Earnings Call Transcript
Eledon Pharmaceuticals, Inc. (ELDN)
Earnings Call Transcript - ELDN Q2 2021
Operator, Operator
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.
Paul Little, CFO
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.
David-Alexandre Gros, CEO
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 (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 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 the 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 US FDA requested 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. As a result, we will both look to complete the FDA requirements as quickly as possible and 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. Regarding 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 blocking CD40 ligand signaling ameliorates disease progression, modifies biomarkers of disease, and improves renal function in autoimmune diseases of the kidney such as IgAn. We selected IgAn because of the unique approach that anti-CD40 ligands bring in targeting both the cellular and antibody-mediated portions of disease pathophysiology. In islet transplantation 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 remained far behind those in the United States, and the number of islet cell transplant procedures performed remained much lower than pre-COVID. As a result, we are still waiting for the 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 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.
Steven Perrin, President and Chief Scientific Officer
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 immune response. The CD40 ligand pathway is an attractive drug development target because the engagement of these receptors plays a pivotal role in immune system activation by mediating both antibody- and cellular immune responses. We are focusing our efforts on the development of an antagonist antibody targeting the ligand rather than the receptors, and targeting the ligand has been shown to be more efficacious in preclinical models of autoimmunity, 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 consist 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 in pro-inflammatory signals in circulation, including TNF alpha, MCP-1, IL-6, and others. We anticipate blocking CD40 ligand will result in an overall decrease in these ALS-related pro-inflammatory markers. Finally, we will also assess other exploratory endpoints, including changes in the ALS functional rating scale, respiratory function, and the levels of neurofilament light chain in 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 therapy in solid organ transplantation and prevent acute and long-term solid organ transplant 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 nephrotoxicity, cardiotoxicity, neurotoxicity, and induction of Type 1 diabetes associated with chronic exposure to CNIs. This study will be an open-label, multi-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 PK/PD endpoints. Regarding starting a trial in the United States, we announced in April that the FDA requested 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 an agreement with the US FDA 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 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 primate 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 model of renal transplantation. In autoimmunity, we will initially focus on IgA nephropathy, one of several autoimmune nephritides that are autoimmune diseases of the kidney. There is a long history of preclinical and clinical data demonstrating 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 glomerulonephritis; disease manifestation and clinical presentation involve renal dysfunction characterized by proteinuria with a slow, relentless progression, 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 the 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 pathogenesis 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 autoantibodies are generated in circulating Gd-IgA1. 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 to chronic loss of kidney function, kidney damage, proteinuria, and end-stage renal disease. There are no FDA-approved therapies for IgAn, and guidelines for the current standard of care for people with IgAn suggest the use of certain classes of antihypertensive medications to modulate hemodynamic stresses on the kidney, resulting in improved glomerular filtration rates and reduced proteinuria. Treatment with either angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockade (ARBs) is the standard of care if proteinuria is greater than one gram per day and is suggested if it is greater than 0.5 grams per day. Treatment with ACEIs and ARBs, along with other molecules in clinical development, focuses on Hit 4, but downstream pathological mechanisms and the disease after immune complex formation in the kidney and decreased kidney function. The exciting opportunity for AT-1501 in 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 autoantibodies 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 amount of IgG synthesized that will be available for improper glycosylation but will also prevent the production of high-affinity IgG1 antibodies that form immune complexes. Blocking CD40 ligand has been shown to decrease immune complex formation 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 impacts the pro-inflammatory polarization of T cells and macrophages and has been shown to decrease immune cell infiltrates and inflammation in the kidney, corresponding to Hit 4. In conclusion, considering the pathophysiologies of IgAn 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, once 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 comorbidities. 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 (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-transplant, which 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 conjunction with induction therapy to animals on tacrolimus and induction therapy in a non-human primate model of islet cell transplants. Her findings indicated that animals on AT-1501 had significantly longer rejection-free survival, significantly longer overall islet cell graft survival, and maintained greater body weight compared to animals on 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 CMV 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, potentially allowing islet cell transplants to become a viable treatment option and even a potential functional 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 study. 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 rollout 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 significantly reduce the number of islet cell transplant procedures being performed so far this year compared to pre-COVID. We are working with the site to facilitate patient recruitment into the study, including reaching out to more endocrinologists across the province in Canada, and beginning to work on ways to allow patients to receive the 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 thus far, they have experienced similar COVID-related issues 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 on islet cell transplants in the first half of 2022. This is based on the timing to assess graft function in acute transplant rejection being 90 days post-transplant on a patient-by-patient basis. With that, I'll turn the call over to Paul for our financial update.
Paul Little, CFO
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, as well as 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 in 2020. R&D expenses were $9.9 million for 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 30, 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 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.
David-Alexandre Gros, CEO
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, along with 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?
Operator, Operator
Our first question comes from Alethia Young with Cantor Fitzgerald. You may proceed with your question.
Unidentified Analyst, Analyst
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 can combine the patients? And also if you can just remind us how many patients that you plan on recruiting? Thanks.
David-Alexandre Gros, CEO
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, as we discussed, we will look, especially as COVID progresses, to see whether there are ways to add additional countries to the trial. What’s nice here is we can begin to get data quickly since patients often need second transplant procedures within 90 days after the first transplant when they receive the current standard of care, which could allow us to quickly assess the impact of AT-1501. We plan on reporting the data that we have on the totality of patients that we'll be able to enroll in the first half of next year. Steve, let me see if you have anything that you’d like to add.
Steven Perrin, President and Chief Scientific Officer
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 has. 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.
Unidentified Analyst, Analyst
Okay. Thank you.
Operator, Operator
Our next question comes from Matt Kaplan with Ladenburg Thalmann. You may proceed with your question.
Matt Kaplan, Analyst
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 the 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 transplant?
David-Alexandre Gros, CEO
Thanks. Thanks, Matt. Why don't I turn that over to Steve to go through the plan?
Steven Perrin, President and Chief Scientific Officer
So I think that there were two questions here, Matt. One was about the non-human primate study and the other was about anticipation on moving into the U.S., correct?
Matt Kaplan, Analyst
Correct. Yes.
Steven Perrin, President and Chief Scientific Officer
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 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 it's a fairly straightforward study given that they're looking to demonstrate that AT-1501 can extend the timeframe to rejection in untreated animals. As far as the clinical plans in the U.S., I think 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 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 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.
David-Alexandre Gros, CEO
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 as soon as the second half of next year.
Matt Kaplan, Analyst
Okay. Makes sense. Thanks. And then a second question. Thanks for all the detail on IgA nephropathy and the potential kind of nodes of impact that AT-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 nephritis?
David-Alexandre Gros, CEO
In terms of specific color on trial design, we'll provide more color 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 CTAs approved 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.
Steven Perrin, President and Chief Scientific Officer
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 am thinking of lupus nephritis, FSGS, IgAn, and others. There are differences within each of these indications, but a common theme here is kidney dysfunction, proteinuria, and ultimately improving eGFR. 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.
Matt Kaplan, Analyst
Great. Thanks. Thanks, Steven and DA.
Operator, Operator
Our next question comes from Thomas Smith with SVB Leerink. You may proceed with your question.
Thomas Smith, Analyst
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?
David-Alexandre Gros, CEO
Yes. So, we've historically spoken about autoimmune nephritis covering the three: FSGS, lupus nephritis, and IgAn. 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 had the greatest chance of success. Let me turn it over to Steve to provide some more color on the potential use of CD40 ligand in IgAn.
Steven Perrin, President and Chief Scientific Officer
Yes. I mean the idea is certainly hit the highlights there. We think that there are opportunities and unmet needs in FSGS, lupus nephritis, and even other autoimmune nephritides. 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. Mechanistically, we’re still trying to elucidate what are the real mechanisms leading to kidney dysfunction and FSGS. When we compare and contrast to the pathophysiology of what we know about IgAn, we just understand more of what causes disease in IgAn. 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 see if blocking immune complex formation downstream—if moving upstream and actually eliminating immune complex formation by eliminating antibody production—can even further upstream from that, ultimately result in modulating the production of IgA by knocking down B cell production and preventing antibody 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 dramatically impact the upstream processes of kidney dysfunction in IgAn.
Thomas Smith, Analyst
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?
Steven Perrin, President and Chief Scientific Officer
Yes. We will look to construct the trial to be able to begin to get some data readouts next year.
Thomas Smith, Analyst
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?
David-Alexandre Gros, CEO
Yes. The presentation will be, again, done by Norma Kenyon from the University of Miami. She'll continue to provide more details on all the work that she has done to date with her non-human primates in AT-1501.
Steven Perrin, President and Chief Scientific Officer
Yes, I mean, Norma continues to be really excited about the data that she has generated thus far. Given her long history going back over 20 years, Norma has had her fingers on a lot of different potential treatments to prevent transplant rejection in her non-human primate model. She continues to look at the data and we'll continue to build her story on how blocking the ligand has the potential to prevent short- and long-term rejection and even induce tolerance in a functional cure in some animals. We're really excited to be working with Norma and her team.
Thomas Smith, Analyst
Okay, got it. Looking forward to the presentation. And thanks for taking the questions.
David-Alexandre Gros, CEO
Thank you.
Operator, Operator
Our next question comes from Rami Katkhuda from LifeSci Capital. You may proceed with your question.
Rami Katkhuda, Analyst
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?
David-Alexandre Gros, CEO
Sure. Rami, thanks for the question. Let me turn that over to Steve.
Steven Perrin, President and Chief Scientific Officer
Yes. So, you're probably specifically talking about APRIL, BAFF, and BCMA inhibitors?
Rami Katkhuda, Analyst
Yes, exactly.
Steven Perrin, President and Chief Scientific Officer
Yes. So the very targeted therapy is much like CD40 ligand. They are targeting the upstream processes of antibody formation and production. The second and third hits, if you will, that I was talking about, are strategies that 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-immune complex deposition. That's one of the things that blocking the ligand allows us to do, which is a little bit mechanistically different than blocking APRIL or BAFF.
Rami Katkhuda, Analyst
Got it. That makes a lot of sense. And then, I guess, switching gears a little…
David-Alexandre Gros, CEO
Said another way, I think back to what Steve had described, 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.
Rami Katkhuda, Analyst
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?
David-Alexandre Gros, CEO
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 while also respecting our regulatory requirements and making sure we do what's right for patients. But the idea is to meet the FDA's requests concerning the non-human primate study and then use the data that we are looking to generate in patients to see what is the fastest next step in terms of the development of AT-1501 in kidney transplantation.
Rami Katkhuda, Analyst
Great. Thank you guys.
Operator, Operator
Our next question comes from Vernon Bernardino. You may proceed with your question.
Vernon Bernardino, Analyst
Hi, DA, Steve, and Paul. Thanks for the update and thanks for taking my question. Most of my questions related to the choice of IgAn and therefore were 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?
David-Alexandre Gros, CEO
So, the work that we'll present is going to be primarily focused on enormous work in islet cell transplants. Let me turn that over to Steve to talk about how that work could impact or read through to other immune conditions as well.
Steven Perrin, President and Chief Scientific Officer
The work that we're doing with Norma is fairly focused on islet cell transplant. Mechanistically, there is probably not a lot of read-through there for understanding 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 at normal rejection, but also immune cell infiltrate and other downstream parameters associated with transplant rejection and function that could be informative in the context of autoimmune nephritis. So that study could provide some information on how blocking CD40 ligand modulates the immune system and may improve renal function in the context of transplant. So that one could have some read-through downstream.
Vernon Bernardino, Analyst
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 at different doses?
David-Alexandre Gros, CEO
So, to your point, this will be a human clinical trial, and we’ll look to do a Phase 2. The specific trial design and the potential to use multiple doses will give more color on that further down the line.
Vernon Bernardino, Analyst
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.
Operator, Operator
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.
David-Alexandre Gros, CEO
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.
Operator, Operator
This concludes today's conference. You may disconnect your lines at this time. Thank you for your participation.