ELDN - NASDAQ

Greetings. Welcome to the Eledon Pharmaceuticals Reports Second Quarter 2021 Financial Results Conference Call. At this time, all participants are in a listen-only mode. A question-and-answer session will follow the formal presentation. Please note that this conference is being recorded. I will now turn the conference over to your host, Paul Little, Chief Financial Officer. You may begin.

Good afternoon, and thank you for joining Eledon Pharmaceuticals' Second 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 second quarter ended June 30, 2021. 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 today during this conference call related 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 SEC on our website under the Investor tab. We encourage you to review these documents carefully. It is now my pleasure to pass the call over to our CEO, Dr. David-Alexandre Gros. DA?

Thank you, Paul, and good afternoon, everyone. We continue to make significant progress during the second quarter, advancing our lead molecule AT-1501. I am excited by the promise offered to us by AT-1501 as a potential therapeutic for organ or cellular transplantation, ALS and serious immunological diseases where patients face limited treatment options. We plan to advance AT-1501 in up to four clinical trials, one, ALS; two, the prevention of kidney allograft transplant rejection; three, autoimmune nephritis, starting with IgA nephropathy or IgAn; and four, the prevention of islet cell allograft transplant rejection for the treatment of Type 1 diabetes. We selected these indications based on preclinical data that was generated with both our molecule, as well as historical anti-CD40 ligand molecules. Steve will give more details about each of these, but at a high level, our recent progress is as follows: In ALS Phase 2 biomarker study, our trial is progressing according to plan. We are completing enrollment of our third of four cohorts and top-line data is expected in the first half of 2022. In renal transplantation, we previously communicated that the USFDA requested that we provide AT-1501 specific renal transplant data in non-human primates prior to initiating a clinical trial in renal transplantation in the United States. And that as a result, we would both look to complete the FDA requirements as quickly as possible, as well as look to initiate a clinical trial outside of the United States. In terms of our US regulatory requirements, we reached alignments with the FDA to conduct a preclinical renal transplant study evaluating AT-1501 as monotherapy in four non-human primates. We anticipate initiating this non-human primate study in collaboration with an academic collaborator with vast transplant experience next quarter with completion of the study in mid-2022. With regards to our ex-US clinical trial, we received a no objection letter from Health Canada in response to our clinical trial application proposing to evaluate AT-1501, replacing tacrolimus as an immunosuppressive regimen component in patients undergoing kidney transplantation. The trial is expected to be initiated in the last quarter of 2021 with interim data readouts expected to begin in late 2022. In autoimmune nephritis, we will be targeting IgA nephropathy. There is a long history of preclinical and clinical data demonstrating the blocking CD40 ligand signaling ameliorates disease progression, modify its biomarkers of disease and improves renal function in autoimmune diseases of the kidney such as IgAn. We selected IgAn, because of the unique approach than in anti-CD40 ligands brings in going after both the cellular and the antibody mediated portions of disease pathophysiology. In islet transplantations for Type 1 diabetes, earlier this year, we initiated a Phase 2 clinical trial of AT-1501 as a replacement for tacrolimus. 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 allowing for the resumption of these procedures. Unfortunately, until late June, vaccination rates in Canada remains far behind those in the United States and the number of islets cell transplant procedures performed remained much lower than pre-COVID. As a result, we are still waiting for first patient to be enrolled. Steve will discuss the steps we are taking to address the pace of this study including making it easier for patients to enroll and looking at additional geographies where islet cell transplants are performed. Steve will also provide an update on AT-1501 in non-human primate islet cell data that was presented at the American Transplant Congress in June. I will now turn over the call to Steve Perrin, our President and Chief Scientific Officer to discuss our clinical programs, afterwards, Paul Little will provide a financial update. Steve, please go ahead.

Thank you, DA. 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 clonal expansion, antibody production and secretion of pro-inflammatory cytokines that amplify an immunoresponse. The CD40 ligand pathway is an attractive drug development target because the engagements of these receptors plays a pivotal role in immune system activation by mediating both antibody and cellular immune responses. We are focusing our efforts on the development of an antagonist antibody targeting in the ligand rather than the receptors and targeting the ligand has been shown to be more efficacious in preclinial models of autoimmunity, and as well as in the prevention of acute and long-term allograft transplant rejection. I'll now dive into four targeted indications, ALS, kidney transplant, autoimmune nephritis and IgAn in particular, and finally, islet cell transplant for the treatment of Type 1 diabetes. Eledon’s ALS trial is a 12-week, open label, dose-escalating study enrolling at 13 sites in the United States and Canada. Our enrollment continues to be on track and we have now enrolled 17 of 18 patients in the third cohort with the last patient in this cohort currently completing the screening assessments. We expect to complete enrollment of the fourth and final cohort by the end of the year enabling the reporting of to-line data in the first half of 2022. This data will consists of safety and tolerability data, 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 will assess biomarker to CD40 ligand target engagement. Mechanistically blocking CD40 ligand has profound effects on B cell maturation, antibody production and antibody class switching. We anticipate that we'll be able to assess CD40 ligand targeting engagement by AT-1501 with markers of B cell functions 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 enraged. We anticipate blocking of CD40 ligand will result in an overall decrease of these ALS related pro-inflammatory markers. Finally, we will also assess the other exploratory endpoints including changes in ALS functional rating scale, or ALS FRS, respiratory function, and the levels of neurofilament light chain and circulation. We consider these exploratory since the short duration of the study of 12-weeks may not provide sufficient time to see changes in clinical endpoints or changes in neurofilament light chain. Moving on to renal transplant, we recently announced that we received a no objection letter from Health Canada to proceed with our first safety, pharmacokinetics and efficacy study of AT-1501 in six to twelve subjects undergoing renal transplant. This is an important study to demonstrate that AT-1501 can safely be utilized to replace calcineurin inhibitors as part of first-line immunosuppressive impressive therapy in solid organ transplantation and prevents acute and long-term solid organ transfer rejection. We expect that replacing calcineurin inhibitors will result in measurable improvements in the quality of life for people undergoing organ transplants and eliminate the nephro toxicity, cardio toxicity, neuro toxicity, induction of Type 1 diabetes associated with chronic exposure to CNIs. This study will be an open-label, multiple site study, which we anticipate initiating by the end of the year with initial interim data expected in late 2022. Endpoints will include biopsy-proven acute rejection, antibody mediated rejection and biomarkers of rejection, as well as safety and PKPD endpoints. In the terms of starting a trial in the United States, we announced in April that the FDA requested that we provide AT-1501 drug-specific renal transplant data in non-human primates prior to potentially initiating a clinical trial in renal transplantation in the United States. We have now reached agreement with the USFDA that this study will consist of evaluating AT-1501 as monotherapy in four non-human primates. To do this, we will be collaborating with a world-renowned expert in the development of new treatments and protocols for the prevention of allograft transplant rejection. We anticipate starting this study in the fourth quarter with the completion in mid-2022. These data will continue to build on the strong foundation that has already been established for AT-1501 in over 60 non-human primates across multiple species including preclinical efficacy data in a non-human permit model of islet cell transplant. Moreover, multiple historical anti-CD40 ligand molecules similar to AT-1501 have demonstrated preclinical safety and efficacy in hundreds of non-human primates, including specifically in a non-human primate model of renal transplantation. In autoimmunity, we will initially focus on IgA nephropathy, one of several autoimmune nephritises which are autoimmune diseases of the kidney. There is a long history of preclinical and clinical data demonstrating the blocking CD40 ligand signaling ameliorates disease progression, modifies biomarkers of disease, and improves renal function in diseases such as focal segmental glomerulosclerosis, lupus nephritis, and IgA nephropathy. Moreover, a soluble CD40 ligand often correlates with disease flares in autoimmune diseases such as these. IgA nephropathy or IgAn is the leading cause of glomerul nephritis, disease manifestation and clinical presentation involves renal dysfunction characterized by proteinuria with a slow relentless with approximately 30% to 40% of patients ultimately reaching end-stage renal disease. The standard-of-care for end-stage renal disease is dialysis or kidney transplant which represents a significant economic burden, as well as a major impact on a patient's quality of life. IgAn is diagnosed via renal biopsy and the presence of IgA containing immune complex deposition in the kidney. At time of diagnosis, renal dysfunction is highly variable with proteinuria levels greater than one gram per day. The formation of glycosylated IgG1 immune complexes in the kidney is hypothesized to be a multi-hit pathogen across pathological process. Hit 1 is the aberrant glycosylation of IgA due to errors in the enzymatic glycosylation of IgG1. Hit 2 is the recognition by the immune system that this aberrant form of IgG1 called Gd-IgA1 is foreign and auto antibodies are generated in circulating gDiGG1. Hit 3 is the formation of Gd-IgA1 immune complexes in circulation and Hit 4 is the deposition of these immune complexes in the mesangial cells of the kidney resulting in immune cell infiltration, cytokine production, complement activation leading chronic loss of kidney function, kidney damage, proteinuria and end-stage renal disease. There is no FDA approved therapies for IgAn, guidelines for current standard-of-care for people with IgAn suggest the use of certain classes of anti-hypertension medications to modulate hemodynamic stresses on the kidney resulting in an improved glomerular filtration rates and reduced proteinuria. Treatment with either angiotensin converting enzymes or ACEs or angiotensin receptor blockade, ARBs the standard-of-care of proteinuria is greater than one gram per day and suggested if it’s greater than zero point five grams per day. The treatment with ACEs and ARBs, as well as molecules and clinical developments are focusing on Hit 4, but downstream pathological mechanism and the disease after immune complex formation in the kidney and decreased kidney function. The exciting opportunity for AT-1501 IgA nephropathy is that AT-1501 has the potential ability to ameliorate pathologies associated with Hits 2, 3 and 4. AT-1501 can prevent the production of autoantibody towards Gd-IgA1 referred to as Hit 2. This is due to the ability of AT-1501 to inhibit B cell maturation thus decreasing antibody production and preventing antibody class switching. The inhibition of antibody class switching at the IgM stage will not only decrease the month of IgG synthesized that will be available for improper act silanization, but it all also prevents the production of high affinity IgG1 antibodies that form the immune complexes. Blocking CD40 ligand has the ability to decrease immune complex in immune complex formation has been shown in multiple animal models of autoimmunity, as well as in the clinic, thus AT-1501 has the potential to reduce pathogenesis associated with Hit 3 immune complex formation. Finally, blocking CD40 ligand and Hit is pro-inflammatory polarization of T cells and macrophages and has been shown to decrease immune cell infiltrates and infiltration - inflammation in the kidney Hit 4. In conclusion, when IgAn’s pathpphysiologies taken as a whole,. AT-1501 has the potential to ameliorate immune cell infiltration subsequent complement activation in the kidney and improve kidney function. We plan to launch an international Phase 2 study by the end of this year and we'll provide more details including trial design when we enroll the first patient. Finally, in diabetes, 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 co-morbidities. Clinical Trials conducted by the Clinical Islets Transplantation Consortium, as well as islet cell transplants in other countries have demonstrated that islet cell transplantation in patients with difficult to control Type 1 diabetes maintains glycemic balance, reinstates metabolic control, and in some cases, even eliminates the need for exogenous insulin. However, the current use of calcineurin inhibitors or CNIs for the prevention of islet cell transplant rejection poses two issues. First, CNIs are toxic towards transplanted islets, potentially resulting in significant islet cell loss post-transplants and may lead to the requirement for multiple islet cell transplants. Indeed in published trials, islet cell transplant recipients typically require multiple transplants with the need for a second transplant, often apparent within approximately 90 days after the first transplant. At the American Transplant Congress in June this year, Dr. Norma Kenyon Director of the Diabetes Research Institute at the University of Miami presented data comparing an aggregated group analysis of animals receiving AT-1501 as either monotherapy or in conduction with induction therapy to animals on tacrolimus and conduction with induction therapy in a non-human primate model of isolate cell transplants. Her findings indicated that animals on AT-1501 had significantly longer rejection free survival, significantly longer overall islet cell graft survival and maintain greater body weight compared to animals on tacrolimus. In addition, C-peptide levels were more times higher for animals treated with AT-1501 compared to animals treated with tacrolimus. In one group of animals receiving AT-1501 monotherapy at 10 mg per kg every 14-days, she decreased the dosing frequency by half starting on day 224 and one of these animals continued with graft function well over 400 days which according to her represented a functional cure of Type 1 diabetes in this animal. Finally, she reported that animals on tacrolimus were more susceptible to life-threatening CMB infections, a common toxicity associated with CNIs. As a result of data such as this, we believe that replacing CNIs with AT-1501 may improve islet cell survival and clinical outcomes associated with islet cell transplant, thus potentially allowing for islet cell transmit to become a viable treatment option and even a potential of function of cure for persons living with high-risk Type 1 diabetes. We currently have an active clinical site in Alberta, Canada seeking to enroll a single arm, open-label stud. Primary endpoints include safety and tolerability, glucose control, insulin independence, reduction of HBA1C, graft survival and function. We will also be assessing hypoglycemic awareness events, as well as renal functions. Unfortunately, Canada and the Province of Alberta were significantly impacted by COVID in the first half of this year and the roll out of vaccinations in Canada was until recently far behind the U.S. This significantly impacted the ability of the staff to work on site and maintain a normal process of patient screening enrollment for islet cell transplant procedures. Moreover, travel between provinces in Canada was seriously impacted, as well as the willingness of patients to take the immunosuppressants necessary for an elective transplant procedure. Taken together, the effect has been to very significantly reduce the number of islet cell transplants procedures being performed so far this year compared to pre-COVID. We are working with the site to facilitate patient recruitment into the study included by reaching out to more endocrinologists across the province in Canada, as well as by beginning to work on a ways to allow patients to receive drug closer to home, thus decreasing their need to travel. Separately, we have assessed the ability to expand the study to sites in Europe, but at pharma to-date they have experienced similar issues with Covid-19 as Canada. As the Covid situation continues to evolve, we will reassess the potential for international expansion. We are still targeting to enroll this trial as soon as possible, which would allow us to meet our goal of generating interim data and islet cell transplants in the first half of 2022. This is based on the timing to assess graft function in acute transplant rejection is 90-days post transplant on a patient-by- patient basis. With that, I'll turn the call over to Paul for our 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 $7.4 million or $0.50 per share for the three months ended June 30, 2021, compared to a net loss of $2.6 million or $2.74 per share for the same period in 2020. Research and development expenses were $4.2 million for the three months ended June 30, 2021, compared to $800,000 for the same period in 2020. The increase in R&D costs primarily reflects clinical and CMC activities as we advance our AT-1501 programs. G&A expenses were $3.7 million for the three months ended June 30 2021, compared to $1.3 million for the same period of 2020. The increase in G&A spend primarily reflects increased personnel and stock-based compensation costs, legal and other professional fees. Now turning to a few key financial metrics for the full year-to-date. The company reported a net loss of $15.9 million or $1.07 per share for the six months ended June 30, 2021, compared to a net loss of $10.8 million or $11.31 per share for the same period of 2020. R&D expenses were $9.9 million the six months ended June 30, 2021, compared to $2.5 million for the same period in 2020. The increase in R&D cost primarily reflects clinical and CMC activities as we advance our AT-1501 programs. G&A expenses were $7.1 million for the six months ended June 30, 2021, compared to $3 million for the same period last year. The increase in G&A spend primarily reflects increased personnel and stock-based compensation costs, legal and other professional fees. The company had $101.1 million in cash and cash equivalents as of June 30th, compared to $108.6 million in cash and cash equivalents as of March 31, 2021. We expect our financial resources to be sufficient to fund operations as currently planned well into 2023. Finally, subsequent to our acquisition of Anelixis in 2020, we undertook a strategic review on the Novus Pharmaceuticals’ legacy assets for Otitis Media. We recently concluded this review and determined that the best path forward was to terminate license agreements associated with these assets and return the rights to the original license holders. We did this in July. There was no financial impact with the return of these assets. With that financial update, let me turn the call back over to DA.

Thank you, Paul. We made significant progress during the second quarter, advancing our lead molecule AT-1501 and look forward to multiple potential upcoming milestones. This year, we expect to present AT-1501 non-human primate data at the International Pancreas and Islet Cell Transplantation World Congress Annual Meeting in October to initiate clinical trials, a clinical trial in the prevention of kidney transplant rejection and a trial in IgAn and to initiate a non-human primate kidney transplant study. We then expect to begin reporting data readouts from these trials starting in the first half of 2022 with ALS and islet cell transplantation for Type 1 diabetes, as well as the non-human primate kidney transplant study. With that, I will now ask the operator to begin our Q&A session. Operator?

Our first question comes from Alethia Young with Cantor Fitzgerald. You may proceed with your question.

Hi. This is Nina on for Alethia. Thanks for taking our questions. We are wondering for the islet cell transplantation program. If you had any idea, at least on when the first patient might be enrolled? And if you think that'll be in Canada or elsewhere in Europe? And how quickly do you think you combine the patients? And also if you can just remind us how many patients that you plan on recruiting? Thanks.

Sure. Hey, Nina. Thank you for the question. We are looking to enroll a first patient as soon as possible. Currently, the trial is only open in Canada and so, that's where we are focused. But as you heard, and as we discussed, we will look especially as COVID progresses to see whether there are ways to add additional countries to the trial, as well. What's nice here is that, we can begin to get data quickly since patients often need second transplant procedures within 90 days after the first transplant when they receive current standard-of-care, which could allow us to quickly see the fact that AT-1501 is having. What's nice here is that, we can get significant learnings with just a few patients. And so we plan on reporting the data that we have on the totality of patients that we'll be able to have enrolled in the first half of next year. Steve, let me see if you have anything that you'd like to add.

Yes, again, I mean, we are working hard with the site to get back up and running. They've had challenges with Covid-19 as everybody. The important thing about the islet cell transplant procedure as DA mentioned is the ability to fairly rapidly assess graft function on a subject-by-subject basis, which could still yield exciting data next year.

Okay. Thank you.

Our next question comes from Matt Kaplan with Ladenburg Thalmann. You proceed with your question.

Hey, guys. Thanks for taking the questions. I apologize if there is some background noise. We're just getting hit with a thunderstorm right now. I wanted to just dig in a little bit more to the renal transplant program. I guess, given the readouts that you expect for the non-human primates in middle of next year and clinical data late next year, when do you think you'll be able to start a U.S.-focused study and meaningful at transplant?

Thanks. Thanks, Matt. Why don't I turn that over to Steve to go through to go through the plan?

So I think that there was two questions here, Matt. One was about the no-human primate study and the other was about anticipation on moving into the U.S.? Correct.

Correct. Yes.

So for the non-human primate study, as we indicated, we had very specific guidance from the agency on what they wanted there, which was monotherapy AT-1501 in a non-human renal transplant model. Because of that guidance, we can reach out and start to work with an excellent collaborator in that regard. We know based on lots of historical data that we've mentioned hundreds and hundreds of animals have undergone renal transplant studies with monotherapy for various anti CD40 ligand antibodies and the absence of any treatment, animals reject very, very quickly, within a few days to a week. Even on monotherapy, there is some variability in the durability of preventing rejection. But typically, average survival times would suggest that we can conduct this experiment fairly quickly. Monotherapy treatments standardly depending upon the types of primates and the types of treatments can go anywhere from 14 days to 30 days with some standard deviations with animals surviving longer than that. But a fairly straightforward study given that they're looking for just to demonstrate that AT-1501 can move out the timeframe to its from a key rejection in untreated animals. As far as the clinical plans in the U.S., I think that that's just very dependent on what the data looks like from Canada. I mean, we're really excited about the study to initiate in Canada by the end of the year, as we know transplant studies are a little bit more complicated in humans than they are in animals. But really, I think the decision to get back to the agency with not only their request for the non-human primate data, but with also some human data from that Canadian study is key. So I think we need to wait until we see what that Canadian data looks like.

And so, we'll look as when we begin to have human data, as well as complete the study to return and reinitiate discussions with the FDA, which could be obviously as soon as in the second half of next year.

Okay. Makes sense. Thanks. And then a second question. Thanks for all the detail on IgA nephropathy and potential kind of nodes of impact that 1501 can have. Can you give us a little bit more color on the study that you plan, the Phase 2 that you plan to start? And also, what kind of read through do you think the study will give to potential other ideologies of autoimmune nephropathy our nephritis, I should say..

And so, in terms of specific color on trial design, we'll give more color as we as we begin to initiate the trial and enroll patients. As you can understand we'd like to finish our discussions with the various regulatory bodies and have our CTA is approved before we go into - before we go into full detail. With regards to the potential read through in autoimmune nephritis, overall and the overlap between various autoimmune nephritis, let me turn that over to Steve.

Yes. It's a great question, Matt, about read through, because, you know, one of the common themes even though these diseases are different, I mean, I am thinking of lupus nephritis, FSGS, IgAn and others. I mean, there is differences within each of these indications, but a common theme here is, kidney dysfunction proteinuria, ultimately eGFR improving all of the above. So there is some crossover, if you will, once you get some data points in one of these indications that if you are improving downstream kidney function by ameliorating immune infiltration, complement activation or a host of other pathophysiologies that could easily read through to other indications. So, the data in IgAn, I think is very important to help us understand mechanistically how the drug is working, but also if we are improving kidney function.

Great. Thanks. Thanks Steven and DA.

Our next question comes from Thomas Smith with SVB Leerink. You may proceed with your question.

Hey guys. Good afternoon. Thanks for the updates and thanks for taking the questions. Just on the autoimmune nephritis, I mean, you’ve previously talked about FSGS and lupus nephritis as potential initial indications. Can you just walk us through how you thought about, IgAn relative to those other two indications and how you ended up settling on IgAn?

Yes. So, we've historically spoken about autoimmune nephritis is covering the three. So, FSGS, lupus nephritis and IgAn, that we ultimately selected IgAn, because as we thought about both our understanding of the disease, as well as the way of using an anti CD40 ligand could impact the disease. That's where we felt that we add the greatest chance of success. Let me turn it over to Steve to just provide some more color on the use of - potential use of CD40 ligand in IgAn.

Yes. I mean the idea is certainly hit the highlights there. I mean, we think that there is opportunities and unmet need in FSGS, lupus nephritis and even other autoimmune nephritises. But really the disease mechanisms for some of these indications are still a little unclear. There is significant heterogeneity, and patient stratification can be a problem in the context of FSGS in particular. I am thinking about all of the above. I mean, mechanistically, we're still trying elucidate what are the real mechanisms leading to kidney dysfunction and FSGS. And when we compare and contrast to the pathophysiology of what we know about IgAn, we just understand more of what causes disease in IgAn. And the fact that blocking CD40 ligand can play a very significant role in multiple parts of that process really makes it an exciting opportunity to really understand it blocking immune complex formation downstream if moving upstream and actually eliminating immune complex formation by eliminating antibody production moving even further upstream from that as really modulating ultimately the production of IgA by knocking down B cell production in antibodies and blocking class switching. AT-1501 has the potential to do all of those things. So, it really is an exciting opportunity to look and see if blocking CD40 ligand function can have a dramatic impact on the upstream processes of kidney dysfunction in IgAn.

Got it. Okay. That's helpful. And then, just a follow-up on an earlier question. I understand you're still working through the details of the study design and you're waiting to hear feedback from some of the regulators. But I guess, do you have any initial sense of when we could see a first look at data from this program?

Yes. So, this - we will look to construct the trial to be able to begin to get some data readouts next year.

Okay. That's helpful. And then, maybe just one last question, just on islet cell and the presentation at the Islet Transplant World Congress coming up here in October. What should we be looking for in terms of the new datasets in that presentation?

Yes. So, the presentation will be again done by Norma Kenyon from the University of Miami. And so, she'll continue to give to give more details on all of the work that she has done to-date with her non-human primates in AT-1501. Steve?

Okay got it.

Yes, I mean, Norma continues to be really excited about the data that she has generated thus far. And given her long history going back over 20 years, I mean, Norma has had her fingers on a lot of different potential treatments to prevent transplant rejection in her non-human primate model. So, she continues to look at the data and we'll continue to build on her story of mechanistically how block in the ligand has the potential to prevent short, long term rejection and even induce tolerance in a functional cure in some animals. So, we're really excited to be working with Norma and her team.

Okay, got it. Got it. Thanks guys. Looking forward to the presentation. And thanks for taking the questions.

Thank you.

Our next question comes from Rami Katkhuda from LifeSci Capital. You may proceed with your question.

Hey, guys. Congrats on all the updates and thanks again for taking my questions. I know, Steve, you touched upon this briefly, but can you guys provide a little more insight on the differentiation between AT-1501 and some of these B cell modulating therapies in development for IgA nephropathy specifically?

Sure. Rami, thanks for the question. Let me turn that over to Steve.

Yes. So you're probably specifically talking about APRIL BAFF BCMA inhibitors?

Yes, exactly.

Yes. So the very targeted therapy is much like CD40 ligand. They are targeting the upstream processes of antibody formation and production. So, the second and third hits, if you will, that I was talking about and the strategies there are probably fairly similar to how we think CD40 ligand would inhibit those two processes. Your modulating B cell function, B cell maturation, antibody production, class switching downstream of IgM, which is critical. I think one of the potential differentiation points is more in the downstream process. But one thing the blocking CD40 ligand does, that the BAFF and APRIL inhibitors may not specifically do is modulating immune cell infiltrate into the kidney post to mean complex deposition. And that's one of the things that blocking the ligand made you that's a little bit mechanistically different than blocking APRIL or BAFF.

Got it. That makes a lot of sense. And then, I guess, switching gears a little…

Said another way, I think back to what Steve had described, which as you think about the four hit hypothesis, what this allows us to do is to potentially have an impact on more hits than other approaches.

Got it. And then, looking at the open-label kidney transplant trial, I know this is somewhat hypothetical, but is there potential for positive data from that program to kind of expedite the development pathway with regards to the FDA?

So, that's what we're looking to do is to see how quickly we can move the program forward and we'll do it in a way that's as expeditiously as possible. We’ll, also, of course, respecting our regulatory requirements and making sure we do what's right for patients. But the idea is to meet the FDA's requests in terms of the non-human primate study. And then, use the data that we are looking to generate in patients to see what is the - assuming that data is positive, what is the fastest next step in terms of the development of AT-1501 in kidney transplantation.

Great. Thank you guys.

Our next question comes from Vernon Bernardino. You may proceed with your question.

Hi, DA, Steve and Paul. Thanks for the update. And thanks for taking my question. Most of my questions we're related to the choice of IgAn. And therefore asked and answered. And then, what to expect at the conference in October, and then you basically mentioned primate work, but will some of that work also be related to the IgAn research?

So, the work in – first, thank you very much for that question. The work that we'll present is going to be primarily focused on enormous work in islet cell transplants, but let me turn that over to Steve to talk about how that work could impact or could read through other immune conditions, as well.

I mean, the work that we're doing with Norma is fairly focused on islet cell transplant. I mean, mechanistically, there is probably not a lot of read through there for understanding mechanistically how it could work or impact autoimmune nephritis indications. Now, the animals that we're talking about doing for monotherapy, for the renal transplant study in non-human primates, we will be looking obviously as normal rejection, but also, immune cell infiltrate in other downstream parameters associated with transplant rejection and function that could be informative in the context of autoimmune nephritis. So that could provide - that study could provide some information on mechanistically how blocking CD40 ligand modulates the immune system and may mitigate improvements in renal function in the context of transplant. So that one could have some read through downstream.

Okay. That's perfect. And then, therefore with the IgAn study, I just want to confirm, is that going to be a Phase 2 study? And are you going to look on different doses?

So, it's going to be, to your point, this will be a human clinical trial. So we'll look to do a Phase 2. The specific trial design and the potential to use multiple doses will give more color on further down the line.

Okay. Just one in queue I will get that. Thanks for taking my question. Everything else was already asked and answered. So, appreciate the update and all the answers. Thank you.

At this time, we have reached the end of the question and answer session. I will now turn the call over back to management for closing remarks.

Thank you, operator, and thank you everyone for joining us today on the call. We are pleased you could join to hear our progress during the second quarter and we look forward to keeping you updated on our company and programs.