Greetings and welcome to the Incyte First Quarter 2018 Conference Call. At this time, all participants are in listen-only mode. A question-and-answer session will follow the formal presentation. It is now my pleasure to turn the call over to your host, Mike Booth, Vice President of Investor Relations for Incyte. Please go ahead, sir.

Thank you, Kevin. Good morning and welcome to Incyte's first quarter 2018 earnings conference call and webcast. The slides used today are available for download on the Investors section of incyte.com. I am joined on the call today my Hervé, Barry, Steven, Dave, and Reed. Before we begin, we'd like to remind you that some of the statements made during the call today are forward-looking statements, including statements regarding our expectations for 2018 guidance, the commercialization of our products, and the development plans for the compounds in our pipeline, as well as the development plans of our collaboration partners. These forward-looking statements are subject to a number of risks and uncertainties that may cause our actual results to differ materially, including those described in our 10-K for the year ended December 31, 2017, and from time to time in our other SEC documents. I'd now like to pass the call to Hervé for his introductory remarks. Hervé Hoppenot - Incyte Corp.: Thank you, Mike, and good morning, everyone. So there is much to be excited about for the future at Incyte with our fast-growing revenue line, late-stage pipeline of compounds that could lead to new marketed products in the next several years, and an earlier stage portfolio of having multiple opportunities for the longer term. That said, it's definitely been a tough few weeks from a news flow standpoint and I would like to briefly share my perspective as we begin today's call. Epacadostat was a pioneering development program and what is true in the biology did not translate into a benefit in patients with advanced melanoma. We have been working efficiently with investigators and our partners to downsize the ECHO program, while still allowing us to ask the right scientific question, but in a much smaller program. Steven will…

Thank you, Hervé, and good morning, everyone. Net product revenue for Jakafi in the first quarter of 2018 grew by 25% over the same period last year. Sales continue to be driven by robust prescription demand and we saw a year-on-year increase of approximately 17% in total patients being treated with Jakafi. We exited Q1 2018 with normal levels of inventory and take the opportunity today to reiterate our Jakafi net product revenue guidance for the full year of 2018, which is in the range of $1.35 billion to $1.4 billion. Slide 8 illustrates the estimated penetration of Jakafi into its two approved indications. We believe that there are approximately 16,000 MF patients and up to 25,000 PV patients that are eligible for Jakafi therapy, and we continue to work to bring Jakafi to more of these patients. We see, therefore, a significant potential growth in both indications, and this potential is augmented because as a proportion of PV in the patient mix rises, so does the average duration of therapy. As you recall, in July last year, Jakafi was included as a recommended treatment for PV in the NCCN guidelines. We believe that there is now a greater awareness of those guidelines among the prescribing community, and also that as more physicians become familiar with the PV guidelines, that usage of Jakafi may increase. I'll now pass the call over to Steven for an update on our portfolio.

Thanks, Barry, and good morning, everyone. As you can see on slide 10, we are making some important changes to the ECHO program, following the recently announced results of ECHO-301, which clearly demonstrated that adding epacadostat to pembro did not add efficacy over pembro monotherapy in patients with advanced or metastatic melanoma. We have also moved very swiftly and with significant cooperation from the investigators, from Merck, and the conference organizing committee to bring the ECHO-301 data to ASCO next month. We think it's very important to share these data as soon as possible. We want to assess the IDO plus PD-1 combination in another tumor type, as well as assessing it in combination with chemotherapy. We can achieve both of these objectives by changing the two ongoing lung studies with pembro into randomized Phase 2 trials. Specifically, we'll be looking at the IDO plus PD-1 combination in tumor proportional score high non-small cell lung cancer versus pembro alone, and thus performing the randomized Phase 2 tests in a second histology after melanoma. And we would look at the IDO, PD-1, plus chemotherapy combination versus pembro plus chemotherapy in an all-comer non-small cell lung cancer population, thereby also asking the chemotherapy combination question in a lung cancer population. Enrollment in all of the other pivotal studies in the ECHO program has been stopped and each of these studies will be amended to enable patients and their physicians to consider alternative therapeutic options. The proposed pivotal study with Dova (00:08:24) will not be initiated. We will continue to investigate the potential utility of IDO1 inhibition in a variety of clinical settings, but these will be conducted in small proof-of-concept trials and where we believe the biology and translational data are compelling. The lower half of the slide describes these updates in…

Thanks, Steven, and good morning, everyone. The financial update this morning will include GAAP and non-GAAP numbers. For a full reconciliation of GAAP to non-GAAP, please refer to our press release. In the first quarter, we recorded $382 million of total revenue on both the GAAP and non-GAAP basis. This is comprised of $314 million in Jakafi net product revenue, $21 million in Iclusig net product revenue, $41 million in Jakavi royalties from Novartis, and $6 million in Olumiant royalties from Lilly. First quarter Jakafi net sales of $314 million represents 25% growth over the same period last year and first quarter Jakavi royalties of $41 million represents 43% growth over the same period last year. Remember that despite significant growth in underlying Novartis sales of Jakafi, the royalties received in the first quarter of 2018 are slightly lower than the fourth quarter of 2017, because the royalty tiers reset each calendar year and we begin each year in the lowest tier. Our gross/net adjustment for the quarter was approximately 16%. This is driven primarily by Jakafi and, as with similar oral oncology drugs, our gross/net adjustment is higher in the first quarter of the year than the rest of the year, primarily because of our share of the donut hole for the Medicare Part D patients. We expect that our gross/net adjustment for the full-year 2018 will be approximately 14%. Our cost of product revenue for the quarter was $13 million on a non-GAAP basis. This includes cost of goods sold for Jakafi, Iclusig, and the payment of royalties to Novartis on U.S. Jakafi net sales. Our R&D expense for the quarter was $266 million on a non-GAAP basis, primarily driven by clinical development programs. Our SG&A expense for the quarter was $109 million on a non-GAAP basis. This…

Certainly. Our first question today is coming from Alethia Young from Credit Suisse. Your line is now live. Alethia Young - Credit Suisse Securities (USA) LLC: Hey, guys. Thanks for taking my question. Just kind of the two big picture. One, with the PD-1 program you have for MacroGenics, well, how do you think about kind of changing or thinking about redefining this program or will you use monotherapy or would you kind of continue with the combinations, which are kind of Phase 1 assets? And then just also, I mean, talking a little bit about the trends that we've seen coming out of AACR , I know that you kind of used the high tumor burdened folks in the non-small cell group. So I just wanted to see kind of how you were thinking about that strategically as well. Thanks.

Alethia, hi, it's Steven. Thanks for your question. So for our MacroGenics PD-1, in many ways it was independent of IDO. We needed that compound internally for upwards of seven combinations to be done. But if you look at the compound at a high level, in terms of monotherapy, we will be pursuing registration strategies likely in the niche tumor initially, and then potentially exploring elsewhere thereafter in bigger tumor types. So, just to reiterate, it will have a monotherapy strategy attached to it, as well as numerous internal combinations that need to be done for proof-of-concept work. In terms of AACR and perspectives on what is the potential best way to select patients for immunotherapy in general and checkpoints, we're following all of what you mentioned, including PDL-1 tumor proportional scores, tumor mutational burden, et cetera. We haven't yet outlined which way we would potentially enrich, but all of the above are interesting. We'll also, obviously, be examining our own data from ECHO-301 to see in that program what biomarkers may or may not help us. Thanks.

Thank you. Our next question is coming from Cory Kasimov from JPMorgan Chase & Company. Your line is now live.

Hey. good morning, guys, and thank you for taking my questions. I wanted to follow-up on your prepared comments for FGFR and cholangiocarcinoma. The comments were helpful in framing expectations for this pivotal 2 trial a little bit, but there's, obviously, a lack of viable options for patients if response rates to current standards are only 10%. But I'm curious how much you think you need to clear this by to have a clinically meaningful single-arm result that would potentially satisfy regulators. And then as a follow-up, can you also describe the market opportunity here a little bit? What's the potential sizing?

Cory, it's Steven. I'll do the first part of your question, and then somebody else will opine on the second. You are right. Combination chemotherapy response rates are around 10% with very short progression-free survival of approximately two months in the set-in. So for us, something north of that that is durable, so response rates 20% to 30% range that are durable would be, for us, a reasonable consideration for an accelerated approval in that setting that's combined with a reasonable progression-free survival. You do have to couple that, additionally, with the likelihood that a single-agent targeted therapy is likely to be a lot more tolerable than combination chemotherapy. So for all of those reasons, should the trial deliver the results we expect, we think we'll have a viable option for a submission there. In terms of the market opportunity, I'll pass it to Barry.

Sure. Remember, this is a subset of patients with cholangiocarcinoma that have FGFR2 translocations that we're looking at. So in the United States, we believe the opportunity is about 1,000 patients with this disease in the translocation and worldwide about 3,000 patients.

And then one quick follow-up on this program, the bladder cancer, the FIGHT trial that you highlighted in your slides, is the intention there also for that to be a pivotal trial?

Cory, it's Steven again. It is a single-arm study in FGFR3 patients with bladder cancer. So, again, should it deliver a response rate that's durable, it would certainly be considered for an accelerated approval opportunity in the U.S. In terms of ex-U.S., that would be a matter for regulators to consider, but we may need randomized data additionally for that.

Okay. Thanks, guys.

Thank you. Our next question today is coming from Ying Huang of Bank of America Merrill Lynch. Your line is now live.

Hi. Good morning. Thanks for taking my questions. My first question is maybe, can you talk about the percentage of R&D in the non-GAAP R&D portion that's allocated to the IDO program now, so we get a sense maybe the run rate for 2019 R&D? And then secondly, if the 2-milligram of baricitinib is approved by FDA, but not the 4-milligram, considering the market size and your (00:21:57) rate, would you reconsider the opt-in for that and the other indications? Thank you.

So, Ying, it's Dave. I'll answer the first part of the question. In terms of the R&D, that is a percent of what is IDO in 2018. We don't break that out separately, but obviously it's going to come down, because we mentioned that will come down in our prepared remarks by about – the overall R&D expense will come down by about $50 million. And, obviously, in 2019 and 2020, it will become very insignificant. There will still be some, but it will be far smaller than we originally thought it would be. Hervé Hoppenot - Incyte Corp.: Yes, regarding baricitinib, frankly, the opt-in option that we have is always open and we look at it by indication. So there is no really direct correlation between that decision for new indication and what could happen in RA. But there is a connection in the sense that it has an impact on the royalty and the amount of royalties that we would be receiving. So it's far, far too early for us today to make speculation about which way it would go. I think we have a month and a half now, up to June, to see how the discussion are going with FDA, and then we will have all the opportunities to make decisions based on that.

Thank you, Hervé.

Thank you. Our next question today is coming from Geoff Meacham from Barclays. Please proceed with your question.

Good morning, guys. Thanks so much for taking our questions. This is Jason on for Geoff. I'm curious with regards to the epacadostat lung cancer trials, I know it's still early days, but were there any clues from ECHO-301 that could give you some insights or provided some suggestions as to what happened there, and then why specifically lung cancer study has a potential? And then you sort of touched upon this, but in terms of patient stratification, again, any clues along that way?

Jason, hi, it's Steven. So, for ECHO-301 itself, as I said in my prepared remarks, we have been able to secure an oral presentation at ASCO on Sunday morning, so the data will be presented there. It is early from the biomarker point of view. As we said repeatedly before and on calls, the biomarker data only comes in through the second half of this year. So, at this junction, I can't tell you whether or not that presentation will have biomarker data within it. In terms of sort of read-through to lung and why lung, so firstly, we step back, we consider either a pre-proof-of-concept asset now, and with Merck we'll be doing randomized Phase 2 tests in the lung cancer setting, in the two settings. So in the tumor proportional score high by the Merck definition of 50% or above, it's a very clean study of pembro monotherapy versus pembro plus IDO and isolates the potential effect of IDO very cleanly in a randomized Phase 2 setting. There's no other enrichment at the current time or any learning that we've read through to that. In terms of second study, again, a different MoA being explored with chemotherapy in an all-comer lung setting, and again a very clean study of pembro/chemo/IDO versus the combination with IDO alone that then allows us to isolate the IDO – versus pembro/chemo. So pembro/chemo/IDO versus pembro/chemo that then allows us to potentially isolate the IDO effect very cleanly there. And again, at this junction, no important biomarker stratification at this point in time.

Great. Thanks for the color. I guess, is there any other potential oncology indication that you might consider following with epacadostat?

In terms of the checkpoint blockade doublet, as I outlined, our principles are pretty clear. We want to test one other histology to rule out a false negative, if you will, randomize Phase 2s, and then the chemotherapy MoA. In terms of beyond that, in terms of other biology, I'll ask Reid to answer your question.

Yes, this is Reid. So we remain, and I think the field remains, interested in IDO1 and maybe the most appropriate place to evaluate an inhibitor. And so in situations where we think the scientific data, either preclinical or translational are strong and we have a clear way to isolate treatment effects to evaluate the molecule in a clinical setting, we look to pursue those. They'll likely be in smaller Phase 1/2 studies, perhaps in randomized Phase 2 studies, like Steven just described, that we're going to conduct with Merck in lung cancer, but I think our thinking around IDO1 is evolving given the ECHO-301 data. But we do absolutely look to study the mechanism in other places, such as with vaccines, perhaps with other immune stimulatory mechanisms, and I think the details on the early stage program for epacadostat will evolve over the coming months.

Great. Thanks so much for the color.

Thank you. Our next question today is coming from Jay Olson with Oppenheimer & Company. Your line is now live. Jay Olson - Oppenheimer & Co., Inc.: Oh, hey, guys. Thanks for taking the questions. Just wanted to make sure that we understand the GVHD opportunity. Can you just walk us through where Jakafi and itacitinib will fit into the current treatment paradigm in light of some recent approvals, such as IMBRUVICA? And then maybe take us through how we should think about the size of the commercial opportunity there?

So, Jay, it's Steven. I'll start off, and then Barry will talk about the commercial opportunity. So, if you step back and look at graft-versus-host disease in its entire spectrum, you're dealing with multiple entities. So there's a steroid-refractory setting, which is where we started with the REACH1 study, and that's a single-arm study that will be delivering data first half of this year, looking at ruxolitinib monotherapy in a single-arm study with a 28-day endpoint in steroid-refractory acute graft-versus-host disease. To back up that study and with Novartis also to get approval ex-U.S. is REACH2, which is a randomized study of ruxolitinib in the same settings, steroid-refractory acute versus best available therapy. And then there's a completely different clinical entity, chronic graft-versus-host disease, which occurs more than 100 days post transplantation, has a different clinical phenotype in terms of it being more fibrotic disease and more skin manifestations. And you're right, ibrutinib has an approval there in that chronic graft-versus-host disease setting. Our randomized Phase 3 study, REACH3, is ruxolitinib versus best available therapy, which could include ibrutinib in that setting and the primary endpoint is response rate at month six. So that's the spectrum of the steroid-refractory setting. And then there's a completely different entity, which is upfront steroid-naïve graft-versus-host disease, so before high-dose dexamethasone is used. And if you remember, our proof-of-concept data with itacitinib, our JAK1 inhibitor, was strongest in the setting, and that's where we're conducting GRAVITAS-301, which is in steroid-naïve graft-versus-host disease in acute setting, 436 patients. It's a randomized study versus placebo in that setting with steroids, so 28-day response rate. If that study is ultimately successful, then itacitinib would be used upfront in the steroid-naïve setting, and that's a compound that's wholly owned by Incyte and is globally ours. And then rux would find its way more in the steroid-refractory setting, as I outlined above. I'll ask Barry to opine on the epidemiology. Hervé Hoppenot - Incyte Corp.: Yeah. Hervé here. Before Barry speaks about the U.S., just to give you the perspective of the potential for us. So the first program is ruxolitinib, where obviously it is Incyte commercializing in the U.S. and our partner Novartis outside in steroid-refractory GVHD, and that is a number of patients that has been estimated, as shown on slide 11. It's around 3,500 new cases of acute GVHD in the U.S., and there is around 3,500 new cases of chronic GVHD also in the U.S. So that's the first thing where we do the work with Novartis, we will commercialize in the U.S., and that's a steroid-refractory setting. In the steroid-naïve GVHD, where itacitinib is developed, we estimate north of 10,000 new cases of acute GVHD between U.S., Europe and Japan, and it's important because it's a project where Incyte will be commercializing itacitinib across U.S., Europe, and Japan. So, Barry, I don't know if you want to speak a little bit about the specific U.S. short-term opportunity for us.

Well, so I think Hervé pointed out the epidemiology for both acute and chronic GVHD in the U.S. I think you asked a question about IMBRUVICA, and obviously it's approved in the chronic GVHD setting. We think that there's an opportunity for both drugs there. We actually don't see the uptick in IMBRUVICA to be that great so far in chronic GVHD, and we think our profile will serve patients well there. Jay Olson - Oppenheimer & Co., Inc.: Great. Thanks for taking the question.

Thank you. Our next question today is coming from Kathryn Xu from William Blair. Your line is now live. Yu Katherine Xu - William Blair & Co. LLC: Good morning. I just have a few questions. First, Barry, can you at this moment comment on the duration of Jakafi treatment in the MF and PV in the marketplace? Just some update there will be very helpful. And then also to Dave, and Hervé I guess, how do you look at the strategy or updated strategy going forward advancing (00:33:01) profitability and investing in R&D going forward for the company?

Yeah. Thanks, Katherine, for the question. So we've said this a number of times, I think, about persistency and in the commercial setting how sometimes it's difficult to actually follow patients as they switch insurance and so forth. So the best evidence is to turn to our trials. If you look at the RESPONSE trial, for example, more than 80% of patients are still on therapy at two years. And if you look at the COMFORT trials, you have more than 50% of patients that are on therapy at three years. So that's sort of our guidepost. There's actually information from our RESPONSE trial from ASH, and there will be an update at ESH, European Society of Hematology, where we've shown the response data that 66% of patients are still either on therapy or have completed at least five years of therapy. So the duration of therapy in PV is clearly longer than MF, but MF patients stay on therapy for a long time as well. Dave? Hervé Hoppenot - Incyte Corp.: Yeah, Hervé here on the R&D and the profit question. We have said – I mean, it is a series of decisions and choices that are made on a product-by-product basis. So the bad part of (00:34:23) what happened with ECHO-301 is that by downsizing fairly drastically our epacadostat program, as we just discussed, in fact, we are improving the profitability for this year, but obviously it was not the goal. I mean, the goal was certainly to develop this in multiple indications very quickly. And it's interesting to look back at this as sort of an example. We have a project here that has a clear safety profile that was very well-established. It's a program where we have good biology. We have early clinical data and where…

Thank you. Our next question today is coming from Carter Gould from UBS. Please proceed with your question.

Good morning, team. Thanks for the color on the R&D spend. I guess, Hervé, I just wanted to follow-up on that prior question. I appreciate your comments that you've taken IDO R&D spend out of the numbers and that you still kind of look at these things on a program-by-program basis. But, I mean, the R&D line is still even – pretty robust, even with kind of IDO coming out. So maybe if you could just expand a little bit more in terms of maybe just the focus on profitability going forward here and to the extent that you feel like you may still need to do work on that end or you feel pretty comfortable after this guidance change. Thank you. Hervé Hoppenot - Incyte Corp.: Yeah. Concerning the epacadostat program, obviously, the first two quarter of this year will still carry the cost of the larger studies that we have ongoing. So don't expect Q2 to be suddenly dropping very quickly. I think you will see most of the effect in Q3, Q4, and certainly in 2019 and 2020. So, just to be very clear, by shutting down or stopping some of the studies in the middle of the quarter, you end up carrying all the cost of the closure. So that's what the perspective looks like. I believe having a robust R&D spending for a company like us is the right thing if the science is good, and I think we'll be following that science as we go. At the same time, I also believe that because we have this growth of our top line, that we would be emerging in sustainable profitability over the next quarters, just as we have always planned for. So there was always a plan in the way we were looking at the number, and specifically on the ratio of fixed cost and variable cost, to emerge into sustainable profitability at some point. The fact that the IDO program has been more or less put back into proof-of-concept stage or a very much smaller investment is just making it happen a little bit earlier.

Thank you.

Thank you. Our next question is coming from Peter Lawson from SunTrust Robinson Humphrey. Your line is now live.

Hervé, just maybe thoughts around kind of M&A that is buying versus building and how aggressive you could get on use of capital structure there. Hervé Hoppenot - Incyte Corp.: Yeah, I think – you know we have been always open to acquiring assets. So you can see that over the past three years it has been fairly selective. It has been targeted to some scientific questions that we were interested in, and you can go back to arginase, or it has been based on portfolio needs, like the MacroGenics PD-1. And then there are some more scientific early-stage research programs, like MIRAS and CYROS (00:40:14), so you can see the appetite for partnership has always been there. I think the portfolio we have today is very full of solid near-term opportunities. We spoke about them, but they are like four molecules that are at the stage of starting and being in the middle of pivotal studies, so we don't lack opportunities to launch new products over the next few years. And at the same time, if we see opportunities that will strengthen that, we will look at them, but we would not look at them at any price. I think it would have to be something that fits with the portfolio and something that is in a price range that is reasonable. We have $1.1 billion, $1.2 billion in cash, so that gives us some flexibility to do that if we see the right opportunity, and that's really the way we look at it.

And the comments around sustained profitability, is that going to be a key part of the corporate and financial strategy going forwards? Hervé Hoppenot - Incyte Corp.: It's always the goal. There is no objective of not being profitable, obviously. So it has always been the goal. It is always the goal. What we see today, because of the technical reduction of our R&D spend with the epacadostat downsizing is that it is, in fact, happening in the short term. If you take the guidance we just gave, maybe, Dave, if you can describe it.

Yeah. So Hervé is mentioning, if you take the guidance we just gave, and we reduced the SG&A guidance and not reduced the R&D guidance, I mean, of course, we don't give guidance on milestones, but if you assumed what the consensus is on milestones of Jakavi royalties of $200 million and $40 million on Olumiant, because that's consensus, we're going to end up with non-GAAP profits of between $200 million to $250 million this year. So, as Hervé has mentioned, we're well on our way to that sustained profitability number and we hope over time that will get better on a yearly basis.

Perfect. Thank you so much. Thanks for taking the questions.

Thank you. Our next question today is coming from Salveen Richter from Goldman Sachs. Please proceed with your question. Salveen Richter - Goldman Sachs & Co. LLC: Thanks for taking my question. So, maybe just transitioning to the early pipeline and your checkpoint strategy here. You've completed these dose escalation studies for OX40 and GITR, could you just comment on what you're looking to combine these with going forward? And it looks like the TIM-3 and LAG-3 studies are progressing to clinic, so how are you prioritizing the relative targets, particularly given competitive feedback?

Salveen, it's Steven. Hi. I'll start. So, for the agonist for OX40 and GITR, they've been in the clinic the longest. GITR is slightly before OX40. And as you pointed out, we've got two recommended Phase 2 doses for the monotherapy. They likely are both combination drugs, should they continue to go forward. Neither us nor our competitors have demonstrated to-date any large amount of monotherapy activity, nor was it expected. And currently, with checkpoint blockade. We hope over the ensuing next half of this year, early next year to get to the ability to discern whether or not there's proof-of-concept with these agonists in combination with checkpoints. In terms of TIM-3 and LAG-3, they're on track to go through their INDs this year and get into the clinic their antagonists. Their field, as a whole, is probably a little more bullish about the antagonists, and again, they're not likely to have a large amount of monotherapy activity based on what we've seen from competitors. So they'll be combination products. One thing we can do when we're not first is learn, hopefully, a great deal from our competitors and see where they go and where they potentially get proof-of-concept, and then jump on that quickly. But as I said, it's very early with those programs and they are only about to go into the clinic. And then I'll just remind you that we are taking another compound, as we speak, into the clinic that also has IO mechanism too, and that's our AXL/MER inhibitor, and we'll be taking that very carefully into the clinic as we speak, and that will round out our current immunotherapy portfolio. Thanks. Salveen Richter - Goldman Sachs & Co. LLC: Great. And then just following up, you had first-in-man data in December for both the bromodomain and the PIM programs. What are the next steps there?

Yeah. So again, those targets, you're right, have completed the early part of their work in terms of getting towards a dose. But for the bromodomain, that program we selected the backup compound to go forward with, because it had a better PK profile than the lead compound. And we're busy looking at that very carefully to see if there is a route for it in terms of a proof-of-concept to work with. It does have on-target toxicity in terms of – and we showed this publicly in our presentations – thrombocytopenia. So that will – we'll have to work very carefully for it. For PIM, again, a program that we've been cautious with. There are not many competitors left. We have a dose, and again, we're looking at where are paths forward there in heme malignancies and in combination. Both of them, by the way, have really good combination data with rux in myelofibrosis. So it's part of our rux combination work in MF. But they are still early programs and can't declare yet where we would be going and haven't reached proof-of-concept yet. Salveen Richter - Goldman Sachs & Co. LLC: Thank you.

Thank you. Our next question is coming from Marc Frahm from Cowen & Company. Your line is now live. Marc Frahm - Cowen & Co. LLC: Hi, guys. Thanks for taking my questions. If we go back to the GVHD, I know that the long-term Jakafi sales guidance includes the GVHD opportunity. Can you talk about kind of the durability that you assume in that guidance, since that's kind of big part of this – what the sales potential is? Are we thinking there's going to be a very transient population of Jakafi or more like MF and PV where people are on for several years?

So, hi, Marc. It's Barry. So I'll try to answer your question is that for acute GVHD, we have to see the final results of the REACH1 study to see how long patients stay on therapy. We believe that in chronic GVHD, the potential could be much greater for persistency and for the provided long-term benefit they have. But remember, patients even with acute GVHD can get retreated with the same product or they can go on to get chronic GVHD. So overall, we think that the opportunity for both acute and chronic GVHD could be quite good. Hervé Hoppenot - Incyte Corp.: But we also see the duration of treatment as being much shorter than what you observe in MF and PV. Marc Frahm - Cowen & Co. LLC: Okay. And then, Hervé, maybe for you kind of strategically, over the last few years you've spent some efforts preparing to be a fully global company both with ARIAD, but also going to other territories like Japan in preparation for epacadostat, and the next things in the pipeline, whether it's GVHD or FGFR, just aren't necessarily the same size and breadth of the opportunity as IDO. Do you still have the same kind of appetite to be a fully global company or is this more of the kind of traditional Incyte model for some of these molecules? Hervé Hoppenot - Incyte Corp.: It's a good question. The way we organize the expansion, and we are happy we did it that way now, was to make it proportional to the existing portfolio. So the way we're organized in the U.S. is basically there is a team working on Jakafi. They have a very fast-growing top line, and all of that is doing well from the commercial standpoint. Same thing in Europe.…

Thank you. Our next question today is coming from Ren Benjamin from Raymond James. Your line is now live. Reni Benjamin - Raymond James & Associates, Inc.: Hi. Good morning and thanks for taking the questions. Just two. One with GVHD. Steven, can you remind us the prior data that led you to this trial design in acute, and what your expectations are and what are clinically relevant expectations in the REACH1 study?

Yeah, Ren, it's Steven. Thank you for your question. So it was very interesting. It actually came from external investigator initiated research from a group of investigators in Germany led by Zysa who showed in their study, which had approximately 60, 70 patients in, 70%, 80% response rates. Not as classic sponsored study with tight controls on how you measure endpoints, et cetera, but very, very encouraging proof-of-concept data. And then we worked to get the rights back to run our graft-versus-host disease program with rux. Now remember, I also teed up the large unmet need here. There's approximately 10,000, 11,000 allogeneic transplants that occur, with more than half of them getting graft-versus-host disease. And then if they aren't steroid responsive, which is about half the patients, they have an extreme morbidity and high mortality rates, as I outlined to you. We got Breakthrough designation here. We are able, with the agency, to run a single-arm study in steroid-refractory acute and where we would like to see the response rate is in the 50% plus territory that's durable. We think if we meet that under the conditions that I've just outlined, then we will have a submission, a supplemental NDA in the United States. The Europeans may also be interested in that single-arm data, by the way, if it's in that territory that I mentioned, but we have a randomized study, REACH2, as well to go to, if need be. So, hopefully, that answers your questions on how we got there on steroid-refractory acute. Reni Benjamin - Raymond James & Associates, Inc.: Yes, it does. I was remembering an investigator sponsored Italian study, but it was probably the German study as well. And then switching gears to PI3K-delta, you have several CITADEL studies that are ongoing. I think there was some interesting data looking at the synergistic effects in combination with a PD-1 inhibitor presented at AACR. Can you talk a little bit about this program right now? Because I thought you were still trying to find the appropriate dosing schedule. How are you thinking about this monotherapy versus combination, and how do these studies kind of fold into a pivotal study?

So, yeah, thank you for the question on our PI3-kinase-delta inhibitor, INCB50465. So, in many ways, we did take a time hit, in that we stepped back and looked at the class in general and said, we have a second-generation compound that seems to have eliminated for the most part the liver toxicity seen with the first-generation compounds, like idealalisib, but there are still long-term toxicities probably from chronic B cell suppression like colitis. We knew we had a very active compound. We presented this data two, three times already. There is very high activity in B cell malignancies, particularly in follicular, mantle, and marginal zone lymphomas. But we also knew with time we were going to see some of that long-term toxicity. So what we did is dose through sort of an induction paradigm to get to the efficacy endpoint you want. And most people respond by the time of the first scans at eight/nine weeks, and then change thereafter to a different dosing schedule and see with ameliorating or changing that dosing schedule, we were able to ameliorate the toxicity profile. And data we showed at ASH last year, again, small numbers and many caveats, that we're able for the most part to ameliorate the toxicity profile. So we think we're in a very good place with our highly active compound and we are able to change the tolerability profile with the dosing scheduling changes. So now we have ongoing efforts in all the B cell malignancies, diffuse large B-cell lymphoma, follicular lymphoma, mantle cell, and marginal. The class as a whole is more active outside of diffuse large. It tends to have more activity in the follicular, mantles, and marginal zones. We're conducting those studies this calendar year, into early next year, and hopefully have data next year. If they again meet the required high response rate that's durable, then there are potential accelerated approval strategies in those settings. So that's where we stand with the program. We're proud of what we did in trying to change the profile. We look like we've been able to and now we have to execute these studies to show both the efficacy and tolerability. Reni Benjamin - Raymond James & Associates, Inc.: And just thoughts regarding combinations?

We'll have to follow all of that work with combinations. In many of those settings you require CD20 antibodies or other compounds. But the initial strategy is monotherapy, and then we'll begin safety with various combinations. We are looking at INCB50465 in combination with rux in myelofibrosis, because there's very good preclinical rationale for that. The pathway is upregulated in myelofibrosis and we're conducting that study now. And then you alluded to a very early dataset that was at AACR with a lower dose of delta INCB50465 to try and change the tumor microenvironment with a PD-1 inhibitor that we're also looking at currently, and there's some early data that there may be some activity with that doublet as well. Reni Benjamin - Raymond James & Associates, Inc.: Great. Thank you, guys.

Thank you. Our next question is coming from Liisa Bayko from JMP Securities. Your line is now live.

Hi. Just a follow-up on GVHD. Can you give us just some sense of how to think about duration of therapy in this population, both frontline and second-line, and maybe the acute and chronic? And I don't know if it's similar across those. And then also for itacitinib, it will be, obviously, positioning against – in the frontline setting and steroids, which obviously are inexpensive. How do you kind of anticipate kind of gaining share there? What's the strategy for going up against steroids? Thank you.

So, Liisa, it's Steven. I'll try to answer your question first, and Barry alluded to this, because we don't have the final data yet. Our expectation is that in acute is once you have the dataset and show what the duration of response is, that physicians will use the compound to get control of the graft-versus-host disease, to then eliminate the steroids, and then eventually potentially eliminate the JAK inhibitor as well, once they know patients are controlled. I don't know what that duration will ultimately be, but it's probably of the order of somewhere around anything between three to nine months approximately, not knowing the data. For chronic, as Barry said, it may be slightly different paradigm. These patients phenotypically have a different disease. They tend to have a lot of skin toxicity and it's a longer endpoint. It's a six-month response rate endpoint. So we feel there that the likelihood, as Barry said, is there will be a longer use pattern of the JAK inhibitor in that setting and in people once they have control of the various organ systems, we'll look at weaning them off the therapy. For Itacitinib, it's steroid-naïve, but it's in combination with steroids. So it's an add-on therapy. You have to use the steroids as well. So it's not versus steroids. It's Itacitinib plus steroids versus steroids in steroid-naïve. So, I hope that's clear in terms of the scheme of the study.

Great. Thank you. It's very helpful.

Thank you. Our next question is coming from Christopher Marai from Nomura Securities. Your line is now live.

Hi. Thanks for taking the question. I was wondering if you could comment perhaps on the arginase inhibitor program with Calithera. Obviously, given the IDO data and sort of the T-cell related metabolic checkpoint hypothesis there, perhaps run us through your thoughts on that program, potential to combination with your now in-house PD-1. Thank you.

Yeah. Thanks, Chris, this is Reid. So the arginase inhibitor program we in-licensed and are co-developing with Calithera. We've completed or are completing now the Phase 1 dose escalation and expansion studies. The mechanism, as you pointed out, does have some similarities to IDO1 and the compound, therefore, to epacadostat, but there's actually some very important differences as well, not the least of which is the cell types that express the enzyme and the types of immune complexities that those patients may have, which are actually quite a bit different than those that are IDO1 positive. So I don't think there's any direct read-through to the arginase from a mechanistic standpoint. Clearly, the epacadostat experience will color the kind of stepwise de-risking that we take to pursue the arginase inhibitor program. And the studies that the clinical team are working on now include both translational studies to look at effects of the molecule on the immune microenvironment, as well as the initial thinking around safety studies to move the agent probably first in the combination with the PD-1 antagonist. But right now it's a pre-proof-of-concept mechanism and the translational data we generate over the coming months will be important to any next steps that we make.

Okay. And then just with reference to that translational data, I guess, biomarker data coming out of the epacadostat program second half, is that something that you think could be informative with respect to the potential clinical fit of this compound? Thank you.

Yeah, again, so the translational work with the ECHO-301 include PDL-1 status, IDO1 status, tumor mutational burden, and RNA seek. To the extent that there are learnings from those trials, it's probably going to apply more to the PD-1 doublet setting and certainly to melanoma. So I think there is a potential for some information content to flow to arginase, but as I mentioned earlier, the types of patients that we believe are likely to have a dependency on the arginase biology are probably not those that you would normally think of as being inflamed tumor types, like melanoma. So, in short, probably some read-through, but not very much.

Got It. Thank you.

Thank you. We have reached end of our question-and-answer session. I'd like to turn the floor back over to Hervé for any further or closing comments. Hervé Hoppenot - Incyte Corp.: Okay. Thank you. Thank you for your time today, for your questions. So we look forward to seeing you at some of the investor medical conferences, but also at the 21st of June meeting we are organizing, where we will do a full company update. But for now, thank you again for your participation in the call today and goodbye.

Thank you. That does conclude today's teleconference and webinar. You may disconnect your line at this time and have a wonderful day. We thank you for your participation today.