Thank you. A press release with our first half 2019 financial results and second quarter business update became available earlier today and can be found on the News and Events section of our website. Before we start, I would like to go to Slide 2 to remind you that forward-looking statements maybe presented during this call. This may include statements about our future expectations, clinical development, regulatory timelines, the potential success of our product candidates, financial projections and upcoming milestones. Actual results may differ materially from those indicated by these statements. argenx is not under any obligation to update statements regarding the future or to conform those statements in relation to actual results, unless this is required by law. I am joined on the call today by Tim Van Hauwermeiren, Chief Executive Officer; Keith Woods, Chief Operating Officer; and Eric Castaldi, Chief Financial Officer. On Slide 3, you will see a brief agenda for the call. We will start with recent news followed by a pipeline update. Keith will talk about commercial preparations for our lead asset, efgartigimod and its first indication, generalized myasthenia gravis. Eric will then provide financial results for the first 6 months of the year and Tim will end the prepared remarks with upcoming milestones before we start the question and answer portion of the call. And with that, I’d like to turn the call over to Tim.

Thank you, Beth and welcome everyone. This past quarter was underscored by our May R&D Day, where we unveiled our argenx 2021 vision, shown on Slide #4. We outlined our intention to expand the building blocks of our growing organization, including our unique innovation engine, our late stage clinical development programs and our people and processes into an integrated immunology company, and more specifically into a commercial organization in 2021. We are building a deep pipeline of highly differentiated molecules that grow from our roots, the innovative access engine and will feed into our commercial franchises, one in neuromuscular and one in Hem/Onc. Through these franchises, we plan to take our pillar of being patient focused and put it into action, launching efgartigimod into its first indication, generalized myasthenia gravis, to serve the persistent unmet needs we have identified in this community. We are devoting resources across the organization to scale up to the demands of a commercial launch. argenx Japan is up and running, solidifying our presence in 3 high priority regions Boston, Ghent and Tokyo. We hired our Chief Medical Officer, Wim Parys, who is very experienced in product development and help bring 7 now commercial molecules to approval. We have made all the key hires across the organization, many in the United States, and are now at 182 total headcounts. And we are expanding our relationship with Lonza to ensure we are operating at commercial scale well ahead of launch. We have Keith on the call today to talk more about the key infrastructure we are implementing to compete as an immunology powerhouse across our key markets. On the call today, we will also highlight each of the four indications from our ambitious efgartigimod program shown in our pipeline on Slide 5. Notably, in our press release…

Thank you, Tim. Today, I would like to talk about the work we are doing on the commercial front, building on the launch preparation we shared during our R&D Day in May. On Slide 16, you can see an overview of our therapeutic franchises. Following the Phase 2 proof-of-concept data in MG, we realized we had a high value multi-indication product that would, assuming success, require a significant commercial infrastructure across several therapeutic areas. We recognized the importance of starting to build this infrastructure early and getting a repeatable formula in place because efgartigimod and MG is just the beginning. Let’s discuss our launch preparation work along two key themes. First, where we will play and second, how we will win? Starting with the where, we are building out a plan to be a fully integrated biopharmaceutical company in 2021. We have three geographic priorities in the U.S., Japan, and Europe. As Tim mentioned earlier, we are making key hires in the U.S. around our first commercial launch in 2021 of efgartigimod and MG. Japan is our second priority, and we do not expect it to be far behind the U.S. in terms of a launch timeline. MG is a very attractive market in Japan due to the high unmet medical need and the concentrated prescriber base with around 200 prescribing physicians. So this is a group we can reach with an efficient argenx team. Rare disease status is similar in Japan as it is to the U.S. and so medications targeting small underrepresented populations are given certain efficiencies. And perhaps most importantly, health insurance coverage is universal in Japan. Critical to the question of where we will play is our commercial franchise model where we can build infrastructure and winning core capabilities within each. We have announced 2 commercial…

Thank you, Keith. So Slide 18 covers our second quarter operating results, which are detailed in today’s press release and regulatory filings. Total operating income reached €51.3 million for the first 6 months of 2019, an increase of €30.8 million for the same period in 2018. The increase is related to the €16 million increase in the recognition of milestone payments from AbbVie, the €7.8 million from the recognition of R&D service fees under the Janssen collaboration and an increase of €5.2 million driven by higher payroll, tax rebates for certain R&D personals. R&D expenses for the first half were €78.3 million compared to €34.4 million for the same period in 2018. Selling, general and administrative expenses were €27.5 million for the first half of this year compared to €11.5 million for the same period in 2018. The increases in R&D and SG&A expenditures over the prior year has been driven by the progress made within our late stage pipeline, including higher consulting and personnel expenses, higher clinical trial costs and manufacturing expenses, and also the recruitment of additional employees to support ongoing activities. We expect operating expenses to increase year-on-year as we further advance our pipeline and prepare for future commercialization. For the first half of 2019, financial income amounted to €7.2 million compared to €1.3 million for the same period in 2018. Exchange gains totaled €2.5 million for the first half of 2019 compared to €4 million for the same period in 2018. The total net loss for the first half of 2019 was €45.1 million, compared to €20.1 million for the same period in 2018. As of June 30, 2019, we ended the first 6 months of the year with €944.3 million in cash, cash equivalence and current financial assets, compared to €564.6 million on December 31, 2018. And with this, I would like to turn back the call to Tim.

Thanks, Eric. We’re expanding quickly in an integrated and deliberate way across our organization. We have several milestones to look forward to in the next 18 months shown on Slide 19. First with efgartigimod, we will report top line data from the Phase 3 ADAPT trial in MG in the second half of 2020. We will initiate the Phase 3 ADVANCE trial in ITP in the second half of 2019 and the second Phase 3 trial with a subcutaneous component will follow. We will report data from the Phase 2 trial in PV in the first half of 2020. We will launch the Phase 2 trial in CIDP in the second half of 2019. We will also report data from the Phase 1 healthy volunteer trial of the efgartigimod ENHANZE combination in the second half of 2019. We anticipate that given efgartigimod’s best in class safety and efficacy profile are validated across multiple clinical trials targeting a well known and clinically relevant biological mechanism, we are in an advantageous position to deliver substantial value in the near and long term from this candidate. With our other assets, we expect the following. Janssen will dose the first patients in a Phase 2 and registration-directed trial of cusatuzumab in newly diagnosed AML patients who are unfit for intensive chemo. We will file the CTA for ARGX-117 before the end of the year and dose subjects in a Phase 1 healthy volunteer trial in early 2020. We will continue to lead optimization work on ARGX-118 and will line up ARGX-119. You can see by the depths in our pipeline and the infrastructure we’re putting in place ahead of our first commercial launch in 2021 that we are dedicated to building an integrated immunology company. We thank you for your time today. And I will now turn the call over for questions. Operator?

[Operator Instructions] And your first question comes from the line of Matthew Harrison. Please go ahead.

Hi, guys. Good afternoon guys. Thanks for taking the question. I guess, probably maybe two from me if I can. So the first one, just – I know you are not ready to talk about the CIDP trial design. Maybe you could just talk to us a little bit about how you’re thinking about the indication and what you think you need to demonstrate in a trial to be able to move this ahead given the results from IVIg as well as steroids? And then a second question from me just on bridging for IV to subQ, could you just maybe briefly talk about what sort of steps you need to take with regulators to have clarity on whether or not a bridging study is appropriate?

Thank you, Matthew and thank you for being with us today. So the detailed CIDP trial design is going to be disclosed in a CIDP KOL event later this year. We’re going to do, again, an educational session on the disease, today’s management of the disease and then of course the trial design and the rationale for the trial design. But let it be clear that we have the ambition to establish, again, a clear signal in this patient population when it comes to establishing the correlation between knocking down IgGs and seeing clear clinical improvement. So as we discussed before, there is precedent on how to do Phase 2 clinical trials in CIDP. There are known clinical and regulatory endpoints. So I think we will be well equipped to set a big competitive trial, which we will disclose later this year. With regards to bridging IV to subQ, I think we are clearly going to try and leverage the unique mode of action of the compound, where we can correlate the IgG reduction to PD effect with clinical outcome. And I think the real discussion with the regulator can start once we have collected solid PK-PD and bioavailability data from the currently ongoing Phase 1 study in healthy volunteer. So I think this is going to be unprecedented. But we will have to enter into the discussion of course to see to what extent we can agree with the regulator on the path forward. So when we have the outcome of that conversation, we will certainly turn back to our stakeholders and communicate about it.

Thank you. Next question comes from the line of Christopher Marai. Please ask your question.

So just with respect to the ITP subQ formulation that you’re using, will it be the Halozyme formulation or the homegrown subQ? And then just to maybe piggyback on that last question, so given the start of the subcutaneous trial with the Halozyme formulation, do you expect data will be available such that it could be used in your first BLA for efgartigimod in MG such that your label would have both IV and subQ formulations?

So clearly we have two different subQ product presentations. It is clear from today’s call that we’re pushing forward with both product presentations. And homegrown maintenance product is a product we’re going to push forward into the Phase 3 registration program for ITP. So that clearly is a product which would come on the back of an IV induction. So the start of the Phase 1 Halozyme combination product will indeed deliver data in time by the end of the year and the company is going to disclose on the back of these data also how it’s intending to take the product forward into patients. But allow me to hold off on answering that question until we have the time to look at the data and then also disclose and discuss the data with you.

Thank you.

Thank you, Chris.

Next question comes from the line of Derek Archila.

Hi, Good morning and, thanks for taking my question. So, Tim, maybe first off, can you just talk about maybe or provide a little color on the endpoints you might use in the ITP Phase 3 to measure durability of response? We’ve seen some of the data from the [indiscernible] Phase 3. So would it be kind of similar or how do you think about that?

So I think the field has clearly demonstrated that a platelet count of 50,000 platelets per micro liter is clinically meaningful. And we also saw that the regulators started to ask for some measure of durability because it’s of little clinical meaning when a platelet count is crossing the 50,000 number just once. What you want to see is a persistent increase in platelet. So I think what we disclosed today is a trial design where we will want to see in 4 out of 6 subsequent visits that platelet count of 50,000 and we also pre-specified the window, the time window in which that should happen. So we allow patients to go through that induction. And towards the end of that induction, we really want to see a sustained increase in platelet counts in order to call that a response.

Got it. Thank you. And then just a follow-up onto the CIDP, so I know you are not going to talk about your trial design, but I just want to see if you had any thoughts or comments on the UCB CIDP trial design? It looks like they’re dosing rozano on top of standard of care IVIg or subQ IG. So I just wanted to kind of get your thoughts on that and whether you think there is a potential benefit of dosing both therapies in those – in CIDP patients?

As you could guess, it’s premature for me to comment on the exact trial design. Remember that I think we always start new indications from the start, which means establish the activity of the compounds, establish a clear correlation between the PD effect and the clinical benefit. So I think that’s also what you’ll see in our CIDP study, that is where we’re going to start.

Okay, alright. Thanks.

The next question comes from the line of Ted Tenthoff.

Hey, thank you very much and I really appreciate the thought for Phase 3 ITP trial design, a lot of progress on a lot of different fronts. I want to come back to pemphigus if I may because it’s a disease I know a little bit less about and obviously kind of heterogeneous in terms of manifestation. So, what should we be expecting from that data next year, what would be a win for you guys that would really show that this is an indication to pursue with efgartigimod? And do you think this is an IV indication or is this one that may be better utilized via subQ?

Hey, Ted. Thanks for being with us. So what to expect from the pemphigus trial, recall the key objectives of that study, right. So we’re seeking to establish the correlation between the reduction of total IgGs and then specifically of course the anti-desmoglein auto antibodies on the one hand and then disease improvements, which we assess along the PDI score on the other hand. And we also want to link that to clinical improvement. Now in pemphigus, let me walk you again through the three meaningful clinical improvements you want to see. First of all, you want to see disease control in a pemphigus patient. Disease control is defined as no new lesions are being formed and you start to see the closing of the existing lesions. That is very important for a PD patient. These lesions are extremely painful and difficult to manage. So you want to stop that. Then secondly, you want to go to consolidation. End of consolidation basically means that 80% of the lesions closed and there are no new lesions being formed. That is a very substantial step on the way to a clinical remission. And the definition of clinical remission basically means that all lesions are gone. And remember that in the interim update, we could already show in the first cohort a speedy disease control, which very nicely correlated with the PDI score improvement and the knockdown in pathogenic IgG4s. The reason we amended the study is we want to now show or hopefully show that with prolonged exposure, we can also go to the second stage and which is end of consolidation and then the final stage, which is clinical remission. To the other question, IV or subQ, I think the jury is out and allow us to do the homework into Phase 1 Halozyme study, and then I think the scientists and clinicians will have all the data in hand to make a deliberate choice.

Next question comes from the line of Jason Butler.

Hi, thanks for taking the questions. First one, just another on the ITP ADVANCE trial design. Specifically, is the trial powered or does the trial has statistical power to show a difference versus control on the secondary endpoint of bleeding event rates? And then my second question is for the real-world study that you’re doing in MG burden of disease. Are you looking at economic burden as well as health burden in that study thanks.

Thank you, Jason. Two great questions and I am going to refer the second question to Keith. We have the benefits of having Keith with us today. He is best placed to talk about the real world evidence too. With regards to the ITP trial design, expect pretty standard endpoints in the secondary endpoint. So, yes, indeed we will look at reduction in bleeding events and we will also look at quality of life at some of these secondary end points, absolutely. Keith, do you want to tackle the real-world evidence question?

Sure. Thank you. In the real world evidence study that we are beginning in the second half of the year, what we are looking at is the true disease burden for these patients with MG. And the data that we’re going to be generating is going to not only be on the impact of the disease, but the patients living with the disease and living on treatment and the responses to various treatment. It will look at really the broader picture that will include their hospitalizations, it will include number of crisis and so we will be able to take into consideration paralleling that with the economics of the therapies that they would be on.

Great. Thanks for taking my questions.

Next question comes from the line of Akash Tewari.

Hey guys. And I apologize if I didn’t hear the window correctly, but why did you choose the particular definition for sustained platelet count for ITP of greater than 50 to the 9th for at least 4 out of 6 visits from weeks, did I hear this correctly, 19 through 24? And then you compare that versus like Riegel’s definition which was similar but it was from weeks 24 – 14 to 24 and the TPO is where it’s kind of a cumulative percentage over a 6-month period. And would that definition of sustained response include without rescue therapy? And then on the Halozyme formulation, just to understand the range of possibilities, is it possible that you could bridge patients from the Halozyme formulation to the Phase 3 myasthenia gravis study, so like the IV to the subQ? And if not, when could we potentially get a subQ myasthenia gravis Halozyme formulation on the market? Thank you.

[Indiscernible] great to have you with us today. So, I think to answer your first question on the time window in which we’re going to measure the sustained platelet count improvement, I think that’s mainly being driven by the learnings from our own Phase 2 study in the PK-PD model. So, I think we had to choose carefully the window where we maximize the chance to see a durable response. And I think that could be different or slightly different for different molecules, but we just wanted to maximize chances to see success. The definition itself in terms of 50,000 in 4 out of 6 visits is indeed something which was pioneered by Riegel. With regards to your second question, I think you have to expect that the ADAPT study is going to sail as fast as possible to conclusion. I do not believe that we are going to try and ride that protocol by bringing in a subQ product. Remember that speed to market is the key strategy here. The key question is what is the minimum dataset, which the regulator will want to see to allow us to comfortably bridge from IV into subQ and there we are going to heavily leverage to PK-PD bioavailability data from the ongoing Phase 1 study, to what extent, the regulator will want to see additional comfort on top of that I think is the very topic of the conversation.

Got it. Really appreciate it.

Thank you.

Next question come from the line of Yatin Suneja. Please ask your question.

Hi guys. Congrats on the progress and thanks for taking my question. The first question I have is on the ITP side. Can you maybe help us understand the scope and size of the second ITP study relative to ADVANCE? I mean, how it might differ from the first study, I mean, or is the main difference only is IV subQ or is it purely a bridging study? And then I have a follow up.

Hi Yatin thanks for being with us today and thank you for this question. So, we haven’t said much about the second study. So, I think today’s call was mainly focusing on the first study. Remember that we did decide to accelerate the subQ product in ITP from what was originally a Phase 2 into a Phase 3 and the only thing I would like to say today is that the concept of the second Phase 3 study will be to give further comfort on study 1 for the IV product, whilst also making use of this opportunity to demonstrate hopefully the power of the subQ product. But more details to follow and we will certainly be happy to enter into the detailed conversation then.

Got it. And then on the MG side, maybe could you talk about what you are seeing in terms of enrollment in the ADAPT trial that sort of enabled you to guide now to second half of 2020, have a more precise guidance now versus the product 2020 guidance that you had in the past?

Remember, Yatin, the conversations we had when we kicked off the ADAPT study in terms of guidance for the duration of that study, the best proxy which we could give was actually the precedent of the REGAIN trial. And it turns out that actually that guidance or that proxy is also applicable to our study. So, what we are announcing today is that we’re on track with enrolling the trial, we continue to stick to the guidance which we gave earlier. And then when you simply do the math, you will see that the study should read out in the second half next year.

Very good. Thank you so much.

Thank you.

Next question comes from the line of Sandra Cauwenberghs. Please ask your question.

Thanks. I have two small questions left. I understand that it’s difficult to give more insight on the second ITP trial. But given the fact that competition is advancing with the subQ alone application, where could the findings of the second ITP trial give you a differentiating factor in terms of patient adoption or commercialization of the drug for that indication? The second question is with regard to 117, so I understand that the first indication would stay in the neuromuscular corner and maybe I missed it during the R&D Day, but is there a biological rationale to also a C2 blocker in a disease like ITP given the fact that there are some historical reportings on C2 deficiency in ITP? Thanks.

Thank you, Sandra. Two good questions, let me start with the second one first. So, when we talk about ITP and our understanding of the pathogenic role of the antibodies, there are at least 4 pathogenic modes of action of these autoantibodies, right. And 1 of the 4 is indeed complement recruitment. So, we cannot quantify exactly how many patients suffer from a complement recruitment as the key mode of action, but it certainly plays a role. In addition, of course, to complement recruitment, we also see the accelerated clearance of platelets, the impaired production of platelets, and the impaired platelet functionality. So, we believe that clearing the pathogenic IgGs is a more profound impact on the disease biology is also extreme by the way of the complement recruitment because complement in ITP is recruited by these autoantibodies. So, yes, complement is involved, but we think that the heart of the biology actually sits with the pathogenic auto-antibodies. With regards to differentiation in the ITP space, I think it’s still early to talk about it. We have only seen our own Phase 2 data and we have seen Phase 2 data in public from one of our FcRn colleagues. I think already there you see a distinct different patent in terms of safety and efficacy, but truly to compete or talk about competition in the global market we would need to see Phase 3 data for both products. So, allow me to hold off on that question and build an answer on that on the back of Phase 3 data.

Sure. Thanks.

Thank you.

Next question comes from the line of Graig Suvannavejh. Please ask your question.

Hi good afternoon, thank you for taking my questions and congrats again on the progress. I’ve got two questions and they are both related to your interest in dermatology. So with dermatology and your decision maybe to move forward as a third therapeutic area or not, is it completely dependent upon whether you have positive data in PV or do you still see an opportunity in dermatology just in case the proof of concept does not read out in the way that you want? And then my second question with regards to, on a similar note, whether you’d move into nephrology, is this an either/or of going into dermatology or nephrology or could it possibly be both?

Yes, thanks for that question. I think that’s a great strategy question. The way we are thinking internally is that only it makes sense to invest in commercial infrastructure if that infrastructure can also be leveraged across multiple indications. So, PV of course would be a great entry point, but we would want to see rationale and/or data in at least second and maybe third indication before we would establish a franchise. And that is the potential of course across our portfolio to play in multiple skin indications. But let the data drive the decision and no dermatology and nephrology are not mutually exclusive. I think they’re both very interesting spaces. And what we said in our R&D Day is that actually we are starting with a neuromuscular and Hem/Onc franchise, but there is expansion possibility in both skin and kidney.

Next question comes from the line of Joon Lee. Please ask your question.

Hi thanks for the question. Regarding pemphigus vulgaris program for which we expect data in the first half of 2020, there are competing mechanism of action like B cell depletion methods. Rituximab for example is now approved for PB and has demonstrated complete remission at month 24 with infrequent dosing of 6 to 12 months. How do you think about competitive landscape versus such modality? And what are some of your tall design strategies to help setup efgartigimod for commercial success in PV? Would safety or convenience be potentially differentiating aspects of efgartigimod? Thank you.

That’s a great question. Thank you. It’s also a question which we tried to address in our KOL during last year’s pemphigus event. So, what you need to remember is that pemphigus is a complete empty space when it comes to therapeutic tools in the toolbox. So, in general, people will be looking for different modalities, different modes of action and they will be looking to use them in concert rather than see one compete with the other one. So, they need more medication, not less. Now when we look at the Phase 3 trial results for the Rituximab trial, a couple of things spring out. So, the first one is, it takes some time for Rituximab to start acting in these patients and of course mechanistically we understand why that is the case. It’s not because you wipe out B cells, that your plasma cells are affected. And also, you have titers of circulating old antibodies, which we all know have a long half-life, thanks to FcRn. So, when it takes 4 months for Rituximab to take an action, question is, how do you control that patient in between period of time? The second thing which is interesting about Rituximab in pemphigus is the high relapse rates. It’s difficult to understand where it is coming from, but there is a substantial relapse rates for patients, which are on Rituximab. And third, I think you’re spot on, we need to keep an eye on safety. We know that in pemphigus there is the 3x higher mortality due to infection compared to the normal healthy population. So, these patients do have an impaired barrier function. And I think [indiscernible] risk of infection and the safety profile of the different modality is making their way into that markets. So, I think early, a point of differentiation visible, but bear in mind this is a very bad disease. These patients are in high unmet needs and therefore people will be looking for multiple modalities in the toolbox, which ideally could be used synergistically or together.

And if I may ask one more question. It’s well known that FcRn is also involved in maintaining albumin homeostasis and your competitors using monoclonal antibodies against FcRn seems to also end up reducing albumin in addition to IgG. At what magnitude of albumin reductions do you start to see clinical sequel of hypoalbuminemia and is there any reason to believe that ITP, gMG and PV or CIDP patients may be particularly vulnerable to low albumin levels?

Thank you for the albumin question. I would like to refer to our Phase 1 publication where we published microscopy data highlighting the difference in behavior between efgartigimod and some of the full-size monoclonal antibodies when it comes to interfering with serum albumin trafficking. So, we haven’t seen any drop in, albumin, whilst indeed some of the high affinity monoclonal antibodies have consistently reported drops between 20% and 30%, I think mainly in healthy volunteers. I am not the best person to talk about potential risks associated with low levels of albumin, but I am aware of publications highlighting the drops, for example, of 50% start to become really problematic in patients. And therefore, I think the jury is out, how big the drop in, serum albumin will really be when we go into chronic dosing regimens for some of these molecules. But I think it’s too early to really comment on that. It’s a watch out. It’s something to work around for those programs, but I think it’s too early to really comment on that.

Thank you.

You are welcome.

Thank you. Next question comes from the line of Emily Field. Please ask your question.

Hi, thank you. I was just wondering if you could comment on the advanced trial design and the thought process behind trialing efgartigimod on top of standard of care and not as a monotherapy. And then also just on each of the subcutaneous formulations, is the intention that these would both be home administered by the patient or would they have to be administered in a physician’s office? Thank you.

Thanks for these questions. And again, I’m going to defer the second question to Keith. We have the benefit of having Keith on the call today. Look, the reason why we’re testing in MG and ITP efgartigimod on top of standard of care is because we’re aiming for a broad label. And actually, the label I’m aiming for is that efgartigimod could be dosed on top of standard of care as soon as patients are no longer adequately controlled by standard of care. And by doing that, you’re actually going for a very broad label instead of niching into a highly relapsed refractory patient population. So, the goal really is a broad competitive label for both indications. I would like to ask Keith maybe to address your subQ home administration question.

Yes, thank you, Tim. So in regard to the two different formulations that we have for the ITP study where we’ll be using, what I heard referred to as the homegrown, but the maintenance subcutaneous dose, during the trial, of course, it will not be administered at home immediately because we’ll be monitoring platelets on a regular basis. But the desire with providing subQ is optionality and convenience for patients. So, the desire, and it will be determined as we meet with the regulatory bodies with successful data, would be that it would be that you could inject yourself at home.

Great. Thank you.

Next question is from the line of Boris Peaker. Please ask your question.

Great. So, I just want to follow up on the prior, I guess, questions. For the ADAPT trial, how they enroll patients to date compared to your expectations? And how do they compare to the Phase 2 study, and more specifically, I just want to get an understanding of how the background therapy compares to the Phase 2 study?

Hi Boris. These are two great questions. So, believe it or not, but the enrollment curve is perfectly matching our forecast. So, I think the strategies which we deployed for recruiting such an ambitious trial, remember this is the biggest and the broadest MG trial ever worked, and I’m very proud of the teamwork behind such an ambitious trial. And the comparison between the Phase 3 patients and the Phase 2 patients is a great question. We believe that the ADAPT study design is substantially de-risked by a couple of factors. One of those factors is indeed that we try to stay as close as possible to the type of patients, which we saw in the Phase 2 study including the severity of the disease, so the MG [indiscernible] cutoff, but also the type of background medication, which we allow. The difference between the ADAPT study and the small Phase 2 trial is that, of course, we will aim to have a better balance in background medication between control arm and study arm. Remember, there was a slight imbalance in the past in the Phase 2 study, which we have of course explained and contextualized, but it’s clearly not something which we wanted to see in the Phase 3 registration trial.

Great. And then my second question, for the Phase 2 study in MG, are there any additional plan updates that you any data cuts or in the future, whether it’s presentation at a medical meeting or publication of any sort or anything like that?

The manuscript is being submitted. So, I think the next data release to be expected will be a peer reviewed publication.

And do you have a tentative timeline for that?

No, that’s in the hands of course of the review process. So very difficult to pin us down on the timing. But you know that this company takes pride to be science based and is typically also announcing publication of key data to its stakeholders. So, we will alert you.

Great. Thanks for taking my questions.

Thank you, Boris.

Thank you. I would now like to hand back the call to Beth DelGiacco. Please go ahead.

This concludes the call for today. Thank you for joining and we look forward to updating you on our progress.

You may all disconnect.