Have Incyte for this session represented by Bill and Pablo. Maybe just a quick disclosure before we get into it. For important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. With any questions, contact your Morgan Stanley sales representative. All right. With that, welcome back. Bill, you joined the company a couple months before the conference last year. Maybe you could provide a brief overview of how the company has evolved, both strategically and in the clinic over the last 12 months or so.
Thanks for having us. I think the most significant change over the past 12 months since I've joined, and to be fair, I inherited a lot of substrate, is that the pipeline today looks fundamentally different than it did 12 months ago. To put a fine point on that, when I joined, we had no proof of concept data on 989, our CALR antibody for MF and ET. We had no proof of concept data on G12D inhibitor for pancreatic cancer, or TGF-beta by PD-1 for colorectal cancer. We didn't even have phase III data for povorcitinib, which is now under review at the FDA. Through the acquisition of Vega, we didn't have latarcibart for von Willebrand disease. Today we have all of that.
I think the point here is that we have much greater visibility into the recovery phase or the growth phase of the company post 2029, after we lose JAKAFI. Now it's our job to convert phase III trials into FDA approvals and ultimately revenue earnings and cash flow. We think about this company right now in two simple pieces. This, I think, is how we should be judged. The first is our core business ex-JAKAFI, which is annualizing at roughly $2 billion in sales. Our job is to get it to $3 billion- $4 billion by 2030, which sets the floor for Incyte.
The second job is to continue to advance the pipeline, which is more de-risked now than it was a year ago, as I said, and launch these products. If we do this right, and it's got to work, we don't expect people to take our word for it, the company has the potential to grow at a 15%-20% CAGR from 2030- 2035. That would increase the value of the company. It'll give us a great deal of sort of breadth and depth in terms of our product line. We'll have dramatically reduced the LOE exposure of the company. That's the basic framework for recovery.
Okay, great. That's a good way to set the stage. We're going to jump around a bit, but figure we'll start with MPN. For the JAKAFI franchise and XR specifically, what will determine whether conversion reaches the low or high end of the 10%-30% pre-LOE target you put out?
Yeah, it's a good question. We have this range of 10%-30%, take the midpoint of 20%. If we're successful there, we preserve almost $750 million in sales as we go through the transition. I think there's two steps. The first is to get formulary coverage. We'll provide an update on the third quarter call where we are. We are ahead of schedule.
Formulary coverage for XR by the end of the year is going to approach 70%-80%. We have all the major PBMs and health plans with XR on formulary at parity with IR and at a price that is acceptable to us and acceptable to them, which is parity to JAKAFI. I think 2027 is going to be about conversion, and you can convert new patients and continuing patients. Both sources of conversion are important. If you're converting at a half a point to a point a month over a 24-month period, w e can preserve a significant portion of this business. It's a bridge. XR is not going to drive the value of Incyte, but it will provide support as we go through the transition.
Okay. That makes sense. Just talking about some of those next-gen assets, specifically for the CALR antibody 989, we'll have frontline phase I data in MF, I believe, later this year. So maybe just help us with efficacy signals you're looking for, what would support further development of the monotherapy and combination approaches, and then we'll have some more specific questions.
I'll turn it over to Pablo.
Let me recap real quick just to expand a little bit on your question. 989 is currently in pivotal trials already for second-line ET. That has been initiated, and we disclosed the design earlier this year. We're in the process of implementing a second-line MF trial. We'll give you full details at the next earnings call on the design of that trial. Roughly speaking, the study will be in second-line MF and with the best available therapy control arm, and it will enroll all comers with a primary analysis probably around Type 1, just to improve the probability of success of that trial. That's already in motion. When it comes to first-line MF, there's a couple things that we need clarity on. One is, as you brought up, we're going to have a data set in frontline MF patients at ASH.
About 2/3 of the patients, single agent 989, about 1/3 with combination with ruxolitinib. That data set, which is maturing as we speak, but we don't have yet, it's critical for us to make a decision, not whether we go into frontline, but what the design of the frontline study is. We're convinced we have a drug here that will be developable in frontline MF, and there's a path on approval with a single-agent combination with JAKAFI. The data will determine. In parallel with that, we have a number of meetings scheduled with the agency, or in the process of scheduling, to continue a conversation that I think we gave you some visibility on whether it is time to really redefine the endpoint for approval in MF drugs, particularly in frontline.
The standard has been now for the past 15 years, since the introduction of JAKAFI, has been TSS50 and SVR35. We think that 989 has a different mechanism of action. It does different things for the patient. It normalizes hematopoiesis, which leads to a dramatic improvement in anemia in more than half the patients, as well as eradication of the malignant clone. That has been reflected in improvements in SVR35 and TSS50 second-line patients. Whether the TSS50 data frontline is sufficient to give us confidence on beating JAKAFI is the question that we need to answer. In parallel with that, we will get the data, we will continue the conversation with FDA, we have a constructive dialogue with them so far, and we will bring those two pieces of evidence together and we will give you clarity on the design of frontline.
Our intention is, in the early part of 2027, to initiate a frontline MF trial with 989. The final piece of the story, if I may, is, and we sort of alluded to this in the last earnings call, at ASH we will present a preclinical data package with our next generation mutant CALR antibody. We think based on what is publicly available, that we have now in our hands not only the first CALR antibody but the best one, with a longer half-life and much, much more increased potency against both Type 1 and Type 2. We think it is going to reset the bar, and we look forward to sharing that data with you.
Okay. Maybe just a couple more on the ASH readout to help folks with framing those. For the combination arm, I know you talked about legacy endpoints being utilized, but for efficacy in anemia, I guess SVR35 range and anemia rates, does comparable to ruxolitinib sound like where investors should be anchored?
Yes. I mean, but look, if you take the JAK ineligible cohort that we presented at EHA, which is technically frontline, it is just a different group of patients. The SVR35 data that we showed there at 24 weeks was, I think, beats JAKAFI in frontline easily. There is not a ton of data sets, but if you look at JAKAFI frontline mutant CALR-positive patients, there is data from the COMFORT-II study and data from the pelabresib control arm study, and that data falls somewhere between 20% and 22%.
We presented data upwards of 45%. I think that is clean. TSS50, our numbers were very strong in the JAK ineligible patients. We need to make sure that that stays above. In order to be JAKAFI head to head there, you have to hit 55%-60%.
That is a little bit harder, which is why we think this dialogue with FDA, number one, or maybe focusing on just Type 1 patients, o r combining with JAKAFI for a predefined period of time and tapering off the JAKAFI. Any of those approaches, I think, could lead to an approval in frontline.
Okay. Just for the monotherapy patients, I guess sort of similar question, but how important is the efficacy profile versus reducing that anemia?
That, I think, is the reason why we think, and we hope the FDA will get there when we continue to build the evidence that we have or present the evidence to them. Because the anemia improvement that we've seen in second-line is dramatic. There were questions about washout. I think we've answered those, and you'll see more data. It doesn't matter how long you follow patients for, the hemoglobin keeps getting better. If you remove the patients that have prior JAKAFI, the anemia improvement is there. So it's very clear. When you look at the bone marrow and you look at markers of erythropoiesis like CD71, there's a clear improvement in those numbers. So this is a true restoration of normal blood red blood cell production. When you give JAKAFI, you're going to blunt a little bit of that.
That's why even in the case that we need to develop this in combination with JAKAFI, one would provide the JAKAFI symptom improvement. In parallel with that, you see an improvement, a growth of the benign clone, and then you taper the JAKAFI and you'll get the anemia benefit. It could take a little bit longer, but you'll get the anemia benefit eventually.
Okay, great. And maybe just a bit more color on those FDA discussions around endpoints. Where do they stand on incorporating hemoglobin improvement, disease modification measures like you said, and how could the regulatory path affect uptake and how important could this be for the broader space going forward?
Yeah, great question. Let's take a step back in what we're trying to do here. We've taken evidence generated independently of Incyte, and I think that's important. There's a publication sponsored by ELN not that long ago, and they show that certain parameters, and specifically we're interested in hemoglobin, platelets, blasts, and spleen size, are independently correlated with improved leukemia progression and survival in these patients. We've taken that and we've built a model that we think is the basis for this composite endpoint. I think the FDA is receptive to the idea.
The question is what's the evidentiary threshold that we need to clear here to convince them that we're ready to put it in a study? I think that's basically what needs to happen honestly. Whether it is immediately or not, our goal, as we made clear a number of times, is to provide a molecular targeted therapy for every single patient with MPN. This is a journey that we are in it as long as it takes. We need to get there with FDA. Hopefully, it will happen in the next three to six months. If it takes longer, it takes longer. We still have a path to approve 989. We are playing the long game, and it is really to try to change the standard of care for MPNs.
Okay, great. We wanted to touch on the Halozyme collaboration you announced relatively recently for an enhanced-enabled sub-Q formulation of 989. I believe the phase I initiated in this past quarter. So how important is that sub-Q dosing to the commercial profile? Would you call it a differentiator or a nice to have as you progress here?
No, I think it is a need to have. Pablo can walk through the aspects of the program, but we expect at this point that at least within the first six to nine months of the ET launch, we will have an on body sub-Q twice a month. I think it's especially relevant in ET. There's several work streams in place, and we'll have more information on the third quarter call about our discussions with FDA. That program, I think, is in a good place right now.
I completely agree, and we have a clear plan, some of which, we've vetted with FDA, and we continue to advance it. The Halozyme collaboration, it's an important part of it, but it's not a necessary element.
We have in parallel a novel formulation. We have an increased concentration formulation. We have a Halozyme formulation that will all be tested, and then we'll select the best one for the next step. We also, as you know, we have a collaboration for an on-body infusion device. To be clear, this has to be applied only every other week, just for 20, 25 minutes. It's not something the patient has to wear continuously. We think that provides a solution for the higher doses that we need to provide to some of the patients on the sub-Q. That's ongoing, and over time, as the data gets generated, we'll provide additional clarity. We have a very clear plan to get there.
Okay. Just to round out 989, just remind us of timing for top line for second-line ET, the phase III data there, and in your mind, what is supportive of expansion to frontline?
We have not provided a timeline. The study is just getting initiated. Let us get going a few more months, and then we will start as we usually do, as enrollment goes well, which we hope it will. Certainly, we will provide additional clarity. The frontline question, there is two components that are important. One is we are not 100% convinced you need a frontline indication in order to build this business. I think that the standard of care frontline, as you all know, is hydroxyurea. It is a poorly tolerated drug that requires multiple dose adjustments, and it does not lead to disease modification. So we think we have a fundamentally different value proposition for patients, and I think that the shift from frontline to second-line therapy will be faster once a great second-line therapy is available.
Then we have the next-generation antibody, which is coming pretty soon, and we think that might be just a better tool to first for frontline ET, and we will just do that with the new antibody.
Okay, great. Maybe just switching gears for a minute to JAK2V. You talked about a next-gen JAK2 V617F inhibitor. What should we be looking for in terms of preclinical translation? When it could enter the clinic? What would you tell investors on that front?
Very important target for us. We remain fully convinced that this is a critical target for a big subset of patients with MF and ET and almost 90%+ of the patients with PV. We terminated the earlier program. We had expressed at the time, I think all of you heard, that while we were optimistic about it, the therapeutic window for that compound, 058, was relatively narrow. It didn't have cell selectivity. It was the best effort we had at the time, and we thought it was important to test it in the clinic. That program has been terminated. The next-generation program, which you will see preclinical package at ASH, is a completely different chemical scaffold. That's really important. Number two, we're starting with an ASD formulation from day one.
That should not be a problem. And perhaps most importantly, it's much more potent than 058. And it has a much wider cell activity window. This is a much better tool for the job. We're convinced of that. Whether it's the perfect tool, time will tell, but it's certainly much better than 058.
Okay, great. Maybe just a competitive landscape question. Within the more targeted MPN therapies. For JAK2 V617F, there are clearly some competitors. I think even for mutant CALR, we are seeing more upstarts. I guess just in terms of differentiation versus those programs, timelines, beyond, how are you thinking about the competitive set there?
I think first on the CALR antibody, it is tough to compare a clinical asset to a preclinical asset until you have human data. We look at it right now, we're two years ahead on one and maybe several or few months behind on the other. I think the way we have to look at, Pablo mentioned this, he just talked about four targeted therapies.
Two CALR antibodies, 617F. We have a T-cell engager. If we're going to win, it's going to come from breadth covering the three MPNs, MF, ET, and PV, multiple driver mutations, multiple lines of therapy. And it's hard when you're in a horse race and it's a single asset versus another single asset. Usually breadth is what's going to decide who's successful long- term, and did you build a real franchise or is it a single asset franchise? You can answer that.
No, I have nothing to add to the general points. We look at everything that it's public in that space. As Bill said, I think with CALR, if we execute on our plan, I think we're optimistic that everything's going to be fine, and we're going to dominate that space. We have the first one. We have the best one. I think execution is key now. On V617F, there are a number of programs out there. We keep an open mind.
The best ideas are not always ours, which is why we put a collaboration in place with Prelude, and we have an option deal to their programs that we'll decide whether to exercise next year. Everything else is out there. We try to keep an eye on it. Right now, I am confident. Our next-generation program and the collaboration of Prelude are the two ways to address this problem.
Okay, great. Moving to your solid tumor programs, you will have an ESMO update of your KRAS G12D inhibitor-734 in about 50 first-line PDAC patients, I believe. Maybe talk a bit about efficacy and durability that would support a best-in-class profile and kind of de-risk the ongoing phase III further.
That is right. We will have a couple of updates. One is the one you mentioned, frontline pancreatic cancer, about 50 patients, half and half in combination with FOLFIRINOX and GemNab. Some of the data are out there. I would tell you the data that we will present at the meeting is a little bit better than what has been put out there. When I look at all the data, efficacy and safety, vis-à-vis our nearest competitor, which I think everyone knows who they are, I think the data are comparable. I will not try to convince you we are better.
I just don't think we are worse. The efficacy data that we will report is very strong. We don't have a mature PFS because we don't have enough progression events. You will see an event-free survival of six months, which I think looks very strong as well. We will give you a full view of the safety as well. Our exposure, based on the data that they presented about a couple to three months ago at ESMO GI, our exposure is about 1.6- 1.8 months longer, so you need to interpret the safety data with that in mind. When you put the safety data side by side, I think they look roughly comparable. Some adverse events are a little bit different.
Roughly the same rates of events are there. When you look at dose intensity or discontinuations, I think it looks similar. We think we have a very competitive program. We think we are as good as the best in class out there, and we look forward to continue to expand the program, and I'll tell you how. The frontline study is ongoing, the phase III. That's accruing very well. We're happy we're expanding it globally. We're going to move in the adjuvant pancreatic cancer setting as well. The other piece of data they're going to see at ESMO, we combined 734, that's our G12D inhibitor, with cetuximab in late-line colorectal cancer. We're going to show you that data. We have a nice-sized cohort. We think we have a very good response rate.
We'll provide an update of what we're going to do, which basically is talk to the FDA, and we have a design for a pivotal trial indication that we intend to launch in the very near- term, assuming we get positive regulatory feedback. On top of that, we are generating data of 734 in combination with FOLFIRI and cetuximab in frontline colorectal. That data will not be at ESMO. We'll disclose at some point next year. It's not mature enough. We're expanding this program in a number of different directions, also combination strategy, which we're happy to talk about.
Okay, great. Maybe just a couple philosophical questions on the program, I guess. How did safety and combinability with chemo factor into program design? Did you consider pan-RAS approaches and then just kind of the on/off mechanism versus on-state only or other on/off inhibitors? I guess how do you feel you're differentiated on that front as well?
Bill said it a minute ago, breadth matters for these programs, particularly in the competitive landscape. You're going to see over the next few months what I would say is a comprehensive combination strategy.
We're not ready to talk a lot about the details. Some are combinations that I think everybody in the room expects. Others might be more creative based on preclinical data. But we'll have novel targets, and we'll have a next-generation EGFR inhibitor as well. So we're putting together a three to five different component combination strategy that we'll roll out over the next few months. So I'm very happy the way that it's going, and we'll tell you more as these agreements are completed with different collaborators, and so as not to get ahead of the curve a little bit.
Okay.
I think when we reverse engineer what we're trying to accomplish at Incyte, which is when you hit 2029, is there a lineup of franchises or individual products that can drive top quartile growth? I think what will become clear as we get through the second half of the year is that if you bet on the G12D class so put pan-RAS aside there's two companies in late-stage development in a phase III trial. There's all these opportunities for lines of therapy, combinations, and tumor types. Right now, the G12D class 2xs the response rate and potentially the PFS of the standard of care chemo.
We're one of two. If you look at this market globally, U.S., international, it becomes a real needle mover. For Incyte as we hit that 2030- 2035 period. The same is true for 989, which is only the starting point for a franchise. If you look across everything that Pablo talked about, that is another franchiser vertical. You stack those two things on top of our core business potential. We have the potential to 2x this company.
Okay, great. And maybe just, you mentioned the cetuximab combo in second-line plus CRC. I guess any thoughts on an ORR durability bar that supports development there?
You'll see ORR. As you know, cetuximab single agent is single digits, so I think you'll see data that very clearly beats that. You'll see a PFS as well. For what it's worth, but it's a mature PFS. I think both give us conviction that we can beat the control arm. I won't talk about details on the control arm until we have a discussion with FDA, but we're confident in the design that we are presenting to them.
Okay. All right, great. Maybe just moving to the bispecific, 890, which is going to be in MSS CRC. Why could TGF-beta receptor II blockade succeed where TGF-beta approaches have failed previously? How does the PD-1 binding affinity factor in?
Yeah, it's a very important point because obviously this has been tried before. The reason why it's been tried before is because arguably TGF-beta is the second most important mechanism of tumor immune evasion after PD-1, PD-L1 axis. People have tried two different types of interventions. Fully systemic interventions, small molecule inhibitors, those have turned out to be toxic, or they can't even be dosed at the right dose.
People have tried traps, which you're trying to grab the ligand, which is a lot harder than block a receptor. Both have failed for different reasons. I think what our team did is a different approach, which is combining bispecific with a PD-1 arm and a TGF-beta receptor II arm. The TGF-beta receptor II arm only engages if the PD-1 arm is fully engaged. That gives you a targeting that you don't get with the programs that have been tried in the past. It's not about blocking TGF-beta receptor II everywhere, it's about blocking it only when PD-1 is present and fully engaged. That has turned out that in a very large phase I program with more than 300 patients, that the safety is very manageable, and it's mostly related to PD-1 related side effects, which you would expect. Is the PD-1 better after all?
The doses we're testing in phase III and we've tested in phase II, 900 mg every other week, the TGF-beta related toxicities don't seem to matter. With that in hand, we run a program in colorectal cancer in a broad set of tumors, but interesting, the most advanced data in colorectal cancer. In about 100 patients with heavily pretreated MSS colorectal cancer, where PD-1s have a response rate of zero, we saw a response rate of 15% with very durable responses.
We combined with FOLFOX/bev chemotherapy. We showed the combination is tolerable, and we are going to present data on about 50 patients at ESMO. With FOLFOX/bev plus TGF-beta by PD-1 frontline to show you why we believe the phase III in that indication has a significant probability of success and we are very optimistic about it and it has been a very important program for us and is enrolling ahead of schedule as we speak.
Okay. Maybe just a minute on attractiveness to those targets versus PD-1/VEGF . This is a good question.
I think both are great ideas. The PD-1/VEGF data continues to evolve. I think that some data was presented at the World Conference on Lung Cancer. In colorectal, I think there's consensus that bevacizumab is a very important drug. We can give our drug with full dose bev. Which you cannot do with a PD-1/VEGF. Doesn't mean it's not going to work. It means that our thesis here is that a PD-1 better that you can give with full dose bev is superior to a PD-1 better than you cannot. Without making predictions, I think it's possible both ideas will be successful.
Okay, great. I want to make sure we touch on the derm franchises also. Maybe we start with povorcitinib in HS. Just as the competitive landscape evolves, how are you thinking about, we'll have RINVOQ phase III data upcoming. How could you see that potentially affecting the broader class? Obviously, there's a black box warning. Could that limit uptake?
I think the best way to think about povorcitinib is HS is one of the most difficult derm conditions you can treat. All you have today are antibiotics and steroid on one side. IL-17s on the other. Antibiotics and steroids are imperfect solutions. IL-17s have made a big difference in patients' lives, but if you look at the HiSCR50 or 75 numbers, they're modest. It's not like you see in psoriasis. Povorcitinib is a multi-cytokine inhibitor. HS is a multi-cytokine disease. There is no oral broad anti-inflammatory for HS. We studied two populations.
We studied pre-biologic and post-biologic. Patients who are on antibiotics and steroids don't have to leap over to an IL-17. You have an oral option. We also have the post-biologic data. I think the drug will get used in both pre and post-biologic patients. I don't think you could have a better setup for an oral anti-inflammatory inhibitor right now. As it relates to AbbVie and RINVOQ, it's one of the most successful products in all of biopharma. Their data will be in a post-biologic population. I don't think dermatologists are going to question whether there's utility of RINVOQ in a pre-biologic population, but we will have both efficacy and safety data in both. I think that is important. Looks like we're going to have about a one-year head start.
I think that also is important. As it relates to JAK safety, the dermatology community now has a much more nuanced understanding of JAK safety. I don't think any company needs to relitigate the warnings and precaution on JAK. The most important thing is first, data from our HS1 and HS2 study, open label extension, over 1,200 people is very reassuring. The second point I'd make is that it comes down to patient selection, dose selection, and monitoring. I think the benefit/risk calculation in an HS population is fundamentally different, for example, than in an AD population years ago when DUPIXENT was out, RINVOQ was out, and then you had the XELJANZ data.
Okay, great. What can you tell us about launch prep for HS in the U.S. and Europe respectively?
Yeah. It'll be fully wired and fully funded and resourced. We'll have a large sales organization covering north of 10,000 HS specialists. We'll have all the appropriate peer-to-peer programs in place. There'll be a consumer advertising campaign. We'll make sure we get the right formulary coverage and price this in a way that makes sense for the PBMs and health plans, and at the same time, makes sense for Incyte. Internationally, we'll launch in Germany, which right now is a target market. Launch execution requires careful management, and we have an experienced group. Povo will be marketed right alongside OPZELURA.
We'll have essentially, and we're getting data on OPZELURA in HS in the fourth quarter. The phase II study with OPZELURA looked very reassuring. The HiSCR50 number was in the 70s. There was a high vehicle response, but the HiSCR50 was very good. We could have a topical to oral solution, which is a logical sequencing in HS, which I think could be a competitive advantage for Incyte.
Okay, great. Thinking about the vitiligo and PN opportunities relative to HS, what would you highlight on that front?
Well, I will tell you, we were just talking about [paragangliomas] with povorcitinib. As you know, it was an itch disease. Some would say that JAKs were made for PN. We know that with OPZELURA, it has a profound and rapid impact on itch. We expect the same with povorcitinib. That could be an outlier for povo.
It is a three-indication oral anti-inflammatory. We start with HS. We will have our PN data in the fourth quarter too, and let us see what those data look like. If the benefit risk profile stands up, w e could secure an approval by roughly the end of 2027, early 2028, and I think it will be an important growth driver. Then of course, y ou have vitiligo.
The key in vitiligo is bridging the gap between the prevalence population and the treated population. The one benefit of an oral for vitiligo, and the same is true for RINVOQ, which will have an indication too, is that 50% of the vitiligo market has BSA involvement of greater than 5%. A topical is a little bit less practical.
An oral systemic could make a great deal of sense, and medicalizing vitiligo is this difference between, I think, where the class is today and where it could be, and our job is just to execute against these three indications.
Okay. I want to make sure before we run out of time, that we touch on the Vega and latarcibart acquisition. So maybe just remind us of the strategic attractiveness of that, how it fits into the broader business, and maybe also if you could loop in just business development thoughts going forward as well.
Yeah. I'll touch on it generally, and I'll let Pablo talk a little bit about scientifically why it was so interesting to us. I think it's a textbook example of the type of deal that makes sense for Incyte in hematology, broadly speaking, not MPNs, which is a sweet spot of the company. We have a great deal of knowledge and capabilities in hematology. A completely novel approach to treating von Willebrand disease. The standard of care today is simply replace a missing protein or factor that you have to take multiple times each week. De-risked phase III.
And we were able to do a staged deal, it will be highly accretive if we're successful getting it through phase III and FDA, highly accretive to the post-2030 growth profile of the company, there's not too many of those any of those out there. I think that my view, if you really step back, is look what HEMLIBRA did to hemophilia A. Now, hemophilia A is a different condition, more severe, but there's a hemophilia A population in von Willebrand, which is sizable. This is to von Willebrand what HEMLIBRA was to hemophilia A, I think scientifically, it's a really interesting concept.
Yeah. It's a completely different approach to treating a bleeding disorder, right? Modulating an anticoagulant protein S, in order to basically activate the coagulation cascade in those patients, but without getting into a true procoagulant or hypercoagulable state. You see this based on the PK/PD data that our colleagues generated, now a part of Incyte, Vega , showing that there's no real movement in D-dimer of F1+2, which tells you there's no evidence of hypercoagulability at all. I think that, as Bill said, we thought this is a completely open opportunity.
There was a presentation recently where they took the Komodo database and applied the standard prophylaxis criteria to that database, they calculated that the population of patients with von Willebrand disease that should be on prophylaxis is about 30,000 patients.
Only 2,000 of them are on prophylaxis, and that is the market that we considered when we did the transaction. This is a really big opportunity for us to enter in a relatively near- term because the trial is accruing very well in what could potentially be a significant opportunity.
As it relates to BD, the way we think about it right now is we have five assets in the company that will drive 80% of the recovery that I would say, relatively speaking, have high [PTS]. If the benchmark is 65%-70% for a phase III, nothing is 100, but it is somewhere north of 65%- 70%, and that is povorcitinib, which is under review, and then you just walk through them. 989 for MF and ET, G12D , TGF-beta by PD-1 , and then latarcibart.
That is very reassuring, but we know attrition can come in lots of different flavors. I do not think we have any zeros on our hands. There can be delays. You can have underperforming launches, so business development is a priority to supplement what we are doing internally. I think there are two types of deals. Vega is the perfect deal. Accretive in that, or there is something even near-term that could be important. The most important thing is just to deploy this capital right and not turn $1 into $0.50. We are doing what every other company is trying to do in that regard.
Yeah. Great. We could keep going, but we are out of time, so thank you again.
Thank you.
Yeah.
Thanks, man. Nice work. That was efficient.