know what was recorded in Q2 for Jyseleca revenue in the EU. And then second, can you remind us on 4399, how the potency of its target engagement for SIK3 compares to the target engagement of 3970 for SIK2/3? Is it significantly more potent? Or is it more on parity? Thanks.

Bart Filius -- President and Chief Operating Officer

Let me quickly answer the question on the revenue. It's correct, Phil. So we will be booking sales as of July and we will be reporting sales ourselves as of the third quarter. Gilead is not, let's say, detailing those sales levels in their reporting. But once we do the Q3 updates, we will make sure to give you a full perspective on sales of the compound also on a year-to-date basis.

Then maybe on 4399, I've give that to Walid.

Walid Abi-Saab -- Chief Medical Officer

Thanks Bart. So, on 4399, I will again ask Piet to comment specifically on the potency. I believe it's in the same ballpark of 3970, but that's not the key point. The key point is whether the -- based on the half-life and the margin -- safety margin, to what degree we can inhibit the SIK3 enzyme. And that will not be known until we finish Phase I, and we will be able to figure out what are the doses that are safe and well tolerated that we can use.

So maybe, Piet, you can say a couple of words if you know about the potency of 4399 versus 3970.

Piet Wigerinck -- Chief Scientific Officer

Okay, thanks Walid. Indeed as you mentioned, both 3970 and 4399, if you look, both at the biochemical or [Indecipherable] level, they are single-digit number more potent compounds. So the big difference is that with 4399, you would only block the secretion of the pro-inflammatory cytokines. You don't play on the second angle where you help the system to rebalance quicker. So it will only inhibit the situation of the pro-inflammatory cytokines. It's a potent molecule, from what we've seen in animal studies. It's going to be once-a-day. And we expect a good coverage of the biomarker in Phase I, but that's an ongoing study, and we'll need to wait until the data to report out on those.

Phil Nadeau -- Cowen -- Analyst

That's very helpful. Thank you.

Operator

Thank you. We have time for one more question, and it comes from the line of Wimal Kapadia from Bernstein. Please go ahead. Your line is open.

Wimal Kapadia -- Bernstein -- Analyst

Great. Thank you very much for taking my question. So, can I actually ask about 2737, please, for PKD? So I know the asset was previously investigated for cystic fibrosis [Indecipherable] primary, didn't show any significant improvement in pulmonary function. And I guess, I'm just curious, what gives you the confidence to start the Phase II trial? Just to get a sense of your conviction will be great, just given some of your earlier comments on risk appetite within drug development. Thank you.

Walid Abi-Saab -- Chief Medical Officer

Yeah. So, I'll start, and if Piet wants to chime in, based on the animal data, but this is a compound that, as you know, we've known for some time and we were working on it in cystic fibrosis. And through the action on the CFTR channel, we were able to surmise that it's going to work in this indication. Our preclinical data actually were quite solid supporting this, both on its own and using also tolvaptan as an active control, but also in addition to -- and based on those, we elected to do the study. Now, of course, this is a long disease. The studies are long. There is huge unmet medical need. And this is our first foray into that space. So, there is an element of learning involved there. But I think the preclinical data are quite supportive.

Piet, do you want to add some more color to the preclinical data?

Piet Wigerinck -- Chief Scientific Officer

Okay. Walid, thanks. So, 2737 is -- as a monotherapy, act as a CFTR blocker. And so, the disease we are investigating, ADPKD, is a disease where processes go wrong in the kidney [Indecipherable] cysts swell. So we expect the compound to block the swelling of those cysts and to completely one of those channels that make those cysts grow. In that sense, we've seen in the clinic signs of target engagement during the CF program, and we believe that it's going to be sufficient to engage the target as well in the kidney in those ADPKD patients. We've tested it in multiple in vitro systems and in vivo systems, and we're always coming up with an efficacy which is close to the only approved drug currently, and that's where we stand today.

Wimal Kapadia -- Bernstein -- Analyst

Great, thank you very much.

Sofie Van Gijsel -- Senior Director Investor Relations

Thank you. So that's all we have time for -- on today's call. Of course, please feel free to reach out to the IR team if you have any further questions. We're happy to help. Our next financial results call will be the Q3 2021 results on November 4. Thank you all for participating today, and have great day. Bye.

Operator

[Operator Closing Remarks]

Duration: 61 minutes

Call participants:

Sofie Van Gijsel -- Senior Director Investor Relations

Onno van de Stolpe -- Chief Executive Officer

Walid Abi-Saab -- Chief Medical Officer

Bart Filius -- President and Chief Operating Officer

Michele Manto -- Chief Commercial Officer

Piet Wigerinck -- Chief Scientific Officer

Brian Abrahams -- RBC Capital Markets -- Analyst

Laura Sutcliffe -- UBS -- Analyst

Dane Leone -- Raymond James -- Analyst

Rosie Turner -- Barclays -- Analyst

Charlie -- Morgan Stanley -- Analyst

Jason Gerberry -- Bank of America -- Analyst

Lenny Van Steenhuyse -- KBC Securities -- Analyst

Phil Nadeau -- Cowen -- Analyst

Wimal Kapadia -- Bernstein -- Analyst

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