Steven Stein: Yes, Michael, thank you for the question. Now we have seen the data. Obviously, it is an impressive data set. At this point, as you know we have a number of studies ongoing povorcitinib. We have had internal discussions about the potential to extending the trials of povo to atopic dermatitis. What I can say right now is we are encouraged by the data from [indiscernible]. I think that it’s an indication that povo could work very well in this disease. We have not made an internal decision that yet as to whether to develop povorcitinib and atopic dermatitis yet, but it’s certainly something we are contemplating.
Operator: Thank you. Next question is coming from Marc Frahm from TD Cowen. Your line is now live.
Marc Frahm: Hi, thanks for taking my questions. Maybe just start. One, just following up on the prior BET question. Can you — were your comments just based on the clinical data you are seeing in those– concern of AML? Or maybe can you speak to preclinically — because I believe that BET inhibitor from a competitor has shown genotoxicity in some preclinical assays. Has your’s shown genotoxicity?
Steven Stein: Yes. It’s Steven answering your question. So just to reiterate Pablo’s remarks and remind you that our BET program was in the clinic a while ago in solid tumors. And then we have obviously pivoted to study myeloproliferative neoplasms. We’ve treated close to 200 patients to-date. And in the clinical data set, which is the most powerful, as Pablo said we have no concern as regards AML transformation or any concerns that we’ve seen in that regard. From a prior preclinical work on things like [AMs assay] (ph) and genotoxicity, et cetera, we also have no issue, and we are aware of the issue with the competitor drug that was seen in preclinical work.
Operator: Thank you. Next question is coming from Brian Abrahams from RBC Capital Markets.
Brian Abrahams: Hi, guys. Good morning. Thank you so much for taking my questions. I wanted to drill down a little bit more on the Jakafi dynamics. What’s your explanation — or I guess what do you think is the best explanation for the sequential downtick in total Jakafi demand? Was that something that’s just seasonally related that you typically see in first quarter? And then I guess, on the competitive front, I am curious why you think you’re not seeing any impact at this point to market share or patient persistence? Is this something you might expect to change going forward? Or would you expect market share and persistence to remain stable based on sort of what you’re hearing in terms of market research and on the ground KOLs discussions?
Hervé Hoppenot: Maybe I can start on the uptick. I mean what we said, and you can see on the slide is that, in fact, there is an increase in the number of patients treated across all three indications in Q1 versus Q4, and there is a growth that you can see on the so-called paid demand graph also that shows that versus last year there is a lot of growth in PV and GVHD. So the unit growth of Jakafi sequential to Q4 and versus Q1 of last year is there and fairly visible. The reason for the sequential growth versus Q4 is what we discussed when we discussed Q4 a few months ago is that there was an abnormal free drug ratio in Q4 that has been completely fixed in Q1. So we are back to normal rates of free drug in Q1. Now on the competitive side, maybe Barry, if you want to speak of why we don’t see the impact of the new competitors.
Barry Flannelly: Sure. I think, in fact, the new competitors, let us take an [indiscernible] and momelotinib as examples, there — as far as we can tell from all of our market research, from all of our experience working with hematologists, they are all being used in the second-line setting or maybe in patients that have very, very low platelets, for example. So we anticipate because of really the overall survival benefit of Jakafi, because of the tolerability of Jakafi, because of the symptom release of Jakafi, it’s a great drug, and it will continue to be very useful to patients who have myelofibrosis going forward.
Operator: Thank you. Next question today is coming from Vikram Purohit from Morgan Stanley. Your line is now live.
Vikram Purohit: Hi, good morning. Thanks for taking our questions. So we had two, one on LIMBER and then one on Opzelura. So on LIMBER, for the ALK2 POC data set we’re expecting to see by the middle of the year, could you just frame for us kind of what the scope and size of the data set is going to be? And what you would define as sufficient for continued development for that program based on what we see for that POC data set? And then secondly, on Opzelura, I just wanted to revisit the topic of potential guidance and see when you think might be a good potential time to provide revenue guidance for Opzelura since you mentioned that it seems like the script shared seem stable between AD and vitiligo? Thanks.
Steven Stein: Hi, Vikram, it’s Steven. So on your first question, just a reminder, ALK2’s mechanism felt to work through hepcidin inhibition and then ameliorate anemia by releasing iron and make it available for hemoglobin production. As we’ve already shown in multiple presentations, we can decrease subsiding levels. The question you get into does this translate to some sort of clinical benefit? Just to remind you of the study, it has 3 groups, treatment group A, B and C. A was monotherapy, B was in combination with RUX, but those were in later line patients. And the real focus right now, as you can see on clintrials.gov is treatment Group C, which is the treatment-naive group of patients to see in combination with RUX, will help make an effect that will be of clinical benefit to patients, either by raising hemoglobin or preventing the decrease that sometimes occurs with JAK2 inhibition.
And then if we’re able to demonstrate that as we dose increase in the second half of this year, then we’ll have a clinical proof-of-concept that we can then potentially take forward to a regulatory environment, but we’ll have to be clear that we are benefiting patients from a clinical benefit point of view in that treatment-naive group, and we’ll have that data set second half of this year. I’ll turn it over for the second question.
Christiana Stamoulis: Vikram, it’s Christiana. I’ll take the second part. As we discussed on our last call, before we provide guidance for Opzelura, we’re looking to have more real world data on utilization, especially for vitiligo. And data that goes beyond that first initial phase of therapy, which may represent a phase of experimentation by patients. So we are still early into the launch. We are still going through that initial phase of patients on therapy. So we are waiting for more real-world data before we are in a position to give you guidance.
Operator: Thank you. Next question today is coming from Derek Archila from Wells Fargo. Your line is now live.
