Greetings ladies and gentlemen and welcome to the Incyte Corporation Third Quarter 2013 Earnings Call. A brief question-and-answer session will follow the formal presentation. (Operator Instructions) As a reminder this conference is being recorded. It is now my pleasure to introduce your host, Ms. Pamela Murphy, Vice President, Investor Relations and Communications. Thank you Ms. Murphy, you may now begin.

Thank you and good morning. Welcome to Incyte’s third quarter 2013 conference call. On the call today are Paul Friedman, Incyte’s President and Chief Executive Officer, Jim Daly, Executive Vice President and Chief Commercial Officer, Dave Hastings, Executive Vice President and Chief Financial Officer and Rich Levy, Executive Vice President and Chief Drug Development and Medical Officer. Paul will begin with a brief overview of the quarter, Jim will follow with an update on the ongoing commercialization of Jakafi, Rich will then highlight progress made in our lead clinical programs and Dave will describe our third quarter financial results. Paul will then open the call up for Q&A. Before beginning, we would like to remind you that some of the statements made during the call today are forward-looking statements including statements regarding our expectations for the commercialization of Jakafi, our development program for Jakafi and other indications and for other compounds in our pipeline and our expectations for net product revenue. These forward-looking statements are subject to a number of risk and uncertainties that may cause our actual results to differ materially including those described in our 10-Q for the quarter ended September 30, 2013 and from time to time in our SEC documents. Paul?

Good morning, everyone. Incyte’s third quarter was a highly productive one. As expected with Jakafi we’re continuing to establish a strong commercial foundation in myelofibrosis. In the third quarter Jakafi experienced solid, consistent growth with steady new patient adds and new prescribers and we’re starting to see physicians become more appreciative of the need to treat patients earlier in the course of the disease. We also continue to see a modest, yet meaningful increase in persistency rates and we believe physicians are hearing and understanding the message that dosing should be individualized for each patient and they’re changing their behavior accordingly. We’re confident that we will reach the high end of our 2013 guidance for net product revenues which we increased last quarter to a range of $220 million to $230 million. In his remarks Jim will provide more color around Jakafi and myelofibrosis as well as the anticipated launch of Jakafi and Polycythemia Vera. With a potential approval in PV on track for late 2014 we see a significant opportunity and continue to grow revenues and to position Jakafi as best in class among emerging MPN treatments. Jakafi shows potential beyond MPNs, recent data from the Phase II RECAP trial in second line pancreatic cancer suggest a significant growth opportunity for Jakafi and pancreatic cancer among a well defined patient subgroup and provide a strong rationale for use in other solid tumors. The growing potential of Jakafi is just one part of our story however. Our core competency in medicinal chemistry tightly integrated with biology has been a primary driver of productivity in drug discovery and we now have a growing robust pipeline that extends far behind one product. In his remarks Rich will discuss several of these clinical programs, but there are few I’ll highlight briefly now. The…

Thank you, Paul and good morning everyone. Our third quarter results reflect continued solid progress in executing our strategy to grow Jakafi in patients with intermediate or high risk MF. In terms of quarter-over-quarter growth net sales grew 11% with the following components of growth. Underlying demand as measured by bottles dispensed to patients grew by 8%. Net price accounted for 3% of growth, inventory levels remained relatively constant and third quarter inventory remains within the normal range of three to three and a half weeks. Our third quarter performance is consistent with our expectations for steady growth in underlying demand. Based upon the trends we are seeing in new patient starts and persistency, we expect to see continued solid growth in the fourth quarter and as Paul indicated to achieve the high end of our current net product revenue guidance of $220 million to $230 million. New patient starts remain consistent with previous quarters and the number of prescribers continues to increase. Through the third quarter more than half of our target prescribers have prescribed Jakafi at least once. We believe these dynamics are driven by a growing recognition of the disease modifying effects of Jakafi in MF as evidenced by survival data and fibrosis data. Physicians are becoming increasingly aware of the medical imperative to treat patients earlier in the disease. With respect to persistency, the expanded dosing guidance in the label for patients with low platelet counts approved by the FDA in June has been well received by physicians and we continue to see 5 milligrams and 10 milligrams strengths representing a growing percentage, nearly 50% of dispensed bottles. While we originally expected to expand our oncology sales force for the PV launch, we’ve accelerated our plans to capitalize on what we see as sustainable longer term…

Thanks, Jim. As Paul said earlier, we’ve made considerable progress with our compounds in development [technical difficulty] The emerging results show great potential for our portfolio in oncology and inflammation. First, with respect to our development in myeloproliferative neoplasms we submitted a number of abstracts for ASH which we expect to reinforce Jakafi’s position as what we believe is the best in class treatment for patients with intermediate or high risk myelofibrosis. Earlier this month we submitted an sNDA for inclusion of survival data into Jakafi’s labeling for myelofibrosis. Based on prior discussions with FDA, I continue to believe the agency is amenable to some display of these data. For our Phase III registration study for Polycythemia Vera, it's being conducted under an SPA. We expect to release top line data in the middle of the first half of 2014 and to submit the sNDA in June. Assuming a six month review we would have potential approval before the end of 2014. The companion study in PV and piled RELIEF is a double-blind study focused on symptomatic improvements. While the study is nearly full year accreted, the results of this 16 week study won’t be included in the original submission for the PV indication, but we expect to submit an sNDA for inclusion of the symptom data into the package insert shortly after the anticipated original approval for PV. Our goal is to present data from both RESPONSE and RELIEF at a scientific session in the second half of 2014. Moving to our other oncology indications for JAK inhibitors, in August we released top line results from our Phase II study of ruxolitinib in combination with capecitabine and second line pancreatic cancer. It was the hazard ratio for overall survival of 0.47 in a prospectively defined sub set of patients…

Thanks Rich. Good morning everybody. Let's start with product revenue. We recorded $60.2 million of Jakafi net product revenue in the third quarter. Our gross to net adjustment for product revenue recognized was approximately $5.6 million or about 8.5% for the third quarter. We still expect that our full-year growth in net adjustment will range from 8% to 9%. In addition, we recorded $8.2 million in product royalties from Novartis for sales of Jakavi outside the United States. Now moving to operating expenses, our cost of goods sold for the third quarter was immaterial. As our [starting] [ph] finished goods inventory was previously expensed as R&D prior to FDA approval. Both R&D and SG&A expenses were within our expectations. Now, moving to the balance sheet, in terms of cash, we ended the third quarter with $291 million of cash and equivalents. In addition, during the third quarter, the company entered into separately negotiated agreements with certain holders of 4.75% convertible senior notes in which such holders agreed to exchange approximately $37 million in aggregate principal amount of the notes for the 4.2 million shares of the company’s stock and to which the notes were convertible. The holders also received $1.5 million, which are recorded debt exchange expense in the third quarter. Now importantly, this amount is significantly less than what we owed in future interest expense on the exchange bonds had those notes remained outstanding. In total of the original $400 million principal balance of these notes, we have now completed separately negotiated exchanges of approximately $181 million of the notes in 2013. So in conclusion, we continue to make solid progress on multiple fronts and I believe we are in a strong financial position. So with that Paul, I’ll turn it back to you.

Operator, let's please go straight to Q&A.

Thank you, we will now be conducting question-and-answer session. (Operator Instructions) Our first question is from the line of Thomas Wei of Jefferies. Please proceed with your question. Thomas Wei – Jefferies & Co.: Hi, thanks. I have a couple of questions on slightly different topics, the first just wanted to find out if you are able to provide any more granular detail on persistence rates and new patient starts on Jakafi? And then, on the solid tumor program that you are expanding into, can you give us a little bit more detail on what percent of non-small-cell lung cancer, colon and breast cancer would qualify for the study based on the criteria from the pancreatic subgroup that would be helpful in terms of sizing those opportunities. And based on the pancreatic press release that you had put out where there is mention of durable tumor responses, I guess I wanted to understand do you think that Jakafi is working predominantly through a direct antitumor effect and would there be actually a potentially big difference between JAK1 and JAK2 in that way? Thanks.

Hi Thomas, this is Jim. I will take the first part of your question. Regarding new patient starts, they have been remarkably consistent quarter-over-quarter. So we have not seen a deceleration in the absolute number of new patients starts quarter-over-quarter. With respect to persistency, we really don't want to get into specific metrics around how long patients are staying on a product, only because it's a moving target. Our best indicator of improved persistency is really looking at the dosing practice of physicians starting at lower doses and titrating as appropriate. So we are using 5 milligram and 10 milligram tablets as an indicator of physicians individualizing dosing and we continue to see that move very nicely upward quarter-over-quarter. So with respect to the specific metrics of persistency, there is a number of different ways you can measure that, you can look at the number of patients who stay on 12 months after initiation. You can look at the number of patients who drop off in a given month. We do have some variability in the data sources particularly as patients switch from plan to plan. So we would prefer to really look at underlying demand as measured by total dispensed bottles and then really let you triangulate between new patients starts and total patients in order to back into the persistency.

So with respect to the clinical questions that you asked, first solid tumors in terms of what percent would qualify, I mean based on what we saw in the pancreatic cancer where we said it would be approximately 50% of patients. We believe that's also true in these other solid tumors, you know within a ballpark. Now the other thing you have to consider in terms of looking at the size of the opportunities there is line of therapy. We haven’t really disclosed where we are looking but it's pretty – it should be pretty clear that we are not focusing initially on first line therapy and so when we talk about the approximately 50% of patients that applies often to the lines of therapy that we are going be focusing on initially and as we move towards first line those numbers could come down a little bit. With respect to the effects within pancreatic cancer, we are seeing survival benefits that I think are beyond what you might expect based simply on response rates even though there were durable responses seen only in the patients that received ruxolitinib in addition to capecitabine. And in terms of the differences between JAK1 and JAK2, our hypothesis is based on everything that we know that the mechanism should be equally applicable to both JAK1 selective inhibitors as well JAK1/2 inhibitors. However, the proof of concept that we have right now is with ruxolitinib which inhibits both JAK1 and JAK2 and that is part of the reason why one of the studies that we are planning to start in the first half of next year is looking at one of our selective JAK1 inhibitors to make sure we can reproduce those results before we make an even larger investment for our JAK1 selective inhibitors in other solid tumors.

Thank you. Our next question comes from the line of Salveen Richter of Canaccord, please proceed with your question. Salveen Richter – Canaccord Genuity: Thanks for taking my questions. I am just wondering what the, if you could just maybe elaborate on the overall strategy with the JAK1, how do we think about that strategy in inflammatory space and then how is it de-prioritized relative to the heme-oncology opportunity and how we should think about solid tumors versus heme opportunities especially with 110? And then, just a competitive question, Gilead just started their Phase III trial with their JAK versus [Rux] [ph], I mean, what are your expectations there and how do you think, if this drug should come to market, it will play out in the marketplace?

Why don’t you take the first part.

Okay. So with respect to our overall strategy for JAK1 we believe that the strongest most, the strongest opportunity and those that we have a clear competitive advantage and lead on are in oncology for both solid and liquid tumors. But we have multiple JAK1 selective inhibitors two of which are already in the clinic and our first goal is to figure out which of the drugs is best suited for use with more highly myelosuppressive chemotherapies and once that decision has been made then pursue the inflammatory indications with the one that is best suited to inflammation either alone or possibly with a partner. And was the next question simply the question on the competition or was there another question in between?

Solid versus –

Solid versus liquid. So I think the opportunities are excellent in both places with the data that we have besides myelofibrosis right now is in pancreatic cancer with ruxolitinib which happens to be a solid tumor. So we are certainly planning to pursue solid tumors with both ruxolitinib and in other cases with a JAK1 selective inhibitor, but as we said we are starting a combination study with a JAK1 inhibitor with 40093 – a PI3K delta Inhibitor because we believe that there will be synergy in the clinic there and there is no reason why the same drug can't be approved, developed and then approved for both solid tumors and liquid tumors so we don’t feel that there is a need to have separate molecules for those and we plan to pursue both.

Salveen, with respect to competition our – we have always expected competition, our view is that competition is good for patients, is good for the market, ultimately more patients will be treated with the JAK inhibitor, so the question really comes down to which product will they be treated with that's the function of product profile, we are absolutely convinced we have a best in class profile with Jakafi. With respect to Gilead having just started their Phase III they’re a long way off from the market. If you look at their study design, they seem to be with a secondary endpoint looking at transfusion independence. From our point of view, cytopenias is an on-target effect with JAK1, JAK2 inhibition, it's predictable, it's manageable and we think between now and when Gilead were to come to the market, cytopenias will be an issue that physicians are very comfortable dealing with through individualized dosing with Jakafi. Salveen Richter – Canaccord Genuity: Thank you.

Our next question is coming from Rachel McMinn of Bank of America. Please proceed with your question. Rachel McMinn – Bank of America: Yes. Thanks very much, a couple of questions. One, Rich, I was hoping you could flash out a little bit more helping to set expectations for your IDO inhibitor at ASCO. Are we looking for just a responses there, would we have any PHS for overall survival data that we could begin to look at and then I don't know either Rich or Paul, if you could talk about the PV read through from Sanofi discontinuing their Phase II monotherapy study, I think that kind of spooked some people. I don't know if you have any futility analysis that was already built into your Phase III that you could speak to that gives you confidence beyond just to be obviously the strong data you have in the Phase I, II study? And then, lastly, how do we think about all of these studies with regards to 2014 R&D. It sounds like you are making a really big push and solid tumor is not surprisingly, but I just want to make sure that we’re kind of well prepared to think about how to model expensive next year? Thanks.

Okay, so with respect to IDO, what we are going to likely present in 2014 are the results of an open label running where everyone is getting both IDO inhibitor 24360 and ipilimumab. And this is a dose escalation to find the proper dosage for the randomized study that will be definitive. What we would expect to be able to show based on what we are seeing now are our response rates. The duration of maintaining therapy before they have to change to something else likely as a result of progression and how long those individuals are living and we are fairly confident based on data that we have right now that, that will compare favorably to historical controls with ipilimumab alone and that is the basis of our level of excitement right now. But in terms of actually having robust data and comparison to ipilimumab alone that will be coming in later years after we really get into the randomized portion of the study. Now, with respect to PV, we have only read the restatement in the Sanofi press release from yesterday saying that they, you know, halted that study and plan on looking a combination therapy. We have no idea and we would be interested in finding out others as well. Rachel McMinn – Bank of America: They said it does that -- Yes, they said it doesn't live up to their internal expectation was the comment that I understand. So, I am assuming that's just a failure to have robust efficacy.

Yes. So I don't know exactly what they – I don't know exactly what their issue is and we still try to find out more about that. But let me just talk about our place. So, first of all the PV data from this Phase II study 256 was just published online yesterday in cancer, so that is out there for people to look at. Secondly, that our registrations study, the response study, not only has been fully enrolled for almost a year, but all of the patient surpassed the primary endpoint now we just need to wait for all, which is basically at 32 weeks, all patients need to have four to eight week data before we have last patient, last visit and look at the data. But we know from a vigilance perspective that there are no issues with the study in terms of safety and we have no indication from the study that there will be a lack of efficacy. I can't imagine why the results would be particularly different from what we saw in Phase II, where we have like 97% of the patients become phlebotomy independent, patients had profound reductions in spleen size at least as measured by palpation, patients demonstrated symptomatic improvement in that study. So, we remain confident in our study and are curious when eventually the data comes out from the Sanofi as to where they ran into problems with their drug. And with respect to R&D expense in ’14, I will turn that over to Dave.

Thanks, Rich. Yes, Rachel, I think you are right, it is an aggressive plan, and rightly so. I mean, we are very confident and optimistic about our portfolio. Like it's pretty consistent with what we’ve said in the past that the return on investment as we invest in our R&D, pipeline is very strong, as I mentioned in my prepared remarks, we’re in a strong financial position, we continue to focus on optimize in the capital structure of the company as evidenced by the recent exchanges we perform. So I think we are in a good position to fund an increased R&D investment next year. Rachel McMinn – Bank of America: Thank you.

Our next question comes in the line of Matt Roden of UBS. Please proceed with your question. Matthew Roden – UBS: Great. Thanks for taking my question as well and Happy Halloween. On the IDO program, can you talk about the evidence that suggested this should be additive or synergistic with the checkpoint inhibitor? Just try to give us a sense for why you think this approach should work and then, related, we all know that Charlie Sawyer has been pushing this idea, the combinations of investigational agency in cancer should be pursued but operationally, can you talk about the password and combining idea, with PD1 or PDL1 inhibitors and then, if I may a follow up?

Okay. So first as I mentioned in response to an earlier question. Just with respect to our drug and checkpoint inhibitor, if you let me map, which is a CTLA4 inhibitor. We are seeing response rates, we are seeing how long patients are taking to progress and we’re seeing survival data that is early and small numbers, but looks to us quite different than the early data with ipilimumab monotherapy and similar patient population. There is also, animal models in vitro data that suggests synergy between our drug and PD1 inhibitors in PDL1 inhibitors, but there is no clinical data there. With respect to the logistics of how this can work, I think companies, in several areas have now become much more amenable to working together at the investigational stage prior to the approval of the either of the drugs. FDA is making that easier, recognize the benefits in cancer as well. And so we have started discussions with other companies, not to partner our program or to sell it to them, but to maintain the program ourselves while looking at combination therapies and I don't want to get into any specifics about that until things have matured, but right now we are reasonably optimistic to that one or more studies might start next year in combination. Matthew Roden – UBS: Okay and then from the regulatory perspective, are they on board with a combinations as well?

So we have had experience with FDA in terms of combinations of investigational drugs. At this stage where we have no specific agreements with any company, no protocols have actually been submitted to FDA or other health authorities to say that those studies can go forward other than the fact that we – I mean, not that ipilimumab isn't an approved drug, but they had no issues with combining those and that data will help us justify those selection and other things for combinations with PD1s and PDL1s or whatever we end up doing. So I don't have specific FDA or other health authority feedback, but I don't think it's going to be a major problem. Matthew Roden – UBS: Okay and then Rich, you also mentioned the JAK1 PI3 Kinase combinations and I think you said B Cell lymphoma, quite a heterogeneous group here. Can you help us where you think this combination might be best applied into rationale for addressing those particular subsets?

So, I mean, the first part of the study will look at a range of B cell lymphoma's, as we try to establish the doses of the two drugs in combination and establish what safe combination can be looked at that study may also give us further hints as to where we would likely focus in the future. Certainly with respect to either the stat more established or further along in development PI3K deltas or BTK inhibitors. There are places where those drugs are active, but we think there's a lot of room for improvement, either in terms of the number of responses or the duration of those responses. And so that need for increased benefit is the key driver now and I can tell you that in vitro synergy studies suggest the potential for benefit in those same indications where you are seeing suboptimal benefit with either BTK or another PI3K delta inhibitor. Matthew Roden – UBS: Thanks for taking my questions and congrats on the pipeline success.

Thank you.

Thank you. Our next question is from the line of Brian Abrahams with Wells Fargo Securities. Please proceed with your question. Brian Abrahams – Wells Fargo Securities: Hi, thanks for taking my question and congratulations on all the progress on multiple fronts. Question on the pancreatic study, I realize lot of the data, you are going to preserve for ASCO but, I was just wondering if you give us any sense to the number of pre-specified subgroups that you looked at and maybe how the hypotheses that these are testing differed or perhaps overlapped? And then, can you give us on any sense on in terms of the bar for label expansion potentially based on those three, Phase II solid tumors studies that you are going to be running for ruxolitinib given the overall survival and point there? Thanks.

Okay. So with respect to the number of subgroup analysis, we actually had, as we’ve said in the past, more than one and less than five, pre-specified analyses based on the potential mechanism of action. There were other subgroup analysis that were kind of routine, like age, gender, things like that, that were not including in the mix because those are just always, always there. And with respect to how those differed, I really would rather not go into what the other two or three or one additional subgroup analysis was, until such time as we actually present the data. Now with respect to, I think your next question is about the Phase II and the expectations from that. So, the studies are really designed not to be registration studies, but if the results are robust and this time, already backing up the same group that, you know, with identified in pancreatic cancer, I can't say that there's no possibility we couldn't go directly to a label expansion, but I think the expectation from the most part should be that these are Phase II which would then lead to larger Phase III registration studies in any of the number of these indications. Brian Abrahams – Wells Fargo Securities: Thanks Rich and congrats again.

Thank you. Our next question is from the line of Navdeep Singh of Goldman Sachs. Please proceed with your question. Navdeep Singh – Goldman Sachs: Hi, good morning and thanks for taking my question. I understand that you can't provide much color on the biomarker for Jakafi and solid tumors given competition, but when you plan to release that information and if I can, how confident are you that biomarker will resonate with the scientific community?

So, in terms of release of the information I mean, it would certainly be no later than when we expect to present the data at ASCO, but we recognize that, that holding it out for that long may not either be possible or appropriate. Depending upon what information seems to be leaking, various other things that could come about where we just feel obligated to do something. So I am not going to put a specific timeline on it. With respect to how well it's going to resonate, I think it's going to resonate, but I think that there are so few people out there that we have actually, community type oncologist that sort of thing that are aware of what's going on that don't have any data to support it one way or the other. Other than to say that it is consistent with the mechanism of action of JAK1 or JAK1 or 2 inhibition and therefore it should not come across in any way as, oh, they just got lucky, they just found some random thing and I think that's the best I can put it at this point in time. Navdeep Singh – Goldman Sachs: Okay and just a quick follow up on your JAK1 inhibitor, I know that they are evaluating JAK1 inhibitor in a Phase I trial on solid humors. And I think that trial was initiated in June. When do you think, you can get some data on that, is ASCO [indiscernible] thanks.

So, you know, it's hard to say exactly when we are going to present data from dose escalation Phase I studies because you never know exactly how many cohorts you are going end up doing before you reach the maximal tolerated dose, they are largely safety studies and so yes certainly it's possible that there will data out there and there is more than one study going on with JAK1 inhibitors right now in solid tumors. There is the combination with gem and paclitaxel as well as just a general solid tumor dose escalation study. And so it's reasonable to expect that you will see something in 2014, but for example, if that was to be submitted to ASCO that means submitting the data in the first quarter of 2014 and we are just not sure yet how robust that data set will be. So we don’t want to make specific predictions and then not follow through on them. Navdeep Singh – Goldman Sachs: Okay thanks Rich and congrats on the progress.

Great, thanks.

Our next question comes from the line of Ying Huang of Barclays. Please proceed with your question. Ying Huang – Barclays: Good morning, thanks for taking my question. Related to the -- on pancreatic cancer. So the first one is when you conducted the subgroup analysis did you spend any offer [ph] in conducting the analysis and then secondly I am sure Novartis has that done a lot of looks into the data here. When do you think Novartis would adopt in and when is the – I guess the latest time frame they could do that. And then on INCB39110 which is solid data from ACR which looks pretty encouraging, but I am not sure whether we see clear doses, among the three lower doses and we did see living lipids elevation at 600 QD dose. I was wondering what your thought is in terms of taking this count forward? Which dose would you likely select? Thank you.

Okay. So thanks. So first of all, in terms of prospective planning of this study which was 120 patients approximately, there was no pre-specified alpha control for subgroup analysis. However, if you do Bonferroni correction which is most aggressive correction for multiple looks at subgroups. Based on those two to four other groups, the statistics of the subgroup does held up with the feedback, corrected value still less than 0.5. So again, we don’t see this as an issue of chance. We see this as a pretty clear finding that's also supported by the mechanism action make sense as opposed to just statistical rigger. With respect to Novartis, they have no limitations as to when they can decide to opt into a program. So we cannot speak to when they may or may not decide to do that. And with respect to the Phase II data of 39110 in RA, we agree that there wasn’t much of a dose response seen other than with the 600 milligram dose that was clearly, I shouldn’t say clearly, in this study it was clearly better than the 100 BID, 200 BID and 300 QD. I think that you just would need larger numbers of patients to really be able to see that as well as potentially studying a lower dose than either 100 BID or 301 today to really see the full view of that dose response. With respect to lipids, I mean all of the drugs that are being developed in the IR6 space, the JAK space, as well as to a lesser extend other anti-inflammatories increase LDL and HDL and so far this has not been a problem for any of them. We are aware that the (indiscernible) has put out data saying that they don’t increase lipids, they actually do at their 300 milligram QD dose which is one that they have said they are not planning to take forward into Phase II. But clearly the effect is still there when you reach levels of the inhibition of the JAK1 target which is related to then inhibiting the signaling of IR6. So I don’t think there are any exceptions to this mechanistic rule. Ying Huang – Barclays: That's fair. Thanks for the color. Very helpful.

Thank you. Our next question comes from the line of Cory Kasimov from JP Morgan. Please proceed with your question. Matt Lowe – JP Morgan: Hi there, it's actually Matt Lowe in for Cory today. You mentioned, you are in ties with the early data in open label study for IDO, I am just wondering if you would characterize that at all and what you are looking at in the study? And then, also at ASH, I believe you’re going to present the three years survival data for Jakafi. I was just wondering is there still a meaningful number of physicians who need to be convinced of the overall survival data. If you can comment on that that would be great? Thanks.

Okay. So I don’t really have much more to say on the IDO plus similar that I have said before but let me just reiterate the bottom line. So the things that we are looking at now in this small dose escalation open label study is comparison to historical controls and what we are seeing are response rates, the duration before someone has a progression event and the duration that those patients are living which we believe compared to published data on ipilimumab monotherapy in melanoma are better. But it's not a statistical comparison, not even a head-to-head comparison, yet it's a comparison to historical controls based on a relatively small number of our patients compared to a large number of patients in the Phase II and III studies with any ipilimumab but this along with some of the pre-clinical data that suggest synergy between these things gives us confidence that this is a real effect and gives us interest not only in following the study with ipilimumab but with other checkpoint inhibitors and putting PD1 and PDL1. With respect to the impact of three year survival data, I will turn that over to Jim.

Yes, there is still a significant proportion of the physicians who are not aware of the survival data with Jakafi so certainly publication and scientific meetings is incrementally helpful, but ultimately we think the major catalyst would be inclusion of the data in the package insert and again we are hopeful for that sometime next year. Matt Lowe – JP Morgan: Okay. Thank you.

Our next question is from the line of Eric Schmidt with Cowen & Company. Please proceed with your question. Eric Schmidt – Cowen & Company: Thanks. Three questions maybe first for Jim, I am having a little trouble reconciling the unit volume growth 8% in the quarter down from 15% last quarter given the comments you made about studying these darts and maybe the increasing persistence, maybe you could clarify that? And for Rich, I think you indicated earlier that the initial focus here with the JAKs in solid tumors is later lines of therapy. Is that based on some mechanistic rationale or it's just because that’s where you fortunate enough to get the first early read? And then lastly for Dave, just wondering if you have tax planning strategies in place for some of these newer assets I guess the JAK1s in particular that you are on worldwide rights to?

Hi Eric this is Jim. Here is an actual rhythm to the business in terms of our demand pattern, if you remember we did 7% dispense bottles in the first quarter and we did 15% the second quarter, 8% in the third quarter and what you will find is typically the first quarter in oncology particularly for orals tends to be one in which you got kind of the win your face with respect to deductibles, donate etcetera. there is also an issue of the number of shipping days and we had fewer shipping days first quarter, more shipping days second quarter. And the third quarter tends to be impacted more by quite frankly vacations whether it be patients or physicians there is reluctance to put patients on new products during the summer period. And typically we see a relatively strong fourth quarter. So that's the natural rhythm of the business. We were expected to repeat this year. So that really is the explanation for the 7%, the 15% and the 8%.

With respect to lines of therapy, I mean with respect to ruxolitinib, we particularly looked for lines of therapy where the current treatment could include an option that was not very highly myelosuppressive and that was the lead basis for making those decisions. With respect to the JAK1s that’s been less of an issue but it's still very hard to get directly into first line therapy. So we are not saying that we are starting each of our studies in last line by any means. I am saying that first line is hard to get to initially. And it just happens that there are in some of these diseases at least, the percentage of patients who would fit into the category where we worked very well in pancreatic cancer is a little bit higher in later lines maybe because their prognosis is not that good in the first place. But there is a number of patients who exists in first line is larger. So the total number of patients that might be available for treatment in the end can still be as larger and larger and they end in first line even if the percentages are little bit lower. So that was not really a key decision make on how we selected our Phase II studies.

And Eric, yes, we are working with our outside professionals service providers on those strategies in addition where you’re actually recruiting internally for a tax director who would lead that role and of course I will remind you in the meantime we have a $1.3 billion NOL that can be utilized as well. Eric Schmidt – Cowen & Company: Thanks a lot.

Our next question is from the line of David Friedman of Morgan Stanley. Please go ahead with your question. David Friedman – Morgan Stanley: Hi, thanks for taking the question. Just wanted to get a sense of two things, one is of all of the Phase II, these randomized Phase II that are starting in long and colorectal, what is the sort of rough time frame to get data from those, is that 2015 or is that 2016? And then, the other question is just around some of the preclinical work that supports the tumors and I was wondering if you could just talk about what you have seen pre-clinically for pancreatic and how that is similar or different to what you see in longer colorectal but also prostate and myeloma where you had trials as well? Thanks.

Okay. So we are not going to get specific about the time lines for the Phase II yet in part because we have not selected centers yet for all the studies to happen completely visibility to determine how many patients might be enrolled for a month or how many of each of those centers. The only thing I would say is that these are pilot studies like the Phase II recap study and the recap study from start to finish was about two years. So I think, assuming we start in first half of ’14 with some of these studies, I think seeing in ’15 is optimistic and seeing data in ’16 is quite reasonable at this early stage of evaluation. With respect to the pre-clinical work, I would really suggest that we’ve a follow up call with you and the scientists. We’ve done that work because I don’t have all that information at hand to go into detail. Other than to say that there were clear pre-clinical models suggesting benefits in terms of pancreatic cancer and some of the other tumors have been well studied and have similar results but I’m not – and that’s not directing our line of responsibility and I don’t have that information at hand today. David Friedman – Morgan Stanley: Okay, thanks.

Thank you. Our next question is with Liisa Bayko of JMP. Please proceed with your question.

Hi, this is [Drew Prigodich] [ph] for Liisa. Hi, there are couple of questions for you. One is, if you could talk a little bit about how the choices were made for the solid tumors you’re developing first and including colorectal and breast? And second question is, where in the information space do you see the best opportunity for a JAK1 specific inhibitor?

So in terms of the choices with respect rectal in there which is the place where we already have clear, perfect concept in pancreatic cancer, we were looking for major solid tumors and certainly the ones we’ve announced that we’re doing, long colon and breast are major solid tumors. But also where there was an opportunity to combine with something that was not very highly myelosuppressive. And with respect to JAK1 inhibitor at this stage, again, the first thing is to try to reproduce the recap results for the JAK1 inhibitor and the second in non-small-cells because it’s a very large opportunity, large unmet need along with similar levels of evidence that this mechanism should work in these patients and that about 50% of the patients would quality into this subgroup that we think we work best in. With respect to choices in inflammation, I mean, there is really a couple of things I would say. One is that one of the potential benefits are the selective JAK1 inhibitor is to go to levels of inhibition that you can’t get to necessarily with a JAK1 and 2 inhibitor because at that point you would start to get into myelosuppression. And so, there are certain diseases psoriasis being one but certainly not the only one, but the place we have data where the data suggest that you do want higher levels of inhibition that is necessarily for maximal affect in something like rheumatoid arthritis. But obviously, something like rheumatoid arthritis is a very large opportunity and nothing to be dismissed off out of pan. So we’ve not decided exactly what we would do in terms of this, our main priority right now is figuring out which molecule would go inflammation. And if we decide to partner the program then our partner would also have some influence on the – or a live influence probably on the choices that would be made in terms of which indications first and which indications would come later.

Thank you.

Our next question is from Skip Klein with Gauss Capital Advisors. Please proceed with your question.

Thanks. Maybe I should start up by trying to soften – sincerely thanking you for all the good progress and execution in sales, balance sheet, clinical front there is lot going on, you guys are really executing. So then, the question I guess is really for Jim, I’m working on the triangulation that he suggest and how much Jim whether you know that I answered to a higher authority. There is some ladies that play mahjong who are big fans of Dr. Friedman and they honestly pester me more than I’ve ever been pestered in my investor life. And this is what I’ve told him and I guess I’m just wondering whether you could tell me whether I’m in line or out of line. I’ve told them that the company has treated about 5,700 patients in myelofibrosis out of about 12,000 available populations. I’m telling him you’ve about 3,300 on therapy, you’re adding about a 120 to 125 patients a month on a net basis. So, I’m telling you about the half way through MF opportunity, PV is to follow and is a bigger available population, I’m telling them that I’ve peak sales in 2025 and they remind me that they’re not going to be alive then, but I tell him it’s going to be 1.8 billion in peak sales at that point with pancreatic probability of technical success of about 60% to 70% so that’s a lot. Am I roughly in line because these ladies I don’t really want to embarrass my mother and they play mahjong with her?

Skip, we haven’t been that precise in communicating our patient numbers, but I think, you may be misleading the ladies with respect to the total addressable population. Again, we see an addressable population of basically 85% of the total MF population of 16,000 to 18,000, so let’s call that 15,000 patients. You can segment pretty much into three groups, high risk 5,000, intermediate 2 5,000, intermediate 1 5,000. To-date I’d say we have less than – considerably less than 5,700 patients who have touched drug for MF. So the way we’re looking at it, we’re probably into third inning, third or fourth inning with respect to our MF gain. And I think we’re in a good position to be almost two years into launch and we’re still characterizing our growth in terms of sequential quarter-over-quarter. Most oncology products experience relatively rapid peak and then a plateau and they’re often taking about year-over-year growth rate at this point. We’re still talking about double digit sequential quarter-over-quarter growth and I think that’s because the nature of the disease. The heterogeneous disease with a spectrum of severity and it’s also managed by community physicians and when you have a low prevalent disease managed by community oncologist it takes them some time to get comfortable with the new therapy and a disease they don’t see that often. And I think we’re seeing that with the solid consistent growth with Jakafi, but I think we have a lot of growth ahead of us with Jakafi and MF.

Great, and then I greatly appreciate handling the fact that I was high on the treated patients, how about 3,300 on therapy and adding about a 120 a month because there is one lady that kind of focuses on that.

Yes, I don’t want to get into the new adds per month, well I can’t say is that the relatively consistent. If you look at the number of patients who are on therapy, I would just suggest that really use your calculator, if we have $60 million in net sales for the third quarter and right now we realize about $7,600 assume 8% discount of a list of $8,300 and then divide by three months you will get closer to about 2,600 or 2,700 on therapy.

Okay. Thank you very much and I guess the most important is peak sales, but I guess, I can’t expect anyone really to comment on that. Is that way out of line if things go right to think that peak sales could be $1.5 billion to $2 billion for ruxo?

Well, I wouldn’t want to comment on anything outside of MPNs, but I think as we’ve said in the past, we see Jakafi being a $0.5 billion opportunity in MF and we see the PV opportunity being at least as big if not bigger than the MF opportunity. And then obviously the programs that Rich has discussed that’s all incremental.

Great, thank you very much.

Thank you. We are in the end of our question-and-answer session and time for one final question. That will be a follow up from the line Matt Roden of UBS. Please proceed with your question. Matthew Roden – UBS: Well actually, it’s been answered, thank you very much.

Thank you. I’ll now turn the floor back to management for closing comments.

This is Paul. Thank you all for dialing in and for the dialogue we’ve had this morning, I think we’re making really good progress and the company looks forward to our next quarterly call and with that I’ll be signing off. Bye, bye.

This concludes today's teleconference you may disconnect your lines at this time. Thank you for your participation.