Hi, everybody and welcome to our audio webcast today. I am Elizabeth Goodwin, Investor Relations. And I'll be hosting the event. You can view the webcast on our website, www.glpg.com. And it will be available for replay on our website later on today. So that your questions can be included, we request that you call into the telephone number given in the press release. I've got one right here for you. 32, for Belgium, 24-00-6926, and the code is 2352766. Moving on, I'd like to remind everyone that we will be making forward-looking statements during today's audio conference. These forward-looking statements include remarks concerning future developments of the 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; Piet Wigernick, CSO; and Bart Filius, CFO. Onno and Piet will go through the operational highlights of the third quarter, and Bart will explain the financial results. Onno will then close with the considerable news flow we expect over the next year or so. You will see a PowerPoint presentation on screen during this presentation, and we estimate that the talk will take about 20 minutes or so, and will be followed by a Q&A session. So at this point, I'd like to hand over to Onno to begin the presentation.

;: But not only that, in filgotinib we're moving forward in IBD, in Crohn's disease and ulcerative colitis, where we are expecting to start Phase 3 dosing very shortly. So really, we're rolling out filgotinib in these diseases and many others to come. At the conference, we discussed the data of filgotinib in Crohn's, especially the endoscopy and histopathology data, which were well looked for, especially in the context of the competition data from Celgene's Mongersen, and our data came out very nicely in comparison. So we were very pleased with that as well. Also in the third quarter, we obtained an orphan status for 1690; it worked with developing idiopathic pulmonary fibrosis, which is currently in a Phase 2 trial. We're also very pleased that we had the first dosing in our antibody that we're developing together with MorphoSys in atopic dermatitis, so a lot of progress in the pipeline. And if we go to the next slide, if you look at that pipeline, you see that it's becoming larger and larger over time, with two new additions compared to the last time we presented this pipeline. At the bottom, you see 2938 for idiopathic pulmonary fibrosis and other mechanisms of action that we're developing, and it's now moving towards Phase 1; and 2534 for atopic dermatitis. This is what Galapagos is about. It's about new mode of actions around targets that we discover with our platform and that we're moving forward through discovery into development. ,: We talked about 1690 in autotaxin, an autotaxin inhibitor that we're developing for IPF. And we're also very excited about the collaboration that we have with Servier in osteoarthritis with 1972 for which we will start, Galapagos will start, a Phase 2 program in the United States next year. With that short overview of the pipeline, I would like to hand it over to our Chief Scientific Officer, Piet Wigernick.

Thank you, Onno. So first highlight of Q3 for us of course was the kickoff of the FINCH program for filgotinib. FINCH is the large Phase 3 program with filgotinib in RA. We developed 100 and 200 milligrams with three different studies, aiming at a broad label across multiple lines of therapy in RA. The FINCH Program will include in total more than 3,000 patients, and has the classic attributes of currently run or recently run Phase 3 programs in RA, meaning active control is included, X-ray endpoints are included, studies with duration of either 24 or up to 52 weeks. So with the FINCH Program first patients have been included in Q3, we will be able to be showing that filgotinib is really the best JAK1 inhibitor in the space, and it will come out as well with probably the best safety profile. So we're very pleased with the progress our partner Gilead has shown over the quarter for RA. So second highlight on the next slide was of course, the data of filgotinib in Crohn's. So at the UEG Week conference in Vienna, we for the first time shared with the outside world the endoscopy data. So the FITZROY study was a 10-week study that we powered to show a difference on the clinical endpoint, the CDAI improvement and the CDAI remission. We've reported those data before. But in Vienna, for the first time we showed the endoscopy data. And for us the critical criteria there is the number of patients with at least 50% improvement. And we've shown clearly independent of the reading, a medical advantage for the treatment group over the placebo group. I can tell you that for the local reading, you're very close to the statistical significance of 0.05. So it was only in…

Thank you very much, Piet. And good morning for those in the U.S. Good afternoon for those in Europe. My name is Bart Filius, CFO of the Company. Let me walk you through the financial results of the third quarter, or I should say the 9 months up until the end of September. So I'll start off with the cash slides that you have seen before. So at the end of September, cash position was about €940 million, resulting from the cash in that we had earlier this year from the Gilead transaction, both through the up-front as well as through the subscription to shares; and the cash burn that was €78 million for the first nine months of this year. That €78 million, if you extrapolate that to the full year, makes us believe that we will be in the range that we provided for before, between €100 million and €120 million of total cash burn excluding income from Gilead. The €940 million that we have at the end of September excludes still tax receivables that will pay up over the next 4 to 5 years from the French and Belgian governments, and a total of €67 million is now on our balance sheets at the end of September. If I then move to the next slide, on revenues, strong increase in revenues, 38% to €65 million over the first nine months. And not only is it a strong increase, but it's also an increase which is to a large extent cash based. And I've tried to picture that through the different color coding. The orange elements are more or less, cash income; whereas the green code, its parts are what I would call accounting income. The accounting income is associated with the up-front that was paid to us…

Thank you, Bart. If we look at the clinical news flow over the remainder of the year and what's already planned for next year, you'll see that it's quite extensive. For the first time we have split the clinical news flow in two slides, because of the number of programs that we'll provide data going forward. You see that there's a lot of news flow around filgotinib. I would like to focus on top of what Piet has said on the start of multiple proof-of-concept studies with filgotinib in other diseases in 2017. That will start early in that year, and we will announce that when those studies start. With CF, Piet has already highlighted the number of programs that are going into various stages of the clinical trials, with the aim to get the triple started midyear next year, so exciting times there as well. If we go to the next slide with the other news flow on the other programs, you see that with 1690 we hope to report the top-line data in the first half next year. We will start Phase 1 with the other IPF program 2938. With Servier, as I said at the beginning, we are moving forward with our OA program, the disease modifying drug here, a very interesting market opportunity, where Galapagos has the unencumbered U.S. rights. And we'll start independently of Servier, a Phase 2 study in the U.S. With MorphoSys, we're looking forward to the data from the first trial in 2017, and hope to follow it up with a start of a Phase 1B study. And then another program in atopic dermatitis, 2534, we'll start Phase 1 in 2017 as well. So a lot data coming up last quarter, but also in 2017. So the investors will be served to what they're looking for. With that, we would like to end the formal presentation. I'm handing it back to Elizabeth.

All right. Thank you, Onno, Piet, and Bart for the presentation. I'd like to invite the operator now to instruct callers as to how they can pose a question.

[Operator Instructions]. We will now take our first question from Tim Woodward from Goldman Sachs. Your line is open. Please go ahead.

Hi there. It's Tim Woodward from Goldman Sachs. Thanks for taking my questions, two, if I may please. The first is on SAPHIRA 2, did you see the efficacy that you would have expected to from your in vitro? The reason I ask is I guess if you decide to go forward with 2451 in the triple combination, then you will be relying on that in vitro data of efficacy, rather than in patients. And so the second is, can you just describe what you can do differently and what you can take across from your findings in SAPHIRA 2 into how you're conducting SAPHIRA 1? Thanks very much.

Okay. But I think your question is for me?

Yes, please.

Yes, please. On SAPHIRA, well, SAPHIRA 1 is concluded, so all patients have been on treatment. So what we're doing is analyzing the study, so there's nothing out of the lessons from SAPHIRA 2 that can change SAPHIRA 1, as it is coming too late. What I said before is that SAPHIRA 1 is exploring a higher dosing, so the dose there is clearly higher in SAPHIRA 1 than compared to SHAPHIRA 2. So patients will be higher exposed. And we remain for the moment blinded for data, and we'll bring them to the world as soon as we know them. And that's foreseen in December this year. On what we've learned from SAPHIRA 2 in the in vitro data, so as I said in this call before, exposure came out at the lower end of our expectations. So, this study SAPHIRA 2 allows us to fine-tune to see where we can improve for the future programs. But quite honestly, we think the SAPHIRA 2 data confirms that our in vitro data translates into clinical activity. Of course, we didn't max out. But we saw with higher exposure we are convinced that we will get to, as well, a maximum of activity. Limitation of SAPHIRA 2, it was a very small patient population. We knew that. But it was one with [Indiscernible] mutation, so it allowed us to explore the lower end of the dose range. So that's why we wanted to do that. So we have those data now, which we need if we want to move forward with 1837. So we will have safety data across a broad exposure range. For 2451, you're correct, if we move forward then in patients that will again start from the pre-clinical in vitro data. And that needs to translate into a dose which will refine our dose prediction models with all of the data coming out of the SAPHIRA 1 and 2. Thank you.

Thank you.

We will now take our own next question from Michael Vlemmix from KBC Securities. Your line is open. Please go ahead.

Good afternoon, everyone. I'll start with two questions. My first one is regarding the safety results of the SAPHIRA 2 study. Can you maybe elaborate a bit on the adverse events, the headaches that were seen with both the low and the high doses in this population? Were these during the entire four weeks of treatment and more of a chronic type, or standalone acute events? I'm just looking at this purely in theoretical, if you were to increase dosage for these patients, how that would potentially evolve. And then, the second question regarding the poster presentation of the Read-Through agents, the addition of those, showing nice results. And I was wondering if adding those types of agents would be a potential add-on in the future trials to increase efficacy? Thank you.

Okay. Thank you again for these quite good questions. Safety, SAPHIRA 2, what we've observed there is what we typically observe in Phase 1 and Phase 2 early studies, when very little is known about [Indiscernible] exposure of the patients. So headaches were transient, and it was not an acute form. But that's what we always see, and observe in almost every study we do, so nothing to worry about there. And as well, we are confident that we can dose higher, which has been done as part of SAPHIRA 1. So we will report those higher doses by year-end, and all that we can indeed confirm that those headaches were something that we see all the time. So on the Read-Through agent additions, so the whole CF field has been sharing one ambition is to find treatments for all of the patients in the CF field. So the main focus of the program and short-term focus of the program is clearly homozygous and it means delta F508. But one another day, we as well want to tackle the class 1 mutations, where indeed by adding a Read-Through agent, we can go and treat those forms as well. So it's on the agenda, but not for the near term. Complexity there is that we probably will have to go with experimental drugs. And then you have to do also combo tox [ph] upfront, so that doesn't make our life easy, if that's with an external compound. But it's on the agenda. But I can't give you any timing there. Thank you.

All right. Thank you.

We will now take our next question from Vamil Divan from Credit Suisse. Your line is open. Please go ahead.

Great. Thanks so much for taking my questions. I just had a couple, more on just the data flow you discussed and when we should expect public disclosure. So for SAPHIRA 1, you mentioned you'll have that by yearend. So should we expect some sort of top-line press release when you have that? And will it be sort of reasonable expectation in terms of a medical meeting to see that data? And then similar for next year, I see all the data that you're laying out between the potentiators and correctors and going into the triple. Is there anything we'll see publicly in terms of the double or anything else, before you move to the triplet in healthy volunteers, or certainly by the time it goes into patients?

Onno, do you want to take that question?

Well, regarding the first question, we anticipate to come out with the top-line data in a press release by the end of this year. Piet, have we decided yet on a scientific conference that we're going to present the data?

Well, normally there is one in June in Europe, a CF conference. So I think the logical thing is that we'll be present there in June. But I don't have the date yet and the place. But there's always a European CF conference first half, and then an American North American in second half. So we should be present there at the European conference.

Regarding your second question, I think we haven't decided yet how we're going to communicate the dual data, at what time, and if we're already in the triple before the dual is going to be published. Piet, that's correct, right?

Yes. What we do there is we're going to try to accumulate as much of the information as we get in terms of safety exposure, and if so, we don't really in there to quickly close those studies. If you want to move quickly forward with our triple combo later, the more safety we can get, the better, and that's where we will open a number of Phase 2 studies, but not with the aim of publishing data quickly, rather with the aim of getting as much safety as we can, and convert those studies from a mono to a dual later, and by expanding those studies. So we don't have a plan there to quickly converge dual data to any conference.

Okay. All right. Thanks so much. I'll jump back in the queue.

We will now take our next question from Phil Nadeau from Cowen & Company. Please go ahead.

Good morning. Thanks for taking my questions. First a follow-up on SAPHIRA 1, given the exposures that you saw here in SAPHIRA 2, where do you think the exposures will be in SAPHIRA 1 at the doses used in comparison to the EC50s and 90s in the G551D population? Do you still feel comfortable that the doses will get you sufficient exposures well into the efficacious range, or are you now worried that the doses might be a little too low?

Okay. Thank you. No. For SAPHIRA 1 it's clear we are confident that we'll get to the exposures where we can be at least as good as Kalydeco and hopefully the in vitro translates that we can show some superiority over Kalydeco. We don't think we'll get up to the EC90s anymore. That's clear. But there is still quite dose range between EC50 and EC90. And so we are confident that we'll get to at least as good, and hopefully better, in terms of efficacy than Kalydeco, if our in vitro data translates into in vivo.

Okay. And then second, on that -- I believe that SAPHIRA 1 also had a dose increase strategy two weeks at a lower dose, two weeks at a higher dose. Can you give us some sense of what sort of chloride changes and FEV1s you'd expect after two weeks at the higher dose? Can you remind us maybe what Kalydeco produced on those two measures after two weeks?

Thank you. So if I understand well, what was FEV increase seen with Kalydeco after two weeks, so the FEV increase was in the range of 3% to 4% after two weeks of dosing in the S1251N population. So we can send that paper out, there's a paper published by the CF work group. And if you only dose for two weeks, a 3% to 5% is a reasonable expectation.

Sorry. Was that for G551D or 1251? I'm actually asking about G551D for the future dataset?

In both 51 patients I mean. So that's what you can compare to today. So in SAPHIRA 2 we dose patients with S1251 mutations. So comparing apples-with-apples, so comparing with the 1251 data of Kalydeco, there you are in the range of 3% to 5% of FEV improvements after two weeks of dosing.

Right. So I guess I was asking about the G551D population. So we can set a benchmark for the data that's coming up at the end of the year. Do you have the equivalent figures for G551D?

We expect somewhat higher. It should be more 6% to 8% and 10% after two weeks. So data that the increases were higher, even after only two weeks of dosing.

That's very helpful. And just one last question on the healthy volunteer study or the healthy volunteer Phase 1 dosing of your triple, it looks like you've allocated about six months to complete that. I think a lot of us also cover Vertex, and just saw them take just about 12 months to complete a healthy volunteer portion for their triple, despite the fact two elements of that combo were basically either approved or already in Phase 3 trial. So what gives you confidence that you can complete the healthy volunteer Phase 1 portion of your triple in just six months?

Based on what we currently see in terms of safety and exposures with the compounds that have either been in Phase 1, 2222, 1837, and what we hope to see with 2737. I think the Vertex program clearly has its complexities, and that never speeds things up. So, clearly I think the way we plan it is how we've planned this before. And our timelines in Phase 1 have been quite constant over the years. So I don't see a reason why this would take longer than what we've planned. So I'm not saying that some groups can't prefer to do much more or longer studies. But the way we built up from one or two dual and then to triple should allow us to perform it within the timeframe foreseen.

Thanks. Thanks for taking my questions and congratulations on the progress.

We will now take our next question from Anastasia Karpova from Kempen. Your line is open. Please go ahead.

Good afternoon. I have two questions, if I may. Can you please comment on the 2222 trial in combination with Kalydeco potentially, how big that would be, and what you would be looking for? And maybe on competitive landscape, does data that Vertex recently published yesterday on the VX-59 [ph] change your view on the required effects you would like to see from your triple combination? Thank you.

Okay. So the first one, the 2222 study and indeed the study in CF patients, thank you for the question-- is a study on top of Kalydeco. So, we expect a couple of things from that study. Safety first, exposure of women [ph] patients, first with 2222. So we have quite of flexibility with 2222. And our hope for that is that the PK will be as expected. But that's the first thing that we expect there. Safety exposure is the second. And then Vertex have shown before that in some of the G551D patients when they did add 661 that they saw a further change, a limited change in sweat, and some further improvements of FEV. There is a debate on those data, whether we still will get that type of improvements when patients have been longer on treatment. That's a possibility. If we see it that's nice, if you don't see that is not a problem, because it's mainly a safety study. But if you see some activity there, we will report, that's for sure. No problem. Then on the pre-clinical data of Vertex, I can add little. I think broadly we go for triple combinations. We both see that we get, if we add the Kalydeco [Indiscernible] we improve efficacy two, three, four fold pending on the donor [ph]. So I really was pleased with what we've learned this week, and we are convinced that we have a competitive or more than a competitive triple in the reach, and that we're going to develop. I didn't see any reason why we would have to change anything on what I have published this week.

Thank you very much for taking my questions.

Thank you.

We will now take our next question from Matthew Harrison from Morgan Stanley. Please go ahead.

Hi. This is Vikram on for Matthew. Just one question from our side. On filgotinib in Crohn's, are you planning to provide a 25% responder rate, just so that people can compare the dataset with the Celgene data that was released? And if so, when could we expect that?

Okay. Thank you for that question. The [Indiscernible] data on the 25%, honestly we don't have any plans to leave those data. Our KOL [ph] said before the 25% doesn't mean anything. So we don't see why we should add data that doesn't mean anything to our KOL. We are very happy with our 60% improvement score, and are confident that that will translate as well into Phase 3. And from a sideline, then my observation is that too many people try to interpret studies which were not designed, which are not powered for [Indiscernible]. So whether you report 25% or a 50% improvement, they are simply were not powerful. So you will always get a number that tells you something, but can't tell the full story. And that's why they advise us to take the most difficult hurdle, 50%. If you see something there, it will give you more confidence as you count powers in the Phase 2 for efficacy and for [Indiscernible]. So, no, we don't plan, in short, to remove those data.

Okay. Thank you.

We will now take our question from Debjit Chattopadhyay from Janney. Your line is open. Please go ahead.

Hey, thank you for taking my questions. Let me start with filgotinib. Could you clarify the plans for the 200 milligram dose in TNF naive patients, male TNF naive patients in the US? Will those patients be rolled over into the maintenance portion of the study, or how do we think about them statistically once they finish the safety portion?

Can you please repeat the question, whether I can explain -- so it's the TNF experience in the FINCH 2 study?

Yes. In the IBD program that 200 milligram dose…

Okay, yes. Sorry.

So, the question is in the IBD program, the 200 milligram dose in male patients who are TNF naive; how are we going to account for them statistically? Are they going to move to the maintenance portion of the study, or the initial -- the 10-week induction phase, once they finish the safety portion?

So, we will not collect as part of the IBD program, data with the 200 milligram in TNF naive patients for IBD in the US. So those data will have to come out of the U.S., where most of these patients are located. So we will make sure that we have sufficient male patients, TNF naive, 200 milligram across the globe to compensate for the few patients in the U.S. that can't be included. So that is the question. But they will be remain in the US on the same dose. So that's how that's going to be taken care of.

Okay. Now moving to the SAPHIRA 2 program, could you comment on the lower sweat chloride response in the SAPHIRA 2 versus the FEV1 response? It seemed to be very much in line with what we have seen for Kalydeco, given the small number of patients in the S125N patients.

Okay. Thank for the SAPHIRA 2 question. Lower sweat chlorides were two possible causes. Either that's what we really think is that exposure was suboptimal, and that as part of SAPHIRA 1, we will do that. We will increase exposure. We should get to a full response there, so that we then get higher sweat chlorides. Second possibility is that lungs and skin differ a bit. So when we predicted those, we really targeted for the lungs. And maybe we did favor a little bit there the skin, and that might be a reason why for a compound that tends to penetrate better in the lungs probably compared to the skin, we see better efficacy compared to sweat chloride changes. But there is no clarity there. Let's be honest. That's the second possibility. That, of course, complicates the whole picture. If you want to later dose range based on sweat, so then you must be sure that your compound penetrates as well into sweat as into the lungs. And so we will have to watch that and analyze carefully as part of the SAPHIRA 1, where we have one more patient, and where we do three dosages rather than two. So we should get a better picture there. But if it's due to the penetration throughout the skin, okay, then we have to think carefully how we're going to design future studies if we want to change our dose type rate [Indiscernible].

And just one clarification on the SAPHIRA 1 study; did I hear you say before the doses that you're evaluating, the higher doses that you're evaluating in SAPHIRA 1 will get you very close to the Kalydeco dose in terms of efficacy?

Yes. So SAPHIRA 1, indeed. Thank you for the question. SAPHIRA 1 we designed to explore whether in vitro we see a higher Emax with 1837 compared to Kalydeco. And the dose range we apply will allow us to see whether indeed that translates in vivo into higher efficacy. So with the current data of SAPHIRA 2, we should not think that we get up to the EC90, where you got up to one on the 50% of the efficacy of Kalydeco. But we should be at least as good, and probably somewhat higher, than Kalydeco as part of SAPHIRA 1.

And one last question. On the second potentiator, do you think you need mono-therapy study in any one of these mutation subgroups, or based on the early volunteer data that you'll present next year, you should have enough to directly start thinking about triple combo? In which case, which one do you really want to take forward, the twice daily or the once daily? Thanks so much for taking the questions.

Thank you for two additional questions. I think for patients that need to be treated lifelong, mono-therapy would be a clear advantage, so there's clearly a preference for once a day. But of course efficacy will trump everything. So if you really need to [Indiscernible] efficacious at the combo. But a once-a-day would have an advantage. And well, we believe that based with the SAPHIRA program, then the 2222, which should start into patients as well, will be able moving without those single-studies, those mono-therapy studies, 2451 if needed, into patients immediately without a need of mono-therapy studies.

Great. Thank you so much.

I think we have time for one last question, if there is still one.

[Operator Instructions] There are no further questions – beg your pardon. Our next is from Hugo Solvet from Bryan Garnier Securities. Please go ahead.

Hi. Hello. Thank you for taking my question. Just if we look ahead in six to nine months, you will moving in Phase 2 trial for the triple combo. What are the interactions you have with the U.S. centers at the moment and how do you anticipate competition with Vertex who might be looking in some centers at the moment? Anything you can share on this subject?

Okay. Thank you for the question. First off, well until now we've run the CF program mainly outside the U.S., so it's clearly part of the program to move quickly into the U.S. And we will use there the different components of the program, the mono, the dual, and the triple as soon as we can. So we don't want to underestimate the competition with Vertex. They are very well-established in the field. They know everybody. So they probably will get access easier to patients than we. On the other hand, the CF community is a very motivated field, and really hopes for a number of drugs, and to be able be to choosing between drugs. And there's only one way that a number of centers are going to include patients in trials of other companies, as well. Otherwise there is -- and they know that if they only test the Vertex, they'll be in the hands of Vertex, and there will be probably little choice later on in the market. And so having the freedom to choose between therapies is what they desire as well. And that desire requires then that also other companies get access to patients, and on the sales part of the SAPHIRA program we've been very pleased with how those teams have been working with us. So, I don't want to underestimate the Vertex advantage they have. Let's be clear. But we believe that -- and we are in the field now. The feedback as well is that we will get access to the patients. Don't forget for the triples you have homozygous population, [Indiscernible] is there, but is not really serving fully that population. So maybe patients are either not taking or either are underserved. So we should be bringing it there to participate, delta F508 [Indiscernible] patients, so there is no treatment. So they as well, we believe there will be sufficient patients who will be included in our studies. But we are not going to underestimate it. Thank you.

Thank you.