Actually allowing for the healing of lungs in IPF patients. I'll tell you about this devastating disease, how this drug is different, and why you should be interested in this company. Sorry, which way does this point? There. This doesn't seem to be advancing slides. There we go. All right. LTI-03 is the drug that we are focused on. This is a novel agent for idiopathic pulmonary fibrosis, has really kind of a dual mechanism in that it inhibits pro-fibrotic proteins. I'll talk about that. That's really kind of the scarring inside the lungs. This is what other drugs in development are trying to do, is to stop or slow down the scarring process. More importantly, however, we are preserving cells in the lung epithelium. They're called Type 2 epithelial cells. These are progenitor cells. They can make new lung tissue. They can restore lung function.
This is something absolutely unseen in this disease, and we believe would add lifespan to these patients. We do have another drug that's a phase II level drug, but really we're completely focused on this IPF asset right now. We have done two clinical trials to get to this phase. Again, we are in a phase II study in IPF. We've announced publicly enrollment is going great. We hit 25% enrollment faster than what we had thought. We did a phase I-A in healthy normals and a I-B study that I will talk about a little bit later. It's a really rigorous trial. We just had this study published in Nature Communications, obviously a very prestigious journal, so we're happy to get that published and to be moving on. Sorry, I always point this thing at the wrong place. Pointing right there. Okay. We've got a great small team.
I just want to point out on our team Dr. Cory Hogaboam. I wish Cory could be here to talk about IPF. He is a preeminent thought leader in the field, a real KOL, and someone I love telling this part of the story. We had been consulting with Dr. Hogaboam like just about every company in IPF about eight years ago. He's someone. He's at Cedars-Sinai Medical Center in L.A., runs a lab where he's done a 30-year career looking at about 45 different novel agents and mechanisms. Somebody that pharma would go to to test their drug in this space. We were working with Cory just like everybody else in the space. We got data on this regenerative part of the drug, the side of the drug where we're preserving lung function, where possibly we can restore the lung.
Cory, we sent this data to him. He said, "No way. I don't believe it. I've never seen this before in my career. I certainly don't think your drug could do it either." Gave me a laundry list of confirmatory experiments, which we ticked through kind of one by one. Ultimately, got all the satisfactory answers, sent all the data back to Cory. He just said, "Wow. I've never seen a drug that could do this before." Six months later, he calls me and asked to join our company as our CSO. He said, "I've been offered this position before. I can never get behind the drugs. I think I could put my career behind LTI-03." A huge vote of confidence. A great person to have on our team.
IPF is a disease that affects about 100,000 people who are living with this in the U.S. alone each year, about 50,000 new cases, so that means about 50,000 deaths per year. This is a completely fatal disease. No one lives with IPF. The only resolution is to get a lung transplant, which obviously you don't want to do. Median time of survival from diagnosis is only three to five years. So worse prognosis than many cancers. A terrible disease with really very few choices. There are three drugs that are approved as of last year. A third drug got approved in 2025. These are kind of what I would consider slow the progression of the disease kinds of drugs. They slow down the disease for about a year or two. They have really terrible side effects.
GI side effects are so bad with the market-leading drug that 50% of the patients that go onto that drug will come off, many within the first month. That's what you get for your $160,000 a year that they charge. So the market-leading drug is doing $4 billion in sales, and half the patients can't tolerate that drug and are off the drug. So there's a real desperate need in this space for novel drugs that can address not only the scarring process, but again, the underlying health of the lung. I just want to point out, we have also tested our mechanism that I'll talk about here in a second in models of fibrosis of the heart, of the kidney, of the liver, the skin, of the eye. It works everywhere. So this is a real untapped mechanism in fibrosis.
Again, just to talk about kind of the competitive landscape real quick, because we get this question a lot. Two of the approved drugs are Boehringer Ingelheim drugs. One is about to go off patent, as is the Roche drug pirfenidone. We do like these drugs in that they address multiple fibrotic pathways. We think this is what you have to do, and this is really where the field has been heading over the past few years. What we've seen is that kind of targeting one pathway, one agent, is just not enough in this very complex disease. A few of the other competitors, this is not comprehensive. There is other competition in the space, but we think that we are alone in preserving the part of the lung that can help heal the lung, provide for new lung tissue. Whoops.
Our drug is focused on a protein called caveolin-1. Caveolin-1, we think of this protein as a regulator of balance in the cell or kind of a regulator of homeostasis in the cell. It keeps pro-fibrotic proteins in check, and it promotes turnover of things like ECM turnover. So it's a really positive protein and works across multiple fibrotic pathways. Again, we think this is really key in this very complex disease. The problem with caveolin-1 is that it's lost in a fibrotic state. So if you're scientific-minded, both at the transcript level and the protein level, dramatically downregulated. So all this regulation that you get is lost with CAV-1, which always, at this point of the presentation, begs the question, okay, if your target is missing, well, then what do you target? Our drug is a mimic drug.
It is actually a portion of the caveolin-1 protein. It is this seven amino acid peptide down here. It is a portion of the region of CAV-1 that binds other proteins and regulates them. We are, in effect, sort of mimicking or replacing the binding effect of caveolin-1. We bind proteins at their caveolin binding domain, affect their phosphorylation. And sort of non-intuitively, we put this peptide into a living system, and it is like caveolin-1 has been restored. We get the same sort of regulation kind of across the board, both in terms of inhibition of bad actors and promotion of things that can help heal the lung. Think of this drug more like, say, Akero's FGF21 mimic that they have had such success with in the liver. We hope to do something similar in the lung. On the anti-fibrotic side, our drug is a powerful anti-fibrotic.
In studies that we have done, it has looked very similar to the market-leading drug, nintedanib or OFEV. We work in a system, a translational system, where we can take a piece of a lung from an IPF patient. This is a lung that has been removed due to transplant. We are able to get a sample of that lung, and then we can test it, in this case, either with LTI-03 or with OFEV, both at concentrations similar to what are given in the clinic, and look for inhibition of a large panel of pro-fibrotic, let us call them bad actor proteins. I know you probably cannot read these down the left, but these are bad actors, interleukins, MMPs, osteopontin, things that you do not want overexpressed in the cell. In this patient sample, you can see we had inhibition virtually identical to the market-leading drug in terms of breadth and strength of inhibition.
Only, again, nintedanib is quite toxic. This dose of nintedanib will light up markers of apoptosis, necrosis, things that you obviously do not want in the cell. We have not had any sort of deleterious effects with LTI-03 thus far. This data here is the one that I believe let us know that this drug is really special. I will spend a minute on this slide here, really kind of panel A. What you are looking at is this tissue culture model, this IPF lung tissue. The lab that works with this tissue, they want to make sure this is precious tissue. Can we get experiments out of it? They will add a dye called LysoTracker to check the health of every culture that they run. LysoTracker is the bright green dots in these panels against the dull green background, and that dye will localize to the progenitor cell in the lung.
It is called a Type 2 or AEC2 cell, and those are the cells that make new lung tissue. They make surfactant. They can restore lung function. This lab just wants to see, do we have any viable cells? Basically, is this a viable culture for us to work with? The technician that ran these studies had a medical emergency. She could not come back to the lab for 48 hours, and when she did, she called us and said, "These are crazy compounds you all sent us. They are keeping Type 2 cells alive." What we could see qualitatively was an increase in the viability of these critical progenitor cells, and I was so excited. This is the data I sent off to Cory. He threw cold water all over my excitement, said, "No way. I just do not believe it." Gave me a whole list of experiments to run.
Are they making surfactant? Yes. We could just tick off all the experiments. These are functional progenitor cells, something this lab had never seen, something Cory Hogaboam had never seen, but something that you have to have in your lung if you are going to get resolution of fibrosis. If you are going to get any kind of healing, this is what is missing from the equation in IPF today, and this is what our drug really provides. Again, we have done two clinical trials to get to this point. A phase I-A in healthy normal volunteers is pretty safe and well-tolerated. The phase I-B study that we have done in IPF patients, there we go, we required a bronchoscopy before and after 14 days of dosing. Again, this is in patients, so we wanted to take lung samples. We used a technique called deep bronchial brushings, which is exactly what it sounds like.
You stick a brush in the lung, you are able to get protein samples. They were willing to do this so that we could look at lung-specific biomarkers. We get a lot of questions. Our drug is inhaled, it is a peptide. How do you know it is even getting to the lung? How do you know it is getting to the fibrosed part of the lung? We have looked in the deeply fibrotic part of the lung at different markers, and we were able to assess seven biomarkers in the lung. All seven of them went in the direction we were hoping they would go, four with statistical significance. This interleukin 11, CXCL7, TSLP, and collectin 7, these are bad actor proteins. These are proteins that we had seen pre-clinically. We can inhibit these with LTI-03.
Now we have evidence in the lungs of IPF patients we are doing the exact same thing that we have done in pre-clinical studies. We are knocking down these bad actor proteins in a way that was statistically significant. That gave us a lot of confidence that in patients we are seeing what we have seen before. Some of these proteins, including IL-11, are indicators of positive effects in Forced Vital Capacity or FVC. That is a lung function measurement. That is what we are going to be measured on in this phase II study and in registrational types of trials. We looked at indicators of, are we going to have positive effects on lung function? The answer was yes, at least for these biomarkers. Again, lots of confidence going into the trial. I am going to skip that one real quick.
We measured a plasma biomarker, so one that we could get from blood samples from patients called Surfactant Protein D or SP-D. This was important because the two approved drugs at the time, nintedanib and pirfenidone, had seen that they could reduce this SP-D by 4% and 5% in 12-week studies. It does not sound like a lot, but for SP-D it is. It is a large amount of reduction. We also were able to reduce SP-D by 5% in just the two weeks of our clinical trial. We feel like if there is a clinical bar for a biomarker, not a lot of companies have done biomarker studies in the IPF space for whatever reason. We wanted to do a really rigorous study to give us a lot of confidence heading into this phase II trial. This is a schematic of our current phase II trial.
It's placebo-controlled, two doses of LTI-03. The low dose is 5 mg a day. The high dose is 10 mg a day. 24 weeks of treatment in IPF patients. This will take us into 2027. We haven't given guidance on end of the study, but it will take us into next year. We want to release some sort of interim data, blinded data. We're not going to unblind the study. We're not going to do stats, but just kind of a blinded look at 12 weeks' worth of data with some portion of patients. We're not sure how many, 30 to 40 patients. Ultimately, we're going to measure changes in Forced Vital Capacity or FVC. This is the lung function measurement, again, the drugs get approved on. We'll also look at high-resolution CT scan, before and after 24 weeks of dosing.
We have an AI imaging platform by Qureight that we're using to assess this. We have announced that we're better than 25% enrolled faster than we thought. Enrollment's going great. We're excited to finally be at the stage where we can help IPF patients. These patients are desperate. They call us. They message us. I know that they're doing the same for other companies. They just need better drugs in this space, and we hope that we are providing one. That's it. I will finally take a breath and let you ask any questions that you may have.