$160 million market cap. We had a fresh 52-week high just this morning, so the timing here is good for me to present at the conference. Let's talk about interstitial lung disease. As I mentioned, a group of diseases that you may not be aware of, but there on the right you see a caricature of an end-stage fibrotic lung. Now, you may have heard of pulmonary fibrosis, IPF, for example. That's one form of interstitial lung disease, but most of these interstitial lung diseases all have a chronic inflammatory signature that progresses to pulmonary fibrosis. What are they characterized with? Worsening lung function, fibrosis, quality of life issues. The issue here is the survival rate. Mortality starts to take off in all of these diseases. The problem is options beyond IPF, they're quite toxic.
Even IPF itself has a number of drugs on the market that generate about $5 billion in sales. These therapies aren't exactly safe, but they extend mortality. No drug is really disease-modifying. We think we have something here with efzofitimod. That's our phase III drug. That's a drug candidate with a novel mechanism of action that we think can be disease-modifying. So it's a real game changer in my mind that we've set up here. We're looking at efzofitimod as standard of care for all interstitial lung disease. So there you see on the bottom a spectrum of inflammation and fibrosis. As I mentioned, IPF, this is a disease that's highly fibrotic, but you see a lot of inflammation in the other forms of interstitial lung disease. IPF itself may present with a little bit of inflammation, but there's a whole host of diseases across a spectrum here.
Sarcoidosis is the most inflammatory form. We're going to talk a lot about that, and you're going to learn about sarcoidosis today. But there's also other interstitial lung diseases such as scleroderma-related ILD, other connective tissue disease-related ILDs like RA ILD, Sjögren's ILD. CHP is a form of interstitial lung disease that's a hypersensitivity pneumonitis. You've probably heard of burn pit pneumonitis from returning vets in Desert Storm, for example, or even vaping-induced lung disease. That's a form of hypersensitivity pneumonitis. All of these diseases have a hallmark of chronic inflammation that leads to fibrosis, and we just don't have good treatment options for these patients. Why wait until we progress to fibrosis and then use pirfenidone and nintedanib? Why not address the inflammation early and really bend the arc of disease? That's what efzofitimod is trying to do here.
Patients have a high degree of morbidity even with the current therapies, which are largely steroids, and the problem is steroids create other problems for these patients, so huge area of unmet need. We're focused on the more inflammatory phenotypes right now, sarcoidosis being the major form of interstitial lung disease. We estimate conservatively that efzofitimod, if approved, could easily generate upwards of $3 billion in sales, so real opportunity here. The upside is to move into systemic indications. We have already demonstrated some rather significant effects in a phase II trial. The question now is, could we move beyond the lung, so I think that's the vision for efzofitimod, but right now ILD is really where we're focused. The basic hypothesis for efzofitimod, it's targeting the innate inflammatory, the immune reaction that's occurring right there in the lungs. It's downregulating a number of inflammatory and fibrotic markers.
It's addressing complex immune pathology. That's the thing that I think what makes this drug unique. It's been described as multinodal. We have a lot of therapies out there, monoclonal antibodies that will be a hammer on one particular cytokine. What I like about efzofitimod and what the experts have conveyed to me is it works in a multifactorial manner. And when you talk about diseases like ILD, they can occur due to environmental stimuli. They can occur due to underlying autoimmune disease. Sometimes you don't know the etiology. So in these multinodal diseases, having a drug that also works to downregulate the immune system in a sophisticated manner across different cytokines, it's really important. We have robust clinical proof of concept. Our phase II data was published in the journal CHEST just last month. It was highlighted in the Best of CHEST session.
This is one of the largest lung disease conferences here in the U.S. Published data is something I ask all of my other biotech companies to really work on a little bit more. We present a lot of slides, but get it into a peer-reviewed journal, see if it actually passes the muster there from your statistical analysis plan, see if you can actually demonstrate that. I think you'll see a lot of biotech companies not do what we do, which is really publish all of our data. We're learning as we go. We're very data-driven, and we also feel very validated to have this publication out there. What did we see with that data? I'll talk a little bit about this. We resolved symptoms. We reduced steroids.
We were the first therapy to actually show that you could improve the patient's quality of life, their symptoms, and their function while reducing steroids. The biggest thing for me, no known safety issues. If we are moving a new therapy forward, we don't want to have to find any new untoward effects. So let's talk about pulmonary sarcoidosis. As I mentioned, it's the most prevalent form of interstitial lung disease. We don't know the cause, but sarcoidosis presents with this characteristic granuloma, a clump of immune cells that you largely see in the lungs. If you remember 20, 25 years ago, 9/11, most of the workers, all of the workers there that cleaned up the debris there in lower Manhattan, they developed sarcoidosis. But sarcoidosis, we still don't know the actual etiologic cause, but it always presents with this characteristic granuloma, largely seen in the lungs.
About 200,000 patients in the U.S. Though we have an orphan designation, it's peri-orphan. What we know is a large proportion of these patients, approximately 75%, based on recent claims analysis that we've looked at, are steroid dependent. It's a really large unmet indication that a therapy that could actually reduce or even eliminate steroids could be really transformative for these patients. What you typically see is when you have this granuloma, you'll do a biopsy. It's a very easy diagnosis once you actually do a biopsy. From there, you can basically look at clinical presentation, which is cough, shortness of breath, and then again, the chronic inflammatory state. A lot of these patients have hot inflammatory biomarkers. This is why steroids actually work pretty well to tamp down on that, but they create other problems. 70% of the patients within the first few years need steroids.
The unfortunate thing is you get 20% of these patients progressing to fibrosis. So steroids are not really disease-modifying. Once you get fibrosis, you need a lung transplant or you might die. So really a higher mortality risk as you start to see more and more of this inflammatory cascade progress to fibrosis. High degree of burden for these patients. Just yesterday, there was a five, six-hour session with the FDA where sarcoidosis was a listening session with patients, and they highlighted a number of challenges they have. First of all, it really robs your quality of life. That cough, that shortness of breath, it's debilitating. It does not allow these patients to really have a quality of life that you and I would expect. A lot of times they have problems even just getting out of bed, moving around.
That fatigue that comes with this persistent dyspnea really affects their ability to even get to work and work. In order to do that, they have to take steroids. What do steroids do? They bring on a whole host of other diseases. We had one expert say, "I really like efzofitimod because it does two things. It treats sarcoidosis as one disease, but it's also treating steroid toxicity, which is another disease." So I think this is something that we are on the forefront of a kind of different sort of transformative therapy, not just basically, as I said, controlling inflammation, but really changing the quality of life for these patients. I mentioned the major socioeconomic impact, the loss of ability.
There was a presentation recently last month that European Respiratory Society says. It said sarcoidosis patients on average take another one to two months of leave every year in their jobs. So it really makes it hard for people to have a productive life with sarcoidosis. And then on top of that, taking steroids. Limited alternative therapies has not been an approved therapy in 60-70 years, and the only approved therapy before was really grandfathered in. That was steroids. And a quarter to a fifth of these patients, as I said, are progressing to fibrosis. That's important to keep in mind here that we're trying to change that dynamic. Efzofitimod targets about 50% of these patients. We've got some very fibrotic patients. We have some mild patients. We're really looking at those moderate to progressive patients.
Once the lung becomes very, very fibrotic, it can be hard to really move those inflammatory cells, and some of those patients who have mild disease may not be on steroids. You're just watching and waiting, but there's a large cohort here within the disease severity that we think efzofitimod could actually gain market share. We think it's a frontline therapy, a steroid-sparing agent. We feel that way based on some of the data that we saw in the phase II trial. Reducing or eliminating steroids is our short-term goal. Long-term goal is to basically blunt that progression of fibrosis. There's an addressable population in major markets, including the U.S. and Europe, of greater than 200,000 patients here. Benchmarks with the types of drugs that are getting approved, more steroid reduction type drugs like Tavneos. I'll highlight that. That's for vasculitis.
That was recently approved, priced at about $180,000 a year. That was a drug that had, as part of its package, a big value proposition that it reduced the steroid burden for these patients. We see ourselves in that same mix, a steroid-sparing agent, a rare disease agent, but also something that can slow down the lung function decline. As I mentioned, Ofev, Actemra, these are drugs that generate multi-billion-dollar drugs. Though I can't say exactly where on the scale the pricing will be, early estimates indicate that we will be priced closer to pirfenidone and Ofev, which are about $100,000-$120,000 a year. It's positioned to be a first approved product here for sarcoidosis in 60 years. So I think we're in really good shape here to basically command the market if we're approved. Let's talk a little bit more about efzofitimod.
A little summary here of about eight years of work that we've been working on in San Diego. Really developed from this innovative platform out of Scripps, as I mentioned. There were some discoveries about 15 years ago by Dr. Schimmel that we have enzymes in all of our bodies called tRNA synthetases. These help us make proteins, but what he discovered is these enzymes break apart into fragments, and the fragments migrate out into different organ systems, and there they play an immune regulatory role, so we are really leveraging this evolutionary intelligence that we have within our bodies to basically create a new modality, so it's quite innovative. A lot of the experts and even basic scientists have found this really intriguing. We've taken the first protein in our IP library, and we have about 200, and we moved it forward here into phase III .
I don't think we've gotten lucky. I think we've always looked at things from a data-centric approach. We have other opportunities with other fragments. Won't talk too much about them today, but we have some in our presentation and preclinical testing right now. Efzofitimod works by binding this receptor called Neuropilin-2. Neuropilin-2 is highly expressed on these cells called macrophages. Macrophages are involved in an inflammatory response. They're generally the marines. They come in early. They leave late, and these are the sort of immune cells that are meant to sort of help signal your T cells and other sort of cells that you've heard of, immune cells. It works quite upstream. What I like about efzofitimod is it's working with those early cells to retune those macrophages.
We've seen this actually visually that in the presence of efzofitimod, a macrophage, which might be highly fibrotic, can start to tamp down and become more restorative. As I mentioned, anti-inflammatory effects, anti-fibrotic effects. We ran about a half a dozen animal models before we moved into the clinic. That's also important. Really understand the translational biology before we jump into the clinic too soon. Happens with a lot of biotech companies jumping into the clinic a bit too quickly. Neuropilin, we wanted to make sure it's expressed in the actual tissue of greatest pathology. As I mentioned, granulomas are the hallmark of sarcoidosis. We see a high degree of Neuropilin expressed both on ISH and in situ hybridization and also immunohistochemistry. You can look last year, we were published on Science Translational Medicine. We made the cover with an immune cell lit up with immunofluorescence with Neuropilin.
So Neuropilin-2 is becoming kind of a hot new target as well. I wouldn't be surprised if the cancer experts also want to sort of activate the immune system using Neuropilin-2 in the coming years. Really nice safety profile thus far. Animals, phase I, phase II. We've got to hope safety, safety, safety is important here as we create a new dynamic therapy. Clinical proof of concept, I'll talk to you a little bit about that. That's actually the molecular structure there for those of you that like crystallography. But the real small protein fragment is that yellow helix-turn-helix domain. That's right now in all of our bodies. I can assay our blood, and I can find it there. In our bodies, it's probably working in the background to kind of keep our lungs nicely restored.
In sarcoidosis patients, for example, where they have this inflammation, I'm in effect resupplementing this protein to try to get that balance again. Here's a basic hypothesis. Interstitial lung disease, you have a loss of immune balance. To prevent that fibrosis, we actually attack the macrophage that's upregulated, bind to this macrophage via this Neuropilin receptor that's expressed on the macrophage. By doing so, we can tamp down the inflammation. When that happens, we're improving lung function, restoring, improving symptoms, and again, preventing that progression of fibrosis. I'll spend a minute here on our phase II data. This really, I think, was the best data in the last 70 years in interstitial lung disease. We had a small trial, 37 patients, where we were testing a number of doses to see could we improve symptoms? Could we see any benefit with lung function?
Could we reduce steroids while doing those two things? As it turns out, in all of those measures, we saw a trend. First off, we reduced steroids. The more drug we gave, the more reduction in steroids we saw. Next, lung function. The higher dose we gave, we started to see better forced vital capacity. This is a measure of how much air you move in and out of your lungs. This was quite surprising to our lead PI, Dan Culver, who's a chair of pulmonary medicine at the Cleveland Clinic. He said, "This is outstanding to see this kind of improvement so quickly." The thing I really like is fatigue, shortness of breath, cough. In all of these measures, the more drug we gave, the better response we gave. And in all of those PROs, we saw a directional improvement.
So in a small trial to see this directionality across subjective and objective endpoints, it's really hard to do. If I have 300 or 600 patients, I can get a trend out of that. 37 patients to see everything move in the right direction was really quite outstanding. And we published our data in the journal CHEST a few years ago. For those of you that really want to read a medical journal, I encourage you to go look that up. Our phase III trial, this is what we're really excited about. This trial has enrolled, fully enrolled in July, 268 patients. And it was the first and biggest phase III trial in sarcoidosis ever. So in that sense, it's accomplishment. Nine countries, 90 centers around the world, we enrolled 268 patients. We over-enrolled by a couple of patients. 88 patients per arm are tested across a year.
We have a placebo arm that we're testing as well. The two highest doses that we saw the best effects in the last trial, that's what we really are looking to see if one of these can actually show stat-sig compared to placebo. What are we looking for? We're looking for steroid reduction again. But we're also looking at key secondary endpoints, the forced vital capacity and symptom control. What I can tell you is some of those patients who have finished thus far, a really nice signal here is they've asked us, we don't know what they're on, but they've been able to get off steroids and stay off for nine months. They are refusing to go back on steroids. So we had to step up with a compassionate use program rather quite early. And that's listed there at the bottom. And Individual Patient Expanded Access Program.
This allows us to give drug to patients who are finishing the trial, who have done well. I'm blinded, we're blinded, we don't know what these patients are on. But these are patients who have been able to get off steroids and maintain that for nine months. So that's really quite intriguing interim biomarker, if you will. Top-line data is expected in Q3 2025. And despite our highs today, I think we are still significantly undervalued as a company who's about to have a major phase III readout. In the last few minutes here, I'll talk about our backup program. We have another follow-on program. I mentioned sarcoidosis as the most inflammatory form. We're also looking at scleroderma-related ILD. Scleroderma is an autoimmune disease, affects the skin. We think that's the next opportunity here for our drug to show some effects.
We had a very, very robust animal model a few years ago that I presented at the Scleroderma Foundation that showed efzofitimod did better than even some of the approved therapies here for scleroderma. This is a disease characterized with really debilitating scarring of the skin, but eventually you may have this attack your lungs. When it attacks your lungs, that's the worst phenotype, a high degree of mortality. If you're a scleroderma patient, you don't want to get diagnosed with scleroderma of the lung. Current treatment, again, toxic or ineffective. So efzofitimod is an opportunity here in a more fibrotic disease to potentially change the morbidity and mortality in these patients. This is a small 25-patient trial that we're reading out. There's a mini catalyst in Q2 next year where I'm looking at an interim readout to see what the drug might do here.
In particular, one thing that's cool about this trial is we can look at the skin biopsy. I don't have as much access to the lung tissue. Patients here in the U.S. don't want a bronchoscopy during a trial. But in scleroderma patients, we can access their skin. We can look at their skin to see if there's any immune improvement there or even some actually physiologic improvement. So that's something that we'll read out in Q3 here. Why am I bullish on the skin? We saw a high degree of Neuropilin expression there too. So think about that. The drug binds this receptor, Neuropilin. We got to see that in the tissue. It's a very precision immunology type of approach that we're taking here. So I'll wrap up here. This is our pipeline.
Efzofitimod is really what we spend a lot of time talking about and what we talked mostly about today. But we have some other protein fragments from our IP library from this really novel platform that Dr. Schimmel discovered that we are right now targeting in other forms of fibrosis. So there's another fragment that seems to do a nice job of controlling fibrosis in the liver and kidney. And then we have another modulator that seems to work through a fibroblast mechanism, FGFR4. So these are preclinical programs we have in San Diego. We have a large lab. We have a lab. We're not a virtual company. And many of the scientists also come out of UCSD. Our head of research, for example, was a postdoc in Paul's lab 15 years ago. Our corporate summary, a real disruptive type of platform biology. It's a new modality.
I think if we're successful here, we can follow the steps of potentially a company like Alnylam that Paul founded. Our lead candidate, large market opportunity, $2-$3 billion. It's just a green space sitting there for a better therapy, a therapy that can control the day-to-day symptom burden that these patients have, but also really prevent that progression of fibrosis. We learned a lot about that even yesterday in this patient session I mentioned. A growing pipeline here. We are really focused on inflammation and fibrosis. That's where this biology seems to have the greatest effects. And I'll end here with the strong financial fundamentals here. With $80 million in cash, with 35% of the company owned by Federated and Fidelity, a good group of investors. I encourage everyone to look at our cap table.
Since we've actually finished enrollment, you've seen a material appreciation in our value. We think we'll see more of that before we have the readouts. Most of the analysts, take it for whatever you think about analysts. We have six or seven analysts with an average price target of about $20 here. So it's going to be a very important year for us. I'll end by saying that our program has been partnered already with a Japanese pharma, Kyowa Kirin. Kyowa Kirin, we had a partnership even before we got into clinical data. We've brought in $20 million of milestone payments from this $175 million partnership. We're eligible for the additional $150 million plus, largely tied to approvals and regulatory approvals. In our 268-patient trial, we have a large cohort of Japanese patients within that trial.
If the phase III trial is successful, we'll also be able to unlock some of these milestone payments. Thank you for your time.