Eledon Pharmaceuticals, Inc. (ELDN) Earnings Call Transcript & Summary

Greetings, and welcome to the Eledon Pharmaceuticals' Fourth Quarter and Full Year 2020 Operating and Financial Results Conference Call. [Operator Instructions] As a reminder, this conference is being recorded. I would now like to turn the conference over to your host, Mr. Jon Kuwahara, SVP of Finance. Please go ahead, sir.

Good afternoon, and thank you all for joining Eledon Pharmaceuticals' Fourth Quarter and Full Year 2020 Financial Results Conference Call. Joining me today are 3 members of our leadership team, David-Alexandre Gros, Chief Executive Officer; Steve Perrin, President and Chief Scientific Officer; and Paul Little, Chief Financial Officer. Earlier today, Eledon issued a press release announcing financial results for the quarter and full year ended December 31, 2020. You may access the release under the Investors tab on our company website, 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 Securities and Exchange Commission. I would also like to note that Eledon uses its investors relations website to publish important information about the company, including information that may be deemed material to investors. Financial and other information about Eledon is routinely posted and is accessible on the company's Investor Relations website at eledon.com. It is now my pleasure to pass the call to our CEO, Dr. David-Alexandre Gros. DA?

Thank you, Jon, and good afternoon, everyone. 2020 was a transformational year for Eledon, punctuated by our recent name change in January. Our new name reflects the company's overall evolution, including our evolution in therapeutic focus to transplantation, immune-related diseases and amyotrophic lateral sclerosis or ALS. This shift came as a result of a diligence and careful exploration of strategic alternatives to maximize shareholder value, which we concluded with the acquisition of Anelixis Therapeutics in September of last year. Through this acquisition, Eledon gained a new lead asset, AT-1501, a next-generation anti-CD40 ligand antibody. As Steve will review shortly, AT-1501 has unique attributes that we believe make it a potential best-in-class molecule targeting a well-validated pathway that has shown promise in multiple indications. Concurrent with the Anelixis transaction, we raised over $108 million in financing. We plan on using the proceeds from this offering to advance Phase II clinical trials of AT-1501 in up to 4 indications: renal transplantation, islet cell transplantation for the treatment of type 1 diabetes, autoimmune nephritis and ALS. During the fourth quarter, we achieved multiple important milestones. We successfully launched and commenced patient enrollment of AT-1501 into a Phase IIa clinical trial for the treatment of adults with ALS. We then received clearance from Health Canada to proceed with the initiation of a Phase II clinical trial of AT-1501 in islet cell transplantation for the treatment of type 1 diabetes. These are important trials for us as a company and for these respective patient communities. In ALS, average survival remains only 36 months after diagnosis. For type 1 diabetes, AT-1501 has the potential to help unlock a functional cure, starting with some of the most at-risk patients, those with a brittle phase of the disease. Finally, we expanded the talent on our team. In December, we appointed Dr. June Lee to our Board of Directors. A few weeks ago, we announced that Paul Little had joined as our Chief Financial Officer; and that Dr. Jeff Bornstein will be joining us in early April as our Chief Medical Officer. We are thrilled to have the opportunity to work with June, Paul and Jeff, and we look forward to benefiting from their extensive expertise. I will now turn over the call to Steve Perrin, our President and Chief Scientific Officer, to discuss our clinical programs in more detail. Afterwards, Paul Little will provide a financial update. Steve, please go ahead.

Thank you, DA. For those of you that are new to Eledon's story, I'll start off by giving a brief overview of our lead asset AT-1501, an IgG1 anti-CD40 ligand antibody locking Fc effector function. Physiologically, the interaction of CD40 ligand and CD40 results in clonal expansion, antibody production and secretion of pro-inflammatory cytokines that amplify an immune response. The CD40-CD40 ligand pathway has been an attractive drug development target for decades, because the engagement of these receptors plays a pivotal role in immune system activation by mediating both antibody and cellular immune responses through the modulation of germinal cell function, the clonal expansion of B cells and T cells, antibody production in class switching as well as the polarization of pro-inflammatory lymphocytes. The initiation of a robust immune response is mitigated by costimulatory signaling when CD40 ligand binds costimulatory receptors, such as CD40 on antigen-presenting cells, as these antigen-presenting cells are simultaneously presenting foreign peptides under MHC receptors to the T cell receptor on lymphocytes. We are focusing our efforts on the development of an antagonist antibody targeting the ligand rather than the receptor, since targeting the ligand has been shown to be more efficacious in preclinical models of autoimmunity and as well as the prevention of acute and long-term allograft transplant rejection. There may be 3 biological mechanisms for the benefit in preclinical efficacy showed by targeting anti-CD40 ligand over targeting the CD40 receptor. The first is differences in cellular distribution, since the ligand is more restricted in its expression present on platelets, endothelial cells and activated lymphocytes, whereas the receptor is present more broadly on all antigen presenting cells, including monocytes, macrophages, dendritic cells and specialized antigen-presenting cells and tissues. Second is that targeting both the receptor and the ligand inhibits B-cell activation and class switching as well as inhibiting the pro-inflammatory polarization of CD4 positive T cells; however, blocking CD40 ligand also inhibits other integral receptors, including CD11 receptors on antigen presenting cells, thus blocking the pro-inflammatory polarization of CD8-positive cytotoxic T cells as well. And finally, third, blocking the ligand also polarizes CD4-positive lymphocytes to become FoxP3-positive Tregs, and thus potentially creating a more tolerogenic environment in the context of preventing allograft transplant rejection as well as autoimmunity. We plan to advance AT-1501 in up to 4 Phase II clinical trials, the prevention of kidney allograft rejection, the prevention of islet cell allograft rejection, autoimmune nephritis and ALS. We selected these indications based on preclinical data that was generated with either our molecule or historical anti-CD40 ligand antibodies. Preclinical data in animal disease models suggest that blocking CD40 ligand is the most efficacious way to prevent acute and long-term transplant rejection in renal and islet cell transplant, and in some cases, can induce long-term transplant tolerance. Blocking CD40 ligand has been shown to be more effective at preventing allograft transfer reduction compared to blocking CD40 receptor. Importantly, targeting CD40 ligand is not associated with systemic lymphopenia. The ability to prevent acute and chronic transplant rejection in the absence of calcineurin inhibitors has the potential to transform the clinical management to preventing graft rejection, thus potentially mitigating the nephrotoxicity, cardiotoxicity, induction of diabetes and increased opportunities in infections associated with calcineurin inhibitors or CNIs. Chronic exposure to CNIs in organ transplantation is associated with an increase in type 1 diabetes. This is due to the toxicity of CNIs on insulin producing beta cells in the pancreas. Similarly, CNIs are toxic to transplanted islet cells and islet cell transplantation, up to 50% of the transplanted islet cells may die within days after transplantation in part due to the CNI toxicity thus exposing subjects to risk of transplant rejection and requiring multiple islet cell transplants in order to obtain a sufficient cell mass to eliminate the requirement for exogenous insulin. Adoption of islet cell transplant as a treatment option and potential functional cure for brittle diabetes is therefore been hampered in part by the toxicity associated with the CNIs that are required to prevent islet cell rejection, yet result in acute islet cell loss and dysfunction. We believe that as a result, replacing CNIs with AT-1501 may improve islet cell survival and clinical outcomes associated with islet cell transplant, thus potentially allowing for islet cell transplants to become a viable treatment option and even a potential functional cure for persons living with type 1 diabetes. In autoimmunity, we are focusing on autoimmune nephritis, which are autoimmune diseases of the kidney. There is a long history of preclinical and clinical data demonstrating that blocking CD40 ligand signaling ameliorates disease progression, modifies biomarkers of disease and improves renal function in diseases such as focal segmental glomerulosclerosis or FSGS, lupus nephritis and IgA nephropathy, for example. Moreover, soluble CD40 ligand often correlates with disease flares in autoimmune diseases such as these. Two clinical development program in ALS is based on positive preclinical data in a rodent model of ALS conducted at the ALS Therapy Development Institute, or ALS TDI. ALS TDI has screened approximately 500 compounds in rodent models of ALS. And according to ALS TDI, blocking CD40 ligand function is one of only a handful of drugs that slows down disease progression, improves survival and improves muscle function. Similarly, how soluble CD40 ligand can correlate with flares in autoimmune diseases, soluble CD40 ligand can also correlate with disease progression in ALS. Shifting to our clinical trials. Eledon initiated a Phase II study of AT-1501 in people living with ALS in October of 2020. The trial is a 12-week open-label dose escalating safety and biomarker study with 4 doses of AT-1501. This is the first multiple ascending dose study of AT-1501 in humans. Thus, the primary endpoint of the study is safety and tolerability. We will also assess multiple exploratory biomarker endpoints, including target engagement, pro-inflammatory signaling and circulation, such as TNF alpha and IL-6 and neurofilament light chain levels as a surrogate marker of neuronal health and disease progression. Finally, we'll be looking at some exploratory efficacy endpoints related to disease progression such as changes in ALS functional rating scale, or ALSFRS as well as respiratory function, although these are not expected to significantly change in the 12-week clinical study. Despite the recent peaks in COVID-19, enrollment in this trial continues to be on track, and we anticipate reporting on top line data from this trial in the first half of 2021. In November of last year, we received clearance from Health Canada to proceed with the initiation of a Phase II clinical trial of AT-1501 islet cell transplantation for type 1 diabetes. This is a single-arm open-label study with primary endpoints assessing safety and tolerability, glucose control and insulin independence, reduction in Hba1c, and graft survival in people with type 1 diabetes. We will also be assessing hypoglycemic awareness events as well as renal function. As we announced previously, we learned in early January that our study site in Canada voluntarily stopped performing islet cell transplants on a temporary basis because of COVID-19, before reinitiating and performing these transplants in February of 2021. Despite this COVID-related delay, we now expect our first patient to enroll in the second quarter of 2021 and we still anticipate that we'll be able to generate interim data in islet cell transplant as planned in the first half of 2022. In terms of renal transplantation, pending regulatory clearance, including from the FDA, we target to initiate the Phase II clinical trial at the end of the second quarter 2021. Finally, we'll discuss our specific fourth indication after we initiated the renal transplantation study. With regards to releasing data, we look forward to having presentations and posters at the American Transplant Conference in June, where we plan to present data from the Phase I clinical study of AT-1501 as well as preclinical data, including characterization of AT-1501 in in-vitro assays and non-human primate studies of AT-1501 in the prevention of islet cell transplant rejection. Let me now turn the call over to our Chief Financial Officer, Paul Little.

Thank you, Steve. In addition to the financial results summarized in our press release, you can find additional information in our Form 10-K, which we will file later today. The company reported a net loss of $5.9 million or $2.13 per share for the 3 months ended December 31, 2020, compared to a net loss of $4.1 million or $5.75 per share for the same period in 2019. Research and development expenses were $3 million for the 3 months ended December 31, 2020, compared to $1.3 million for the comparable period in 2019. General and administrative expenses were $3.3 million for the 3 months ended December 31, 2020, compared to $1 million for the comparable period in 2019. Now turning to a few key financial metrics for the full year. We reported a net loss of $22.8 million or $15.72 per share for the year ended December 31, 2020, compared to a net loss of $16 million or $24.42 per share for the year ended December 31, 2019. R&D expenses were $6.1 million for the year ended December 31, 2020, compared to $8.1 million for the year ended December 31, 2019. G&A expenses were $10.1 million for the year ended December 31, 2020, compared to $6.1 million for the year ended December 31, 2019. The company had approximately $114.2 million in cash and cash equivalents as of December 31, 2020, compared to $8.8 million in cash and cash equivalents as of December 31, 2019. Concurrent with our predecessor company's acquisition Anelixis Therapeutics in September 2020, we raised gross proceeds of $108 million through a private placement of shares to several highly regarded institutional investors. Based on our current clinical and operating plan, we believe our current cash resources will fund operations well into 2023. As is common for biotechs of our size and with our current S3 expiring in the coming months, we are filing a new S3 and establishing an at-the-market equity facility, or ATM. As DA indicated earlier, we are well financed to advance up to 4 clinical trials of AT-1501 and fund our operations as currently planned well into 2023. However, we believe this ATM is prudent financial housekeeping and gives us the flexibility to raise additional capital, should circumstances arise that would allow us to do so on terms favorable to the company. Eledon has no obligation to sell shares under the ATM, and we currently have no plans to utilize either the shelf or the ATM. With that financial update, let me turn the call back over to DA.

Thank you, Paul. We are excited to close out a transformational year in 2020, a year where we acquired Anelixis Therapeutics, completed a private placement financing with a blue-chip group of investors, advanced AT-1501 into our first Phase II trial in adults with ALS, and received clearance from Health Canada to proceed with initiation of a Phase II clinical trial of AT-1501 in islet cell transplantation for type 1 diabetes. Now with ALS enrollment continuing, multiple Phase II trials planned to start this year, pending clearances from regulatory agencies, and are planning to present data on our work to date, starting with the American Transplant Congress in June, we believe we have set the stage for numerous, potentially value-creating catalysts both this year and next. With that, I will now ask the operator to begin our Q&A session. Operator?

[Operator Instructions] Your first question comes from the line of Alethia Young with Cantor.

Congrats on a good amount of progress that you've made over 2020. A couple of things from me. Just one for AT-1501, can you talk a little bit about what autoimmune indications you might prefer, is lupus kind of the lead one? Or are there kind of others? Just thinking about where kind of -- I think there are now some lupus drugs in the market. The second question is, have there been -- have you provided like any kind of evidence around target engagement from either like [ SAT ] study or anything? And then the last question is just, can you just talk a little bit about kind of the dynamics which have been underpinning transplant trials during COVID?

Alethia, it's DA. Thank you very much for the questions. So maybe I'll start with the first one, and then I'll turn it over to Steve to talk about target engagement as well as ongoing dynamics. In terms of the autoimmune indications, we are looking at indications in autoimmune nephritis. So as we mentioned, autoimmune disease of the kidney. There are 3 primary types of autoimmune nephritis that we're considering, lupus nephritis, which you mentioned, as well as FSGS and IgA nephropathy. There's a good amount of historical preclinical data in the space of using anti-CD40 to tackle these indications. And at this stage, considering that this would be our potential fourth trial that we'd be starting, we haven't finalized, which specific indication we'd be going after. In part because, as you mentioned, this is a rapidly evolving field. So with that, let me turn it over to Steve to talk about target engagement as well as what we're seeing with COVID-19 impact.

Sure. Thanks, DA. So on target engagement, Alethia, we did in our Phase I study at the highest dose, just 1 of the doses, 8 mg/kg, doing immune challenge with KLH. And we showed that we can attenuate an immune response for the KLH challenge. We completely attenuated it in 2 of 3 people. So that was a very good demonstration to us that we had target engagement because, we completely blocked an antibody response to a foreign antigen. On the third question as far as COVID-19 impacting transplant studies, I guess there's a couple of pieces of data there. So although the site in Canada in Alberta did shut down temporarily for islet cell during the peak of what we consider the COVID spike very early in the year this year. They reopened up their site as soon as they felt that COVID-19 was better managed up there at that point. We also did look into the impact of COVID-19 in the first half of last year, particularly in the context of renal and liver transplant. And amazingly enough, sites learned to mitigate the risk of organ transplant pretty quickly during spikes. And given the precious nature of matching recipients and donors in the context of organ transplant, sites, for the most part, did very well mitigating those risks and did not really stop performing those procedures. So I think we're anticipating the same thing here as the vaccine rolls out. I think sites have already had an experience on how to manage COVID-19 last year, and I think they're doing a better job with that. And I think that they're going to manage that fairly effectively as far as we can tell.

Our next question comes from the line of Rami Katkhuda with LifeSci Capital.

I guess to start you've shown some very compelling preclinical data with AT-1501 in ICT. Can you kind of walk us through how translatable the nonhuman primate model has been in transplantation?

Thanks, Rami. Let me turn that over to Steve.

I mean with the specific question and translatability to the clinic based on preclinical transplant data, the only data point we have currently for blocking the pathway would be Novartis's molecule, Iscalimab. And so anti-CD40 as well as anti CD40 ligand antibodies have been tested going back 30 years preclinically in multiple species, demonstrating that they can prevent both acute and long-term transplant rejection. But Iscalimab, Novartis' anti-CD40 antibody is the first antibody with substantial data in renal transplant. They reported out their Phase II data last year showing noninferiority to standard of care. So that's the first good sign of translatability of blocking this pathway in the context of organ and cellular transplant.

That's helpful. And then one more, if you don't mind. But with regards to ALS, is neuro inflammation present throughout the course of disease or more so during periods of progression?

So unlike autoimmune diseases like lupus where flares and then holiday periods, if you want to call them that, are very common, and people can become fairly asymptomatic during non-flare periods. ALS is much more progressive of a disease once symptom onset starts. And so in the longitudinal studies that have been completed in ALS, the inflammatory signature that we see is measurable throughout disease course. And that's probably due to the fact that it's a more progressive disease.

Our next question comes from the line of Thomas Smith with SVB Leerink.

Congrats on all the progress. Maybe you could just talk about your planned data presentation at the American Transplant Congress here in June. What are you expecting to present? And what can we expect to learn about AT-1501 at the conference? And then secondly, on the islet cell trial, congrats on getting the green light to resume recruitment there. I know you're targeting a total enrollment of around 12 patients into the study, but it's an open-label trial, and you've guided to taking an interim look at the data, I think, in the first half of 2022. How many patients do you think you'll need for the interim? And what are you looking for specifically in that analysis?

DA, do want me to take the conference question first?

Yes, why don't you do it.

You want me to do both?

Okay.

So we submitted 4 abstracts to the American Transmit Congress and really excited. We actually got all 4 of them accepted. So 2 of them got accepted for presentations and 2 of them got accepted for posters. And so we're really going to unveil the whole history of AT-1501, which we've never published. So the first poster is going to talk about design of the antibody, in-vitro characterization for Fc effector function, in-vitro data to demonstrate lack of platelet activation, and other cell-based assay showing functional activity of the antibody in blocking an immune response. So that was kind of the first part of making the antibody and making sure it had the binding efficiency and everything else that we wanted in the antibody. The second poster is focused on the nonhuman primate tox data. We did 3 different nonhuman primate studies. We did a PK study just to look at -- quickly look at pharmacokinetics of the antibody in primates. The second study was a 12-week tox study. And then the third study was a 6-month, 26-week tox study. So we'll be presenting all of that data in the second poster. The 2 presentations, one of them is focused on work that was done by Norma Kenyon at University of Miami. It's the islet cell transplant data in her nonhuman primate model. And actually, Norma is going to present that data herself. And then the other presentation is a presentation of all of our Phase I data that was primarily in healthy volunteers, but with 1 cohort of ALS patients, and I'm presenting that presentation. The Congress hasn't giving out the full agenda yet, so I don't know what days and times those are. But I heard that they're coming out the first week of April. So either way this week or next week, we should have better ideas on days and the timing. DA, do you want me to answer the second question or do you want to take that one?

Please, go ahead.

So for the interim analysis that we're planning for next year, we think that if we can look at interim data with about 4 subjects. With 4 subjects of people that are at least 90 days post transplant, that's going to provide a lot of valuable information for us. As you can imagine, we're focusing on a patient population of type 1 diabetes that's been on exogenous insulin for a very long period of time, decades. The islet cell transplant allows us to very quickly look at islet cell function noninvasively, because we can look at C-peptide levels. We can monitor if we get these people off of exogenous insulin with a single islet cell transplant, rather than historically with calcineurin inhibitors. It often takes 2 or 3 transplants to get people a big enough islet cell mass that survives. In order to get them off exogenous insulin, we're hoping to decrease that number. And typically, surgeons will evaluate that at around 75 to 90 days post transplant. So we'll have a pretty good idea, not only of islet cell function, we'll know if we've gotten people off exogenous insulin post transplant. And then long term, we're going to be looking at other outcome measures that are really important to patient quality of life, such as have we modulated the number of glycemic awareness events that people encounter over some period of time. We'll be looking at continued long-term islet cell function. Clearly, we're still looking at safety and tolerability in studies like this, but with 4 subjects, we should get a pretty good idea about islet cell function and the ability to get people off exogenous insulin.

Congrats on the upcoming data presentations, looking forward to that in June.

Our next question comes from the line of Matt Kaplan with Ladenburg.

Just wanted to dig in a little bit further, Steve, perhaps, if you could. In terms of 1501 and how it differentiates potentially from other programs targeting CD40 or really CD40 ligand and how you see it kind of perhaps separating from those?

So Matt, we look at those with 2 different questions. So I'm going to answer them sequentially. The first one is really what do we think the difference is between targeting the ligand and the receptor. And the second one is how do we think AT-1501 might be different than the other antibodies that are out there. Is that correct?

Yes, exactly. Yes.

So on the first one, we think about it in a few different ways. We know based on 20 to 30 years of working on the receptor ligand pathway, that they're both really critical to mediating full immune function. However, we do know that these receptors in the ligand are expressed very differently in the body. CD40 ligand has a much more restricted expression pattern. It's on platelets, endothelial cells and activated lymphocytes, whereas the receptor is much more ubiquitously expressed. It's on every antigen presenting cell in your body, B cells, monocytes, macrophages, dendritic cells, and every one of your tissues has specialized antigen presenting cells, including your gut and your skin. So when you think about the biodistribution of antibodies that are blocking the ligand and the receptor, we're probably going to see some differences on receptor occupancy and dosing in order to block the receptor versus the ligand. The second one, biologically is that we always think that CD40 ligand only binds CD40 on antigen-presenting cells to activate co-stimulatory signaling and that's not true. It actually binds to multiple integrins, multiple different receptors on antigen presenting cells, and as an example, it also binds CD11. So when you block CD40 ligand signaling, you're blocking multiple different co-stimulatory pathways. And in the context of CD 11 as an example, it's really important for the activation of CD8-positive cytotoxic lymphocytes in the context of acute transplant rejection. So when you block the ligand, you're getting multiple different costimulatory blocks, whereas you don't get that with the receptor. And then the third one that's very unique to blocking CD40 ligand, and it's because it's expressed on CD4 positive lymphocytes. When you block CD40 ligand on CD4 positive cells, not only are you blocking the pro-inflammatory differentiation, you actually convert them into Treg cells, which are tolerogenic T cells that secrete IL-10, TGF beta and other chemokines that create a localized tolerogenic environment. So again, this is one of the reasons why we think blocking the ligand might be very effective compared to blocking the receptor in the context of preventing acute and long-term transplant rejection. So as far as your second -- does that make sense?

Yes. No, that's very helpful. Yes.

So as far as your second question on differentiating AT-1501 from some of the other antibodies, there's lots of different antibody formats that are out there, if you will, or I should probably call them biological formats to block the ligand. So we went with a full antibody. AT-1501 is a full IgG1 with point mutations in the Fc to cripple Fc effector function. But [ Eledon's ] experiments back in the early 2000 showed that you could block CD40 ligand signaling without Fc effector function by using FABs, so just the head of an antibody. And then to make them have better drug like properties, people pegylate them, and that's where UCB has done with their pegylated FAB that's been in the clinic for lupus. You can work with domain antibodies, which are single chain antibodies that don't have Fc effector function. Abatacept is an example of that. So domain antibodies commonly made by BMS is another way to do that. And then you can make fusion proteins. So in the case of Yellow Bio, they made a Tn3 fusion protein with Tn3 scaffolds that have high affinity to blocking the ligand and then to give them better drug like properties. They fuse them to things like human serum albumin to give them a better half-life. So those are the ways -- those are the other formats that are currently out there. And of course, we went with a full antibody, because of manufacturability and predicting that an antibody has very good predictable drug like properties. And in the case of AT-1501, those things have really panned out for us. We have a very good robust manufacturing process with Lonza, high-yield cell line, and our antibody has a half-life of 18 to 26 days, which is 2 to 2.5x longer than some of the other formats that are out there.

Okay. Yes. And then you provided some details in terms of the interim look in the islet cell transplant. How should we think about the study that you plan to initiate, I guess, in the middle of this year's second quarter for renal transplantation? And will you take an interim look there? And what should we look for, if you do?

Yes. So the plan is to try to design the study that we'd be able to take an interim look during that trial as well. It would -- for obvious reasons, we wouldn't look at the primary endpoint, but likely rely on biomarkers for that look. But right now, all of that is really pending ongoing regulatory discussions, starting with getting the regulatory clearance to proceed. So soon as we have that, and we begin to launch the trials, we'll come back and provide just a lot more color in terms of trial design and what to expect when. But the goal is to be able to have an interim look during that trial as well.

[Operator Instructions] Our next question comes from the line of Vernon Bernardino with H.C. Wainwright.

Congrats on the progress. Looking forward to the gates being opened for the studies to advance this year. Most of my questions have been asked. Just one follow-up regarding the pursuit of autoimmune nephritis indication. What work still needs to be done? Because as you've guided, you will look to initiate the Phase II with 1501 in late 2021.

So in terms of the ongoing work, I think the preclinical work that we've done is largely complete in terms of what we expect to need to do. The cadence here has more to do with our company size and being able to launch trials in a way where we can manage them effectively. So we started with ALS. We then moved into islet cell transplant. We're now in the process of -- we're now in the process of hopefully being able to start renal transplantation. And once we have that ongoing, we'll then be able to shift focus and resources to the fourth indication. So the field is progressing quite quickly, and we're seeing even some drugs get approved, for example, in lupus nephritis for the first time. We're following those evolutions carefully as we consider which specific subindication of autoimmune nephritis we should focus on. And so it really has to do with the strategic decision tied around the timing when we have to make that decision.

Is part of that requiring Jeffrey Bornstein to get onboard and hiring a team?

So we have a team that we've been building, and we've been expanding our team since the acquisition of Anelixis. So today, we have a well-built out clinical development and operations organization, but Jeff will definitely be an important addition to the team.

And early insights you can provide as far as Vertex efforts with islet transplantation?

Yes. So Vertex, which used to be acquired a company called Semma. And what they're looking to do is stem cell -- stem cell derive islet cells. So it's -- while we're looking at the therapeutic approach, so thinking about the immunomodulator immunosuppressive regimen that needs to be given concurrently with islet cell grafts. Vertex is looking at the supply of those grafts and working on developing an approach where those cells could be manufactured as opposed to needing to come from a donor. Since -- especially with the first generation cells, those continue to need -- our understanding is that those continue to need immunosuppression. The 2 approaches are quite complementary. So that if -- since any issues that may exist with CNIs in the past, one may expect that they would occur again even with Vertex's or other companies that are doing similar things cells.

Ladies and gentlemen, we have reached the end of the question-and-answer session. And I would like to turn the call back to Dr. Gros for closing remarks.

Thank you again to everyone joining us on our first quarterly call as Eledon Pharmaceuticals. We look forward to the continued advancement of our programs and to keeping you updated of our progress. Have a great evening.

This concludes today's conference. You may disconnect your lines at this time. Thank you for your participation.