Q3 2022 Eledon Pharmaceuticals Inc Earnings Call

November 14, 2022

Operator: Good day, and welcome to the Eledon Pharmaceuticals Q3 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 Pharmaceuticals, Inc. Mr. Little, please go ahead.

Good day and welcome to the Eligon Pharmaceuticals third quarter 2022 financial results Conference call all participants will be in a listen only mode.

So you need assistance. Please signal contract specialists by question Starkey I'll, let IC Ro.

After today's presentation there'll be an opportunity to ask questions. Please note. This event is being recorded I would now like to turn the conference over to Paul Lytle, Chief Financial Officer of elegant Mr. Little Please go ahead.

Paul Little: Good afternoon, everyone, and thank you for joining Eledon's Q3 2022 operating and financial results conference call. Today, I am joined by David-Alexandre Gros, Chief Executive Officer, Steve 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 Q3 ended 30 September 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.

Good afternoon, everyone and thank you for joining <unk> third quarter 2022, operating and financial results Conference call.

Today, I am joined by David Alexandra grow Chief.

Chief Executive Officer, Steve <unk>, our President and Chief Scientific Officer, and Jeff Bornstein, Our Chief Medical Officer.

Earlier today <unk> issued a press release announcing financial results for the third quarter ended September 32022, you may access the release under the investors tab on our company's website at <unk> Dot com.

I would like to remind everyone that statements made during this conference call relating to <unk> 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 1095, 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.

Paul Little: 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. D.A.

The impact of many factors beyond the control of <unk>.

<unk> 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 <unk> reports filed with the U S Securities and Exchange Commission.

Now I would like to pass the call to <unk> CEO , Dr. David Alexander grow.

Yeah.

David-Alexandre Gros: Thank you, Paul, and thank you all for joining the call today. Following the positive phase 2a ALS results in Q2, we continue to make important progress in our three 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 two subjects in this phase 1b 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 Q1 2023.

Thank you Paul.

And thank you all for joining the call today.

Following the positive phase Iia ALS results from the second quarter, we continue to make important progress in our three ongoing clinical trials evaluating <unk> in kidney transplantation.

Hey, nephropathy, or all again and I'll, let cell transplantation.

Before I turn the call over to Steve I'd.

I'd like to provide a brief recap on the new developments across our <unk> pipeline.

In renal transplantation.

We successfully dosed our first two subjects in this phase <unk> open label study of <unk>.

Given our enrollment rate to date, we are on track to provide initial three month and six month open label data across multiple available transplant participants in the first quarter of 2023.

David-Alexandre Gros: Additionally, in Q3, we received FDA clearance of our IND application for a phase 2 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 1b ex-US trial. The phase 2 will enroll approximately 120 subjects, and we anticipate initiating the study next year. Moving to IgAN. In Q3, 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 US sites as part of our ongoing global phase IIa clinical trial. With addition of the US, the trial has now received regulatory clearances in 11 countries.

Additionally, in the third quarter, we received FDA clearance of our IND application for a phase II trial up to go provide for the prevention of Oregon rejection in subjects, receiving a kidney transplant in the United States.

This trial is designed as a superiority study versus standard of care with C&I.

And we will run in parallel to the ongoing phase one be ex U S trial.

<unk> II will enroll approximately 120 subjects and we anticipate initiating the study next year.

Moving to all again in.

In the third quarter, we received FDA clearance of our IND application, allowing us to evaluate to go provide in again and do not it states.

Given this clearance we're now in the process of opening U S sites as part of our ongoing global Phase II Phase Iia clinical trial.

With addition of the U S. The trial has now received regulatory clearances in 11 countries.

David-Alexandre Gros: 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 H1 next year and anticipate sharing available six months open label data from this study in Q1 2023. Turning to islet cell transplantation. After receiving orphan drug designation from the FDA in Q2, we opened our first US clinical site at the University of Chicago. The site has been actively engaging with potential participants to evaluate tegoprubart in a phase IIa study for the prevention of allograft rejection in islet cell transplantation, and we continue to expect the first subject to be dosed by year-end.

Enrollment in the <unk> trials continues with multiple new subjects dose and 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 six months open label data from this study in the first quarter of 2023.

Turning to our lead 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.

<unk> has been actively engaging with potential participants to evaluate to go for Barton and the phase Iia study for the prevention of allograft rejection in islet cell transplantation.

And we continue to expect the first subject to be dosed by year end.

David-Alexandre Gros: We plan to enroll up to six participants with type one diabetes at this site, and we anticipate reporting initial three-month open label data from the first subject in the study in Q1 2023. Finishing with ALS. Following our announcement of positive top-line data in our phase IIa 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 Steve Perrin, our President and Chief Scientific Officer, to provide additional details on our development programs. Steve?

We plan to enroll up to six participants with type one diabetes at the site.

And we anticipate reporting initial three month open later.

The first subject in.

In this study in the first quarter of 2023.

Finishing with AOS.

Following our announcement of positive top line data in our Phase Iia study is to go for Bart 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 acting in 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 Steve <unk>, our President and Chief Scientific officer to provide additional details on our development programs.

Steve.

Steven Perrin: Thank you, D.A. 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.

Thank you D a.

So I'll begin by providing an overview of our progress evaluating <unk> 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 23000 performed every year.

Our goal in this indication is to use today go part to reply.

C&I is the current standard of care.

Although C&I as are the most widely used immunosuppressive therapy and kidney transplants that are often toxic to the kidneys theyre intended to predict protect resulting in shortened graft function.

It also caused numerous other side effects, including nuance of diabetes and cardiovascular disease.

Our hypothesis for targeting CD 40 ligand as first line immunosuppression for kidney transplant.

From a large amount of nonhuman primate data generated both by our company with <unk> as well as with historical anti CD 40 ligand antibodies.

Steven Perrin: 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 two subjects in our phase 1b clinical trial of tegoprubart in kidney transplantation since the initiation of the study in July. The cadence of enrollments is consistent with expectations since the initial three participants in the study require a safety monitoring 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.

In these studies nonhuman primates treated with anti <unk> antibodies.

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 two subjects in our phase <unk> clinical trial of Teikoku Rotten kidney transplantation. Since the addition of this study in July .

The cadence of enrollment is consistent with expectations since the initial three participants in the study.

Requires safety monitoring committee meeting to review the first months of data after each transplant.

Higher to the enrollment of the next participant.

Given the enrollment progress we are making we believe we can generate meaningful data on graph function quite quickly in this population given that acute rejection. Most often occurs within the first 90 days after transplant.

Steven Perrin: We remain on track to provide initial data from key three-month and six-month time points across multiple transplant participants in Q1 2023. In addition to the ongoing Phase Ib trial in kidney transplantation, this quarter we were very excited to announce the clearance of our US 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.

We remain on track to provide initial data from key three month and six month time points across multiple transpire participants in the first quarter of 2023.

In addition to the ongoing phase one b trial in kidney transplantation. This quarter, we were very excited to announce the clearance of our U S. IND application to evaluate <unk> for the prevention of kidney transplant rejection and patients undergoing de novo kidney transplant.

The study will be a multicenter open label active control study to assess the safety and efficacy of <unk> compared with <unk> and the preservation of allograft function and approximately 120 patients undergoing kidney transplantation.

Participants participants will be randomized one to one to receive either <unk> or active comparator to coronavirus as part of an immunosuppressive regimen.

Steven Perrin: The study's primary objective is to evaluate the efficacy of tegoprubart against standard of care, and the primary endpoint is the mean eGFR 12 months post-transplantation. Secondary objectives include safety, incidence of new onset diabetes, biopsy-proven rejection in participants, 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 2 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 1b study. We expect to run both the phase 1b and the phase 2 studies in parallel, so we can continue to report data and insights on tegoprubart from the phase 1b study while the phase 2 is running. Next, I'll move on to IgA nephropathy.

The study's primary objective is to evaluate the efficacy of <unk> against standard of care and the primary endpoint of the mean each year Egfr 12 months post transplantation.

Secondary objectives include safety incidence of nuance that diabetes biopsy proven rejection.

And participants as well as graft survival.

We are excited to investigate takeover Barton 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 <unk> study.

We expect to run both the phase <unk> and the phase two studies in parallel. So we can continue to report data and insights onto <unk> from the phase <unk> study, while the phase two is running.

Next I'll move on to Iga Nephropathy will remain excited about <unk> potential ability to show beneficial effect, both on the upstream and the downstream pathophysiology of the disease.

Steven Perrin: 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.

<unk> is the most common primary equal marilee in nephritis. It occurs in about 150000 Americans and a significant portion of these patients will end up progressing to end stage renal disease, where we'll need dialysis or transplant.

We believe <unk> 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 and nickel married itself.

In animal models of glomerular nephritis blocking CD 40 ligand is shown to be effective in reducing proteinuria.

Decreasing inflammatory infiltrate into the kidney and improving survival.

Steven Perrin: 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 H1 of next year.

We recently presented a poster at ASN kidney week, describing the trial design of our open label Phase Iia clinical trial in subjects with IGN 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 has a 96 week open label trial that will include 42 participants.

Or a high dose or low dose cohort.

The primary endpoint is change in proteinuria or 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 hydrous cohort of 21 participants at 10 Meg per kg in the first half of next year.

Steven Perrin: Additionally, we'll be providing an initial six-month open-label data from the study, including change in proteinuria from multiple subjects at six months in Q1 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 I 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, we are providing an initial six month open label data from this study including change in proteinuria from multiple subjects at six 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 C&I as the first line immunosuppressive regimens for islet cell transplant procedures.

There are over $1 3 million Americans living with type one diabetes.

We believe islet cell transplants could reduce or eliminate the need for <unk> insulin injections, but adoption is hampered by the toxicity of C&I is the current standard of care to prevent islet cell transplant rejection.

I'll, let cell transplant in nonhuman primate models have shown that animals treated with <unk> versus those C&I had longer rejection free survival as well as improved overall graph function.

Steven Perrin: 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 Q3, we opened our US site at the University of Chicago, where we are focusing our resources for the study. This site plans to enroll up to 6 Type I 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.

Additionally, animals <unk> regimen demonstrated better metabolic control and were healthy risk 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 the site plans to enroll up to six type one diabetes patients with hypoglycemic on awareness, who experienced significant swings in glucose levels that are associated with serious risk and co morbidities.

Our goal is to evaluate <unk> as the backbone of maintenance anti rejection therapy similar to assign for kidney transplantation.

And 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 III study by the end of the year.

Steven Perrin: 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 Q1 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 four distinct programs readout 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.

Given most subjects required multiple transplants in this indication by day 75, we believe we can generate meaningful data quickly with limited subjects and aimed to provide available three month data in the first quarter of 2023.

Okay.

I'll wrap up my update by turning to AOS, a program in which we announced positive topline 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 our carriage by the reception and excitement is generated.

These data marked a significant milestone for <unk> as the first of our four distinct programs readout and is further validated the favorable safety and tossed toxicity profile of taiko, Peru, Bart 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.

Steven Perrin: 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 DA mentioned, we have been deeply engaged with the ALS community, including key opinion leaders on potential next steps.

Lastly, the data was meaningful in providing potential read throughs for.

<unk> in Iga nephropathy, as well as kidney transplant.

Observed reductions in the levels of Iga AGM.

<unk> 40, and <unk>, Biomarkers, which are associated with class switching and b cell maturation with potential relevance to IGN given that reduction in Iga should result in decrease Iga levels, thus, reducing the pathogenic form of Iga and a reduction in circulating immune complexes.

There was also a reduction in propylene Batori chemo <unk> 10, as well as complement C. Three biomarkers associated with signs of renal transplant rejection.

As <unk> mentioned, we've been deeply engaged with the analyst community, including key opinion leaders on potential next steps.

Steven Perrin: 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.

Given the data we observed in the phase Iia, we're excited to explore other promising results reserve will translate into a larger study designed to measure clinical benefit and we are actively evaluating a range of approaches to fund potential future trial pending available financing.

With that I'll now turn the call over to Paul for our financial update.

Paul Little: Thank you, Steve. In addition to the financial results summarized in our press release, you can find additional information in our Form 10-Q, which we will file later today. The company reported a net loss of $10.5 million, or $0.73 per share for the three 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 three months ended September 30, 2022, compared to $7.7 million for the comparable period of 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.

Thank you Steve and.

In addition to the financial results summarized in our press release, you can find additional information in our Form 10-Q, which we'll file later today.

The company reported a net loss of $10 5 million or <unk> 73 per share for the three months ended September 32022.

Third to a net loss of $9 8 million.

<unk> 66 per share for the same period in 2021.

Research and development expenses were $7 5 million for the three months ended September 32012.

Two compared to $7 7 million for the comparable period of 2021, a decrease of 200000 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 head count.

Paul Little: G&A expenses were $3.1 million for the three months ended September 30, 2022, compared to $2.8 million for the comparable period in 2021, an increase of $300,000. 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 2 trial of tegoprubart for the prevention of organ rejection in subjects receiving a kidney transplant. Additional financing will be required to fund any future ALS clinical trials. With that financial update, let me turn the call back over to D.A.

G&A expenses were $3 1 million for the three months ended September 32022, compared to $2 8 million for the comparable period of 2021, an increase of 300000. The increase was primarily related to an increase in professional service costs general operating costs and stock based compensation costs.

As of September 30 of 2022, Hello, Don 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 runaway allows us to initiate the phase II trial of <unk> 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 <unk>.

David-Alexandre Gros: Thanks, Paul. I am highly encouraged by the progress our team has made across our clinical programs. With three 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 Q1 of next year, we look forward to providing meaningful initial data updates for three of our four programs, kidney transplant, IgAN, and islet cell transplant. In addition, next year, we expect to launch our phase 2 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?

Thanks, Paul.

I am highly encouraged by the progress our team has made across our clinical programs with three ongoing clinical trials, we remain committed to strong execution and our development efforts to close out the year, which we believe will leave us well positioned entering 2023, a potentially transformative.

Year for all of them.

In the first quarter for next year, we look forward to providing meaningful initial data updates for three of our four programs.

Kidney transplant again, and I'll, let 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 ILS program.

I'll now ask the operator to begin our Q&A session.

Operator.

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.

Thank you we will now begin the question and answer session to ask a question you May press.

Alright, then one on your Touchtone phone, if you're using a speaker phone please pick up your handset.

To withdraw your question please.

Then too.

Our first question today.

Sandra correct with Cantor Fitzgerald.

Gerald please.

Pete Stavropoulos: 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 percent 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 percent 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?

Good evening and thank you for taking our questions.

So.

At the American Society of Nephrology, you recently presented data for the ALS study showing a percent change from baseline for pro inflammatory biomarkers, including markers of B cell activation and T cell activation.

Just wanted to get your thoughts your perspective on the percent change of Iga and <unk>.

If you see similar changes in <unk> patients would it be enough to translate to clinical benefit.

David-Alexandre Gros: Steve, let me turn that over to you. Thanks for the question, Pete.

Steve Let me turn that over to you. Thanks for the question Pete.

Steven Perrin: 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 within 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 percent 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.

Yes, it's a good question I mean for Iga levels in AOS, we don't know what baseline levels mean.

We'd never I don't think any companies ever shown a reduction in iga levels, but the reductions were fast they occurred within right. After the first dose before subjects received second doses.

So the mechanism was very quick much like we've seen in the prevention of transplant rejection in primates.

And we saw a double digit percent reduction so as we dose escalated. So I would anticipate that those levels are meaningful but hardly trends for into <unk>. I think is unknown at this point.

Pete Stavropoulos: 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 benefits seen broadly across, you know, all IgAN patients?

Alright, and then again for I guess you know.

What is the target population that you believe.

<unk> benefited from Tango when you take into account.

The mechanism of action and its a potential disease modifying properties would it be earlier stage patients later stage patients.

Benefits seen broadly across all <unk> patients.

Yeah.

Steven Perrin: 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. 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.

I mean, I'll give you my perspective, and Jeff can jump in but I think across almost any disease indication at this point. The early you see interventions the better off you are outcomes tend to be.

We know that <unk> is a long term disease right I mean, it's chronic it last 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.

Pete Stavropoulos: Jeff, anything to add or?

Jeff anything to add.

Jeff Bornstein: Yeah. Thanks. Thanks, Pete. Well, I concur with Steve. As the disease progresses, if glomerular loss 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.

Yeah. Thanks, Thanks Pete.

Well I concur with Steve.

As the disease progresses, and <unk> lost in fibrosis that's in.

None none of these agents are going to reverse that.

So.

Earlier intervention is probably better across the board.

Our mechanism of action does doesn't work, both upstream and downstream so in patients where others could deal.

Information on the kidney itself, we would expect to see benefit not just in disrupting the upstream process at Iga, but there is that that distinction there the drug does work both upstream and downstream.

Patients who are too too far advanced.

Any of the mechanisms will work.

Pete Stavropoulos: 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 three initial data sets in Q1 2023?

Alright, thanks for the color and sorry last question is how many patients can we expect to see data for across the three initial datasets and <unk> 23.

David-Alexandre Gros: 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, which of the conferences we'll be able to present the data at.

So I mean.

We will share everything that we have that's available at the time it depends a little bit on.

When we when we end up presenting the data and so which of the conferences.

Will.

We'll be able to present to present the data at.

Pete Stavropoulos: Okay. Well, thank you. Thank you for taking my question.

Okay well. Thank you. Thank you for taking my there'll be there'll be a number similar to what <unk> seen other companies presents for their initial phase II data.

David-Alexandre Gros: It'll be a number similar to what you've seen other companies present for their initial phase two data.

Pete Stavropoulos: All right. Look forward to it. Thank you.

Alright look forward to it thank you.

David-Alexandre Gros: Thanks, Pete.

Thanks Pete.

Operator: The next question comes from Matthew Kaplan with Ladenburg Thalmann. Please go ahead.

The next question comes from Matt Kaplan with Ladenburg Thalmann. Please go ahead.

Matthew Kaplan: Hi, good evening, and 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 1b, 3- and 6-month data. What read-through will that data provide to the potential for the phase 2 superiority study that you plan to start next year?

Hi, good evening.

Congrats on the progress.

To follow up on Pete's question with.

With respect to the renal transplant program.

You announced that Youre going to report initial data from our first two subjects in the phase one b.

I mean six months data.

What lead through will that data provided to the potential for the phase III superiority study that you plan to start next year.

David-Alexandre Gros: Thanks, Matt. Jeff, why don't I turn that over to you?

Thanks, Matt.

Jeff why don't I turn that over to you.

Jeff Bornstein: All right. Thank you, D.A. Thanks, Matt. It's, you know, the study, the stage of 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, and potentially more like on point for your question is how is that graft functioning? What do their GFRs look like? And, 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.

Alright. Thank you, yes, thanks, Matt.

The study state.

The pilot study designed to show safety and also preliminary efficacy rates in what we expect to see is that we can administer we can administer this regimen safely do these patients and it prevents rejection and potentially more like on point for your question is how does that graph functioning.

What do you what do their GFR is look like and how is that going to inform our our endpoint for the next study. So it will be a few patients only so.

But we will start to get a sense of how they're doing how well they're doing how they're functioning.

Jeff Bornstein: Of course, 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.

Of course, when you look at the side effect profile right to make sure that.

We're looking at whether or not theyre, developing diabetes or whether it's preventing it.

Matthew Kaplan: Okay. That's helpful.

Okay. That's helpful.

David-Alexandre Gros: The phase 2 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 tegoprubart, that's the same.

And that these are designed are designed in a similar manner.

So other than the fact that one of them is open and the other one is control.

In terms of how the patients are being treated and how theyre getting to go for Bart.

Yeah.

Matthew Kaplan: Okay. Then 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 three-month data that you're going to report in Q1, what we should be looking for there?

Okay.

And then just with your your islet cell transplant program I guess youre expecting.

First patient enrollment in the near term.

You already have shown strong preclinical data there.

Help us think about the initial data of the three month data that you know you're going to report in the first quarter, what we should be looking for there.

Yeah.

David-Alexandre Gros: Thanks, Matt. Jeff, let me turn that to you.

Thanks, Matt Jeff.

Turning now to you.

Jeff Bornstein: Right. Thank you. You know, similarly to our kidney transplant study, we'll 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.

Alright, thank you so.

Similar to similarly too.

Our kidney transplant study, we will we'll give an update of.

Who has been.

The number that's been transplanted and how <unk>, how theyre doing so.

The adverse event profile.

Graft function and rejection.

Okay.

David-Alexandre Gros: Here we'll look at, as part of that, we'll also see, right, with regards to graft function, whether those, 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 to 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.

We'll look at as part of that we'll also see right with regards to graft function.

Whether those are.

Those patients are doing in terms of glucose control of the need for exogenous insulin.

So recall that most patients today, if they get a islet cell transplant require repeat transplant typically about 75 to 90 days later.

In order to have sufficient glucose control.

So our hope is that with only one transplant, we might be able to achieve that.

Matthew Kaplan: Great. Thanks, guys. Look forward to the readouts in Q1.

Alright, great.

Thanks, Thanks, guys look forward to the Readouts in the first quarter.

Yes.

Operator: The next question comes from Thomas Smith with SVB Securities. Please go ahead.

The next question comes from Thomas Smith with <unk> Securities. Please go ahead.

Thomas Smith: Hey, guys. Good afternoon, and 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?

Hey, guys. Good afternoon, thanks for taking the questions.

Just wondering if you could comment on some of the latest developments here across the CD 40 landscape.

I know back in September we saw some positive topline data from her.

Horizon CD 40 ligand in Shogun syndrome, 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 integrated indication like sugar.

David-Alexandre Gros: Sure. Steve, do you wanna talk about some of the recent data? I'm happy to talk about how we think about indications.

Sure Steve do you want to talk about some of the recent data and then I'm happy to talk about how we think about indications.

Steven Perrin: 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. 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.

Yes. Thank.

Thank you thanks, Great question.

We're excited about the data it really continues to validate the mechanism of action for the pathway.

They showed data that was similar to what Novartis had presented with their earlier <unk>.

Our study compared to what they are running today.

So classic auto antibody mediated diseases like showrooms in lupus continue to be aligned with.

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. So we thought that data was encouraging.

David-Alexandre Gros: All right. Then in terms of how we approach thinking about indications, when we picked our initial indications, we looked at three different things. One 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 approvals, the regulatory path would look like. And 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.

Alright.

And then in terms of how we approach thinking about indications.

We picked our initial indications we looked at three different things. One was we want indications where there was a good understanding of the pathophysiology of the disease and how an anti CD 40 ligand would play into that indication.

We then looked at indications, where we had a good understanding of what the path two approvals the regulatory path would look like.

And third we saw it out indications that could be executed by a smaller biotech.

And its 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 CD 40 ligand could make sense, including Sjogren switch you just would you just brought up.

David-Alexandre Gros: Right now from our perspective, we remain focused on our indication. Today we don't have the financial flexibility to add another indication. Obviously, in the future as we grow, we could consider adding other indications as well.

But right now from our perspective, we remain focused on our indication in <unk>.

Today, we don't have the financial flexibility.

To add another indication.

But obviously.

In the future as we grow.

Consider adding other indications as well.

Thomas Smith: Got it. Okay, that's helpful. 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.

Got it Okay. That's helpful. And then I was just wondering if you could comment on the.

The latest developments with Novartis and their anti <unk> 40, a gallon math it seems like they have.

Recently stopped.

Second solid organ transplant study and liver transplant.

It would be helpful. If you just share your thoughts around this program and maybe just remind US why you think targeting CD 40 ligand is a superior approach in solid organ transplant.

David-Alexandre Gros: Sure. Let me turn that over to Steve to go through the CD40 versus CD40L in transplant.

Sure.

Let me turn that over to Steve to go through the CD 40 are versus CD 40 outlet and transplant.

Steven Perrin: 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. One is that the receptor and ligand have very different expression patterns in the body.

Yes, so great question I'll answer that and then maybe I'll hand, it over to Jeff to talk about the skull Mab liver.

Recent results there. So so the history there as we know for a long time, we've known 30 years. They are blocking the ligand tends to be more efficacious than blocking the receptor not only in the context of preventing a short and long term transplant rejection, but similar data exists for our 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. One is that the receptor ligand have very different expression patterns in the body.

Steven Perrin: 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, and then there's mechanisms to remove it from the cell surface to actually prevent autoimmunity. That's one. 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.

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 interesting presenting cells, including b cells dendritic cells NK cells and specialized intra presenting cells in your organs, whereas the ligand that's expressed on T cells.

Constituent if it's not there all the time, it's only on the surface transiently when the T cell is activated after entrant antigen presentation, and then theres mechanisms to remove it from the cell surface to actually prevent autoimmunity.

That's one one rationale is up the expression patterns are very different so that antibodies targeting these will have different biological outcomes for.

The second one is that when people think about blocking this pathway and blocking CD 40, login. They think youre only blocking co stimulatory activity via CD 40 receptor and Thats not true CD 40, logging can actually activate multiple different co stimulatory pathways on antigen presenting cells not only through CD 40 receptor.

Steven Perrin: 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.

But as an example through the Mac complex, which has been shown to be very important to the CD eight cytotoxic CDA positive transplant rejection theres a couple of other integrant that CD 40 ligand also can control and activate subpopulations, including various integral and so that's the second one is that blocking the ligand.

Can block multiple co stimulatory pathways and then the third one which is probably the most unique to see 40 ligand and potentially the most exciting.

Steven Perrin: 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 D.A. on iscalimab and liver? I'm happy to as well, but if one of you guys wanna take it.

<unk> on the cell surface of CD four positive T cells, not only does it block their pro inflammatory differentiation when you block the log in at actually re polarized them to become regulatory T cells, which can secrete.

All are going to keep the conflict TGF beta IL 10, and create this tolerant environment in the context of preventing rejection. So those are probably the biggest differentiation points.

Jeff did you want to comment or da on a scale of <unk> and liver I'm happy to as well, but if one of you guys want to take it.

Jeff Bornstein: 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 that 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 that program.

If 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 the study design features that we might.

And you are doing differently in our program going forward.

It's difficult to comment on our competitor program, especially when they haven't made any of the actual trial results public.

But I think there's still opportunities for us to learn from what they've done and.

<unk> tightened things up and study design around things like induction agents and also the role of the bias players in.

These open label studies, and who gets biopsied.

I think we are 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 that program.

David-Alexandre Gros: 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. There is an upside to that, is that it's this wasn't stopped for a safety reason. It continues to underscore just as to date, the safety of the class.

Just a final thought.

Novartis has said is that they showed.

Inferiority they stopped the study's early because of the trend.

Trending towards inferiority versus C&I.

But there is a an upside to that is that it's this wasn't stopped for a safety reason.

So it continues to underscore just as to date the safety of the class.

Thomas Smith: 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 2 kidney transplant study in the US, and I guess elaborate on what other gating factors are there to getting the study up and running in 2023.

Got it okay I appreciate the color guys and then.

Maybe just lastly.

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 up and running in 2003.

David-Alexandre Gros: Thank you. I mean, right now we're just working with our CROs on beginning to execute the study. So it's really, we're working towards that goal, so there aren't any major, large gating items.

Thank you.

I mean, right now were just working with our Crows on.

And beginning to execute the study.

So it's really.

We're working towards that goal there arent any major large gating items.

Thomas Smith: Okay. Got it. Awesome. Thanks, guys. Appreciate you taking the questions.

Okay got it awesome. Thanks, guys I appreciate you taking the questions.

Yes.

Operator: Again, if you have a question, please press star then one. The next question comes from Rami Katkhuda with LifeSci Capital. Please go ahead.

Again, if you have a question. Please press star and one the next question comes from Ramey, Canada with lifestyle capital. Please go ahead.

Rami Katkhuda: 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 three-week dosing frequency were chosen for the phase 2a study in IgAN? I realize it's quite different from the ALS study.

Hey, guys. Thanks for taking my questions as well just a quick one for me, but can you touch upon how the pending <unk> doses as well as the every three weeks dosing frequency were chosen for the phase III study and again I realize it's quite different from the Alpha study.

David-Alexandre Gros: Great. Hey, Rami. Thank you for the question. Steve, let me turn that over to you.

Great Hey, Rami. Thank you for the question Steve.

Steve Let me.

Let me turn that over to you.

Steven Perrin: Yeah. I mean, we learned a lot from the phase 2 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. So 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. So in order to start to increase exposure levels early on while being very cautious about safety profile, we decided to dose every other week.

Yes, I mean, we learned a lot from the phase two study is to remember that was our first multiple.

Sending dose study in humans. The other study we had done was a single ascending dose dose in healthy volunteers for the most part.

So we're learning a lot about the pharmacokinetics of the drug.

We kind of knew from our Primate studies study that were two week dosing, which we had planned.

It was due to the fact that we had started dosing in that study. If you remember very low the lowest dose cohort was one meg per kg. So in order to start to increase exposure levels early on while being very cautious about safety profile, we decided to dose every other week and we hypothesize that by doing that we've really never reached steady state.

Steven Perrin: 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 three-week dosing. Jeff, I don't know if you wanna add some color to that, but that's kind of a high level summary.

That exposure levels would increase over time, which is what we observed in the study even up to eight Meg per kg.

But we utilize that data to start to think about how one would design the appropriate exposure levels for autoimmune indications like Iga nephropathy.

It's how we selected the five and 10 mid dose and renewed based on that data we could grow it every three week dosing.

I don't know if you want to add some color to that but that's kind of a high level summary.

Jeff Bornstein: No, I just, I concur. The doses translate actually pretty well from ALS to IgAN.

I concur.

Does this translate actually pretty well from AOS again.

Rami Katkhuda: Got it. I guess is the end goal to make a subcu formulation of tegoprubart for diseases like ALS and IgAN?

Got it and I guess is the end goal to make a sub Q formulation of scope apart for you.

It means like Alan I am.

David-Alexandre Gros: Thanks, Rami. We're working on a subcutaneous formulation as well. There are certain diseases where, for example, transplant, or ALS, or an IV formulation from a competitive perspective could be acceptable. For example, in IgAN, over time, we would look to use a subcutaneous formulation.

So we are.

Thanks, Rami, we're working on a subcutaneous formulation as well.

So there are certain diseases, where for example, transplant, where a or ALS, where an IV formulation from from a competitive perspective could be acceptable.

But for example in Oregon.

Over time, we would look to use a subcutaneous formulation.

Rami Katkhuda: Got it. Thank you.

Got it thank you.

Operator: This concludes our question and answer session. I would now like to turn the conference back over to D.A. Gros for any closing remarks.

This concludes our question and answer session I would now like to turn the conference back over to Dr. Rolf any closing remarks.

David-Alexandre Gros: Thank you for your assistance, operator, and thank you all for joining us on today's call. Have a great evening.

Thank you for your assistance operator, and thank you all for joining us on today's call have a great evening.

Okay.

Operator: This conference is now concluded. Thank you for attending today's presentation. You may now dis-

This conference has now concluded. Thank you for attending today's presentation you may now.

Okay.

Q3 2022 Eledon Pharmaceuticals Inc Earnings Call

Request a DemoDemo

ELDN

Eledon Pharmaceuticals

Earnings