Greetings and welcome to the Incyte Corporation Second Quarter 2017 Earnings Call. At this time all participants are in a listen-only mode. A question-and-answer session will follow the formal presentation. As a reminder, this conference is being recorded. I would now like to turn the conference over to our host, Mr. Mike Booth, VP of Investor Relations. Thank you. You may begin.

Thank you, Diego. Good morning and welcome to Incyte's second quarter 2017 earnings conference call and webcast. The slides used today are available for download on the Investors section of incyte.com. And I'm pleased – and I'm joined on the call today by Hervé, Barry, Steven, Dave, and Reid. 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 2017 guidance, the commercialization of our products, and our 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-Q for the quarter ended March 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. We appreciate you all taking the time to participate in the call today and we are very excited to share with you the significant progress we have made during the second quarter. First, Jakafi continues to show strong sales growth of 33% in its sixth year on the market as the number of patients benefiting from this treatment continues to increase. Importantly, total revenue in Q2 also grew by 33% year-over-year as strong royalties from Jakafi, sales from Iclusig, and the first full quarter of royalties from Olumiant resulted in a total revenue of $326 million for the quarter. Speaking of Olumiant, it's now approved in Europe, in Switzerland and Japan, and let me quickly address the updates that we along with Lilly provided last week. Based on feedback from the FDA to…

Thank you, Hervé, and good morning, everyone. Jakafi sales in Q2 were strong at $276 million, a 33% increase over Q2 of 2016 and a 10% increase over the first quarter of this year. Demand growth was up Q2 versus Q1 by over 7%. We believe this momentum is due to both the quality of the data underlying Jakafi and to the efforts of our U.S. team here at Incyte. Jakafi's performance in the quarter was driven by strong patient demand for both indications, while total PV patient growth continues to outpace the MF patient growth. We believe that a key driver of demand in MF is the impact of the NCCN guidelines that were published last year, which first included Jakafi as a recommended treatment for MF. Updated NCCN guidelines for MPNs were published late last week and for the first time these guidelines now cover polycythemia vera. Jakafi was included as a recommended treatment for patients with PV, who had inadequate response to first-line therapies, such as hydroxyurea. We are very pleased that the NCCN guidelines for MPNs now include Jakafi for both myelofibrosis and polycythemia vera. A quick word on inventory, which has been fairly steady within a range of 2.5 to 3 weeks. Last quarter, we stated that we exited Q1 at the high-end of a normal range for inventory. This has now been normalized in the second quarter. Lastly, as a result of our strong sales growth, we are pleased to raise our full-year 2017 net product revenue guidance for Jakafi from a range of $1.020 billion to $1.070 billion to a new range of $1.090 billion to $1.120 billion. Jakafi commercial momentum is clearly very strong, and now I'd like to share a slide on how we plan to further grow the brand. We…

Thanks, Barry, and good morning, everyone. We've made significant progress in the clinic since we updated you on our first quarter call in May of this year. Shown here on slide 10 are our five key programs in development, within which we have initiated multiple trials in the last few months. In addition to Barry's comments on ruxolitinib's comprehensive clinical development program in graft versus host disease and essential thrombocythemia, you can see that we have now initiated the pivotal program for itacitinib in patients with treatment-naïve acute graft versus host disease. In the coming months, we expect to initiate multiple trials with our PI 3-kinase delta inhibitor, INCB50465. Following positive proof-of-concept data presented at both ASH last year and ASCO this year, we intend to study this compound in follicular lymphoma, marginal zone lymphoma, and mantle cell lymphoma. Let me provide a little extra color on our expanding ECHO development program for epacadostat. As a reminder, we are planning to initiate six Phase 3 trials of epacadostat in combination with pembro in four different tumor types. And we are also planning to launch Phase 3 trials of epacadostat in combination with nivo in two tumor types. On the epacadostat studies in combination with pembro, I am pleased to confirm that, together with Merck, we have obtained all the necessary regulatory feedback and it remains our aim to open and achieve first patient initiated in all six studies before the end of this calendar year. With Bristol-Myers Squibb, we are in earlier stage in our planning, but are still targeting the planned initiation of these studies before the end of this calendar year. As we get a little closer to sites initiations and first patient initiated, all of these designs will populate to CT.gov. But you can appreciate that for…

Thanks, Steven, and good morning, everyone. The second quarter was very strong. We recorded $326 million of total revenue. This was comprised of $276 million in Jakafi net product revenue, $16 million in Iclusig net product revenue, $34 million in Jakavi royalties from Novartis, and $1 million in Olumiant royalties from Lilly. Jakafi's net product revenue of $276 million represents 33% growth over the same period last year. Based on Jakafi's performance for the first six months of the year, we are increasing our full year Jakafi net product revenue guidance to a range of $1.090 billion to $1.120 billion. Our gross-to-net adjustment for the second quarter was approximately 12%. We expect the total gross-to-net adjustment for the full year to be approximately 13%. Our cost of product revenue for the quarter was $20 million. This includes the cost of goods sold for Jakafi and Iclusig, the payment of royalties to Novartis on U.S. Jakafi net sales, and the amortization of acquired product rights related to the Iclusig product acquisition in Europe. Our R&D expense for the quarter was $202 million, including $23 million in non-cash stock compensation. For the full year, we expect R&D expense to be in the range of $1.050 billion to $1.150 billion. This is an increase from the previous guidance last quarter. The increased R&D expense guidance is related to the acceleration of the Phase 3 plans for epacadostat. Our SG&A expense for the quarter was $90 million, including $11 million in non-cash stock compensation. We recorded $7 million in expense related to the change in the fair market value of the contingent consideration for the Iclusig royalty liability. Moving on to non-operating expenses, we recorded $20 million unrealized loss on our long-term investments in Merus and Agenus, and a one-time debt exchange expense of…

Thank you. At this time we will be conducting the question-and-answer session. Our first question comes from Geoff Meacham with Barclays. Please state your question.

Hey, guys. Good morning and thanks for the question. Just on epacadostat, I want to get your perspective on the MYSTIC results and long (18:31) as it relates to epacadostat. Does it hurt the potential for triple combos? Does it give you an opportunity to substitute CTLA-4 for IDO and doublets or none of the above? And I have a follow-up.

Hi, Geoff. It's Steven answering your question. So, obviously, whenever a Phase 3 reports out negative, this is disappointing for patients and investigators involved. From our perspective with epacadostat and the planning there of our studies, it was an eventuality we, obviously, considered may happen, and it hasn't affected our plans to-date. In terms of triple combinations going forward, that's really more in its infancy right now with us and we're still doing enabling Phase 1 work looking at that, and we haven't decided whether we'll be progressing there or not. And there is no other substitution potential, to answer the third part of your call. So the simple answer to your question is, it hasn't impacted in terms of our execution of IDO going forward and, in our view, opens up the potential for I-O/I-O doublet now to be cornerstoned by IDO with PD-1s in many diseases, and that's positive. In melanoma, we've always said that the PD-1 CTLA-4 doublet data, as regards response rate in PFS, is a clinical benchmark that we wanted to attain with that data. At the same time, we've always been very encouraged by the tolerability profile of our own doublet, of PD-1 and IDO. So that's my comments as regard MYSTIC right now.

And then, Steven, just a follow-up to that. When you look in melanoma Phase 2 results, you guys have seen some pretty durable responses with PFS data that – I guess, someone said it took a little bit longer to mature. I wanted to get your perspective on how much of a hard stop is the assumption for ECHO-301 Phase 3 results for the first half of next year. What would you highlight as the major differences between Phase 2 and 3 in melanoma in terms of the population and things like that?

Yeah, it's me again. Thank you for your question. We updated our data last year at ESMO and, as I just said on the call, we'll be doing it at this ESMO in Madrid in September with more patient data. And you'll get some idea, albeit in a single-arm study, of what our potential progression-free survival rates are with our doublet, and I'll point you towards that meeting itself. In terms of the ECHO-301 study and the readout, obviously, it's event-driven and we need to wait for the events to occur. All our – looking at the operational characteristics of the study point to us getting data in the first half of next year, and that's when we are expected. The benchmark there, just to be clear, is against PD-1 monotherapy, in that case pembro per their labels, which are in the 5.5 to 6-month range is what we have to beat.

Okay. Thanks a lot.

Thank you. Our next question comes from Alethia Young with Credit Suisse. Please state your question. Alethia Young - Credit Suisse Securities (USA) LLC: Hey, guys. Thanks for taking my question. Just a couple. One, do you plan on updating kind of the ASCO dataset we saw any time this year or is it more of a expectation for 2018? And then the second question is just, why did you kind of pick one bromodomain over the other? Thanks.

Alethia, hi. It's Steven. I'll start up with your ASCO question, and then turn it to Reid on the two bromodomain inhibitors. The intent would always be at an appropriate time to update those datasets in terms of more mature data, just as we've done for melanoma, by the way, a year apart now, ESMO last year and then this ESMO. Each time it involves collecting the data, cleaning it, and doing data cuts, so it's not something we do in real time or on an constant basis. But the intent would be to update it at a time point in the future. I can't commit on this call to you for each dataset when that will be, but it will be some time in the next 24 months or so.

Yeah, Alethia, this is Reid. I'll take your BRD question. As we often do for our programs, we'll progress more than one molecule into the clinic, and that can be for various reasons. Sometimes it's a different structure, to safeguard against a safety problem that could arise with the lead compound. Other times, it can be for differential pharmacokinetics and pharmacodynamics, so that we can evaluate the safety and early signs of efficacy of very different clinical drug profiles. And actually, both of those reasons underlie our decision some time ago to progress INCB57643 and INCB54329 into the clinic. Those Phase 1 dose escalations are all wrapping up now, and we'll present data from each of those in the second half of the year. I don't want to get ahead of what those data show, but suffice it to say that we became quite comfortable with INCB57643 is having a more optimal profile and, because of that, it's the compound that will now progress forward into both liquid and solid tumor combination studies, and you'll learn more about those over the coming months.

Thank you. Our next question comes from Cory Kasimov with JPMorgan Chase & Company. Please state your question.

Hey. Good morning, guys. Thanks for taking my questions. I have two of them as well. First I wanted to ask about the ECHO-110 combo trial with atezo, and if you can talk a little bit more about the recruitment issues you ran into there? I mean, what do you think the problem was, and have you seen anything similar in your other PD-L1 combination trial? And then, the second question was just with regard to that pending update on melanoma that we'll see at ESMO. Can you comment on how many patients' worth of data we can expect to see, and how much follow-up you'll have? Thanks.

Cory, hi. It's Steven. In terms of ECHO-110 and the Roche-Genentech collaboration with atezo, as spoken about on the earnings call in the last few quarters, it has been one of the studies that has been a laggard in terms of enrollment. Initially the study included non-small cell lung cancer patients alone, and then was amended to try and capture metastatic bladder cancer as well. And it never took off in terms of enrollment. It's hard to give you all – the reasons related to that, whether it was lack of interest in that particular PD-L1 combination or not. But it was always one of our collaborations because, at the time of NewLink and other reasons, that we knew that would be the case. And I don't think there is any read-through at the moment and, obviously, we'll commit to presenting that data when it's brought in and cleaned in the future. In terms of the melanoma, I can't comment until the meeting itself, other than what I said on the actual call, that it will include both the initial patients and now the dose expansion phase as well. We will look at data in all comers in treatment-naïve setting and at the 100-milligram dose, and present what we think is mature and adequate follow-up for those populations for you. Just getting back to your question and Geoff's question, we'll also try – show the different prognostic subgroups there as regards some of the known prognostic factors, to try and ascertain and give you clarity as to what impacts prognosis here. And then to your question and Geoff's, which I didn't answer clearly in the beginning, the Phase 3 study is in more than 600 patients and we have every belief, because of its size or – it'll be representative of a melanoma population, and will mirror what we saw in ECHO-202.

Great. Thank you.

Our next question comes from Katherine Xu with William Blair & Company. Please state your question. Yu Katherine Xu - William Blair & Co. LLC: Yeah, hi. Good morning. I'm just curious about the PI3K delta inhibitor. Can you talk a little bit about what kind of scheduling you're going – taking into further studies and also, how do you position this particular mechanism in the face of the competition, in those indications that you're going into?

Katherine, yes, hi. It's Steven. As you and others are aware, with this particular class, they're all very active compounds, and we've shown activity at our compound now at multiple meetings across B-cell malignancies, whether it's diffuse large B-cell lymphoma, marginal or mantle cell lymphomas, they're highly active. The challenge becomes tolerability for the class and, as you alluded to, how can you avert some of the longer-term toxicities? With our second generation inhibitor, we now have enough cumulative data that we look like the liver signal seen with the first generation inhibitors is not present with our particular compound. So that's very encouraging. But in terms of on-target B-cell effects, which tend to occur later on, there are two really things you can attempt to do, either change dose or change schedule or change both. And we're looking at – without giving away everything, at trying to maintain efficacy for what we know is a very active compound. And once we have that efficacy achieved, then change in either the dose or the schedule or both, to change the tolerability profile over time. And as we gather that data, we'll be able to prove to you whether or not we can do that, because that I think is the central challenge with this class. We think we have a best-in-class highly active compound, and I'll just point you to the activity data we've shown to-date. Yu Katherine Xu - William Blair & Co. LLC: Well then, if I may, on the melanoma front, if you add epacadostat to the anti-PD-1 agents, it looks like it elevates – the response rate is potentially also prolonged PSIs (28:48) to a new level. And then, what are next steps that you think could further elevate from there, any thoughts on that?

In terms of oncology drug development, obviously, we're always trying to move the benchmarks and increase either response rate or progression-free survival or survival itself to move the field forward. So currently it's about I-O/I-O doublets with, in our case, PD-1 plus IDO. And then looking forward beyond that is trying to work out the populations who work in versus where you may not work in at a biomarker perspective. Then there are multiple other targets. In our own shop, we already have GITR and OX40 in the clinic, and to come next year there'll be further I-O compounds coming into our clinic. We've an arginase inhibitor in the clinic, which is certainly interesting in terms of its biology and potentially being able to address myeloid-derived suppressor cells, and then potentially other new exciting mechanisms of action, which we may explore in combination with PD-1 and IDO or with IDO alone going forward to move that benchmark further. But it's – you have to do the slow iterative experiments and prove first where you're heading, and then execute on a Phase 3 trial to get there. You can't jump ahead of yourself. I'll leave it at that. Yu Katherine Xu - William Blair & Co. LLC: Thank you.

Thank you. Our next question comes from Ian Somaiya with BMO Capital Markets. Please state your question.

Thank you and congratulations on a great quarter. I had a question in regards to the epacadostat Phase 3 program. I know you're not going to be able to speak to the design, but I was hoping you could speak to the goal. And specifically, how do you balance potentially improving on the PD-1 response in populations where KEYTRUDA and OPDIVO are effective versus potentially enhancing or entering into populations where those drugs have been ineffective? And again, the challenge we face from an investor standpoint is the predictability of small Phase 2 studies as we move on to Phase 3s and we haven't had much success yet. Just trying to get – I was hoping to get your take on how do you balance those with the risk and the opportunity that's available to you.

So, Ian, I'll start and others may want to add to what I say afterwards. Obviously, you have to aim at – in these studies at improving the event-driven endpoints, whether they're progression-free survival, overall survival, or combinations thereof, depending on the settings. Sometimes the OS is short enough that that may be the point you're trying to achieve, and that's in terms of demonstrating value for your doublet over the PD-1 alone in the settings we've selected to go after. In terms of the therapeutic ratio, though, once you hit efficacy, obviously, tolerability comes into the equation as well. And I don't want to forget that. I've said it repeatedly. It's one thing now we have hundreds of patients worth of data with some longer-term exposures and we're very confident in our tolerability profile, and that's going to be really important going forward in I-O/I-O doublets in general, but certainly as you compare to CTLA-4 combinations potentially. There are populations where the tumors are either colder or where things don't work, and then it's around trying to ascertain at a biomarker level why that may not be potentially working, and then trying to address it with new MRAs (32:36), things like arginase inhibitors or other things will then weigh in. But to be clear, the Phase 3 programs are going after established entities where PD-1s, for the most part, are the care standard and now trying to improve that in terms of time-to-event endpoints, and then weighing in the tolerability profile. And if Reid wants to add anything to what I said.

Yeah, just a couple of things. I think, Ian, we sometimes forget that even in the so-called inflamed or hot tumors, where PD-1 antagonists are quite effective and are approved for use, generally your objective response rate in those populations, save melanoma, is in the 20% range. And so there is still a substantial unmet need in those populations and, obviously, our goal with the IDO1 epacadostat program is to improve those response rates, improve the patient benefit, and be able to capture a larger proportion of the patient pool to drive benefit. So that's kind of one question and it's the central question in the epacadostat development program now. There is a separate question around what drives PD-1 resistance, either intrinsic or primary or secondary resistance, and that's very much an important focus of our discovery efforts right now as we look at multiple mechanisms that could be operative in that space and even molecules like arginase were in part brought into the portfolio and attempt to address some of the immune-suppressive mechanisms that may lead to T cell exclusion and a cold tumor phenotype. So I think both of them are actively being pursued at Incyte, some in development, some in research, and hopefully in the coming years we'll see the needle being moved in a positive way in both of those tumor settings.

And when can we hear more about just the biomarker work that you've been doing, your biomarker that's specific to IDO that will be utilized in the Phase 3 program?

Yeah. So the translational aspects of the ECHO program are very important. That does include assays to assess IDO1 expression directly. It also includes assessments of PD-L1 status, as you might imagine. It also includes quite a bit of RNA sequencing work to look at things like mutational burden and the inflammatory state of the tumor more generally. I think this is probably one area where we and the whole field have the most ground to make up, and it's very important for us to be able to be smarter when we select our patient populations for these doublets and ultimately triplets. And I think the translational dataset that can emerge out of the ECHO program just is one example where you have five tumor histologies and hundreds and hundreds of patients, you can imagine what a rich status that that will be for us to mine, and hopefully, be able to help move the field forward on the translational aspects of patient selection.

Okay. Thank you very much.

Thank you. Our next question comes from Eric Schmidt with Cowen & Company. Please state your question. Eric Schmidt - Cowen & Co. LLC: Thanks. Maybe another question for Steven. Are we still to expect opt-in or go/no-go decisions on epacadostat and DLBCL MSI-high patients and in combination with the AstraZeneca PD-1? Thanks.

Eric, this is Steven. Very much so, all – the ongoing work will be looked at and examined on its own for signals that potentially we can pursue the two tumor types you alluded to immature at our last presentation, diffuse large B-cell and MSI colorectal. With AstraZeneca, it's the same thing as we're looking at the data now and over the ensuing months we will make decisions on whether or not there are go-forwards there. So the answer is a strong yes from my perspective. Eric Schmidt - Cowen & Co. LLC: Will those be second half, Steven?

In terms of – assuming second half of 2017, in terms of decisions on the AstraZeneca program, yes, that is a potential timeframe we'd have the data to look at and make decisions. I think that's a fair statement. Eric Schmidt - Cowen & Co. LLC: Thank you.

Our next question comes from Ying Huang with Bank of America Merrill Lynch. Please state your question.

Hi. Good morning. Thanks for taking the questions. Maybe first one on baricitinib. If Lilly does start Phase 3 trial at the suggestion of FDA, would the Incyte actually co-fund that Phase 3? If not, do you expect, I guess, downward move on your royalty rate from baricitinib? And then second question on the Phase 3 melanoma trial in combination with Merck's KEYTRUDA. Can you talk about the powering assumption? And also based on the PFS you have seen from the ECHO-201 trial, do you think your assumption when you started a trial in Phase 3 was little bit conservative on PFS? Thank you. Hervé Hoppenot - Incyte Corp.: Maybe – Hervé here. I will take the Lilly question. As you know, as we discussed, I mean, there are lot of decisions that has to be taken on the path forward for RA. One of these decisions have not yet been made, and obviously, based on that, we will have on our side to decide what is Incyte's position today. We are all-in co-funding the development of baricitinib. That's the situation we have today, and depending on how the plans are developing, we will have to make further decisions, but none of them have been made yet.

And then, Ying, in terms of the statistical questions related to the ECHO-301 melanoma study, we don't address the statistics specifically of any – in any study, other than what's already been said. The primary endpoint is a co-primary of progression-free survival and overall survival. We said we can get potential approval on either and on the study the go in was 600 to begin with. So you can read into that anything you want, but we don't know any data yet and I can't comment on the actual powering assumptions around it. The conservative nature of your question is you have to build a design on what you think, what you know for the PD-1 alone and what you think you can achieve with your doublet, but that doesn't always be what's in the end, and I think that underpins your question. But I'm not going to comment further.

Thank you.

Thank you. Our next question comes from Carter Gould with UBS. Please state your question.

Good morning guys. Congrats on the nice Jakafi number and your progress. Thanks for taking the question. I guess two. First, the paired biopsy trials with the I-O doublets appear to have been pushed out or are at least sort of trending right where it's on slide 11. Can you provide some color on the status here? And then I guess also for Steven, on the RESET study, what's the expectation on when that might read out? I know ClinicalTrials.gov says sort of mid-2020, but I guess the most comparable Novartis study is two times the size of yours, and is expected to read out in second half of 2018. So is there any nuance we're missing in the timeline here, or is this just sort of conservatism? Thank you.

Carter, hi. It's Steven. On your paired biopsy question, it's – the studies have – in terms of enrollment, we've done really well. It's now collecting the tissue, analyzing what we have, doing the required testing, and then reporting it out. And that part is still underway, and there are some tricky natures to understanding, do you have adequate representative tumor samples. So we need a little bit longer, you're correct, and we expect to be able to show that data to you sometime during 2018. In terms of the timeline for the RESET program in essential thrombocythemia, and I just want to make sure you understand that this is in a patient population who have either progressed on hydroxyurea or are intolerant of it, and then are randomized to either, in our case, ruxolitinib or the control in this case, anagrelide, with an endpoint that is a composite around platelet control and white blood cell control, and the goal is 120 patients there. And we'll have to just see. Obviously, we always want to do better on operational enrollment than what we anticipate, but we don't expect this to be an incredibly easy population to find, and that's why we have guided to mid-2020 at the moment.

Thank you.

Our next question comes from Michael Schmidt with Leerink. Please state your question.

Hey, guys. Good morning. Just a couple of quick ones. Regarding the ECHO-301 trial, is it correct to assume that the un-blinding will be triggered by PFS, and/or will you provide both data points in the first half of 2018, PFS and OS? And the second question is regarding your FGFR1/2/3 inhibitor, as well as the PI 3-kinase delta inhibitor, I think you've always talked about those as kind of the next wave of potential agents that could reach the market. I'm just wondering how we should think about the sort of potential NDA filing timelines for those two, either in DLBCL or in iCCA? Thank you.

Hi, Michael. It's Steven. In terms of the dynamics around how you conduct endpoint analysis and un-blinding, it's a co-primary endpoint. Obviously, for a large Phase 3, there is a Data Safety Monitoring Board who conduct these analyses to begin with. And they will, as is – I mean, it's not a secret here, PFS would always be triggered before overall survival in terms of doing the analysis, because it delivers earlier. So, I guess the simple answer to your question is, yes, in terms of having mature overall survival data at that point in time, it will be whether it exists or not. Just going to the part two and part three of your questions, yes, we very much like both those programs. We feel, as we've said before, for INCB54828 FGFR1/2/3 inhibitor, that we have a best-in-class compound. We understand the compound. We dose the patients to the pharmacodynamic endpoint of hypophosphatemia there. And we have three open studies, all of which could serve as registration potential, should they reach high response rates that are durable, and all of them are biomarker-driven in terms of targets. So metastatic bladder cancer for FGFR3, cholangiocarcinoma for FGFR2, and for that rare myeloproliferative neoplasm that's driven by chromosome 8p11, those studies are all underway and enrolling well, and we really like the compound. I think it's premature to talk about potential NDA dates there, or accelerated approvals. For the delta inhibitor, just to reiterate the comments I said earlier, I think we've been more step-wise and careful, because of the tolerability profile and needing to understand how we can get the efficacy we know we can get, but then keep patients on therapy long enough. And so it's a little bit early to also comment on when those may potentially deliver, but we have programs in diffuse large B-cell and now in additional B-cell malignancies, like marginal and mantle cell lymphoma.

Great. Thank you, Steven.

Thank you. Your next question comes from Ren Benjamin with Raymond James Financial. Please state your question. Reni Benjamin - Raymond James & Associates, Inc.: Hi. Good morning. Thanks for taking the questions and congratulations on a great quarter. Maybe for Steven, can you remind us the REACH trial design? And since you're not necessarily commenting on the underlying assumptions, can you talk maybe a little bit about what's a clinically relevant results, and do the peak RUX numbers include the potential in GVHD and ET?

So, Ren, I'll do the first part of your question, then turn it to Barry for the second part. So the REACH programs are comprehensive program. There are three pivotal studies there, REACH1, REACH2 and REACH3. REACH1 is a single-arm study of RUX in steroid-refractory acute graft versus host disease. The go in is 70 patients. The response rate, as you can see on – the primary endpoint, as you can see on CT.gov, is a 28-day response rate that would need to be durable to reach an acceptable file for a supplemental NDA, and that's felt to be an endpoint that would point to patient benefit in this particular setting, in high unmet need. REACH2 is in the same setting, but is randomized against best available therapy, is a global study with our partner Novartis and incorporates the same endpoints. And then REACH3, again, in partnership with Novartis, is a randomized study with best available therapy as a control by physician's choice and incorporate chronic graft versus host disease, longer endpoints in terms of being able to show that you can control the disease for longer. All are acceptable endpoints and there is a lot of regulatory feedback on all those studies. As regards the numbers in terms of predicting a revenue for RUX, I'll turn it to Barry.

Yeah, Ren, so we've said in the past that our top net sales for Jakafi will reach at least $2 billion net for MF, PV, and GVHD. We haven't included the numbers yet for ET. Reni Benjamin - Raymond James & Associates, Inc.: Got it. And maybe just as a follow-up. And I know we've been talking about this throughout the call, but insights on how to tackle I-O combinations, just sort of based on what you're seeing right now and how a lot of the competitors, how their trials are unfolding. Do you guys dig into that quite a bit as you're meeting up with Merck and your other partners and deciding which trials to move forward with, or strategically does it kind of just makes sense to have a brute force effort, given the pre-clinical work and early stage work that you've done and tested it out yourself in Phase 3?

Hi, Ren. This is Reid. I'll pass it over to Steven if he has anything to add. The evaluation of clinical trials and prioritization within the I-O/I-O doublet space is an important one for us to get our hands around in the field, because I think we have enough mechanisms now, even within our own portfolio, that you can't do everything in a paired-wise comparison and just have a purely probabilistic approach to drug development. So we do hold the high bar for the preclinical data, one. And so that necessarily allows some mechanisms to move forward at a faster pace than others. Second, in the clinic, we will demand that we see the requisite pharmacodynamic activities early on in the studies to take one step towards de-risking the activity of those doublets. And the third, and this is the most difficult one, is trying to have an underlying assumption as to the patient population that's most likely to respond or benefit from the therapy. We can think of a mechanism like arginase as a good example. Arginase is released from intratumoral myeloid cells, and it's believed that that can be an important immune suppressive mechanism that decreases immunogenicity of the tumor. So you can imagine studying an arginase inhibitor in populations, either individuals or in histologies, which have an abundance of myeloid-derived suppressor cells and intratumoral neutrophils. That will be the approach that we'll take and based on the preclinical studies, we know that arginase inhibition can synergize with PD-1 access blockade and it can synergize with IDO1 inhibition. So you can imagine taking the right patient population and walking through first a doublet study, and then ultimately trying to get to a triplet study. Those are the kinds of activities we have ongoing all the time and we try to always make sure that the programs that we're transitioning into the clinic and investing in meet all three of those ends in terms of underlying preclinical data, mechanistic pharmacology in the clinic and pharmacodynamics, and then finally a patient population that's appropriate. Reni Benjamin - Raymond James & Associates, Inc.: Great. Thanks for taking the questions.

Thank you. We have time for one more question. And our final question comes from Liisa Bayko with JMP Securities. Please state your question.

Hi. Great. Just two parts to my question. First, congratulations on a great quarter with Jakafi. Maybe you could just talk about where you see growth coming from at this point going forward. Obviously, with surpassed expectations multiple times and curious as to what's driving that and where the growth is coming from and where you think it will be coming from. And then just turning to baricitinib, outside of RA maybe you can talk about the commitment to starting some of the other studies and things like lupus and atopic dermatitis, psoriatic arthritis, stuff like that. Thank you. And I guess to that point, would those studies provide any additional safety information to satisfy FDA? Thank you.

Liisa, it's Barry. I'll take your first question and then hand you over to Steven for the baricitinib question. So on Jakafi, we continue to see growth in both MF and PV. We get new MF patients and new PV patients. As we said in the past, PV percentage-wise continues to outpace MF in terms of total growth, but MF patients continue to stay on drug therapy for a long time. So for the future, we see that will continue to grow and continue to penetrate the markets for both MF and PV, and then we'll wait for future indications for GVHD and ET, hopefully. Steven?

Thanks, Barry. Liisa, in terms of programs outside of rheumatoid arthritis, we just feed off what Lilly has already told you on their call. But to reiterate, the diseases that are being considered psoriatic arthritis, atopic derm, and lupus are the ones most often mentioned. At this juncture it's just hard to comment on anything further, other than what Lilly has already told you, and all are still being considered. Your comment around would this be able to contribute safety data to a potential resubmission on a file is also I'm unable to comment on at this time. Other than any data would, obviously, be additive from a safety point of view.

All right. Thanks.

Thank you. I will now turn the floor back to Hervé Hoppenot for closing remarks. Thank you. Hervé Hoppenot - Incyte Corp.: Thank you. Thank you. And thank you all for your time today and for your questions. We look forward to seeing some of you at upcoming investor and medical conferences, including ESMO in Madrid. And for now, we thank you again for your participation in the call today. Thank you and goodbye.

Thank you. This concludes today's conference. All parties may disconnect. Have a great day. Thank you.