Hello, and welcome to the Eledon Pharmaceuticals third quarter 2021 earnings call and webcast. At this time, all participants are in listen-only mode. A question and answer session will follow the formal presentation. If anyone should require operator assistance, please press star zero on your telephone keypad. As a reminder, this conference is being recorded. It's now my pleasure to turn the call over to CFO Paul Little. Please go ahead. Good afternoon, and thank you for joining Eledon's third quarter 2021 financial results conference call. Joining me today is David-Alexandre Gros, Chief Executive Officer, Steven Perrin, President and Chief Scientific Officer, and Jeff Bornstein, Chief Medical Officer. Earlier today, Eledon issued a press release announcing financial results for the third quarter ended September 30th, 2021. You may access the release under the Investors tab on our company's website at eledon.com. Before we begin, I would like to remind everyone that statements made during this conference call relating to Eledon's expected future performance, future business prospects, or future events or plans may include forward-looking statements as defined under the Private Securities Litigation Reform Act of 1995. All such forward-looking statements are intended to be subject to the safe harbor protection provided by the Reform Act. Actual outcomes and results could differ materially from these forecasts due to the impact of many factors beyond the control of Eledon. Eledon expressly disclaims any duty to provide updates to its forward-looking statements, whether as a result of new information, future events, or otherwise. Participants are directed to the risk factors set forth in Eledon's reports filed with the U.S. Securities and Exchange Commission. It is now my pleasure to pass the call to Eledon's CEO, Dr. David-Alexandre Gros. DA? Thank you, Paul, and thank you all for joining us this afternoon. We formed what is now Eledon just one year ago when we acquired Anelixis and concurrently executed a financing with leading life science investors. Since then, we have built a world-class team and strove towards initiating clinical trials in three therapeutic areas: transplantation, focusing on kidney and islet cell transplantation, autoimmunity, focusing on IgA nephropathy, and neurodegeneration, focusing on ALS. I'm proud of the progress our team has made over the past year and especially the past months, underscoring our focus on operational execution. Specifically, we are nearing completion of enrollment in our phase II trial of AT-1501 in adults with ALS, with 16 of 18 subjects enrolled in the fourth and final cohort. We received a no objection letter from Health Canada allowing us to initiate our open label clinical trial evaluating AT-1501 in kidney transplantation, and we are in the process of opening our first site in Canada. We received IND clearance from the FDA to proceed with a clinical trial to assess the safety and efficacy of AT-1501 in the prevention of rejection in patients undergoing islet cell transplantation for the treatment of Type 1 diabetes. We initiated an AT-1501 monotherapy kidney transplantation study in non-human primates as requested by the FDA in advance of a potential IND application for AT-1501 in kidney transplantation in the United States. We announced a research collaboration with CareDx, a world leader in transplant diagnostics and services, and we recently announced IgAN as the next indication for development of AT-1501, and remain on track to begin opening sites for the phase II study by the end of this year. Finally, we presented additional data at the International Pancreas and Islet Transplant Association World Congress from our non-human primate islet transplantation study, focusing on the potential benefit of using AT-1501 in transplantation versus traditional immunosuppression, including calcineurin inhibitors. Before Steve and Paul dive into last quarter in more detail, I'd like to talk about the importance of our upcoming work with CareDx, as well as share some thoughts about 2022 since the new year is quickly approaching. We recently announced a research collaboration with CareDx in October. This multi-year and multi-trial collaboration enhances our capabilities for our upcoming and potential future clinical trials of AT-1501 in kidney transplantation for a number of reasons. First, it gives us access to CareDx's Kidney Care Suite, including AlloSure, a non-invasive cell-free assay that looks for donor-derived double-stranded DNA in the blood as an indicator of graft rejection. Second, it gives us access to algorithms including iBox, a predictive algorithm that provides a prognostic indication of allograft survival. When possible, we plan on integrating biomarkers and algorithms such as these into our renal transplant studies as exploratory endpoints to allow us to better characterize AT-fifteen oh one's performance and its differentiation from current standard of care, and potentially allow us to do so at earlier time points than was historically possible. Finally, as we plan and execute our trials, we will benefit from CareDx's large footprint, experience with kidney transplantation clinical trials, and its established relationship with both key medical institutions and opinion leaders. I'll end by talking about 2022. With our ALS phase II study enrollment nearly completed, enrollment in other trials is expected to begin in the near term. Starting with ALS in the first half of 2022, we are approaching a very busy year of sequential clinical data readouts from ALS, renal transplantation, IgAN, and islet cell transplantation. With that, I'll turn the call over to Steve Perrin, our President and Chief Scientific Officer, to review our lead asset and clinical indications. Steve? Thank you, D.A. As a brief reminder, our lead asset, AT-1501, is an IgG1 anti-CD40 ligand antibody lacking Fc effector function. Physiologically, the interaction of CD40 ligand and CD40 results in T and B-cell clonal expansion, antibody production, and secretion of pro-inflammatory cytokines that amplify an immune response. The CD40/CD40 ligand pathway is an attractive drug development target because the engagement of these receptors plays a pivotal role in immune system activation by mediating both antibody and cellular immune responses. Our programs are centered around development of antagonistic antibodies that target the ligand rather than the receptor, since inhibition of the ligand has shown greater efficacy in preclinical models of autoimmunity, as well as in the prevention of acute and long-term allograft transplant rejection in animal models. I'll begin my program updates with ALS, our most advanced indication. Previous research has found the costimulatory pathway to be an overactive pathway involved in more than half of people with ALS. Preclinical work has demonstrated that stopping or delaying immune system activation by inhibition of CD40 ligand can improve muscle function, slow disease progression, and improve survival in an ALS animal model. This provides strong scientific rationale for the development of AT-1501 in this challenging indication. We are in the midst of a 12-week open-label dose-escalating study, enrolling up to 54 patients at 13 sites in the United States and Canada. Enrollment in the fourth and final cohort is nearly complete, with 16 of 18 patients enrolled, and we remain on track to report data from this study in the first half of next year. Data that we are looking to obtain includes safety and tolerability, as well as multiple categories of biomarker endpoints, with each subject serving as their own control by comparing changes from baseline. In the first category of biomarkers, we'll assess CD40 ligand target engagement. Mechanistically inhibiting CD40 ligand function has profound effects on B-cell maturation, antibody production, and antibody class switching. We anticipate we'll be able to assess the inhibition of CD40 ligand target engagement by AT-1501 with biomarkers of B-cell function such as CXCL13. The second category of biomarkers are changes in pro-inflammatory chemokines and cytokines upregulated in people living with ALS. There is a long history of ALS data describing increases of pro-inflammatory signals in circulation, including TNF-alpha, MCP-1, IL-6, and EN-RAGE as examples. We anticipate the inhibition of CD40 ligand will result in an overall decrease of these pro-inflammatory markers. Finally, we will also assess exploratory endpoints, including changes in ALS, functional rating scale, or ALSFRS, respiratory function, and levels of neurofilament light chain in circulation. We consider these endpoints exploratory since we do not know if 12 weeks of therapy is sufficient time to see an effect. Of note, seeing an effect on neurofilament light chain would be particularly exciting because of this biomarker's association with neuron health and may allow us to be the first company to both show that a therapeutic can lower inflammatory biomarkers of ALS, as well as lower neurofilament light chain in patients where they are elevated. We're in the process of opening our first site in a phase I-B de novo transplant study in Canada, enrolling up to 12 subjects undergoing renal transplant. Our goal in this study is to demonstrate that AT -1501 is safe, achieves predictable drug levels, and can prevent allograft rejection when used as a preclinical replacement for CNIs as a component of an immunosuppressive regimen in this patient population. As D.A. mentioned, we'll also be looking at exploratory endpoints, including biomarkers. The reason we're looking to replace CNIs with AT- 1501 as the backbone of transplant immunosuppression is that CNIs have been shown to be beta cell toxic, thus causing diabetes, neurotoxic, thus causing neurological symptoms, including tremors, cause of hair loss, associated with increased risk of heart disease, infection, and cancer. Moreover, the chronic utilization of CNIs to prevent graft rejection has been associated with nephrotoxicity in up to 30% of patients after one year, 50% of patients after five years, and 100% of patients after 10 years. These toxicities can ultimately shorten graft survival, while others may lead to dose lowering or patient becoming less compliant, thus indirectly increasing the chance of rejection. By improving the safety and tolerability of first-line immunosuppression, we believe that AT-1501 has the potential to both improve patient quality of life and overall morbidity in the near term, as well as ultimately improve graft survival rates in the longer term. In parallel to this clinical trial, we have initiated a non-human primate kidney transplant study with AT-1501 as monotherapy, as requested by the FDA as a prerequisite to a potential future U.S. kidney transplantation IND. We've begun the transplants as planned and on track with our initial data from this study expected in mid-2022. Now turning to islet cell transplantation. We are focusing on people living with high-risk Type 1 diabetes who are on chronic treatment with exogenous insulin and experience severe swings in blood glucose levels, hypoglycemic unawareness, and associated comorbidities. Clinical trials conducted by the Immune Tolerance Network, as well as islet cell transplant in other countries, have demonstrated that islet cell transplants in patients with difficult-to-control Type 1 diabetes can maintain glycemic balance, reinstate metabolic control, and in some cases, even eliminate the need for exogenous insulin. However, the current use of calcineurin inhibitors, or CNIs, for the prevention of islet cell transplant rejection poses challenges as CNIs are toxic towards transplanted islets, potentially resulting in significant islet cell loss post-transplant, and thus potentially leading to the requirement for multiple islet cell transplants in order to reduce insulin dependence and improve hypoglycemic unawareness. Earlier this year, we initiated a phase II clinical trial of AT-1501 in Canada as a replacement for CNIs in a single center at the University of Alberta in Edmonton, which is historically the most active islet cell transplant site in North America. Unfortunately, COVID spikes in Alberta have led to the site temporarily suspending elective procedures, including islet cell transplants twice this year, most recently in August. In addition, due to the COVID environment, it's been challenging to find patients willing to undergo the procedure considering the necessity for immunosuppression. As a result, we announced last quarter that we were considering other geographies for potential expansion. We are proud to announce that the FDA has cleared our IND and provided us with a path forward for the clinical development of AT-1501 in islet cell transplantation in the United States. This IND clearance is particularly important since, one, it covers both AT-1501 as well as a method to purify cadaveric islets necessary for transplantation. Two, it represents the same dosing level as we are using in our Canadian transplantation studies and expect to use in future kidney transplantation studies. Three, provides us with another geography for islet cell transplantation. Finally, in Canada, we are happy to report that the site in Edmonton has recently reopened and is restarting to screen subjects for elective procedures. In terms of data, we presented additional non-human primate data at the International Pancreas and Islet Transplant Association World Congress in October. In a non-human primate model of islet cell transplantation, animals treated with AT-1501 versus those treated with standard of care, including CNIs, demonstrated longer graft survival, better graft function and glycemic control, and healthier, as demonstrated by post-transplant weight gain. I'll now turn to IgA nephropathy or IgAN. IgAN is the leading cause of glomerulonephritis. Onset usually occurs in younger adults, often while the patient is in their twenties, and is characterized by the presence of protein in the urine. Without effective treatment options available, up to approximately 40% of patients will progress to end-stage renal disease within 15-20 years, with patients who have the highest levels of urine protein being at the greatest risk of progression. The treatment for end-stage renal disease is lifelong dialysis or kidney transplant, both of which bear significant patient and healthcare system costs. There is currently no approved therapy for the treatment of IgAN. We believe there is a strong mechanistic rationale for pursuing CD40 ligand inhibition in IgAN, since AT-1501 has the potential ability to ameliorate pathologies associated with three of the four so-called pathological hits associated with the disease. The planned phase II study is an open label study expected to enroll up to 42 patients with a confirmed diagnosis of IgA nephropathy and significant proteinuria. Patients will be sequentially enrolled in two different dose cohorts and receive AT-1501 by IV infusion. The primary endpoint will be% reduction in proteinuria at 24 weeks as compared to baseline. There will also be a continued patient dosing out to 96 weeks to assess changes in rate of disease progression as measured by the estimated glomerular filtration rate or eGFR. We have elected to do an open-label study for this proof-of-principle study since historical IgAN clinical trials have demonstrated that proteinuria in IgAN patients would not be expected to change in any meaningful way over a 24-week assessment period. We anticipate having over 30 countries active and enrolling patients in multiple countries, particularly where IgAN is most prevalent. We expect to have our first CTA approved and site open by the end of the year, thereby allowing us to target getting initial data in late 2022. That concludes my clinical and scientific update. I'll now turn the call over to Paul for a financial update. Thank you, Steve. In addition to the financial results summarized in our press release, you can find additional information in our Form 10-Q, which we will file later today. The company reported a net loss of $9.8 million or $0.66 per share for the three months ended September 30th, 2021, compared to a net loss of $6.1 million or $5.51 per share for the same period in 2020. Research and development expenses were $7.7 million for the three months ended September 30th, 2021, compared to $615,000 for the same period in 2020. The increase in R&D costs primarily reflect clinical and CMC activities as we advance our AT-1501 programs. G&A expenses were $2.8 million for the three months ended September 30th, 2021, compared to $3.7 million for the same period of 2020. The decrease in G&A reflects prior year restructuring charges totaling $2.2 million, partially offset by increased personnel and stock-based compensation costs, legal and other professional fees in the current period. I'll turn to a few key financial metrics for the full year to date. The company reported a net loss of $25.7 million or $1.73 per share for the nine months ended September 30th, 2021, compared to a net loss of $16.9 million or $16.81 per share for the same period of 2020. Research and development expenses were $17.6 million for the nine months ended September 30th, 2021, compared to $3.1 million for the same period in 2020. The increase in R&D costs primarily reflect clinical and CMC activities as we advance AT-1501 programs. G&A expenses were $9.9 million for the nine months ended September 30th, 2021, compared to $9.7 million for the same period last year. The increase in G&A spend primarily reflects increased personnel costs, stock-based compensation expenses, legal and other professional fees. The company had $94 million in cash and cash equivalents as of September 30th, compared to $101 million in cash and cash equivalents as of June 30th, 2021. We expect our financial resources to be sufficient to fund operations as currently planned well into 2023, thereby allowing us to generate data across all of our currently planned trials and still have a year of cash on hand. With that financial update, let me turn the call back over to DA. Thank you, Paul. We have made significant progress during the third quarter, advancing our lead molecule AT-1501 with our nearly completing enrollments in our ALS phase II study and are receiving regulatory clearances to begin clinical trials for kidney transplantation in Canada and islet cell transplantation in the United States. We're now approaching what should be a very busy year of sequential clinical data readouts in 2022, including for our phase II ALS study, followed by interim data readouts for our islet cell transplantation, kidney transplantation, and the IgAN trials. With that, I will now ask the operator to begin our Q&A session. Operator? Thank you. We'll now be conducting your question and answer session. If you'd like to be placed in the question queue, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star two if you'd like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing star one. One moment please while we poll for questions. Our first question today is coming from Alethia Young from Cantor Fitzgerald. Your line is now live. Hey, guys, thanks for taking my questions and congrats on the forward progress here. I guess on the ALS front, I'm curious about if you think a neurofilament light chain could potentially be like a biomarker that, you know, maybe a regulatory body recognizes. To that point, kinda, can you frame kind of what kind of levels and what might be interesting, like what baseline levels people have and how you think about that, if there's any kind of information related to that? On IgAN, I guess, obviously there's some medicines in development there. I guess I kinda wanted to talk about how you think CD40 mechanism might be differentiated versus some of the other plays out there in the universe. Thanks. Alethea, thank you for the questions. Let me turn it over to Steve to talk about ALS and IgAN. Great question on neurofilament, Alethea. As you know, neurofilament light chain is a fairly new biomarker in neurodegeneration, not just ALS, but multiple sclerosis and Alzheimer's and others as well. Historically, we know from lots of studies that neurofilament light chain is elevated in adults with ALS, but the levels are very variable, and they tend to correlate with prognosis more than anything at this point, where at time of diagnosis, if you have high levels of neurofilament light chain, you tend to be a fast progressor, and if you have lower levels of neurofilament light chain, you tend to be a slower progressor. The only data we have with therapeutic intervention at this point is the recent data from Biogen with their antisense oligonucleotide that's been in phase II studies in adults with ALS. There, they showed decreases in neurofilament light chain, but they didn't necessarily correlate with clinical outcomes or survival. We all agree, I think, in the community in neurodegeneration, that neurofilament light chain is a marker of neuron health and ends up in CSF and circulation. Therapeutically, we need to demonstrate that does correlate with other biomarkers, such as pro-inflammatory markers as well as clinical outcomes, and that's one of the goal of the exploratory component of our study. Did that answer your first question on ALS? Yeah. That's helpful. It seems like, yeah, you just have to do the correlations, and it's not really hard and fast numbers and, you know, reductions. You kinda have to see what you see since the Biogen data kinda is a little bit confusing. Yeah, I mean, we're doing a 12-week study, which may not be a long enough duration of treatment to impact neurofilament light chain or clinical outcomes in ALS, but it would be an incredible finding if there was a correlation between reduction in proinflammatory markers, neurofilament light chain, as well as disease progression. We'd be the first company to really show that a change in proinflammatory markers with therapeutic intervention could correlate with a change in neurofilament light chain level. That would be a very big finding if we ended up hitting that one. Okay. That's helpful. Your question about IgAN with mechanism, I'll just review the scientific part of that answer. As far as differentiation goes, I mean, there's a pretty well-validated model of IgA nephropathy. As far as the pathophysiology, it's a multiple hit model, where the first hit is deficiencies in the enzymes that actually put appropriate sugars on IgA, and those deficiencies result in a improperly glycosylated IgA that is recognized by the immune system because it's foreign. That's really step two in the process, where antibodies are made and recognized and made by B- cells towards that improper sugared IgA. Ultimately, that results in immune complex formation and circulation. You get complexes that have recognized that protein that's not normal, and those end up getting deposited in the kidney over time. That's what results in kidney damage, proteinuria being present in the urine, and then progressive fibrosis and further damage to the kidney chronically over time. Other therapies that are in clinical development that are targeting various aspects are not hitting all aspects of that multiple hit, four-hit process. Blocking CD40 ligand, in theory, should hit three out of the four. Because it inhibits class switching at the IgM level, it should lower overall production of IgA, so there's not as much IgA around to be misglycosylated. Secondly, because blocking CD40 ligand blocks B -cell maturation, germinal center formation and antibody production, it will ultimately result in less immune complex formation and circulation 'cause you're not gonna make antibodies. You're not gonna recognize that misglycosylated IgA is foreign, so there'd be less immune complex formation and circulation. Then ultimately, even after deposition in the kidney, blocking CD40 ligand has been shown because it blocks proinflammatory differentiation of T cells and cells of the monocyte lineage, you'll get less immune cell infiltrate into the kidney, and thus you'll get less progressive damage and fibrosis as the result of deposition of immune complexes that might be there. We think that blocking CD40 ligand compared to other modalities in the clinic block three of the four hits. Great. That's helpful. Just another one. On the primate study, have you guys said how many primates you need to enroll or anything about that or where you're at in that? Thanks. We said that the guidance we received was that we needed a minimum of four non-human primates. As we've just announced today, we have begun the trial. We have begun doing kidney transplantations on the primates. Great. Thanks. Thank you. Our next question is coming from Thomas Smith from SVB Leerink. Your line is now live. Hey, guys. Thanks for taking the questions and congrats on all the progress. A couple questions. I guess first, just on ALS, you know, sounds like you're making some good progress there on enrollment. Just in thinking about some of the efficacy markers you're measuring in the study, obviously you called out neurofilament light chain, and I appreciate the color on that. In terms of some of the other exploratory endpoints, you know, things like change in ALS FRS, respiratory function, can you just help frame, I guess, what you'd be looking for within the twelve-week treatment period? Understand it's a, you know, it's a short treatment period, but it is. Is it essentially any signal on those functional endpoints would be considered, you know, a positive signal in your view? Maybe secondly, turning to the islet cell program and the U.S. IND clearance, can you just give us a little more color on how you're thinking about enrollment in the U.S.? Obviously islet cell is still considered an experimental procedure in the U.S. Just want to get your sense for how many study sites you think you could target and I guess your sense of expectations relative to your expectations for enrollment in Canada. Sure. Maybe let me start by turning it over to Steve to talk about ALS and then I can take over and talk about islet cell. Thanks a lot for your question, Tom. It's good to talk to you. Steve? Yeah. Tom, the question on ALS for the exploratory endpoints, the clinical endpoints, as you know, a 12-week study in ALS is fairly short. ALS is a really heterogeneous disease as far as disease progression, and at time of diagnosis, it's very difficult to understand the differences in progression rates. In a 12-week study, we'd probably be surprised to see significant changes in ALSFRS across the cohort or respiratory function or muscle function. Typically, those types of clinical endpoints are looked at as endpoints in longer studies. Six months, 12 months, 18 months are study durations where typically we'd be looking at those types of clinical endpoints for ALS. If we saw something, it'd be incredibly exciting, especially if it correlated with any of the biomarkers that we've described. In such a short study, it would be. I'd be surprised if we see something there. Does that answer your question, Tom? The primary focus here is going to be obviously around safety and tolerability, but then looking for changes in terms of the inflammatory biomarkers. Maybe Steve, do you wanna add some color on the inflammatory biomarkers we're looking at and what's been historically found in ALS? Yeah. The two types of markers that we're looking for that are directly related to immune cell function, one is target engagement. As I mentioned on the call, blocking CD40 ligand has a very profound effect on B-cell development and germinal cell formation, and it can really block many of the chemokines that are associated with that aspect of an antibody response. We can measure target engagement by looking at B-cell markers, including CXCL13, which is a potent chemokine associated with B-cell activation. For the pro-inflammatory markers, I mentioned TNF-alpha, IL-6, MCP-1 as examples, there's a long, long history going back decades of people measuring pro-inflammatory markers in patients with ALS in not only the clinical setting, but just in general studies. Those have been very well characterized. Because of the fact that those are elevated and they're pro-inflammatory, if we block CD40 ligand signaling and block pro-inflammatory differentiation of T-cells and B-cells, we should see a decrease in pro-inflammatory markers like TNF-alpha, IL-6, MCP-1, and others. Got it. Okay. Super helpful color on ALS. On islet cell. Great. On islet cell, you know, as you mentioned, islet cell transplant is considered experimental here in the U.S. A path forward for a clinical trial in this country is a big step forward for us. In terms of the design, we'll start right now, the plan will be to start with a single site in the States. In terms of enrollment, as you've seen with us, and as we've seen with some other ICT trials that are being done, enrollment has been relatively slow. What's good here is that we need few patients in order to be able to have some data that could be meaningful, and that data can come relatively quickly. We're looking forward to getting our first patients, hopefully enrolled in the U.S. and Canada. Once they get enrolled, once they get transplanted, what's nice is that within about 90 days, we'd be able to see how well the grafts are doing, and the impact that AT-1501 might be having in terms of protecting that graft and potentially allowing patients to be insulin independent. Okay, got it. In terms of opening the U.S. site, we just recently got the feedback from the agency, so, you know, we'd expect that site to open probably towards the middle of next year. Understood. All right. Thank you guys for taking the questions and thanks for the color. Thank you. As a reminder, that is star one to be placed into question queue. If you'd like to be placed into question queue, please press star one at this time. Our next question is coming from Matt Kaplan from Ladenburg Thalmann. Your line is now live. Oh, hi, guys. This is Raymond in for Matt. Thanks for taking our question and congrats on all the progress. Just, I guess, maybe just a quick question on the islet cell transplantation program. I was wondering, I guess, since you have a U.S. site and a Canadian site, would the data readout be kind of combined, or would it be kind of similar to the initial Canadian design for the U.S. trial? First, Raymond, thank you very much for the question. Let me turn that over to Steve or Jeff just to talk about the similarities between the programs. Yeah. Jeff here on the call. The protocols are slightly different, so why don't you explain the nuances? Yeah, sure. Thank you. Thanks, DA. Thanks, Steve. Hi, it's Jeff Bornstein. They are separate trials. The trial in Canada has been open for some time now, but as Steve talked about earlier, we ran into issues with COVID, and we're optimistic that now that that seems to be behind them, that they can start recruiting. The U.S. trial is a separate protocol, quite similar in design. Really, we're recruiting very similar patient populations. Although they're separate protocols and they're meant to be managed and analyzed separately, the totality of the data we can look at comprehensively to give us an overview of how well AT-1501 is performing in this population. We will be able to look at the comprehensive set of the data, even though they are separate studies. Thanks. That's very helpful. Just a quick follow-up. I was wondering, you mentioned the dosing was similar, and I was wondering, can you characterize kind of your interaction with the FDA and their thinking on how this islet cell program might be? Any additional color would be helpful. Thanks. What do you mean? Sorry, what do you mean by that question? Oh, sorry. I'm more like you mentioned that, it's kind of the clinical trial path in the U.S. is kind of still experimental. I was wondering if perhaps the FDA had changes in thinking or something kind of in that line or so, as such. Yeah. That has to do with the procedure itself and the purification of the cells. It's considered experimental here in the U.S. The FDA has taken a different approach than some other regulatory agencies around the world. That's not specific to our drug. That's more specific to the procedure. In terms of AT -1501, we're using the same dosing regimen and schedule in both Canada and the U.S. In Canada it's the schedule and dose that is the same that we're using for kidney transplantation as well as islet cell transplant. Okay, thanks. Thank you. Next question today is coming from Rami Katkhuda from LifeSci Capital. Your line is now live. Hey, guys. Thanks for taking my questions as well. I guess first, can you walk us through how you're thinking about dosing of AT -1501 in the IgA nephropathy trial compared to studies in ALS or transplantation? Secondly, is there a potential for the FDA to consider AlloSure and iBox as approvable endpoints in future renal transplant studies, or has there been no indication of that? Rami, thanks for the question. Maybe I can tackle both of them. In terms of your second question with regards to FDA guidance on the use of other endpoints, right now, the current guidance from the agency is to look at non-inferiority in terms of biopsy proven rejection. We don't know whether the agency will allow other endpoints in the future. Right now, that is what we're considering to be the primary endpoint. What we can do is use novel biomarkers and novel algorithms from an exploratory perspective in order to learn more about our asset and potentially in order to be able to help predict how well our asset might be doing or might be able to do versus standard of care. In terms of IgAN dosing, we haven't disclosed specifically how we'll be dosing in IgAN. But at a high level, the dose will be slightly higher, about the same, in the same range as for ALS. As you know, that dose level is lower than we're using for transplant. Got it. That makes a lot of sense. Thank you. Thank you. We've reached the end of our question and answer session. I'd like to turn the floor back over to management for any further closing comments. Thank you very much to everyone for joining us today, and we look forward to talking to you in the future as we continue to make progress as a company and with AT-1501. Thank you. That does conclude today's teleconference and webcast. You may disconnect your line at this time and have a wonderful day. We thank you for your participation today.