Hi, everyone. Welcome to the third day of the Jefferies Healthcare Conference. My name is Michael Furnas. I'm part of the healthcare investment banking team here at Jefferies. I'm here today with David-Alexandre Gros, CEO of Eledon, who will walk you through a quick presentation. Thank you.
Good morning, and thank you for the introduction, Michel. It's always nice to be back here in London at the Jefferies Conference. Thank you for inviting me. I will be making some forward-looking statements, so please make sure to check our forward-looking disclosures. We founded Eledon to focus on organ transplantation. The unmet need in organ transplantation is that the cornerstone immunotherapies that are used to prevent rejection, the calcineurin inhibitors, are both toxic to the kidneys as well as have a number of other toxicities which leave significant room in order to improve upon them to allow better outcomes for patients that have received organ transplants, in particular, patients that have received kidney transplants, which is also the highest population of organ transplant patients. We focused on transplantation because of the unmet need.
One of the core issues that we're looking to solve by seeking to extend how long organs, in particular kidneys, function is the following: today, the average patient that gets a kidney transplant is 50 years old, but the average transplanted kidney only functions for about 10 or 12 years. And so doing simple math, it's easy to see that for a transplant patient to live a regular lifespan, especially if they're 20, 30, 40, 50, even if they're above the average at 60, they may need two or more organ transplants, two or more kidney transplants. But as we all know, those are kidneys that oftentimes don't exist. In fact, today, for every five kidney transplants that we do, one person dies waiting for a transplant that they are not able to get. We also focused on transplant because of the science.
Our lead asset is Tegoprubart, an anti-CD40 ligand, and in preclinical models, anti-CD40 ligands have shown the best efficacy at protecting transplanted organs. And we'll walk through this in a few slides. Transplant also has a clear regulatory pathway with some upside. And finally, the transplant market, while it is large from a dollar perspective, indeed, the drugs that we're looking to replace, many of them have been blockbusters and continue to be blockbusters even after they've gone off patent. So while the market is large from a dollar perspective, it is a small market from a calling perspective. There are only about 750 transplant surgeons in the United States, about 150 centers that do transplants. So this is a market that can be tackled by a small biotech like ourselves.
Our pipeline is focused around our lead asset, Tegoprubart. We are currently in two clinical trials, a phase 1b single-arm open label study in kidney transplantation, as well as a phase 2 superiority study. So this is a study, a phase, that has a control arm, where we're looking to show superiority in terms of kidney function at 1 year versus tacrolimus, which is standard of care. We have a third related study ongoing, which is an open label extension, where patients from the phase 1b or the phase 2 study can enroll after they complete a year on drug. We're developing Tegoprubart in xenotransplantation as well. As you might have seen, about 2 months ago, a second person received a pig heart, so a pig xenotransplant. What makes that possible is twofold.
One, obviously, the technology improvements in the xeno organ itself, but also the therapeutics that are given along. And so we were the core immunotherapeutic that was given as part to that person as part of their regimen. We have a number of preclinical collaborations really around the globe, from the United States to Europe to China, on xenotransplantation today, including one of the largest player, eGenesis, where we have a collaboration and are used across their pipeline. We are also looking at liver transplantation after kidney. That is the largest market, 25,000 kidney transplants a year in the U.S., 7,000 liver, and we are in preclinical work there. And finally, we've completed a positive phase II study in ALS, although ALS is currently on hold as we seek non-dilutive financing in order to advance it.
The mechanism that we're looking at is one that has been very well elucidated, one that is that we've known about for a long time as a scientific community. It was first described in the late 1980s. We're looking at the costimulatory blockade by the interaction between T-cells and either antigen-presenting cells, or B-cells. So anti-CD40 ligand is really found only in two places in humans. It's found on platelets, but principally on top of T cells. Anti-CD40 receptor is much more broadly distributed, and primarily on antigen-presenting cells as well as on B cells. So this is this is part of how the human body is able to identify self versus non-self.
There's a handshake, if you will, where proteins are presented to the T cells, and in parallel, you have a second handshake, if you can imagine that in your mind's eye, using CD40, CD40 ligand. And by interfering with that communication, we can change at how T cells consider the protein that they're looking at. So we make it less likely that they recognize that protein as foreign, and as a result, more likely that they look at that protein and, and decide that it is actually self. So what does that mean from a slightly more technical perspective? It means that we inhibit T cell polarization into CD4 positive and CD8 positive T cells, and by doing that, we in turn inhibit the polarization of B cells, since helper T cells polarize B cells, so that decreases the amount of antibody that's made.
And when T cells are not polarized to become CD4, CD8 positive cells, what's interesting is that a subset become T regulatory cells. They polarize into Tregs, and those are the brakes of the immune system, and the Tregs in transplant play an important role in the induction of tolerance. We went after the ligand versus the receptor for a number of reasons. One of the primary ones is what I went through, which is just how localized the ligand is. That has dosing advantages. Also, when one goes after the ligand, the ligand doesn't just block CD40 receptor, it actually blocks other interactions, including CD11, which is why one sees the Treg effects with by going after the ligand and not the receptor, as an example. We picked to go with an IgG1.
We took a traditional antibody, humanized antibody approach, as opposed to some other ways, such as fusion proteins or pegylated Fabs, which others in the field have used, in order to take advantage of better manufacturing, better half-life, which we've shown, as well as less anti-drug antibodies that have been seen by some of our competitors. Indeed, to date, we have not seen any significant ADAs. To go back to the transplant market, as I mentioned, it is a large market from a dollar perspective, and here's why. So there are 25,000 kidney transplant patients transplanted every year in the U.S., about 19,000 in Europe. There are 10 times as many people in those geographies living, currently living with a kidney transplant. The market today is part...
If we look at kidney transplant, in particular, is part of end-stage kidney disease. End-stage kidney disease is interesting because in the United States, it's actually covered by Medicare. So any patient in the U.S. that has end-stage kidney disease and that needs dialysis or kidney transplant, if they can't get private, private payer insurance, they can apply, regardless of their age, for Medicare, and the federal government will cover the cost of their care. That includes immunosuppression, and as of 2025, that, out-of-pocket expenses for medications for Medicare patients will be capped at $167 a month. So this is an interesting market that provides very nice, very nice coverage. It's also a market, as I mentioned, where past drugs have been blockbusters. The drug we're looking to replace is tacrolimus.
Tacrolimus is used in most of transplants around the world today to prevent chronic rejection. Tacrolimus, last year, this is a drug that was approved in 1994, and it was invented by Astellas. Last year, tacrolimus generated $1.5 billion in revenues for Astellas, which is pretty remarkable for a drug that's now been generic for over a decade. In fact, if we look at the drug that was the cornerstone immunosuppressants before tac, there was a drug called cyclosporine. Cyclosporine was invented by Sandoz, which is, of course, now Novartis. Cyclosporine was a billion-dollar drug in the 1990s, back when a billion dollars meant something. But cyclosporine last year still did $300 million in branded revenues for Novartis, and this is 40 years after it was approved.
So this is continues to be a large market, but as I mentioned, one where it's quite small in terms of the calling points. Now, there's the economics here favor nice reimbursements, since the cost of care of these patients is so much. The alternative to getting a transplant is to remain on dialysis. Dialysis has an average survival rate in the United States of less than 5 years. So one is better off having cancer than needing to go on dialysis, because most cancers today are associated with a lifespan of above 5 years. Dialysis is also very expensive. Dialysis itself costs over $120,000 per year in the States, and organ transplants are expensive as well. So it's over $400,000-$500,000 in costs for an organ today.
Of course, if someone needs another transplant, that cost needs to be paid anew. While they wait for that transplant, they may need dialysis. This is a very expensive population to take care of, and as a result, we believe that by extending the lifespan of those kidneys, that will allow more people to have access to kidneys, since every year there'd be fewer people that would need repeat transplants. Beyond extending life, allowing people to have their life saved by getting an organ that they otherwise would not have gotten, we should also be in a position to save the system substantially from an economic perspective. Why is it that kidneys only survive 10-12 years after organ transplant? As I mentioned, it has to do with the toxicity of the calcineurin inhibitors, these cornerstone immunosuppressants.
So CNIs are toxic to kidneys, both directly as well as indirectly. They're directly toxic to kidneys. They're a nephrotoxin. They're also indirectly toxic to kidneys because they are associated with causing diabetes and hypertension. So as an example, they're toxic to the beta cells of the pancreas that produce insulin, and hence the hyperglycemia and new-onset diabetes that we see after patients receive transplants. Now, this is ironic because diabetes and hypertension are the primary reason why patients end up going into kidney failure and needing kidney transplants in the first place. Interestingly, we not only see this nephrotoxicity in kidney transplants, we actually see it in other transplant types as well. So if we think about heart transplants, 1 in 11 patients that gets a heart transplant will be in end-stage kidney disease after a decade, and at that point, they may need dialysis or transplant themselves.
But they don't lose their kidney function because of the underlying heart disease that they had that led them to get a cardiac transplant. They lose it because of the immunosuppressants, because the calcineurin inhibitors that we put them on to protect their heart, that in turn end up destroying those kidneys and then forcing those patients to need very significant care over the long term. You can see the impact on this slide of the calcineurin inhibitors on kidneys. So if you look at the right hand, my right, your left, the left-hand chart, as you're looking at it, of the graph there, what you see is the reasons why grafts fail over time. This was last presented at the American Transplant Congress, which is the big kidney the big transplant conference in 2018.
What you'll notice are the bars that are the yellow, the blue, and the greens. So those are rejection, that you're looking at the percentage across time of transplants that are lost because of rejection, so the body attacking the organ itself. So early on after a kidney transplant, when someone loses an organ, that is typically because of rejection in the first 90 days, 180 days, 270 days. But notice how that changes. So the moment we get out a year and going out increasingly to 10 years, the reasons those kidneys start to fail is no longer because of rejection. It's not because the immune system is attacking the transplanted organ. It's because of the CNIs and the toxicities that we just discussed.
And so our hypothesis is that we can remove those red lines, and if we remove those red bars, kidneys should be able to function better and longer. Now, this, what we're looking at here, is a meta-analysis of all of the published literature that looked at anti-CD40 receptors and anti-CD40 ligands with non-human primates. When this was done, what it showed, as you can see, is the following: You're looking at how many monkeys, how many non-human primates remain alive over time when they're treated with a monotherapy. The first thing you'll notice is that if animals are not treated, they end up dying almost immediately. 100% of those animals will die within a week. There's no placebo effect in transplantation.
You can see the effect of CD40, the receptor, which is the T line, CD40 ligand, and notice the differences in survival between TAC, which is today's standard of care, the gray line and the red line. This was the data that we used to do our initial raise in 2020, when we raised about $116 million to get Eledon in its current phase going. We're running two studies in parallel, as I mentioned. The key difference between the two studies is that the phase II is a superiority study, and since it's a controlled study, we won't be looking at that data until we finished enrollment and have a year's worth of data on all of those 120 patients.
What we're doing in both of these studies, of course, is only replacing tacrolimus with tegoprubart. So other than replacing the calcineurin inhibitors, the patients remain on standard of care. The phase Ib allows us to report data, and this is the data that we can report, and we've been reporting about twice a year. We've started the phase II. We opened up our first site in June, started enrolling in the summer, and we expect to complete enrollment in that study at the end of next year. So what has our phase Ib data shown us to date? Before, let's take a step back and talk about eGFR, glomerular filtration rate, for a second. Our primary endpoint in the phase II is kidney function.
That is measured as glomerular filtration rate, how well the kidneys filter, which is a measure of how well kidneys function. eGFR, GFR is a number between 0 to 120. Anything above 60 is considered normal. 60-80 is low normal. Your healthy young person will typically have a GFR of above 100. Think if you're a teenager. As we age, our kidneys stop working as well. So someone of retirement age will normally have a GFR of about 80. Anything less than 60 is kidney disease. Less than 20 or 15, someone would typically need either dialysis or a kidney transplant in order to survive. Now, there's been tremendous consistency across clinical trials and large studies looking at eGFR after transplant. This is the latest database that we found that's been published.
It looks, as you can see, initially, at 23,000 patients, so very large population. As you can see, the mean, the median GFR after 1 year, but it really starts after a month on standard of care, is about a 50, 51. If you have a normal GFR, you're in the top 25% of patients. If you're above a 60, if you're in the true normal, above an 80, that's really only 5% of transplant patients get there. And GFR is important because it's the best predictor of how long kidneys are likely to function. And you can see this here. This is based on the data we just reviewed. You can see the bell curve distribution of GFRs, and notice the dark line with the exponential increase. That's the risk of graft loss in the following 12 months.
So as one goes down in eGFR, as one gets below normal, so below 60, you can see how that relative risk of losing that graft increases exponentially. But that's important because it also shows the potential of what improvements in eGFR could do. Since moving patients to the right, which is what we're looking to do, moving them from a 20 to 30, a 30 from a 40, a 40 to 50, as a result, could dramatically reduce the risk of losing, of losing that organ. Moreover, we've seen even in large algorithms that have now been created to predict the life of grafts, in particular, iBox, the primary variable that they look at remains GFR. So turning to the data that we've presented, we presented at Kidney Week, two weeks ago, the results from our first 11 patients on drug.
You can see the demographics here. We had 11 patients, with one patient having completed a year on drugs, so going out to 380 days. Two of the patients had discontinued the study. Our first patient discontinued after about nine months. That subject complained or reported of mild alopecia. It was visible where she parted her hair, as well as mild insomnia. The PIs did not consider that those were due to our drug, tegoprubart, but she still elected to leave the study. After she left the study, her symptoms did not change. So her alopecia did not get better, and her, neither did her, her insomnia, which isn't surprising because these patients are on polypharmacy, and other drugs, such as the steroids, are typically associated with the side effects that she reported.
But we were still extraordinarily grateful to her that she volunteered to be the first person to take tegoprubart after a kidney transplant. We had another patient that was withdrawn from the study by the PI. That patient experienced a BK viral infection. It's a very common infection after kidney transplant. The infection was resolving, but nevertheless, it was the first time we were seeing it, and the PI elected to withdraw that patient and to put that patient back on standard of care. All other patients were on trial at when we reported this data. In terms of safety, overall, the safety looked good. The primary safety issue that we saw was GI related. These patients are on polypharmacy, including MMF, and the GI side effects were consistent with what is seen with MMF. We did have one patient experience a rejection.
It was the mildest form of rejection, a Banff 1A, and it was treated. The patient continued to be on drug. Importantly, we did not see a lot of the side effects that are typically seen with the CNIs. So we did not see hyperglycemia or new-onset diabetes. We did not see CMV infections. We did not see the tremors, which are oftentimes the primary complaints that patients on CNIs get. And in terms of hypertension, we saw as much hypertension as we did hypotension in this trial, but we've now had 100 human subjects on our drug, and we have not seen hypertension or typical CNI side effects across those 100 patients. Turning to efficacy, so remember, this is our primary endpoint, is GFR. As you can see, the GFRs here are quite encouraging.
Recall that the mean or median GFR after transplant is about a 50 or in the low 50s. We were at a 60 at 30 days, going up to a 90 at 365. Small n, but it's still encouraging to see such nice kidney protection and performance. And to give you a sense of the patient that went out 1 year, this was a 77-year-old woman, long-term diabetes, who had been on dialysis and received a deceased donor kidney. So someone died to give her that kidney. So about as difficult a patient as one could think of, and yet today, she has better kidney function than your average person her age without diabetes and two native kidneys walking down the street here in London. So this brings us back to where we started.
We are a biotech that is very focused on the organ transplantation market. Currently have a phase II that is running with a phase Ib running in parallel to generate data. We'll be able to report out data from that over time. We look forward to the next update we'll give. It will be towards mid-2024, when we'll be able to give an update on our phase Ib and how those patients are doing. And with that, I will end my presentation, and I'm happy to take any questions here or answer them in a one-on-one session. Thank you.