Good afternoon, everybody. Thank you so much for joining us on day three of the JP Morgan Healthcare Conference. My name is Bhavana Balakrishnan. I'm an Associate from the Healthcare Investment Banking team. We are here today for the presentation of Disc Medicine, and we're joined by John Quisel, Chief Executive Officer. I'll turn it over to you, John.
Great. Thank you. All right. Great to be here. Thanks, everyone, for taking some time today. I guess Wednesday afternoon, we've reached maybe the exhaustion stage of the conference. But thanks to the JP Morgan team for providing a speaking slot for us here. Okay. So it's about three years publicly listed here at Disc. It's been an exciting run, highly productive. We look forward to next year being a really exciting year. We're on the cusp of approval of our lead program, and then we have a whole pipeline behind that progressing well. So we'll walk through all that today. First, a few disclaimers. We'll be making forward-looking statements. Everything should be taken in context with what we filed on our website and with the SEC. Three clinical programs we'll be talking about: sorry, bitopertin, DISC-0974, and DISC-3405.
These are investigational agents, and they're not approved as therapies anywhere in the world, so quick rundown. For those less familiar with the story, I'll give a brief intro of who we are here at Disc, and then we'll run through our lead program, some of the background, the progress towards approval, and then some launch strategy and launch dynamics to talk about, then we'll go through the pipeline and wrap up with the overview for the year. Okay, so who we are at Disc. We're focused on red blood cell biology. Our programs all manipulate heme and iron metabolism. The theory is that by manipulating those components, you can control a lot about red blood cell biology, how red blood cells form, how they function. Many of the targets are genetically validated. At this point, of course, we've proven most of them out in the clinic as well.
And our goal was always to go broad, right? If we can control red blood cell biology, we should be able to deploy that against a wide range of diseases. And so we've had for years now, the bottom of this slide is a list of diseases running from the left-hand side, very rare like Diamond-Blackfan anemia, up to very common diseases like anemia of chronic kidney disease. And we set out to address each of these with one of the molecules in our pipeline. And happy to say we've almost knocked off the whole list at this point, with a lot of exciting data to go with that along the way. But actually now, for the first time, this is going to be the least science you'll ever hear out of a Disc presentation. We're transitioning now to a commercial company.
We're going to talk a lot about the market opportunities that we're looking at. What this slide shows is that we are progressing from launching our lead program, assuming approval, into this erythropoietic protoporphyria disease, or EPP, which we estimated about 14,000 patients in the U.S. Our pipeline of two hematology-oncology programs taking aim at a pool of about 175,000 patients. From there, there are expansion opportunities into various anemias of inflammation, other disorders, where we hope in the end to address more than a million. We've designed this company to progress through this focus on hematology, iron, and heme biology from a rare disease focus initially into heme-onc, and from there into broader markets. We think this build can all be achieved as a standalone company. This can be viewed as a pipeline chart, of course.
This is not our full pipeline chart. You can find that on our website. I would view this as a pipeline chart that shows what we view as the major opportunities or the places that we're really deploying the most capital. Our lead program called bitopertin in EPP is now the NDA is submitted. We're under review on an accelerated basis under this Commissioner's National Priority Voucher program, looking forward to getting to target approval date, hopefully end of this month, early in February. Then the second program, DISC-0974, targeting something called hemojuvelin. Here, we're in late stages of phase II development, looking to present additional data later this year and move to phase III next year. There's a second-generation antibody with an extended half-life that gives us some optionality, some life cycle management.
And then we have DISC-3405, an antibody against a target called TMPRSS6, designed to restrict iron and address disorders like polycythemia vera and sickle cell disease. So these are where we're active right now. And I'm going to move into bitopertin. So first, let me talk about the patients, the disease we're trying to treat, erythropoietic protoporphyria, really a rare, debilitating, lifelong disease. It arises from a genetic mutation in the last enzyme, typically in the last enzyme of the heme biosynthetic pathway. And it leads to a buildup of a toxin called protoporphyrin IX. And that toxin then wreaks havoc throughout the body.
First and foremost, it absorbs sunlight energy. So as it's flowing through the blood, that blood flows through the skin. Light excites this molecule and gives patients this sense of excruciating pain, as if they describe variously as like you have boiling oil flowing through your veins.
On average, patients can only tolerate maybe even less than 30 minutes of sunlight exposure, can even be through a window before they experience these excruciating pain attacks. This metabolite also builds up in the liver with devastating consequences, leading in 1%-5% of patients to overt liver failure, which can be a fatal complication of the disease. And the visuals are just striking. We have on the slide here just an image of what a healthy liver looks like, and then what a liver of an EPP patient looks like. And you can see this horrific purple color that builds up over time as this compound crystallizes in the hepatobiliary system, ultimately driving severe liver damage in many patients. And so that's the basic description. The other consequences, patients can't live by not going outside, can't live a normal life, a lot of psychosocial complications.
There's no disease-modifying therapy. Generally, the treatment is recommended to just stay indoors, come get your liver monitored on a yearly basis, and design your entire life, your career choices, sports, whatever, all around, just never being outside. There's one FDA-approved agent called afamelanotide, surgically implanted, works by tanning. We're hoping to bring now the first molecule that has the potential to reduce the level of that toxin. Our clinical data, we've studied this in two phase II programs. We actually in-licensed the molecule from Roche, who had tested it in over 4,000 patients pursuing other indications before we picked it up. Our trial data have been fantastic, right? We've shown our primary endpoint in both was reducing protoporphyrin IX. We reduced that by between 50% and 60%.
The two trials here that we've just kind of quick hits on the data, AURORA was placebo-controlled with about 75 patients in the U.S. BEACON was an open-label study in Australia with about 20, 25 patients, so either way, we saw this highly statistically significant reduction in PPIX, that toxin that drives the disease. So if you're reducing that meaningfully, probably more than 30% is meaningful, you would predict to see major improvements in the disease pathology, and that is what we see. Can measure various ways, light tolerance, sunlight tolerance, and we saw two to threefold improvements of those, slightly different numbers depending on whether you compare to baseline, compared to placebo.
We saw, if you look at these phototoxic reactions, right, these pain events that are probably the central feature for these patients' lives, we saw a 75% reduction of that against placebo in the AURORA study, 92% reduction from baseline in the open-label study. In the placebo-controlled trial, actually at the top dose, 60 mg once a day, we saw after four weeks on drug, or sorry, after eight weeks on drug, reduction of PPIX is complete, and at that point, there were actually zero phototoxic reactions, so remarkable effect, and then if you just ask patients how they felt, did they experience an improvement in their disease state, that was statistically significant, and nearly everyone reported seeing major improvements. We also had almost everyone, or over 80%, rolled over into our HELIOS long-term extension study.
We've reported data from that where people go on to maintain that reduced PP IX level and continue to report, I think it's like more than 90% of patients saying they feel much better. So we seem to have a drug that's long-term. The safety has been excellent. It's well-characterized in the safety database of over 4,000 patients. And this once-daily oral actually is a big deal for the patients who otherwise the only therapy requires a surgical implantation every two months at a specified center that they have to travel to. And travel is not easy if you can't go out in the sunlight. So really exciting set of data. We've reported it extensively in the past. So that's probably all I'll talk about today. Today, we're going to talk about our anticipated approval and launch plans. So we filed that NDA at the end of September.
The NDA was accepted at the end of November. If you think of this through a regular way PDUFA, we were given priority review. A PDUFA date would be late May. But in the meantime, we were awarded one of the first Commissioner's National Priority Vouchers, something we're very proud of. Sets up the timeline now where we anticipate an action, an approval, we hope, at the end of January or early February. And then meanwhile, the premise for approval here is an accelerated approval using the PPIX reduction as the surrogate endpoint. So as part of that, we have a confirmatory trial running as well. This is called the APOLLO trial. That's been received with a lot of enthusiasm, 150 patients to enroll here in the U.S., Europe, Australia. And we expect to have the top-line data from that by late this year or early next year.
All progressing well. I'm going to just touch on the CNPV, the Commissioner's National Priority Voucher, for a moment. I think this has become, I would acknowledge, a politically hot issue. We've seen a lot of critiques of that coming from folks, ex-FDAers, folks in the industry. I think from our point of view, it's been a fantastic program. We're just so delighted and pleased to have been chosen for this. And I would highlight that the day that announcement came out, the patient groups that represent EPP patients just were overjoyed to have that kind of recognition for a rare but severe disease that is often overlooked and ignored.
As an effort here by the FDA to bring drugs to patients more rapidly, we think it's been fantastic and rigorous and really hope that this becomes something that's ultimately viewed as very positive for the industry as another path to get more rapid approval of drugs and also as a way for patients to get access to drugs more quickly than they would have otherwise. So back to our launch. One of the things, the consequence of all of this acceleration is that our launch timelines moved in substantially. And when we first got the award, there was a moment of absolute celebration and then a moment of sheer terror. Oh, we're going to have to launch this drug about four or five months quicker than we thought we would. So what are going to be the stumbling blocks? Can we meet those events? First thought was CMC.
Can we have a drug supply available if we're launching this drug at the end of January? And we've now, happy to say, we've worked through all that, received alignment with the FDA that yes, the supply we have on hand is qualified for launch. We're ready to go. The other area is, of course, building the access and reimbursement team. That team is seated. They're working with payers. So that's all going very well. We do anticipate that that will phase in a little slower than it would have otherwise. A lot of payers, we typically would have had four-to-six months of conversations to establish reimbursement policies. Those won't be established at launch. So we anticipate there may be some larger than usual lag between when patients get access to the drug, which we're going to prioritize, versus when they start to see the reimbursement roll properly.
Sales team, we've accelerated that by about a month, and we will have that team seated. They've been hired. We'll talk a little bit about that in a minute. 24 reps ready to go the day of launch. We're again missing about four months of disease state education that would have happened, but I think overall, a lot of folks at the top accounts understand our drug, its mechanism very well, and are very excited, so we think that sales team's deployment is going to go smoothly and drive a smooth launch process, and then lastly, our marketing materials, as typical in an accelerated approval process, we'll be using just the label itself as the marketing material initially, while the FDA prospectively reviews the other marketing materials, and then everything will be fully available by the middle of the year, so overall, we'll be well prepared to launch the drug.
And then essentially all of the full launch capabilities will kind of blossom by the middle of the year. So moving to the launch dynamics in this disease, what's the opportunity here? So the genetics would say there's about 20,000 patients. We went to the claims databases, and we found there are 14,000 patients with a lookback of about eight years. There is an ICD-10 code for EPP, and it looks back about eight years. And in that time, we saw 14,000 patients hitting that diagnosis code. And of those, we see about 6,000 that have had care in the last three years around their EPPs. We view those as the engaged patients. And I'm happy to say now we have an MSL team that's been out in the field for about six months.
One of their jobs is to go to the top accounts and start validating the claims data. Are these patients not just digital signatures in the claims, but actually acknowledged by the doctors in the field? And so we've been working through that. And we've also been using a variety of digital tools to help assess the quality of this claims data and corroborate independently. And by and large, it really does seem to be checking out as we work through this. So again, our team, it's going to be 24 reps, going to be six MSLs, six field-based access team members to help break through barriers of access for the patients. We'll have full patient services, both internally and externally. We're going to be working with one of the top exclusive rare disease-focused specialty pharma partners. So all of these components are now in place and ready to go.
And we'll obviously be focusing first on the top 15 centers of excellence. I think that's going to drive the initial phase of the launch. But this 24 reps is sized to call on essentially 1,500 key accounts. So if we break that down, and this is now at least the top two boxes based on work done by our MSL team, we can now validate that the 15 centers of excellence for this disease have about 600 EPP patients. And that includes also the clinical trial patients who are going to presumably roll over onto commercial product. And we have 105 additional high-volume accounts. These are typically large academic institutions where we've identified another 1,000 patients. So that total of 1,600 patients identified at the top 120 sites, that's more or less what would have been predicted from the claims data as well.
We're delighted to see that correlation or relationship between what we see in the claims data and what we see from the boots on the ground, the MSLs going to the physicians. And that gives us a lot of confidence that the rest of this data is true as well. There'll be 1,500 community specialists. These are dermatologists and hematologists who also are seeing a total of an additional 4,000 patients. That'll be the focus of the launch. It'll be the top 120 accounts for this year. We did size the sales team, 24 reps, to call on this total of almost 6,000, the accounts that see these 6,000 patients. And there's the final about 8,000 patients where we will do, these are GPs, one patient, one doctor. We're taking a variety of tactics to activate those patients as well.
That's already started and actually already yielding identified patients and prescribers. So very exciting. We think this sets up a stage for a rare disease launch that will be consistent with a lot of other successful launches in our industry. Last piece of information, we now have some insight into the payer mix that we'll be dealing with. I think it's very favorable. About 16% will be commercial payers, 25% Medicare, 15% Medicaid. So those are the launch dynamics we're looking at. Again, we're designing this program to aim at an anticipated action date from the FDA coming late in January, early in February, consistent with the original timeline guidance from the FDA around this program. If all goes well, we get through that and looking forward to what should be an exciting launch later this year. I'll move to the pipeline. Our ticker symbol is iron.
You might be saying, "Where's the iron?" It's in the pipeline. The two targets here are well-known genetically validated targets that control the fundamental regulator of iron in the body. This is called hepcidin. We have DISC-0974, an anti-hemojuvelin antibody on the left side of the slide. This suppresses hepcidin, makes iron more available, and this is useful to treat anemias of inflammation. Myelofibrosis has been our lead indication. We're looking at a variety of large indications that we can also expand into. I'll talk about the third program in the pipeline, DISC-3405, against a target called TMPRSS6. What this does is actually increase hepcidin, restricting iron. When you restrict iron, actually it inhibits red cell formation. This has been demonstrated as an effective way of managing polycythemia vera. We're also probing its efficacy in sickle cell disease.
So DISC-0974, anti-hemojuvelin antibody, reduces hepcidin, increases iron. And with the flush with iron, that enables red blood cell production, right? Because iron is, of course, one of the critical nutrients that's necessary to make heme, which is a building block of red blood cells. So we've been focusing in a disease called myelofibrosis. This is a sort of precancerous myeloproliferative disease. There are driver mutations. It leads to, it can start with an overproduction of cells with polycythemia vera, for example, can be a lead-in. But it also can just arise directly in the bone marrow where you get this scarring and fibrosis, ultimately leading to what can be a very severe anemic state, as well as enlarged spleen and other symptoms of inflammatory disease. So we think this is a very significant unmet need. There's actually no therapy approved to treat anemia of myelofibrosis.
There have been, unfortunately, a variety of failures recently. So there's actually almost nothing in the pipeline even to try to treat this. We are essentially the only product now that I'm aware of in clinical development to manage anemia in these patients. So if you look at kind of a treatment algorithm and patient distribution, we see that there's probably about 25,000 myelofibrosis patients in the U.S. A substantial number of them are being treated with a JAK inhibitor. Jakafi is kind of the standard of care. It's designed to manage spleen size and symptoms, but actually exacerbates the anemia. So we see that about 87% of these patients are anemic, meaning there's 22,000 addressable patients.
If you figure in some kind of estimated oncology pricing, you could look at luspatercept, a program approved to manage anemia in a different precancerous disease called myelodysplastic syndrome that prices in the ballpark of $200,000-$300,000 per year. So it implies altogether, roll that up, a $4 billion+ total U.S. opportunity here. And as I mentioned, really essentially no competition. And when we say no competition, meaning no good solution for these patients coming on the horizon. So we've seen a lot of excitement around the data that I'm going to show you. We presented data at ASH. We're in phase II. We call it the RALLY-MF phase II trial. The drug is designed to reduce hepcidin. The left panel shows profound hepcidin reduction. This is elevated in essentially all of these patients.
Our drug, as you would predict from the genetics, is just very powerful at reducing that. We've seen it in healthy volunteers, chronic kidney disease patients, and myelofibrosis patients as well. The consequence of suppressing hepcidin is you mobilize iron. That's the middle panel. You see extraordinary increases in the serum iron levels. That means that ensures that the red cell compartment is flush with iron to help support erythropoiesis. That ultimately translates to a hematologic response, which, depending on the patient type, is calculated differently. If we have a major response, that's using the criteria that are defined by all the KOLs and guidelines. We see that we get to about 50% major response rate. That's a response rate that's never been seen in this disease within anemia therapy.
So we're truly excited about that and really looking to progress forward as fast as we can. To dive in a little bit more deeply, I can share, if you break these down into the non-transfused patients, right? Anemic patients run the gamut from non-transfused all the way to heavily transfused. Our most numerous patients, which match the market expectations, are the non-transfused. That's about 60%-70% of the market. The low transfusion patients represent probably 25%. You can see in the NTD group, very nice hemoglobin increases. We show the red line is the major responders. The blue is the average. And then interestingly, we see great improvements in fatigue. So this is, it's important when you're developing an anemia product to show that there's a clinical benefit, like a real patient can feel type benefit. And we see great fatigue improvements.
It seems to be associated with the level of hemoglobin improvement. We also see in the TD low populations really spectacular effects. These patients, their hemoglobin typically starts around seven or eight. So they're getting occasionally transfused one or two units every 12 weeks. And we see on average about three and a half, somewhere between three and four grams per deciliter increase in hemoglobin, which is a very marked response. And with that larger hemoglobin response, we see also a larger increase in the fatigue scores. So again, confirming that these hemoglobin increases are translating into benefit for the patient's overall health, as would be predicted. Because by the way, I'll note that anemia is well documented to correlate with poor disease outcome and a worsening disease state.
And then for those myelofibrosis aficionados, JAK inhibitors, like I mentioned, ruxolitinib, Jakafi, as well as momalotinib, Ojara, these are used to manage spleen size and symptoms in these patients. They also have effects on erythropoiesis. So there's a common question about how well does our drug work on top of this. Jakafi, in particular, exacerbates anemia. So there's a very strong need to manage anemia in those patients to help them reach their optimal Jakafi dose and just generally live a higher quality life. Ruxolitinib is what we would call anemia sparing. So it's more benign on that front. But we've seen a lot of patients in our trial, actually, who are on momalotinib needing anemia therapy. So we were curious to see how well the drug would work in combination. And the answer, it works very, very well. This is the same dynamics are at play.
The drug, these patients come in with elevated hepcidin levels, as is typical in myelofibrosis. Our drug reduces that. It mobilizes iron, and then you can see the different hematologic responses depending on patients who are not on JAK, on ruxolitinib, on momalotinib. It's basically the same across the board, circling around a 50% major response rate, so really robust, working across a broad range of patients, appears to be broadly active all the way from the non-transfused patients down to the heavily transfused patients, and so with this kind of data set, we're just pushing as fast as we can to get this into a pivotal trial, so we'll continue to run the RALLY-MF trial. It was designed to enroll about 90 patients. As of last October, about 45 had been enrolled, including essentially the entire non-transfused cohort.
We'll have another data cut as we come into the end of the year. I don't think it's going to really change much about the data. The end is already pretty substantial. Nonetheless, for completeness, and actually that extra data does help us when we're designing our proposed pivotal trial. That was the major goal for the year for this program, is to get to an end of phase II meeting with the FDA and look to start up a pivotal trial as early next year as we can. Meanwhile, we're also looking at other anemias of inflammation, right? Hepcidin, this iron regulator, it's known to be elevated in almost any inflammatory disease. Many of those come with an anemia that can be difficult to manage. Inflammatory bowel disease has been identified as one of those.
The patients have attributes that would suggest they should be responsive to our drug. We know now that high EPO levels are a predictor of responders, and these patients, just like MF patients, have very, very high EPO levels, so we're excited about getting that trial started. By the way, the mouse data were spectacular, like we saw six gram per deciliter increases, so a lot of reasons to believe this is going to be exciting. We're doing this as a signal-seeking study, planning placebo control, but planning to start off sometime in the first quarter here, and then we have a second-generation antibody called DISC-0998, extended half-life. Could be used for life cycle management. Could also be used as the differentiating molecule to approach some of these larger indications like inflammatory bowel disease and chronic kidney disease.
So that's the second pipeline program, again, aiming to be into pivotal by next year. The third program, pushing iron in the other direction, anti-TMPRSS6, another genetically validated target here with this antibody. We're trying to increase hepcidin, decrease iron availability, and this modulates red blood cell production in a way that has already been proven out by the Protagonist team, fantastic work with a molecule called rusfertide, showing that restricting iron in polycythemia vera patients delivers a meaningful therapeutic effect. So that is where we're going to go first. We think we have what will be a great presentation for patients. This is a simple antibody subq injection projected to be once every four weeks, maybe every two weeks. We're probing those two doses in our phase II trial. If we think about the market opportunity here, this is actually the exact same prescriber group as myelofibrosis.
These all fit into the myeloproliferative disease world broadly in hematology-oncology. There's probably about 75,000 patients who are in this PV population who are treated, most of them with phlebotomy, a way of drawing blood off to basically crudely create iron deficiency in these patients, and again, we're trying to supplant that with a drug that will just create pharmacologically an iron restriction, and so we think that among these patients, some are treated with phlebotomy, some with hydroxyurea, ruxolitinib, interferons. These are all used sometimes in combination. This iron-based mechanism, we expect, it doesn't really interact with these, meaning it can be used on top of any of these. So essentially, I think any patient who's being phlebotomized as a way of controlling the excess red blood cell production in this disease would find considerable benefit from going on a therapy like this.
So with that number of patients, it ends up being a very attractive market. The drug's doing what it's supposed to do. It's really not a surprise when you work with a genetically validated target. It does limit the surprises. So we've done and published our healthy volunteer work here. The concept is to actually increase hepcidin, not decrease it. I'm sorry, the first two slides here are actually the PKPD and then, yeah, the percent change from baseline in the hepcidin that we see going down in the left-hand panel. And then the serum iron trace is in the second panel. You can see it going down below the baseline. So significant reduction in serum iron as expected. And then that leads to decreases in hemoglobin and hematocrit. And in polycythemia vera, the therapeutic objective is to achieve decreased hematocrit.
The healthy volunteers tells us the drug is doing what it's supposed to do, affecting the hematocrit in the desired way. So I think significant de-risking coming from this healthy volunteer study. Based on this, we opened up a phase II trial in polycythemia vera at the end of 2025. We actually designed it to be an initial cohort of 20 patients using them to explore a variety of doses. We had an overwhelming response to the trial, and we took advantage of that to double the size, anticipating rapid enrollment and also trying to satisfy demand from the sites. There's just a lot of excitement about iron restriction for these patients. And so that has allowed us to accelerate all of our timelines for this program.
We hope then in 2026, this year, by the end of the year, to present a very significant data package, proving out proof of concept in the disease population. And then that should enable an end of phase II meeting early and progression to pivotal trials early in 2027. So all told, the pipeline situated in hematology-oncology is coming together beautifully. We expect to progress through clinical and regulatory activities this year and look to have both kick off as pivotal programs next year. So this leads to how this all rolls up into our milestone and catalyst chart. Needless to say, the most important of which is an anticipated FDA action date coming in just a matter of weeks now. That would be followed by launch. You'll start to get the kind of launch characteristics, revenue, patient starts, prescriptions. That'll run on a quarterly basis.
But in terms of clinical catalysts, then we'll also have the top-line data from our confirmatory APOLLO study, and then in 2027, we'll start to, with a successful APOLLO readout, we would start to approach ex-U.S. markets and get those regulatory filings in place. On the pipeline, we expect to start up first half of the year, the IBD study I talked about, then get top-line RALLY -MF data and progress to that end of phase II meeting with the FDA, phase III initiations penciled in for 2027, and then PV, again, the initial and hopefully pretty substantial set of data from the RESTORE-PV trial. That's our phase II trial, and then I didn't even really talk about sickle cell disease, but it's another place where phlebotomy is used clinically, and we expect iron restriction therefore to be an effective therapy.
We started just a pilot study there, but we'll get some data from that this year as well and that all rolls up into then hopefully a phase III startup for PV in 2027, so a lot going on and I'm delighted to say we're well capitalized. We have about $791 million on the books right now or as of year-end and that provides us runway into 2029. That runway assessment assumes all of these activities are carried out, phase III myelofibrosis, having the commercial team in place for bitopertin, phase II for PV, as well as these signal-seeking studies and that runway does not assume any revenue from bitopertin yet, right? So essentially, it's an all-burn, no revenue type model, very conservative, takes us into 2029. Of course, as we start to get revenue off that program, we can reassess that.
But I think that runway will reach far into the future at this point. So bottom line summary, we built this company always wanting a business plan that would allow us to be standalone with sustainable growth. We now are so happy to have bitopertin on the cusp of potential approval through the CNPV program, launch ready, strong product profile. We think we see a lot of potential benefit for these patients. And we think the overall addressable market is actually $2 billion+ , right? If all 14,000 of those patients can be found, we think this could be a really big rare disease program. We have now DISC-0974, DISC-0998, DISC-3405. We've established proof of concept in the clinic, in the patients with myelofibrosis, mechanistically in healthy volunteers with the third program. And these are also very large hem-onc type opportunities.
We assess $4 billion+ in myelofibrosis anemia and even larger in the polycythemia vera market. So that's everything I wanted to run through today. I really appreciate your attention. I think it's going to be an exciting year at DISC.
Thank you very much, John. We have time to take questions from the audience, if any. Maybe one question from me. You talked about the funnel a little earlier, about the funnel for EPP, and we said there were about 20,000 patients who are predicted with genetic prevalence and then 14K who are diagnosed and addressable, and then 6K who are engaged. What could we do to bring more patients down the funnel? And how is your launch accounting for that?
Oh, yeah, that's a great question. Yeah, we're going to try to make sure those 8,000 patients have access to what we think is going to be important therapy. So some things are happening organically. The patient advocacy groups are just really excited and engaged on this program. And maybe as a result of that work, we've actually seen a number of media articles coming out, patients kind of stepping up and saying, "Hey, this has been a really rough disease for me, and I got into a trial with bitopertin," and they're talking about how exciting the results have been for them. And that kind of publicity actually has caused some patients to come out of the woodwork that we hadn't otherwise identified. So I think there's kind of an organic thing going on, which is super exciting.
We're also using a variety of digital tools to try to help identify where there might be doctors that we can go call on. The claims data is part of that as well. And then we also are just setting up basically call centers to try to just reach out to the 8,000 prescribing physicians who are identified through the claims as having those patients. And we'll just try to make sure we call them all. And that process has started as well and already yielding some physicians who are taking the call. First of all, that's the hard part, but then saying, "Oh, yeah, in fact, I do have a patient and would be interested to learn more about this disease," right?
So I think there's a lot of efforts we're going to make to try to ensure that at least the word gets out and patients have a choice across that full set of 14,000 diagnosed patients.
We have time for maybe one question. Maybe very briefly, if you could tell us more about your ex-U.S. strategy and how we should think about that.
Yeah, yeah. So ex-U.S., it's going to be a traditional approval path, meaning we have the APOLLO trial, which is confirmatory for U.S. purposes, is actually a phase III for ex-U.S. markets. There are a lot of EPP patients in Europe. It's actually a very concentrated market. Those patients all come to single centers. For example, there's a KOL at the Parisian Center who will tell us he has 400 patients at this one center. So very concentrated market. Our intention is once we get that APOLLO trial data, then we'll use that to file the MAA and then move ahead from there. Japan also represents a country with a lot of patients with this disease as well. So those are probably the first two regions we'll look at, and we're projecting that those filings will start to roll in 2027.
Thank you so much for your time, John.
Yeah, thank you.