Good day, and welcome to the Eledon Pharmaceuticals third quarter 2022 financial results conference call. All participants will be in a listen-only mode. Should you need assistance, please signal a conference specialist by pressing the star key followed by zero. After today's presentation, there will be an opportunity to ask questions. Please note this event is being recorded. I would now like to turn the conference over to Paul Little, Chief Financial Officer of Eledon. Mr. Little, please go ahead.
Good afternoon, everyone, and thank you for joining Eledon's third quarter 2022 operating and financial results conference call. Today, I am joined by David-Alexandre Gros, Chief Executive Officer, Steven Perrin, our President and Chief Scientific Officer, and Jeff Bornstein, our Chief Medical Officer. Earlier today, Eledon issued a press release announcing financial results for the third quarter ended September 30, 2022. You may access the release under the Investors tab on our company's website at eledon.com. I would like to remind everyone that statements made during this conference call relating to Eledon's expected future performance, future business prospects, or future events or plans may include forward-looking statements as defined under the Private Securities Litigation Reform Act of 1995. All such forward-looking statements are intended to be subject to the safe harbor protection provided by the Reform Act.
Actual outcomes and results could differ materially from these forecasts due to the impact of many factors beyond the control of Eledon. Eledon expressly disclaims any duty to provide updates to its forward-looking statements, whether as a result of new information, future events, or otherwise. Participants are directed to the risk factors set forth in Eledon's reports filed with the U.S. Securities and Exchange Commission. Now, I would like to pass the call to Eledon's CEO, Dr. David-Alexandre Gros.
Thank you, Paul, and thank you all for joining the call today. Following the positive phase II-A ALS results in the second quarter, we continue to make important progress in our 3 ongoing clinical trials evaluating tegoprubart in kidney transplantation, IgA nephropathy, or IgAN, and islet cell transplantation. Before I turn the call over to Steve, I'd like to provide a brief recap on the new developments across our tegoprubart pipeline. In renal transplantation, we successfully dosed our first 2 subjects in this phase I-B open label study of tegoprubart. Given our enrollment rate to date, we are on track to provide initial 3-month and 6-month open label data across multiple available transplant participants in the first quarter of 2023.
Additionally, in the third quarter, we received FDA clearance of our IND application for a phase II trial of tegoprubart for the prevention of organ rejection in subjects receiving a kidney transplant in the United States. This trial is designed as a superiority study versus standard of care with CNIs and will run in parallel to the ongoing phase Ib ex-U.S. trial. The phase II will enroll approximately 120 subjects, and we anticipate initiating the study next year. Moving to IgAN. In the third quarter, we received FDA clearance of our IND application, allowing us to evaluate tegoprubart in IgAN in the United States. Given this clearance, we're now in the process of opening U.S. sites as part of our ongoing global phase IIa clinical trial. With addition of the U.S., the trial has now received regulatory clearances in 11 countries.
Enrollment in the IgAN trial continues with multiple new subjects dosed in the high-dose cohort of the study. We remain on track to enroll the full cohort consisting of 21 subjects by the first half of next year and anticipate sharing available 6 months open label data from this study in the first quarter of 2023. Turning to islet cell transplantation. After receiving orphan drug designation from the FDA in the second quarter, we opened our first U.S. clinical site at the University of Chicago. The site has been actively engaging with potential participants to evaluate tegoprubart in the phase II-a study for the prevention of allograft rejection in islet cell transplantation. We continue to expect the first subject to be dosed by year-end.
We plan to enroll up to 6 participants with type 1 diabetes at this site, and we anticipate reporting initial 3 month open label data from the first subject in the study in the first quarter of 2023. Finishing with ALS. Following our announcement of positive top-line data in our phase II-a study of tegoprubart in adults with ALS, we have been working closely with key stakeholders on potential next steps, as well as evaluating a range of approaches to fund a potential future trial. We have been active in sharing our phase II data with the scientific community across multiple medical conferences, and we look forward to continued engagement with the ALS community as we work to advance this exciting program. I'll now turn the call over to Steven Perrin, our President and Chief Scientific Officer, to provide additional details on our development programs. Steve.
Thank you, DA. I'll begin by providing an overview of our progress evaluating tegoprubart for the prevention of allograft rejection in kidney transplantation.
Kidney transplantation is the most commonly performed solid organ transplant procedure in the United States, with about 23,000 performed every year. Our goal in this indication is to use tegoprubart to replace CNIs, the current standard of care. Although CNIs are the most widely used immunosuppressive therapy in kidney transplants, they are often toxic to the kidneys they are intended to protect, resulting in shortened graft function. They also cause numerous other side effects, including new-onset diabetes and cardiovascular disease. Our hypothesis for targeting CD40 ligand as first-line immunosuppression for kidney transplant stems from the large amount of non-human primate data generated both by our company with tegoprubart, as well as with historical anti-CD40 ligand antibodies. In these studies, non-human primates treated with anti-CD40 ligand antibodies as monotherapy demonstrated protection from rejection for months at a time versus only days in untreated animals.
We are pleased to report that we dosed our first 2 subjects in our phase Ib clinical trial of tegoprubart in kidney transplantation since the initiation of the study in July. The cadence of enrollment is consistent with expectations since the initial 3 participants in the study require a safety monitor committee meeting to review the first month of data after each transplant prior to the enrollment of the next participant. Given the enrollment progress we are making, we believe we can generate meaningful data on graft function quite quickly in this population, given that acute rejection most often occurs within the first 90 days after transplant. We remain on track to provide initial data from key 3-month and 6-month time points across multiple transplant participants in the first quarter of 2023.
In addition to the ongoing phase Ib trial in kidney transplantation, this quarter we were very excited to announce the clearance of our U.S. IND application to evaluate tegoprubart for the prevention of kidney transplant rejection in patients undergoing de novo kidney transplant. The study will be a multicenter, open-label, active control study to assess the safety and efficacy of tegoprubart compared with tacrolimus and the preservation of allograft function in approximately 120 patients undergoing kidney transplantation. Participants will be randomized 1:1 to receive either tegoprubart or active comparator tacrolimus as part of an immunosuppressive regimen. The study's primary objective is to evaluate the efficacy of tegoprubart against standard of care and the primary endpoint of the mean eGFR 12 months post-transplantation. Secondary objectives include safety, incidence of new-onset diabetes, biopsy-proven rejection, and participant as well as graft survival.
We are excited to investigate tegoprubart in this larger controlled setting and anticipate initiating this trial next year. Of note, the phase II program includes an open-label extension study allowing for the collection of long-term efficacy and safety from both of these studies, as well as the ongoing phase Ib study. We expect to run both the phase Ib and the phase II studies in parallel so we can continue to report data and insights on tegoprubart from the phase Ib study while the phase II is running. Next, I'll move on to IgA nephropathy. We'll remain excited by tegoprubart's potential ability to show beneficial effect both on the upstream and the downstream pathophysiology of the disease. IgAN is the most common primary glomerulonephritis.
It occurs in about 150,000 Americans, and a significant portion of these patients will end up progressing to end-stage renal disease, where they'll need dialysis or transplant. We believe tegoprubart has the potential to impact multiple pathways in the pathophysiology of the disease by reducing production of IgA antibodies, reducing immune complex formation, and reducing cellular inflammation in the glomeruli itself. In animal models of glomerulonephritis, blocking CD40 ligand has been shown to be effective in reducing proteinuria, decreasing inflammatory infiltrate into the kidney, and improving survival. We recently presented a poster at ASN Kidney Week describing the trial design of our open-label phase IIa clinical trial in subjects with IgAN and are happy to report that we continue to make progress on the enrollment front.
We received IND clearance from the FDA in September, bringing our total to 11 countries, with plans to expand into China in 2023. This global study is a 96-week open-label trial that will include 42 participants in either a high-dose or a low-dose cohort. The primary endpoint is change in proteinuria at week 24, and secondary endpoints include change in estimated eGFR at week 96, as well as safety and tolerability. With study approval in 11 countries, we remain on track to enroll the full high-dose cohort of 21 participants at 10 mg per kg in the first half of next year. Additionally, we'll be providing an initial 6-month open-label data from the study, including change in proteinuria from multiple subjects at 6 months in the first quarter of 2023.
Next, I'll move over to islet cell transplant and our phase IIa trial for the prevention of allograft rejection. Like in kidney transplantation, our goal here is to replace CNIs as the first-line immunosuppressive regimen for islet cell transplant procedures. There are over 1.3 million Americans living with type 1 diabetes. We believe islet cell transplants could reduce or eliminate the need for exogenous insulin injections, but adoption is hampered by the toxicity of CNIs, the current standard of care to prevent islet cell transplant rejection. Islet cell transplant in non-human primate models have shown that animals treated with tegoprubart versus those with CNIs had longer rejection-free survival as well as improved overall graft function. Additionally, animals on tegoprubart regimen demonstrated better metabolic control and were healthier as measured by weight gain after transplant compared to standard immunosuppressive regimens.
In the third quarter, we opened our U.S. site at the University of Chicago, where we are focusing our resources for the study. This site plans to enroll up to 6 type 1 diabetes patients with hypoglycemic unawareness who experience significant swings in glucose levels that are associated with serious risk and comorbidities. Our goal is to evaluate tegoprubart as the backbone of maintenance anti-rejection therapy, similar to design for kidney transplantation. In ICT specifically, we're also evaluating the ability of subjects to achieve insulin independence, as well as the number of islet cell transplants required to achieve that dependence. We anticipate achieving first patient enrollment in this phase IIa study by the end of the year.
Given most subjects require multiple transplants in this indication by day 75, we believe we can generate meaningful data quickly with limited subjects and aim to provide available 3 month data in the first quarter of 2023. I'll wrap up my update by turning to ALS, a program in which we announced positive top-line data from our phase IIa trial in May. We've been fortunate enough to share these data with the scientific community at multiple medical conferences this quarter and are encouraged by the reception and excitement it has generated. These data marked a significant milestone for Eledon as the first of our 4 distinct programs read out, and has further validated the favorable safety and toxicity profile of tegoprubart, provided insights into the mechanism of action through dose-dependent target engagement, as well as demonstrated reductions in pro-inflammatory markers, including biomarkers of T-cell and B-cell activation.
Lastly, the data was meaningful in providing potential read-throughs for tegoprubart in IgA nephropathy as well as kidney transplant. We observed reductions in the levels of IgA, IgM, IgE, CD40, and CXCL13 biomarkers, which were associated with class switching and B-cell maturation with potential relevance to IgAN, given that reduction in IgA should result in decreased IgA levels, thus reducing the pathogenic form of IgA and a reduction in circulating immune complexes. There was also a reduction in pro-inflammatory chemokines such as CXCL9 and CXCL10, as well as complement C3, biomarkers associated with signs of renal transplant rejection. As D.A. mentioned, we have been deeply engaged with the ALS community, including key opinion leaders on potential next steps.
Given the data we observe in the phase IIa, we are excited to explore how the promising results we observe will translate into a larger study designed to measure clinical benefit, and we are actively evaluating a range of approaches to fund a potential future trial pending available financing. With that, I'll now turn the call over to Paul for a financial update.
Thank you, Steve. In addition to the financial results summarized in our press release, you can find additional information in our Form 10-Q, which we will file later today. The company reported a net loss of $10.5 million, or $0.73 per share for the 3 months ended September 30, 2022, compared to a net loss of $9.8 million or $0.66 per share for the same period in 2021. Research and development expenses were $7.5 million for the 3 months ended September 30, 2022, compared to $7.7 million for the comparable period in 2021. The decrease of $200,000 was primarily due to lower CMC costs recognized during the quarter, partially offset by an increase in clinical development and personnel costs due to increased headcount.
G&A expenses were $3.1 million for the 3 months ended September 30, 2022, compared to $2.8 million for the comparable period in 2021, an increase of $300 thousand. The increase was primarily related to an increase in professional service costs, general operating costs, and stock-based compensation costs. As of September 30, 2022, Eledon had $65.9 million in cash and cash equivalents, which we expect to be sufficient to fund our clinical trial operations as currently planned into 2024. As a reminder, this cash runway allows us to initiate the phase II trial of tegoprubart for the prevention of organ rejection in subjects receiving a kidney transplant, but additional financing will be required to fund any future ALS clinical trials. With that financial update, let me turn the call back over to DA.
Thanks, Paul. I am highly encouraged by the progress our team has made across our clinical programs. With 3 ongoing clinical trials, we remain committed to strong execution in our development efforts to close out the year, which we believe will leave us well positioned entering 2023, a potentially transformative year for Eledon. In the first quarter of next year, we look forward to providing meaningful initial data updates for 3 of our 4 programs: kidney transplant, IgAN, and islet cell transplant. In addition, next year, we expect to launch our phase II kidney transplant study, as well as provide further clarity on the next steps for our ALS program. I'll now ask the operator to begin our Q&A session.
Operator?
Thank you. We will now begin the question and answer session. To ask a question, you may press star then one on your touchtone phone. If you're using a speakerphone, please pick up your handset before pressing the key. To withdraw your question, please press star then two. Our first question today comes from Pete Stavropoulos with Cantor Fitzgerald. Please go ahead.
Good evening and thank you for taking our questions. At the American Society of Nephrology, you know, you recently presented data for the ALS study, you know, showing a % change from baseline for proinflammatory biomarkers, you know, including markers of B-cell activation and T-cell activation. Just wanna get your thoughts, your perspective on the % change of IgA and you know, if you see similar changes in IgAN patients, you know, would it be enough to translate to clinical benefit?
Steve, let me turn that over to you. Thanks for the question, Pete.
Yeah, it's a good question. I mean, for IgA levels in ALS, we don't know what baseline levels mean, right? I don't think any company has ever shown a reduction in IgA levels, but the reductions were fast. They occurred right after the first dose, before subjects received second doses. The mechanism was very quick, much like we've seen in the prevention of transplant rejection in primates. You know, we saw double-digit % reductions as we dose escalated. I would anticipate that those levels are meaningful, but how they transfer into IgAN, I think is unknown at this point.
All right. Again, you know, for IgAN, you know, what is the target population that you believe would most benefit from Tego? You know, when you take into account, you know, the mechanism of action and its potential disease-modifying properties. You know, would it be earlier stage patients, later stage patients, or broad or benefits seen broadly across, you know, all IgAN patients?
I mean, I'll give you my perspective, and Jeff could jump in, but I think across almost any disease indication at this point, the earlier you see interventions, the better off your outcomes tend to be. We know that IgAN is a long-term disease, right? I mean, it's chronic. It lasts for decades, but I would assume that the earlier interventions one could get on reducing proteinuria, that would translate into better kidney function and less long-term kidney damage.
Jeff, anything to add or?
Yeah. Thanks. Thanks, Pete. Well, I concur with Steve. As the disease progresses, if glomeruli are lost and fibrosis sets in, none of these agents are gonna reverse that. Earlier intervention is probably better across the board. Our mechanism of action does work both upstream and downstream. In patients where there's a good deal of inflammation in the kidney itself, we would expect to see benefit, not just in disrupting the upstream process at IgA. There is that distinction there, where the drug does work both upstream and downstream. You know, patients who are too far advanced, I don't think any of the mechanisms will work.
All right. Thank you for the color. Last question is, you know, how many patients, you know, can we expect to see data for across the 3 initial data sets in 1Q23?
I mean, we'll share everything that we have that's available at the time. It depends a little bit on when we end up presenting the data and so which of the conferences we'll be able to present the data at.
Okay. Well, thank you. Thank you for taking my question.
It'll be a number similar to what you've seen other companies present for, you know, their initial phase II data.
All right. Look forward to it. Thank you.
Thanks, Pete.
The next question comes from Matthew Kaplan with Ladenburg Thalmann. Please go ahead.
Hi, good evening. Congrats on the progress. Just to follow up on Pete's question, with respect to the renal transplant program, you announced that you're going to report initial data from the first few subjects on the phase Ib 3- and 6-month data. What read-through will that data provide to the potential for the phase II superiority study that you plan to start next year?
Thanks, Matt. Jeff, why don't I turn that over to you?
All right. Thank you, DA. Thanks, Matt. It's you know the study is a pilot study designed to show safety and also preliminary efficacy, right? What we expect to see is that we can administer this regimen safely to these patients, that it prevents rejection. Potentially more like on point for your question is, how is that graft functioning? What do their GFRs look like? You know, how is that going to inform our endpoint for the next study? It'll be a few patients only, but we will start to get a sense of how they're doing, how well they're doing, how well their grafts are functioning. Of course-
Okay.
We'll look at the side effect profile, right, to make sure that we're looking at whether or not they're developing diabetes or whether it's preventing it.
Okay. That's helpful.
The phase II studies are designed in a similar manner. Other than the fact that one of them is open and the other one is controlled. In terms of how the patients are being treated and how they're getting to go for biopsy, that's the same.
Okay. Just with your islet cell transplant program, I guess you're expecting first patient enrollment in the near term. You already had shown, you know, strong preclinical data there. Help us think about the initial data, the 3 month data that you're going to report in the first quarter, what we should be looking for there.
Thanks, Matt. Jeff, let me turn that to you.
Right. Thank you. You know, similarly to our kidney transplant study, we will give an update of who's been, like, the number that's been transplanted and how they're doing. Adverse event profile, graft function, and rejection.
Here we'll look at, as part of that, we'll also see, right, with regards to graft function, how those patients are doing in terms of glucose control and the need for exogenous insulin. Recall that most patients today, if they get an islet cell transplant, require repeat transplant typically about 75-90 days later, in order to have sufficient glucose control. Our hope is that with only one transplant, we might be able to achieve that.
Great. Thanks, guys. Look forward to the readouts in the first quarter.
The next question comes from Thomas Smith with SVB Securities. Please go ahead.
Hey, guys. Good afternoon. Thanks for taking the questions. I was just wondering if you could comment on some of the latest developments here across the CD40 landscape. I know back in September, we saw some positive top-line data from Horizon's CD40 ligand and Sjögren's syndrome. You know, you don't currently have any studies there, but can you just comment on that data set and how you think about the potential to pursue development in a large indication like Sjögren's?
Sure. Steve, do you wanna talk about some of the recent data? I'm happy to talk about how we think about indications.
Yeah. I mean, thank you. Thanks. Great question. You know, we're excited about the data. It really continues to validate mechanism of action for the pathway. They showed data that was similar to what Novartis had presented with their earlier, smaller study compared to what they're running today. So, you know, classic autoantibody-mediated diseases like Sjögren's and lupus continue to be aligned with, you know, what has been a long-standing knowledge of the mechanism of action of the drug being able to hit both T-cell mediated as well as B-cell mediated diseases. We thought that data was encouraging.
All right. Then in terms of how we approach thinking about indications, when we picked our initial indications, we looked at 3 different things. 1 was we want indications where there was a good understanding of the pathophysiology of the disease and how an anti-CD40 ligand would play into that indication. We then looked at indications where we had a good understanding of what the path to approval, to the regulatory path would look like. Third, we sought out indications that could be executed by a smaller biotech. It's really looking across all of those things that led us to pick our indication. Now, I think there are a number of other larger indications where using an anti-CD40 ligand could make sense, including Sjögren's, which you just brought up.
Right now, from our perspective, we remain focused on our indication, and today we don't have the financial flexibility to add another indication. But obviously, you know, in the future as we grow, we could consider adding other indications as well.
Got it. Okay. That's helpful. Then, yeah, I was just wondering if you could comment on the latest developments with Novartis and their anti-CD40 iscalimab. It seems like they've recently stopped a second solid organ transplant study and liver transplant. I guess, it'd be helpful if you just share your thoughts around this program and maybe just remind us why you think targeting CD40 ligand is the superior approach in solid organ transplant.
Sure. Let me turn that over to Steve to go through the CD40R versus CD40L in transplant.
Yeah. Great question. I'll answer that, and then maybe I'll hand it over to Jeff to talk about the iscalimab liver recent results there. The history there, as we know, for a long time, we've known 30 years that blocking the ligand tends to be more efficacious than blocking the receptor, not only in the context of preventing short and long-term transplant rejection, but similar data exists for animal models of autoimmunity as well. I think a lot of color has been added to the rationale on why we see a better therapeutic effect with blocking the ligand, and it comes down to a couple of different functional differences. 1 is that the receptor and ligand have very different expression patterns in the body.
The receptor is constitutively on the cell surface of antigen-presenting cells, meaning it's always there on the cell surface, and it's present on a host of antigen-presenting cells, including B cells, dendritic cells, NK cells, and specialized antigen-presenting cells in your organs. Whereas the ligand that's expressed on T cells is not constitutive, it's not there all the time. It's only on the surface transiently when the T-cell is activated after antigen presentation. There's mechanisms to remove it from the cell surface to actually prevent autoimmunity. That's one rationale is that the expression patterns are very different so that antibodies targeting these will have different biological outcomes. The second one is that when people think about blocking this pathway and blocking CD40 ligand, they think you're only blocking costimulatory activity via CD40 receptor, and that's not true.
CD40 ligand can actually activate multiple different costimulatory pathways on antigen-presenting cells, not only through CD40 receptor, but as an example, through the MAC complex, which has been shown to be very important in CD8 cytotoxic CD8 positive transplant rejection. There's a couple of other integrins that CD40 ligand also can control and activate cell populations, including various integrins. So that's the second one, is that blocking the ligand can block multiple costimulatory pathways. Then the third one, which is probably the most unique to CD40 ligand and potentially the most exciting, because it's on the cell surface of CD4 positive T-cells, not only does it block their pro-inflammatory differentiation when you block the ligand, it actually repolarizes them to become regulatory T-cells, which can secrete tolerogenic chemokines like TGF-beta, IL-10, and create this tolerogenic environment in the context of preventing rejection.
Those are probably the biggest differentiation points. Jeff, did you wanna comment or DA on iscalimab and liver? I'm happy to as well, but if one of you guys wanna take it.
I can. I'm happy to chime in. In addition to what Steve said about mechanism, I think we have the opportunity to try to learn about study design features that we might consider doing differently in a program going forward. It's difficult to comment on a competitor program, especially when they haven't made any of the actual trial results public. I think there's still opportunities for us to learn from what they've done and tighten things up in study design around things like induction agents and also the role the bias plays in these open label studies and who gets biopsied. I think we're carefully studying what's been done, and I think we can incorporate some elements into our future studies to try to learn from what happened with their program.
Just a final thought. You know, what Novartis has said is that they showed inferiority. They stopped the studies early because they were trending towards inferiority versus CNIs. But there is an upside to that, is that this wasn't stopped for a safety reason. It continues to underscore just to date the safety of the class.
Got it. Okay. Yeah, appreciate the color, guys. Then, maybe just lastly, you know, now that you have FDA clearance, can you expand on the plans for starting the phase II kidney transplant study in the U.S. and I guess elaborate on what other gating factors are there to getting the study up and running in 2023?
Thank you. I mean, right now we're just working with our CROs on beginning to execute the study. We're working towards that goal, there aren't any major large gating items.
Okay, got it. Awesome. Thanks, guys. Appreciate you taking the questions.
Again, if you have a question, please press star then one. The next question comes from Rami Kado with LifeSci Capital. Please go ahead.
Hey, guys. Thanks for taking my questions as well. Just a quick one from me, but can you touch upon how the 10 and 5 mg per kg doses as well as the every 3-week dosing frequency were chosen for the phase IIa study in IgAN? I realize it's quite different from the ALS study.
Great. Hey, Rami, thank you for the question. Steve, let me turn that over to you.
Yeah, I mean, we learned a lot from the phase II studies. Remember, that was our first multiple ascending dose study in humans. The other study we had done was a single ascending dose in healthy volunteers for the most part. We're learning a lot about the pharmacokinetics of the drug. We kind of knew from our primate studies in the ALS study that we're at 2-week dosing, which we had planned, was due to the fact that we had started dosing in that study, if you remember, very low. The lowest dose cohort was 1 mg per kg. In order to start to increase exposure levels early on while being very cautious about safety profile, we decided to dose every other week.
We hypothesized that by doing that, we would really never reach steady state, that exposure levels would increase over time, which is what we observed in the study, even up to 8 mg per kg. We utilized that data to start to think about how one would design the appropriate exposure levels for autoimmune indications like IgA nephropathy. That's how we selected the 5 and 10 mg dose. We knew based on that data we could go to every 3-week dosing. Jeff, I don't know if you wanna add some color to that, but that's kind of the high-level summary.
No, I concur. The doses translate actually pretty well from ALS to IgAN.
Got it. I guess, is the end goal to make a subcu formulation of tegoprubart for diseases like ALS and IgAN?
Thanks, Rami. We're working on a subcutaneous formulation as well. There are certain diseases where, for example, transplant or ALS, where an IV formulation from a competitive perspective could be acceptable. For example, in IgAN, over time, we would look to use a subcutaneous formulation.
Got it. Thank you.
This concludes our question and answer session. I would now like to turn the conference back over to D.A. for any closing remarks.
Thank you for your assistance, operator, and thank you all for joining us on today's call. Have a great evening.
This conference is now concluded. Thank you for attending today's presentation. You may now disconnect.