Greetings, and welcome to the Eledon Pharmaceuticals first quarter financial results conference call. At this time, all participants are on a listen-only mode. A question and answer session will follow the formal presentation. As a reminder, this conference is being recorded today, May 12th, 2022. I would now like to turn the conference call over to Paul Little, Chief Financial Officer of Eledon. Please go ahead. Good afternoon, everyone, and thank you for joining Eledon's first quarter 2022 operating and financial results conference call. I'm joined on today's call by 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 first quarter ended March 31st, 2022. You may access the release under the Investors tab on our company's website at eledon.com. 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 recent reports filed with the U.S. Securities and Exchange Commission. Now I would like to pass the call to Eledon's CEO, Dr. David-Alexandre Gros. DA. Thank you, Paul, and thank you all for joining the call today. We made important progress during the first quarter of 2022 and look forward to continuing this momentum through the remainder of the year. Our priority this year has been and remains executing on our four clinical trials in three therapeutic areas, neurodegeneration focusing on ALS, transplantation focusing on kidney and islet cell transplantation for type 1 diabetes, and autoimmunity focusing on IgA nephropathy or IgAN. Before I turn the call over to Steve to discuss our clinical development pipeline, I would like to provide a brief recap on our recent progress. In our phase II-A study of tegoprubart in adults with ALS, we completed dosing and visits for all subjects enrolled and remain on track to report top-line data from this study this quarter. In our phase II-A study in tegoprubart in adults with IgAN, we recently announced that we have begun dosing patients. We have regulatory approval for clinical trial sites in five countries with plans to expand to additional countries, and we are therefore on track to have six-month data available later this year. In transplantation, we now have active sites for kidney transplantation in Canada and the United Kingdom, have an open Canadian site for islet cell transplantation, and are preparing to open up a U.S. site for islet cell transplantation in the middle of the year. Similar to our IgAN trial, we plan to communicate our available transplant data at the end of the year. Finally, we recently published a meta-analysis demonstrating the benefits of targeting anti-CD40 ligand as opposed to targeting anti-CD40 receptor in non-human primate models of kidney transplantation. The meta-analysis found a median rejection-free survival of 352 days in anti-CD40 ligand-treated animals versus 131 days in the anti-CD40 treated animals and only six days in the untreated animal control group. Moreover, the median rejection-free survival after cessation of treatment was 230 days in anti-CD40 ligand-treated animals versus 60 days in anti-CD40 treated group. I'll now turn the call over to Steven Perrin, our President and Chief Scientific Officer, to provide more details on our development programs. Steve? Thank you, DA. As DA mentioned, we currently have four open clinical programs exploring the treatment of ALS, the prevention of allograft rejection, both in kidney and in islet cell transplantation, and IgA nephropathy. In the ALS phase II trial, all patient visits are now complete. All patient samples have been analyzed, and we're approaching database lock, thus keeping us on track to provide top-line data this quarter. The study is an ascending dose trial that evaluates four dose levels of tegoprubart administered for 12 weeks. Data from this study will include safety and tolerability of tegoprubart, 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 because 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 tegoprubart with biomarkers of B cell functions, including CXCL13 and others. The secondary biomarker categories, 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, MCP1, IL-6, IL-1, and EN-RAGE. We anticipate that in subjects with elevated levels, the blocking of CD40 ligand will result in an overall decrease of these and other pro-inflammatory markers in circulation. We anticipate in subjects with elevated levels of pro-inflammatory chemokines and cytokines, the blocking of CD40 ligand will result in an overall decrease of pro-inflammatory markers in circulation. As such, as part of our biomarker strategy, we'll look at a comprehensive panel of more than 30 chemokines and cytokines to assess dose response and ALS patient response to tegoprubart exposure levels. Finally, we will also assess exploratory endpoints, including changes in ALS functional rating scale or ALSFRS, and levels of neurofilament light chain in circulation. We deem these endpoints exploratory given the uncertainty that 12 weeks of therapy is sufficient time to see an effect on these endpoints. There are several critical objectives associated with the ALS trial. Confirmation of safety and tolerability through the highest dose cohort is important not only for the ALS program, but also for our other programs. The first objective beyond safety and tolerability is to demonstrate target engagement with exposure to tegoprubart. CD40 ligand is on the surface of activated T-cells in the context of antigen presentation and germinal center formation. During the process of germinal center formation, B-cell proliferation, maturation, and the generation of high-affinity IgG antibodies occur, induced by the expression of chemokines and cytokines such as CXCL13. As a result, based on CD40 ligand's mechanism, we expect tegoprubart to inhibit germinal center formation and B-cell maturation and thus decrease the generation of cytokines such as CXCL13. There is a significant body of published literature showing increased levels of pro-inflammatory chemokines and cytokines such as TNF-α, MCP1, IL-1, IL-6, and EN-RAGE, as well as others in patients with ALS. Based on years of experimental data elucidating the role of CD40 ligand activation in inflammatory induction, the inhibition of CD40 ligand signaling by tegoprubart should thus reduce pro-inflammatory cytokine production. In sum, an exciting positive outcome from this clinical program would be a demonstration of both target engagement and a reduction in pro-inflammatory cytokines. Observing target engagement and reduced inflammation would demonstrate tegoprubart's best-in-class immune modulatory potential in ALS. In addition to these biomarkers, we are collecting monthly ALS functional rating scores or ALSFRS, a common endpoint in ALS clinical trials, as well as measuring neurofilament light chain or NfL levels in circulation. NfL is a prognostic marker of disease progression in ALS, and at higher levels correlate with faster disease progression, but it's unclear at this point if levels of NfL will correlate with therapeutic benefit. Because of the relatively limited number of subjects and duration of the trial, however, we view these endpoints as exploratory. While not expected, given the relatively small size and limited duration of the study, if we are able to show a relationship between target engagement, reduction in pro-inflammatory markers in either a change in disease progression measured by ALSFRS or a reduction in NfL levels, we would consider this a tremendous win that further validates that a reduction in pro-inflammatory markers by tegoprubart may provide therapeutic benefit for people living with ALS. I'll now switch to discuss our transplantation studies. The cornerstone for the prevention of transplant rejection is the utilization of calcineurin inhibitors or CNIs. Although CNIs are associated with significant side effects including hair loss, beta cell toxicity causing new-onset diabetes, neurotoxicity causing neurological symptoms including tremors and decreased cognitive function, and CNIs are also associated with increased risk of heart disease as well as increase in infections and malignancies. Additionally, the chronic utilization of CNIs to prevent graft rejection has been associated with nephrotoxicity in up to 100% of patients after 10 years, which can paradoxically shorten graft survival in the same organs that CNIs are being taken to protect. By improving the safety and tolerability of first-line immunosuppression, we believe that tegoprubart has the potential to both improve patient quality of life and overall morbidity in the near term, as well as ultimately improve graft survival and rates in the long term. Only a few patients are needed to provide an early assessment of the prevention of acute rejection in the absence of CNIs, which have been the mainstay of immunosuppressive regimens to prevent acute rejection for the last 25 years. We have active sites in both Canada and the United Kingdom to conduct a phase I-B clinical trial of tegoprubart in kidney transplantation. This open label study is planning to enroll up to 12 patients undergoing renal transplant with primary endpoints of safety and pharmacokinetics as well as exploratory endpoints including biopsy-proven rejection, change in eGFR, and biomarkers of inflammation and kidney rejection. Our goal is to demonstrate that tegoprubart can be safely utilized to replace CNIs as part of first-line immunosuppressive therapy in solid organ transplantation and prevent acute and long-term solid organ transplant rejection without the use of CNIs. Switching over to islet cell transplantation, we have an open site in Canada and are expecting to open our first U.S. site mid-year. Here we are looking at patients with type 1 diabetes with hypoglycemic unawareness who experience significant swings in glucose levels that are associated with serious risk and comorbidities. Our goal is to evaluate tegoprubart in the backbone maintenance of anti-rejection therapy, similar to the rationale I just described for kidney transplant rejection. In ICT specifically, we are evaluating the number of patients that achieve insulin independence, and we are also assessing the number of cell transplants required to achieve independence. Our hypothesis is that by removing CNIs, which are directly toxic to the islet cells, and replacing it with tegoprubart, more patients could achieve better glycemic control and have fewer islet cell transplants. We are currently looking to enroll our first patients in both the renal and islet cell transplantation trials with the goal of providing available data from these two studies later this year. I'll conclude with our program in IgAN. IgAN is the leading cause of glomerulonephritis, a chronic autoimmune condition resulting in progressive kidney damage. 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. Currently, approximately 40% of patients will progress to end-stage renal disease within 15-20 years, indicating a significant unmet need because the treatment for end-stage renal disease is lifelong dialysis or kidney transplant, both of which bear significant patient and healthcare system costs. We believe there is a strong mechanistic rationale for pursuing CD40 ligand inhibition in IgAN, since tegoprubart has the potential to modify disease progression by reducing the formation of IgA via the inhibition of antibody class switching, a decrease in immune complex formation via the inhibition of B cell maturation, and a reduction in immune cell infiltration and subsequent complement activation in the kidney. In other words, we believe that tegoprubart may have a beneficial effect on both the upstream and downstream pathophysiology of IgAN. We are happy to report that we've begun dosing patients in our open label Phase 2a clinical trial in patients with IgAN. In this trial, patients with a confirmed diagnosis of IgAN and significant proteinuria will be subsequently enrolled in two different dose cohorts of up to 21 patients each. The primary endpoint will be% reduction in proteinuria at 24 weeks compared to baseline, and we expect to communicate available data later this year. With that, 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 $9.9 million or $0.69 per share for the three months that ended March 31st, 2022, compared to a net loss of $8.5 million or $0.57 for the same period in 2021. Research and development expenses were $6.6 million for the three months ended March 31st, 2022, compared to $5.6 million for the comparable period in 2021, which was an increase of $1 million. The increased R&D spend primarily reflects an increase in clinical development costs and costs related to the production of clinical trial materials as we advance tegoprubart into the global phase I and phase II clinical trials. General and administrative expenses were $3.2 million for the three months ended March 31st, 2022, compared to $3.3 million for the comparable period in 2021, a decrease of $100,000. As of March 31st, 2022, Eledon had $76.7 million in cash and cash equivalents, which we expect to be sufficient to fund all clinical trial operations as currently planned into 2024. With that financial update, let me turn the call back over to DA. Thanks, Paul. We remain focused on executing our trials, including generating our ALS data and opening more clinical sites to facilitate quicker patient recruitment to help us generate meaningful initial data in our trials this year. Our goal remains to develop a best-in-class therapeutic targeting the CD40 ligand pathway, which we believe can transform treatment options for patients living with ALS or IgAN or undergoing organ or cellular transplantation. We are proud of the progress across our clinical development programs. As we enter a potentially transformational period for Eledon, we look forward to the multiple potential value-creating milestones ahead of us. With that, I will now ask the operator to begin our Q&A session. Operator? Thank you. We will now be conducting a question-and-answer session. If you'd like to ask a question, please press star one on your telephone keypad, and a confirmation tone will indicate that your line is in the queue. You may press star two if you would like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment please while we poll for questions. Our first question is from Pete Stavropoulos from Cantor Fitzgerald. Please proceed. Hi, DA and team. Congratulations on all the progress on this past quarter. First question I have is, you know, with respect to a kidney transplant, I guess, you know, what are the next steps and, like, your thoughts on a potential interaction with the FDA and moving forward in renal transplant in the U.S., you know, given the initial results that you have from the non-human primate study. Will you share the ALS safety data with the agency to help support the IND? Hey, Pete, thank you for the question. In terms of our immediate plans in kidney transplantation, we now have, as I mentioned, sites open in Canada and the U.K. We're looking to begin enrolling patients into that trial. As you alluded to, during discussions with the U.S. FDA last year, the agency had asked us to do a non-human primate study of tegoprubart as monotherapy in kidney transplantation. We've successfully completed that study. The results showed efficacy consistent with what's been historically shown with anti-CD40 ligands. At this stage, what we'll do is look to complete the current ALS study so that we have that safety data available, and then re-approach the agency, including both the data that will be generated from ALS, as well as with the non-human primate data that they requested. Okay, thanks for the color. You know, another question regarding ALS. You know, just asking you to speculate if you think there are different mechanisms by which the nerve cells are dying in the ALS patients with like elevated pro-inflammatory cytokines, you know, versus those without elevated inflammatory cytokines. You know, do you believe you know you may be able to see a differential response between those patients with 1501 or tego? Can you also speculate if there's any way that you can potentially enrich for patients that may respond to 1501, perhaps a certain cytokine profile or levels of soluble CD40 ligand? Thank you. Let me turn that question over to Steve. Steve? That was a lot of questions, so I'll try to summarize as best I can. Clearly ALS is a very heterogeneous disease. It's a spectrum disorder, you know, all the way from people that have just motor deficits, all the way to people that just have cognitive impairment and a mixture of everything between. You overlap that there's also heterogeneity in the genetics associated with the disease. When we think about the impact of blocking inflammation, one of the common themes that's been is that inflammation is present in pretty much everybody with ALS. About 60% of people have a clear co-stimulatory signal, but most people at some point in time do show some level of pro-inflammatory chemokines or cytokines in circulation. No one's really learned how to leverage a biomarker set in inflammation to predict patient response. Obviously, one of the goals of our study is because of the mechanism of action of tegoprubart as a blocking CD40 ligand, which is one of the most important mediators of pro-inflammatory signaling. Our biomarker plan is to elucidate not only target engagement, which is very specific effort, but to also look at the pro-inflammatory markers that are not only associated with ALS, but also downstream markers associated with CD40 ligand activation. So it's potentially a very rich data set, but I don't know that we can speculate what we'll find out of it at this point as far as being able to predict drug response. That's part of the efforts of the data analysis plan. All right. Thank you for the added color, and, thanks for taking our question. Thank you. Our next question is from Nat Charoensook with SVB. Please proceed. Hi, this is Nat Charoensook on for Tom Smith. I have one quick question on the ALS data coming out in June. Do you expect to see significant or complete target engagement with doses used in the phase II-A trial? Do you think whether you need only a complete target engagement to see clinical benefits such as reduction in pro-inflammatory biomarkers? Thank you for the question, Matt. Let me turn that over to Steve, please. In the dose ranging that we're doing in the study and based on what we know about target engagement, with tegoprubart, we should hit full target engagement in our study over that dose range that we're looking at. I think ultimately the answer to your question is yes, we anticipate that we would. We won't know, of course, until we actually have database lock, look at exposure level, pharmacokinetics, and other aspects of the trial that are part of the safety tolerability goals. Got it. Thank you. Ultimately, what we'll look to do is to show both target engagement, and as we mentioned, the win would be able to then associate that with changes of inflammatory biomarkers. Our next question is from Rami Katkhuda with LifeSci Capital. Please proceed. Hi, guys. Thanks for taking our question. This is Myriam for Rami. Just two quick questions for us. With regards to the upcoming data in ALS, how large of a decrease from baseline are you hoping to see in these pro-inflammatory biomarkers to classify the study as a win? And, quickly, Horizon recently announced positive data with their anti-CD40 ligand and rheumatoid arthritis. Is this an indication you could envision pursuing with tegoprubart in the future? Thank you very much for the questions. Maybe in terms of your question with regards to ALS, I'll turn that over to Steve. I'll start as a result by answering your second question in terms of the positive data in RA that was demonstrated by Horizon Therapeutics. I think in the long term, there are many indications that we could consider using an anti-CD40 ligand. As we go back to when we first merged the companies to create what is now Eledon, RA was a natural potential use of an anti-CD40 ligand like ours. What we've done since was to really focus on indications where we felt that a smaller biotech could succeed in, both in terms of clinical development as well as commercially, because we'd be able to to potentially build the sales force that would be necessary. In order to do that, when we're thinking about our indications, we really focused on three things. We started by focusing on the biology and thinking about indications where the biology was well understood and the potential role of an anti-CD40 ligand therapeutic was well understood as well, so that we would have as high a likelihood of success as possible. We also focused on indications where there was a clear regulatory pathway, so that we could feel comfortable that the data would. We could generate would be supportive if we had positive data, potential approval. We prioritized indications, as I mentioned, that could be commercialized by a smaller company. Typically, orphan indications like the ones we're looking at, since these wouldn't require a large sales and marketing organization. We think RA is a good indication for a drug like ours and one in which our drug might have a good chance of succeeding. From a strategic perspective, RA is not indication that to date we focused on. Thank you. Makes sense. Thank you. For your second question, this is Steve. A great question on how we're thinking about changes in the biomarkers that we're looking at. When you visualize what the data analysis plan looks like for this study, it's multidimensional, and we've alluded to that, so I'll try to describe it in a little bit more detail. You know, obviously we're looking at target engagement. We're looking at multiple downstream pro-inflammatory markers that have been well described not only being present in people with ALS, but also related to CD40 ligand and inflammatory activation that would, if you block CD40 ligand signaling, you should mediate those. Also looking across dose response. It's a multidimensional analysis plan because there is going to be variability across doses, across patients, we've mentioned it's a heterogeneous disease, and across markers. I don't think it's as easy as saying what will we anticipate or what is the percent change we're looking for. It's more of a series of outcomes that we're looking for downstream of target engagement. We wanna see target engagement, which we can measure in circulation. We wanna see changes in the pro-inflammatory biomarkers that are downstream of CD40 ligand signaling, and some of them have been characterized in ALS. Then we wanna look at individual dose response across each patient cohort. Does that answer your question? She has exited the queue. Our next question comes from Matt Kaplan with Ladenburg Thalmann. Please proceed. Hi, Steve. Thanks for that explanation. Just to follow up on the prior question. Can you help us understand potential read-through for the ALS results to other indications that you're looking at? I guess obviously the kidney transplant and transplant and IgAN as well. Thanks, Matt. That is a terrific question and quite insightful. To your point, since we are looking at a range of biomarkers, inflammatory biomarkers associated with ALS, some of those are also seen in some other diseases. For example, both MCP-1 as well as soluble CD40 ligand have been associated with proteinuria in IgAN. There are other biomarkers that are associated with transplant rejection. We would look at the beginning, of course, safety and tolerability. There may be some other biomarkers that could help us understand how tegoprubart is impacting cytokines and chemokines that have been associated with other indications as well. Okay. Okay, great. No, that's helpful. One question on the IgAN study. I guess with you're looking at the percentage decrease in proteinuria as the primary endpoint, would you expect to see a corresponding impact on eGFR, if you see a reduction in proteinuria as well? Let me turn that over to Jeff. Jeff? Yeah, thank you, DA. Hi, Matt. It's complicated because the proteinuria predicts a slowing of the decline in eGFR. If you reduce proteinuria, you would expect to see less decline in eGFR, but not at the same time. The proteinuria predicts it in the future. Our study is designed to look at change in urine protein at 24 weeks, but we continue to dose the patients and follow them up for 96 weeks, and we'll be looking at the eGFR at the end of the trial. All right. Okay, great. Thanks for taking the questions. Yeah. Thank you. Ladies and gentlemen, this concludes our question-and-answer session. I would like to turn the call back to DA Gros for any closing remarks. Thank you, operator, and thank you all for joining us on today's call. Have a great evening. This concludes today's conference. Thank you for your participation. You may now disconnect.