Great. Thanks, everyone, for joining us. Thanks for joining us for the conference overall, and for joining us for our next session. I'm Vamil, one of the bio-pharma analysts here at Guggenheim. Edward Malarkey from the team, also. Next in this room, we have the team from Eledon Pharmaceuticals, a company we actually just launched coverage on not too long ago. We have D.A. Gros, the CEO of the company, Steve Perrin, the President and Chief Scientific Officer of the company. D.A., I was just going to start by, if you can just give, for people who maybe don't know the story that well, just an overview on the story, the history, and how we've gotten to this point. Obviously, important year coming up with some data releases and as you guys progress forward here. Maybe you can just set the stage for everyone first. Sure. And Vamil, good to see you. Thank you very much to Guggenheim for inviting us to the conference. It's our first time here, and we're very excited to be here and be able to join. In terms of the history, I think you'd like me to go through the history and kind of how we got here. We are a company that is focused on transplant immunosuppression. Steve and I founded what is today Eledon about four and a half years ago. We did it by taking tegoprubart, which is an anti-CD40 ligand, from an ALS-focused nonprofit and combining it into a public company. The reason we, at the time, initially, the asset had been focused on ALS, and we shifted the focus to transplant. We did that for three primary reasons. The first reason was that it was the data. In preclinical models, really, regardless of whether we're looking at allotransplantation or xenotransplantation across organ types, pretty much the best data, bar none, has been generated using an anti-CD40 ligand. The second reason we did it was the proven market size. The drug that we're looking to replace as the standard of care, tacrolimus, has been around for about 30 years, 35 years. It peaked back in the day at over $3 billion, $3.5 billion of sales. In fact, branded tacrolimus still does $1.5 billion in sales 30 years after launch. The prior drug, cyclosporine, which was launched in 1983, in the 1980s was doing $1.5 billion of sales. We had this large market with an established drug, but one that hadn't changed in 30 years. We believe this is a market, as a result, that's ripe for innovation. There are very few things, almost nothing, that we do in medicine the same way that we used to 30 years ago. The third reason why we picked transplant was because it's rare disease-like. It's a very concentrated market. There are few transplant centers in the country, maybe 200, 250. You probably only need a sales force of 25 people or so to cover. We can do that as a smaller biotech. For those three reasons, we shifted the focus. Since then, we've now generated some data in ALS, but that was important for the biomarkers that showed that we were getting target engagement and very broad and deep decreases in pro-inflammatory biomarkers. Afterwards, we've started to generate data in transplant. We've now presented data in kidney transplantation from our phase I-B study. We did that in the middle of last year. Later in the year, we presented data in islet cell transplantation. At a high level, that is the history of where we are and how we got here. Yeah, perfect. Maybe we could talk about the I-B data you've released to date. I know you have more coming this year, but just again, as a sense of what you saw in that initial data release and what excitement it led to here. Sure. Steve. Sure. Yeah. The phase I study is an open-label study that we have been enrolling for a couple of years, ex-U.S. The primary endpoint since our first phase I study is safety tolerability. We have been using kidney function as measured by eGFR to look at how well the transplanted kidneys are doing. We are also collecting other data that would be typical of looking at transplant, including rejection, patient survival, graft survival, as well as some of the biomarkers and clinical outcomes that are associated with long-term CNI toxicity. Last year, we released data on our first 13 patients at ATC. The eGFR data, the kidney function data, was really compelling. Our mean eGFRs in that study were floating around 70, starting at about 30 days post-transplant. Some of the patients were out past a year. It was very exciting and very encouraging to see eGFRs at that level, probably about 20 points above what we would currently consider standard of care. With tacrolimus, eGFRs typically are around 50, 52. OK. Now we have more data coming in the middle of this year. Maybe you can just give us a sense of patient numbers or what you expect to see from this upcoming year. The big data is obviously going to be ours. We're running phase II in parallel. That's a controlled study looking to show superiority to standard of care. That data will be out in the fourth quarter. That's really the important data that we have in kidney transplantation this year. We'll give an update on the phase I-B. We'll share the data that we have available, probably up to 12 months. We'll share all the patients that got out there. Obviously, we don't know what that data is going to show in six months. I think regardless of where that data comes out, obviously, the data that regulators are going to focus on, and that's the most important, is going to be the phase II. OK. Yeah. Maybe let's talk about that one, then the phase II at the end of the year. Again, obviously going against tacrolimus, we're looking to replace. What would you need to show? I think some of it is just the safety and tolerability of tacrolimus to be there. What do you think you need to show efficacy-wise? What do you need to show safety-wise? Sure. There are two things where we hope to beat tacrolimus. We hope to beat tacrolimus on efficacy. We hope to beat tacrolimus on safety. When we talk about efficacy, we're talking about kidney function. Kidney function today has the provable endpoint in many kidney diseases. This phase II study is 80% powered to show a nine-point difference between ourself and tacrolimus. A nine-point difference is clinically meaningful. I mean, to give you a sense, for the patient population that's less than 50, which is about half of patients that have eGFRs under 50, a nine-point delta would be at least a 25% reduction in the risk of losing their organ over 10 years. If we were able to hit that and to be stat sig above where tacrolimus is, we'd be the first company or be the first drug in 30-plus years to show that. It would mean a clinical benefit, likely mean a clinical benefit over the long term to patients. The second issue with tacrolimus, it's safety profile. Tacrolimus is directly nephrotoxic. It causes hypertension. It causes hyperglycemia and diabetes because it's beta cell toxic. It is CNS toxic. It causes brain fogs and tremors. Those are the things that patients typically hate the most. We hope to also show a benefit when it comes to those side effects. There is no reason, based on our mechanism, that we should have any of that, the hypertension, the hyperglycemia, or any of the CNS effects. OK. We've been in over 100 humans, and we haven't seen any of those side effects. OK. No, that's great. I think as we've been doing, you know, mentioned, we just initiated recently in speaking with all leaders. I think they definitely agree with the limitation of ta crolimus. The other point they make, well, we've sort of managed over the last decade or so to, we got to monitor patients. We got to figure all this out. I guess the question I have is, both from a regulatory side and then maybe more from a commercial side, what would you need to show to get actual approval of the product, but then also get doctors comfortable that to shift from what they've been doing for these years, even if it's not ideal, at least they've sort of figured out a way to do it? What would you need to have in terms of a data set to? I think we would need to show that we are superior in an endpoint that is prospective and would indicate an increased length of survival of the organ. I mean, today, the average person getting a transplant in the United States is 51. The average organ, kidney that gets transplanted, only lasts 10-12 years. We do not have enough organs. The other alternative, by the way, is dialysis. Average survival in the U.S. on dialysis is less than five years. People have one shot pretty much when they get a transplant. If the average age is 50, the patients that are 20, 30, 40, 50, even 60, for them to live a regular lifespan to get to 80, they are going to need more than one organ. That is more than one organ that just number-wise, they are likely not to be able to get. Extending the functional life of a transplanted organ will most likely translate into extending the life of that actual patient. Being able to show superiority in an endpoint that predicts, helps predict how long an organ is likely to work, is going to be very meaningful. I mean, I can ask you the question. If you needed a transplant, would you rather get a drug that's been around for 30 years or one that's newer and is likely to allow your transplant to survive for longer? I think we'd all agree we'd rather go with the latter. We believe, as a result, physicians will prefer the latter as well. From a regulatory perspective, I guess, if you're assuming positive data into the year in the phase II, is there a path to get this to the market sooner, or do you need to do a longer phase III where you would then maybe need to show outcomes, benefit, or something beyond the eGFR? Yeah. We're definitely going to have to run another study, a single phase III study following up based on the phase II results. Probably a very similar design, more powered, more patients, but a very similar design. OK. The endpoint, and I think you were alluding to the endpoint, there is a new endpoint that's being considered by the FDA, which is called iBox. It's an algorithm that helps predict how long an organ is likely to survive. The important thing in iBox is that its primary variable is eGFR. Whether it ends up, the primary endpoint ends up being eGFR or iBox, they're very similar. We're going to capture all of that data in our phase II. OK. Let me turn over to Edward to talk a little bit more. Maybe turning a bit more to the commercial side. We had the most recent commercially launched agent in kidney transplant was Bristol-Myers Squibb, also known as belatacept, which underperformed commercially. What are your learnings from the belatacept launch, and what do you think you can do differently to make tegoprubart more successful? Sure, so, b ela is an interesting drug, and there's a lot that we can learn. When one looks at the bela launch, which I think we can all agree underperformed, one needs to notice a few things. The first one was that Bristol, and I don't know why they did it, but Bristol ran their phase III as a non-inferiority versus cyclosporine. Remember, the standard of care was tacrolimus. When they launched, they could say that they were non-inferior to a drug that was no longer being used as the standard of care. That puts the reps, as you can imagine, in a pretty weak spot. What they hoped to differentiate themselves on was safety. They hoped that they'd be able to have better safety, which they did when it came to the CNS effects or the hypertension. Unfortunately, Bristol, in with bela, saw rare cases of PML and PTLD, which are rare types of cancers that are always deadly. As a result, there was this overhang because we did not know at the time, the field did not know at the time, whether how common these rare cancers would be. Also, bela in the trial for liver transplant underperformed and actually has a black box against its use in liver transplantation. As a result, it made for a tough launch. Now today, 15 years later, we know bela is a very good drug. Bela helps show how higher eGFRs translate into better organ survival over time. All of that in terms of the importance of eGFR, which we know today as an example, that was n't known to Bristol when they launched in 2011. Of course, that will be known to us. We're looking at a very different environment. What we hope to do is to show not only non-inferiority, but superiority, and not to an older drug, but to the current standard of care. How should we think about potential pricing in this market? We did a number of doc calls and KOL calls when we were looking at your company. A lot of them mentioned that they thought that Nulojix was priced too highly. It sort of inhibited patient access. How are you thinking about pricing in this market? Bela is priced at about $40,000 a year. I don't think we're in a position today when we don't even have phase II data to provide guidance in terms of pricing. It's hard because I don't know when physicians say that how much of that access is, how much of that is really occurring out in the field. That said, what's nice in this space is that in the United States, all patients, regardless of their age or their income, are eligible to have the federal government pay for their immunosuppressants post-transplant. There is a federal law that covers all immunosuppressants. That federal law also has implications in terms of payers needing to cover all immunosuppressants. That's quite favorable. As you know, there are almost no other spaces in medicine in this country where that's the case, where you know any patient who gets prescribed the drug will have a means to get coverage to help them pay for that drug. OK. Maybe last one for me before turning it back to Vamil, but how should we think about sort of the future commercial dynamics in the kidney transplant space, the number of prescribers, infrastructure needed? I know you touched on it a bit earlier. Also maybe just from the competitive sense, what are you seeing in the competitive space that potential competitors that are coming or that could affect tegoprubart? What's nice is that this is a space that's had a dearth of innovation over the past 30 years, which is why we look, and as you brought up Belatacept, we're talking about a drug that was launched in 2010, 2011. Aside from us today, there really isn't much that's in the clinic in terms of the specific de novo kidney transplant indication that we're looking at. I think from a transplant risk or competitive risk, what could be most likely would be one of the other anti-CD40 ligands. If we show the potential here, potentially one of them could decide to enter the field. OK. Maybe let me just shift gears a little bit because this is all we've been talking about, renal transplant. There are other transplants where the product could be effective. Xenotransplantation is something that you've talked about. We've heard United Therapeutics and others talk about it. Maybe you just talk about the potential to move your asset into these other indications. Sure. Steve, do you want to talk about xeno? Sure. Xenotransplantation, as everybody has seen, is really making significant progress with the development of genetically modified pigs that could be amenable to utilize as organs in humans. The two leaders there are Revivicor and eGenesis. They both have done a significant amount of preclinical work in xenotransplant in non-human primates and are now getting compassionate use cases set up where they've demonstrated at University of Maryland a xenocardiac transplant. Massachusetts General Hospital did the first human kidney xenotransplant. There was an announcement yesterday that both of the companies now have INDs to start moving those technologies into a more formal clinical trial setting. One of the things that's been pretty evident with the preclinical data over the last five to six years is that blocking CD40 ligand needs to be a component of that translation into humans. We're supportive of all of the xenotransplant technologies right now. We're trying to be as helpful as we can, trying to get the preclinical work to now translate into humans. As we look at the market, our goal is to be the cornerstone immunosuppressant in transplant, the same way TAC is today. To be what gets used first, regardless of organ type. Today, it's obviously kidney, but we think in the future it could be liver, heart, lung, et cetera, regardless of whether it's a solid organ or a cell transplant. As we discussed, we're also doing islet cell transplantation. Also, regardless of the source of that organ, whether it's living donor, deceased donor, or in the future xeno. What you're seeing us do is work on each one of those silos so that we can be in a place where in the future we're ready to move forward for clinical trials wherever they go. Yeah. I guess my follow-up question was going to be around the preclinical data. Is there any reason why this would not, anything you've seen as to why this could not be used across the range of transplants or anything you can comment on there, what you've seen preclinically beyond the kidney? I mean, the preclinical data going back on blocking CD40 ligand to this day is the most potent way to prevent transplant rejection in multiple different species and pretty much every organ that's been looked at. There is no reason why it wouldn't work for any type of organ cellular transplant as far as preventing both short-term and long-term transplant rejection. For us, although some of it hasn't been presented yet, we've now, we've said publicly that we are IND ready in liver transplantation. We've completed work with preclinical work in liver transplantation. Obviously, we've been in humans with cardiac, in terms of cardiac xeno. We've done preclinical cardiac as well. In our hands, we've seen tegoprubart show efficacy now in multiple different types of organs, both in humans as well as in non-human primates. OK. Maybe just to round out the discussion here, so one, so obviously you laid out these upcoming data releases, but just maybe summarizing for everyone kind of the catalyst path from here over the next 12 - 24 months. Sure. The big catalyst, as I mentioned, is going to be in the fourth quarter, which will be our phase II data. Shortly before that, in the third quarter over the summer, we expect to release an update on our phase I-B data. We also expect towards the end of the year to give an update on our islet cell transplantation. That is a potential functional cure in type 1 diabetes. During the year, investors should expect to see more news coming in xeno. This will be a big year for us where we'll be able to advance across all of the programs where we've been showing progress. Maybe one other thing, going back to the commercial side, we touched on the U.S. market. What are your thoughts at this point in terms of outside the U.S. for this? We're looking at being able to commercialize globally. We run our trials globally. Our phase I-B is being run in three countries, all ex-U.S., although we are going to open up a U.S. site. Our phase II is run in the United States and then, I believe, six other countries, including in four continents, so including Brazil and Latin America, a number of European countries, and Australia and North America. OK. Maybe lastly, just around the cash position for the company now and your runway. We raised about $140 million in two raises in 2024. That gives us sufficient capital to get to the end of 2026. In other words, we can get our phase II data, and we should have at least over a year of cash at that time left. OK. Sorry to come back to where we started with the ALS program. That is still listed in your presentation. What's the any update? You know, our ALS is in the DNA of this company. It's thanks to patients with ALS and families of patients with ALS that funded the development of tegoprubart, and we believe that tegoprubart and anti-CD40 ligand mechanism will work ultimately in ALS. For a number of reasons, it's not our principal focus, but it is something where we would like to advance the study. What we'd like to do is to move it into phase III. We think that there are a lot, typically ALS clinical development is done with underpowered studies. And so, there are results that then are very hard to interpret. We don't believe that that's what's best for the field, and so, for us to move ALS forward, we would want to do a fully powered study that would help deliver a single answer of whether or not tegoprubart can help these patients. In order to do that, ideally, we do it with non-dilutive capital. To date, we haven't located that capital yet, but we do hope that at some point in the future we will be able to do so. OK. All right. Thanks again for joining us in the conference. Thank you. Look forward to seeing all the progress over the year. Thank you for having us. Thank you.