Q1 2022 Eledon Pharmaceuticals Inc Earnings Call

May 12, 2022

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Operator: Greetings, and welcome to the Eledon Pharmaceuticals' Q1 financial results conference call. At this time, all participants are in a listen-only mode. A question and answer session will follow the formal presentation. As a reminder, this conference is being recorded today, 12 May 2022. I would now like to turn the conference call over to Paul Little, Chief Financial Officer of Eledon. Please go ahead.

Greetings and welcome to the <unk> Pharmaceuticals first quarter financial results Conference call. At this time all participants are in a listen only mode. A question and answer session will follow the formal presentation. As a reminder, this conference is being recorded today May 12, 2022, I would now like to turn the conference call.

Greetings and welcome to the Ellendal Pharmaceuticals first quarter financial results conference.

At this time, all participants are in a listen-only mode. A question and answer session will follow the formal presentation.

As a reminder, this conference is being recorded today, May 12, 2015.

I would now like to turn the conference call over to Paul Little, Chief Financial Officer of Elle Donne. Go ahead.

<unk> over to Paul Little Chief Financial Officer of Eldar. Please go ahead.

Paul Little: Good afternoon, everyone, and thank you for joining Eledon's Q1 2022 operating and financial results conference call. I'm joined on today's call by David-Alexandre Gros, Chief Executive Officer, Steve Perrin, President and Chief Scientific Officer, and Jeff Bornstein, Chief Medical Officer. Earlier today, Eledon issued a press release announcing financial results for the first quarter ended 31 March 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 Elanon's first quarter 2022 operating and financial results conference call. I'm joined on today's call by David Alexander Groh, chief executive officer, Steve Perrin, president and chief scientific officer, and Jeff Borenstein, chief medical officer. Earlier today, Elanon issued a press release announcing financial results for the first quarter ended March 31, 2022.

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

I'm joined on today's call by David Alexandra <unk>, Chief Executive Officer, Steve Perrin, President and Chief Scientific Officer, and Jeff Bornstein, Chief Medical Officer.

Earlier today.

<unk> issued a press release announcing financial results for the first quarter ended March 31 2022.

you may access the release under the investors tab on our company's website at elodont.com.

You may access the release under the investors tab on our company's website at Amazon Dot com.

I would like to remind everyone that statements made during this conference call relating to Elodom's expected future performance.

I would like to remind everyone that today that statements made during this conference call relating to <unk> expected future performance fees.

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 Eladon. Eladon expressly disclaims any duty to provide updates to its forward-looking statements.

<unk> 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.

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 recent 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.

Actual outcomes and results could differ materially from these forecasts due to the impact of many factors beyond the control of Olive Garden Hello.

Hello, Don expressly disclaims any duty to provide updates to its forward looking statements, whether as a result of new information future events or otherwise.

whether as a result of new information, future events, or otherwise.

Participants are directed to the risk factors set forth in the Illinois reports filed with the U.S. Securities and Exchange Commission.

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 Eladon CEO , Dr. David Alexander-Grow, DA.

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

David-Alexandre Gros: Thank you, Paul, and thank you all for joining the call today. We made important progress during Q1 2022, and look forward to continuing this momentum through the remainder of the year. Our priority this year has been and remains executing on our four clinical trials in three therapeutic areas. Neurodegeneration, focusing on ALS, transplantation, focusing on kidney and islet cell transplantation for type 1 diabetes, and autoimmunity, focusing on IgA nephropathy, or IgAN. Before I turn the call over to Steve to discuss our clinical development pipeline, I would like to provide a brief recap on our recent progress. In our Phase 2a study of tegoprubart in adults with ALS, we completed dosing and visits for all subjects enrolled and remain on track to report top-line data from this study this quarter.

Thank you Paul.

Thank you, Paul. And thank you all for joining the call today.

And thank you all for joining the call today.

We made important progress during the first quarter of 2022 and look forward to continuing this momentum through the remainder of the year.

Our priority this year has been and remains executing on our four clinical trials in three therapeutic areas.

Our priority this year has been and remains executing on our four clinical trials in three therapeutic areas. Neurodegeneration focusing on ALS, transplantation focusing on kidney and islet cell transplantation for type 1 diabetes and autoimmunity focusing on IgA nephropathy or IgAM.

Degeneration, focusing on a L S.

Plantation, focusing on kidney and islet cell transplantation for type, one diabetes and autoimmunity, focusing on Iga nephropathy or <unk>.

Before I turn the call over to Steve to discuss our clinical development pipeline, I would like to provide a brief recap on our recent progress.

Before I turn the call over to Steve to discuss our clinical development pipeline.

I would like to provide a brief recap on our recent progress.

In our Phase 2A study of the Goprobart in adults with ALS, we completed dosing and visits for all subjects enrolled.

In our phase Iia study is to go.

In adults with AOS, we completed dosing in visits for all subjects enrolled.

and remain on track to report top line data from this study this quarter.

And remain on track to report topline data from this study this quarter.

David-Alexandre Gros: In our Phase 2a study in tegoprubart in adults with IgAN, we recently announced that we have begun dosing patients. We have regulatory approval for clinical trial sites in five countries with plans to expand to additional countries, and we are therefore on track to have six-month data available later this year. In transplantation, we now have active sites for kidney transplantation in Canada and the United Kingdom, have an open Canadian site for islet cell transplantation, and are preparing to open up a US site for islet cell transplantation in the middle of the year. Similar to our IgAN trial, we plan to communicate our available transplant data at the end of the year. Finally, we recently published a meta-analysis demonstrating the benefits of targeting anti-CD40 ligand as opposed to targeting anti-CD40 receptor in non-human primate models of kidney transplantation.

In our phase <unk> study in <unk> in adults with <unk> again.

In our phase 2A study into goprobart in adults with IGAN, we recently announced that we have begun dosing patients. We have regulatory approval for clinical trial sites in five countries with plans to expand additional countries. And we are therefore on track to have six month data available later this year.

Recently announced that we have begun dosing patients we have regulatory approval for clinical trial sites in five countries with plans to expand to additional countries and we are therefore on track to have six months data available later this year.

In transplantation, we now have active sites for kidney transplantation in Canada, and United Kingdom have an open Canadian site for islet cell transplantation and are preparing to open up our U S site.

In transplantation, we now have active sites for kidney transplantation in Canada and the United Kingdom, have an open Canadian site for islet cell transplantation and are preparing to open up a US site for islet cell transplantation in the middle of the year.

For islet cell transplantation in the middle of the year.

Similar to our again trial, we plan to communicate our available transplant data at the end of the year.

Similar to our ARGUN trial, we plan to communicate our available transplant data at the end of the year.

Finally, we recently published a meta-analysis demonstrating the benefits of targeting anti-CD40 ligand as opposed to targeting anti-CD40 receptors.

Finally, we have recently published a meta analysis, demonstrating the benefits of targeting anti CD 40 ligand as opposed to targeting anti CD 40 receptor.

in non-human primate models of kidney transplantation.

Nonhuman primate models of kidney transplantation.

David-Alexandre Gros: The meta-analysis found a median rejection-free survival of 352 days in anti-CD40 ligand-treated animals versus 131 days in the anti-CD40 treated animals and only 6 days in the untreated animal control group. Moreover, the median rejection-free survival after cessation of treatment was 230 days in anti-CD40 ligand-treated animals versus 60 days in anti-CD40 treated group. I'll now turn the call over to Steve Perrin, our President and Chief Scientific Officer, to provide more details on our development programs. Steve?

The meta analysis found a median rejection free survival of 352 days in the anti CD 40 ligand treated animals versus 131 days in the anti CD 40 treat the animals and only six days in the untreated animals control group.

The meta-analysis found immediate rejection-free survival of 352 days in the anti-CD40 ligand treated animals versus 131 days in the anti-CD40 treated animals and only 6 days in the untreated animal control group.

Moreover, the median rejection free survival after cessation of treatment was 230 days in anti-CD40 ligand treated animals versus 60 days in anti-CD40 treated group.

Moreover, the median rejection free survival after cessation of treatment was 230 days and the anti CD 40 ligand treated animals versus 60 days and anti CD 40 treated group.

I'll now turn the call over to Steve <unk>, our President and Chief Scientific officer to provide more details on our development programs.

I'll now turn the call over to Steve Perrin, our President and Chief Scientific Officer to provide more details on our development programs.

Steve.

Steve Perrin: Thank you, D.A. As D.A. mentioned, we currently have four open clinical programs exploring the treatment of ALS, the prevention of allograft rejection, both in kidney and in islet cell transplantation, and IgA nephropathy. In the ALS Phase 2 trial, all patient visits are now complete. All patient samples have been analyzed, and we're approaching database lock, thus keeping us on track to provide top-line data this quarter. The study is an ascending dose trial that evaluates four dose levels of tegoprubart administered every four 12 weeks. Data from this study will include safety and tolerability of tegoprubart, as well as multiple categories of biomarker endpoints, with each subject serving as their own control by comparing changes from baseline. In the first category of biomarkers, we'll assess CD40 ligand target engagement because mechanistically inhibiting CD40 ligand function has profound effects on B-cell maturation, antibody production, and antibody class switching.

Thank you D a.

As Jay mentioned, we're currently have four open clinical programs exploring the treatment of AOS, but prevention of allograft rejection, both in kidney and in islet cell transplantation.

As DA mentioned, we currently have four open clinical programs exploring the treatment of ALS, the prevention of allograft rejection, both in kidney and in islet cell transplantation, and IGA nephropathy.

And Iga nephropathy.

And they gave us phase two trial all patient visits are now complete.

In the ALS phase 2 trial, all patient visits are now complete.

All patient samples have been analyzed and we're approaching database lock, thus keeping this on track to provide top-line data this quarter.

All patient samples have been analyzed and we're approaching database lock thus keeping us on track to provide top line data this quarter.

The study is an ascending dose trial that evaluates four dose levels of <unk> administered every 12 weeks.

The study is an ascending dose trial that evaluates four dose levels of Tegoprubar administered every for 12.

Data from this study will include safety and tolerability of TIGO proof art, as well as multiple categories of biomarker endpoints with each subject surfing as their own control by comparing changes from base to base.

Data from this study will include safety and Tolerability of to go prove art as well as multiple categories of biomarker endpoints with each subject surfing as their own control by comparing changes from baseline.

In the first category of biomarkers, we'll assess CD40 ligand target engagement.

And the first category of Biomarkers with a C. D 40, <unk> target engagement, because mechanistically inhibiting CD 40 wagon function.

because mechanistically inhibiting CD40 ligand function has profound effects on B-submatturation, antibody production, and antibody cluster.

As profound effects on B cell maturation antibody production and antibody class switching.

Steve Perrin: We anticipate we'll be able to assess the inhibition of CD40 ligand target engagement by tegoprubart with biomarkers of B-cell functions, including CXCL13 and others. The secondary biomarker category is changes in pro-inflammatory chemokines and cytokines upregulated in people living with ALS. There is a long history of ALS data describing increases of pro-inflammatory signals in circulation, including TNF-α, MCP-1, IL-6, IL-1, and EN-RAGE. We anticipate that in subjects with elevated levels, the blocking of CD40 ligand will result in an overall decrease of these and other pro-inflammatory markers in circulation. We anticipate in subjects with elevated levels of pro-inflammatory chemokines and cytokines, the blocking of CD40 ligand will result in an overall decrease of pro-inflammatory markers in circulation.

We anticipate we'll be able to assess the inhibition of CD 40 ligand target engagement by tube Gopro, Bart with Biomarkers of B cell functions, including <unk> <unk> and others.

We anticipate we'll be able to assess the inhibition of CD40 ligand target engagement by Tobog to go pro-BART with biomarkers of B-cell functions, including CXCL13 and all that.

The secondary biomarker, Karen Gert categories changes in pro inflammatory chemo kinds in cytokines up regulated in people living with a loss.

secondary biomarker categories, changes in pro-inflammatory chemokines and cytokines upregulated in people living with ALS.

There is a long history of ALS data describing increases of pro-inflammatory signals in circulation, including TNF-alpha, MCP-1, IL-6, IL-1, and in RAID.

There was a long history of AOS data describing increases a pro inflammatory signals in circulation, including TNF Alpha MCP, one IL six IL, one and enraged.

We anticipate that in subjects with elevated levels, the blocking of CD40 ligand will result in an overall decrease of these and other pro-inflammatory markers in circulation.

We anticipate that in subjects with elevated levels of blocking of CD 40 ligand will result in an overall decrease of these and other pro inflammatory markers in circulation, we anticipate in subjects with elevated levels of pro inflammatory chemo kinds of cytokines blocking of CD 40 ligand.

We anticipate in subjects with elevated levels of pro-inflammatory chemokines and cytokines, the blocking of CD40 ligand will result in an overall decrease of pro-inflammatory markers in circulation.

<unk>, an overall decrease of pro inflammatory markers in circulation.

Steve Perrin: As such, as part of our biomarker strategy, we'll look at the comprehensive panel of more than 30 chemokines and cytokines to assess dose response and ALS patient response to tegoprubart exposure levels. Finally, we will also assess exploratory endpoints, including changes in ALS functional rating scale or ALSFRS and levels of neurofilament light chain in circulation. We deem these endpoints exploratory given the uncertainty that 12 weeks of therapy is sufficient time to see an effect on these endpoints. There are several critical objectives associated with the ALS trial. Confirmation of safety and tolerability through the highest dose cohort is important not only for the ALS program, but also for our other programs. The first objective beyond safety and tolerability is to demonstrate target engagement with exposure to tegoprubart.

As such, as part of our biomarker strategy, we'll look at a comprehensive panel of more than 30 chemokines and cytokines to assess dose response and ALS patient response to go provide exposure levels.

Such as part of our biomarker strategy will look up a comprehensive panel of more than 30, 30, chemo constant cytokines to assess a dose response and ALS patient response to ticket to go promote exposure levels.

And finally, we will also expect exploratory endpoints, including changes in ALS Functional Rating Scale, or ALSFRS, and levels of neurofilament, light chain, and circulation.

Finally, we were also a sucks exploratory endpoint endpoints, including changes in ALS functional rating scale or <unk> for us and levels of neuro filament light chain in circulation, we deem these endpoints exploratory given the uncertainty the 12 weeks of therapy is sufficient time to see an effect on these endpoints.

We deem these endpoints exploratory given the uncertainty that 12 weeks of therapy is sufficient time to see an effect on these endpoints.

Yeah.

There are several critical objectives associated with the ALS trial. Confirmation of safety and tolerability through the highest dose cohort is important not only for the ALS program, but also for our other programs.

There are several critical objectives associated with the AOS trial confirmation of safety and Tolerability through the highest dose cohort is important not only for the Airbus program, but also for our other programs.

The first objective beyond safety and Tolerability is to demonstrate target engagement with exposure to ticket to go for Bart.

The first objective beyond safety and tolerability is to demonstrate target engagement with exposure to go pro-BART.

Steve Perrin: CD40 ligand is on the surface of activated T cells in the context of antigen presentation and germinal center formation. During the process of germinal center formation, B-cell proliferation, maturation, and the generation of high-affinity IgG antibodies occur, induced by the expression of chemokines and cytokines such as CXCL13. As a result, based on CD40 ligand's mechanism, we expect tegoprubart to inhibit germinal center formation in B-cell maturation and thus decrease the generation of cytokines such as CXCL13. There is a significant body of published literature showing increased levels of pro-inflammatory chemokines and cytokines such as TNF-α, MCP-1, IL-1, IL-6, and EN-RAGE, as well as others in patients with ALS. Based on years of experimental data elucidating the role of CD40 ligand activation in inflammatory induction, the inhibition of CD40 ligand signaling by tegoprubart should thus reduce pro-inflammatory cytokine production.

The CD4-UI GAN is on the surface of activated T cells in the context of antigen presentation in germinal cells.

For you I can just on the surface of activated T cells in the context of antigen presentation and Germinal Center formation.

During the process of germinal center formation, B cell proliferation, maturation, and the generation of high affinity IgG antibodies occur induced by the expression of chemokines and cytokines such as CXEL13.

During the process of Germinal Center formation, B cell proliferation maturation and the generation of high affinity antibodies.

Antibodies occur induced by the expression of chemo kinds in cytokines, such as <unk> <unk> <unk>.

As a result, based on CD40 ligand's mechanism, we expect TIGO-PROBAR to inhibit germinal center formation and B-cell maturation, and thus decrease the generation of cytokines such as CXL13.

As a result based on CD 40 ligand mechanism, we expect to go back to inhibit Germinal Center formation in B cell maturation and Thats decreased the generation of cytokines, such as <unk> <unk>.

There is a significant body of public researchers showing increased levels of inflammatory chemokines and cytokines, such as TNFL for MCP1.

There is a significant body of published central showing increased levels of telemetry chemo karnes and cytokines, such as TNF Alpha MCP, one IL, one IL 600 reached as well as others in patients with ALS based.

IL-1, IL-6, and enraged as well as others and patients with ALI.

Based on years of experimental data elucidating the role of CD40 ligand activation in inflammatory induction, the inhibition of CD40 ligand signaling by Tegel-ProBart should thus reduce pro-inflammatory cytokine.

Based on years of experimental data elucidating the role of CD 40 block C. D 40 ligand activation inflammatory induction.

Ambition of CD 40 ligand signaling by ticket per Bart should thus reduce pro inflammatory cytokine production.

Steve Perrin: In sum, an exciting positive outcome from this clinical program would be a demonstration of both target engagement and a reduction in pro-inflammatory cytokines. Observing target engagement and reduced inflammation would demonstrate tegoprubart's best-in-class immune modulatory potential in ALS. In addition to these biomarkers, we are collecting monthly ALS functional rating scores or ALSFRS, a common endpoint in ALS clinical trials, as well as measuring neurofilament light chain or NFL levels in circulation. NFL is a prognostic marker of disease progression in ALS, and at higher levels correlate with faster disease progression, but it's unclear at this point if levels of NFL will correlate with therapeutic benefit. Because of the relatively limited number of subjects and duration of the trial, however, we view these endpoints as exploratory.

And some and exciting positive outcome from this clinical program would be a demonstration of both target engagement and a reduction in pro inflammatory cytokines.

In sum, an exciting positive outcome from this clinical program would be a demonstration of both target engagement and a reduction in pro-inflammatory cytokines.

Absorbing target engagement and reduced inflammation would demonstrate to go pro to best in class immune modulatory potential in ALI.

Absorbing target engagement and reduce inflammation would demonstrate to gopro to best in class immune module toward potential in AOS.

In addition to these biomarkers, we are collecting monthly ALS functional rating scores for AOS off for us a common endpoint in AOS clinical trials as well.

In addition to these biomarkers, we are collecting monthly ALS functional rating scores or ALS FRS, a common endpoint in ALS clinical trials, as well as measuring neurofilament light chain or NFL levels in circulation.

What was measuring nerf <unk> light chain or NFL levels in circulation.

NFL as a prognostic marker of disease progression in ALS and at higher levels correlate with faster disease progression, but it's unclear at this point to have levels of NFL will correlate with therapeutic benefit.

NFL is a prognostic marker of disease progression in ALS, and at higher levels correlate with faster disease progression, but it's unclear at this point if levels of NFL will correlate with therapeutic benefits.

Because of the relatively limited number of subjects and duration of the trial, however, we view these endpoints as exploratory.

Because of the relatively limited number of subjects and duration of the trial. However, we view these endpoints is exploratory.

Steve Perrin: While not expected, given the relatively small size and limited duration of the study, if we are able to show a relationship between target engagement, reduction in pro-inflammatory markers in either a change in disease progression measured by ALSFRS or a reduction in NFL levels, we would consider this a tremendous win that further validates that a reduction in pro-inflammatory markers by tegoprubart may provide therapeutic benefit for people living with ALS. I'll now switch to discuss our transplantation studies. The cornerstone for the prevention of transplant rejection is the utilization of calcineurin inhibitors or CNIs. Although CNIs are associated with significant side effects including hair loss, beta cell toxicity causing new-onset diabetes, neurotoxicity causing neurological symptoms including tremors and decreased cognitive function. CNIs are also associated with increased risk of heart disease as well as increase in infections and malignancies.

while not expected given the relatively small size and limited duration of the study, if we were able to show a relationship between target engagement, reduction in pro-inflammatory markers, and either a change in disease progression measured by ALS, FRS, or reduction in NFL levels, we would consider this a tremendous win that further validates that a reduction in pro-inflammatory markers by Take-O-Pro-Bart may provide therapeutic benefit for people living with ALS.

While not expected given the relatively small size and liberate duration of the study.

We were able to show a relationship between target engagement reduction in pro inflammatory markers and either a change in disease progression measured by ILS FRS or reduction in <unk> levels were considered a tremendous win that further validates that our reduction in pro inflammatory markers by take hold for Bart may provide therapeutic benefit for people living.

With a loss.

I'll now switch to discuss our transplantation studies.

The cornerstone for the prevention of transplant rejection is the utilization of <unk> inhibitors, where C&I, although C&I are associated with significant side effects, including hair loss beta cell toxicity, causing a new insight diabetes.

Cornerstone for the prevention of transplant rejection is the utilization of calcineurin inhibitors or CNI.

Although CNIs are associated with significant side effects including hair loss, beta cell toxicity causing new inside diabetes, neurotoxicity causing neurological symptoms including tumors and decreased cognitive function, and CNIs are also associated with increased risk of heart disease, as well as increase in infections and malignant symptoms.

<unk> toxicity, causing neurological symptoms, including Termers and decreased cognitive function and C&I is are also associated with increased risk of heart disease as well as increase in infections and malignancies.

Steve Perrin: Additionally, the chronic utilization of CNIs to prevent graft rejection has been associated with nephrotoxicity in up to 100% of patients after 10 years, which can paradoxically shorten graft survival in the same organs that CNIs are being taken to protect. By improving the safety and tolerability of first-line immunosuppression, we believe that tegoprubart has the potential to both improve patient quality of life and overall morbidity in the near term, as well as ultimately improve graft survival and rates in the long term. Only a few patients are needed to provide an early assessment of the prevention of acute rejection in the absence of CNIs, which have been the mainstay of immunosuppressive regimens to prevent acute rejection for the last 25 years. We have active sites in both Canada and the United Kingdom to conduct a Phase 1b clinical trial of tegoprubart in kidney transplantation.

Additionally, the chronic utilization of CNIs to prevent graft rejection has been associated with nephrotoxicity in up to 100% of patients after 10 years, which can paradoxically shorten graft survival, and the same organs of CNIs are being taken to protect.

Additionally, the chronic utilization of C&I is to prevent graft rejection has been associated with nephrotoxicity it up to 100% of patients after 10 year towards paradoxically shortened graft survival and the same organs of C&I are being taken to protect buying.

By improving the safety and Tolerability of first line immunosuppression, we believe that <unk> has the potential to both improve patient quality of life and overall morbidity in the near term as well as ultimately improve graft survival and rates in the long term.

By improving the safety and tolerability of first-line immunosuppression, we believe that Tag-O-ProBot has the potential to both improve patient quality of life and overall morbidity in the near term, as well as ultimately improve grass survival and rates in the long run.

Only a few patients are needed to provide an early assessment of the prevention of acute rejection and the absence of Cni's, which had been the mainstay of immunosuppressive regimens to prevent acute rejection for the last 25 years.

Only a few patients are needed to provide an early assessment of the prevention of acute rejection in the absence of CNIs, which have been the mainstay of immunosuppressive regimens to prevent acute rejection for the last 25 years.

We have active sites in both Canada and the United Kingdom to conduct a Phase 1B clinical trial to go for rotten kidney transplantation.

Active sites in both Canada, and the United Kingdom to conduct a phase <unk> clinical trial of <unk>.

To go right in kidney transplantation.

Steve Perrin: This open label study is planning to enroll up to 12 patients undergoing renal transplant with primary endpoints of safety and pharmacokinetics, as well as exploratory endpoints including biopsy-proven rejection, change in eGFR, and biomarkers of inflammation and kidney rejection. Our goal is to demonstrate that tegoprubart can be safely utilized to replace CNIs as part of first-line immunosuppressive therapy in solid organ transplantation and prevent acute and long-term solid organ transplant rejection without the use of CNIs. Switching over to islet cell transplantation, we have an open site in Canada and are expecting to open our first US site mid-year. Here we are looking at patients with type 1 diabetes with hypoglycemic unawareness who experience significant swings in glucose levels that are associated with serious risk and comorbidities.

This open label study is planned to enroll up to 12 patients undergoing renal transplant with primary endpoints of safety and pharmacokinetics as well as exploratory endpoints inclusion, including biopsy proven rejection change in Egfr and biomarkers of inflammation and kidney rejection.

This open-label study is planning to enroll up to 12 patients undergoing renal transplant with primary endpoints of safety and pharmacokinetics, as well as exploratory endpoints, including biopsy proof and rejection, change in EGFR, and biomarkers of inflammation and kidney rejection.

Our goal is to demonstrate that to go pro-BARC and be safely utilized to replace C&Is as part of first-line immunosuppressive therapy and solid organ transplantation and prevent acute and long-term solid organ transplant rejection without the use of C&Is.

Our goal is to demonstrate that <unk> can be safely utilize to replace eni's as part of part of first line immunosuppressive therapy, and solid organ transplantation and prevent acute and long term solid organ transplant rejection without the use of C&I.

Switching over to Islet's Hall of Transplantation, we have an open site in Canada and are expecting to open our first U.S. site mid-year.

Switching over to islet cell transplantation, we have an open site in Canada and are expecting to open our first U S site in mid year here.

Here we are looking at patients with type 1 diabetes with hypoglycemic unawareness, who experience significant swings in glucose levels that are associated with serous risk and comorbidity.

Here, we're looking at patients with type one diabetes with hypoglycemic on awareness, who experienced significant swings in glucose levels that are associated with serious risk and comorbidities. Our goal is to evaluate take Oprah Barton the backbone maintenance of antique rejection therapy similar to the rationale I just described for kidney transplant rejection and ice.

Steve Perrin: Our goal is to evaluate tegoprubart in the backbone maintenance of anti-rejection therapy, similar to the rationale I just described for kidney transplant rejection. In ICT specifically, we are evaluating the number of patients that achieve insulin independence, and we are also assessing the number of cell transplants required to achieve independence. Our hypothesis is that by removing CNIs, which are directly toxic to the islet cells, and replacing it with tegoprubart, more patients could achieve better glycemic control and have fewer islet cell transplants. We are currently looking to enroll our first patients in both the renal and islet cell transplantation trials with the goal of providing available data from these two studies later this year. I'll conclude with our program in IgAN. IgAN is the leading cause of glomerulonephritis, a chronic autoimmune condition resulting in progressive kidney damage.

Our goal is to evaluate K. Gopelbart and the backbone maintenance of antidejection therapy similar to the rationale I just described for kidney transplant rejection.

In ICT specifically, we are evaluating the number of patients that achieve insulin independence and we are also assessing the number of cell transference required to achieve.

Specifically, we are evaluating the number of patients that achieve insulin independence. We're also assessing the number of cell transplants required to achieve independence.

Our hypothesis is that by removing CNIs, which are directly toxic to the islet cells and replacing it with Tobtego Prubart, more patients could achieve better glycemic control and have fewer islets all trans-

Our hypothesis is that by removing C&I, which are directly toxic to the islet cells and replacing it with to take over for Bart more patients could achieve better question with control and have fewer islet cell transplants.

We are currently looking to enroll our first patients in both the RINO and ILOT cell transplantation trials with the goal of providing available data from these two studies later this year.

We are currently looking to enroll our first patients in both the renal and islet cell transplantation trials with the goal of providing available data from these two studies later this year.

I'll conclude with our program and again.

IGIN is the leading cause of glomerular nephritis, a chronic autoimmune condition resulting in progressive kidney damage.

<unk> is the leading cause of millions of freight is a chronic autoimmune condition, resulting in progressive kidney damage.

Steve Perrin: Onset usually occurs in younger adults, often while the patient is in their twenties and is characterized by the presence of protein in the urine. Currently, approximately 40% of patients will progress to end-stage renal disease within 15 to 20 years, indicating a significant unmet need because the treatment for end-stage renal disease is lifelong dialysis or kidney transplant, both of which bear significant patient and healthcare system costs. We believe there is a strong mechanistic rationale for pursuing CD40 ligand inhibition in IgAN, since tegoprubart has the potential to modify disease progression by reducing the formation of IgA via the inhibition of antibody class switching, a decrease in immune complex formation via the inhibition of B cell maturation, and a reduction in immune cell infiltration and subsequent complement activation in the kidney.

Onset usually occurs in younger adults, often while the patient is in their 20s and is characterized by the presence of protein in the urine.

Onset usually occurs in younger adults often while the patient is in their twenties and is characterized by the presence of protein in the urine.

Currently approximately 40% of patients will progress to end-stage renal disease within 15 to 20 years, indicating a significant unmet need because the treatment for end-stage renal disease is lifelong dialysis or kidney transplant, both of which bear significant patients

Currently approximately 40% of patients will progress to end stage renal disease within 15 to 20 years, indicating a significant unmet need because the treatment for end stage renal disease is a lifelong dialysis or kidney transplant, both of which bear significant patient and health care system costs.

We believe there's a strong mechanistic rationale for pursuing CD40 ligand inhibition in Iganson. Tagore Prubart has the potential to modify disease progression by reducing the formation of IGA via the inhibition of antibody clotswitch.

We believe there is a strong mechanistic rationale for pursuing CD 40, ligand inhibition and <unk> has the potential to modify disease progression by reducing the formation of Iga via the inhibition of antibody class switching a decrease in immune complex formation via the inhibition of B cell maturation and a.

a decrease in immune complex formation via the inhibition of B cell maturation and a reduction in immune cell infiltration and subsequent complement activation in the kidney.

<unk>, an immune cell infiltration and subsequent complement activation in the kidney and.

Steve Perrin: In other words, we believe that tegoprubart may have a beneficial effect on both the upstream and downstream pathophysiology of IgAN. We are happy to report that we've begun dosing patients in our open label Phase 2a clinical trial in patients with IgAN. In this trial, patients with a confirmed diagnosis of IgAN and significant proteinuria will be subsequently enrolled in two different dose cohorts of up to 21 patients each. The primary endpoint will be percent reduction in proteinuria at 24 weeks compared to baseline, and we expect to communicate available data later this year. With that, I'll now turn the call over to Paul for a financial update.

In other words, we believe that Tegopru Bart may have a beneficial effect on both the upstream and downstream pathophysiology of eye cancer.

In other words, we believe that <unk> may have a beneficial effect on both the upstream and downstream path the pathophysiology of IGN.

We are happy to report that we've begun dosing patients in our open label, phase two A clinical trial in patients with I-

We are happy to report that we've begun dosing patients in our open label Phase Iia clinical trial in patients with IBM in.

In this trial, patients with a confirmed diagnosis of IGAN and significant protein will be subsequently enrolled in two different dose courts.

In this trial patients with a confirmed diagnosis of IGN and significant purchasing Aruba will be subsequently enrolled in two different dose cohorts.

of up to 21 patients each. The primary endpoint will be percent reduction in protein urea at 24 weeks compared to baseline, and we expect to communicate available data later this year. With that, I'll now turn the call over to you.

Of up to 21 patients each the primary endpoint will be percent reduction in proteinuria at 24 weeks compared to baseline and we expect to communicate available data later this year.

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 $9.9 million or $0.69 per share for the three months that ended 31 March 2022, compared to a net loss of $8.5 million or $0.57 for the same period in 2021. Research and development expenses were $6.6 million for the three months ended 31 March 2022, compared to $5.6 million for the comparable period in 2021, which was an increase of $1 million. The increased R&D spend primarily reflects an increase in clinical development costs and costs related to the production of clinical trial materials as we advance tegoprubart into the global Phase 1 and Phase 2 clinical trials.

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 will filed later today. The company reported a net loss of $9 9 million or <unk> <unk> per share for the three months ended March 31, 2022 compared to a net loss of $8 five.

Thank you, Steve. In addition to the financial results summarized in our press release, you can find additional information in our form 10Q, which we will file later today. The company reported a net loss of $9.9 million or $0.69 per share for the three months in March 31, 2022 compared to a net loss of $8.5 million or $0.57 for the same period of 2021.

Our 57 cents for the same period of 2021.

Research and development expenses were $6 6 million for the three months ended March 31, 2022, compared to $5 6 million for the comparable period in 2021, which was an increase of $1 million the.

Research and development expenses were $6.6 million for the three months ended in March 31, 2022, compared to $5.6 million for the comparable period in 2021, which was an increase of $1 million.

The increased R&D spin primarily reflects an increase in clinical development costs and costs related to the production of clinical trial materials as we advance to go prove art into the global phase one and phase two clinical trials.

The increased R&D spend primarily reflects an increase in clinical development costs and cost related to the production of clinical trial materials as we advanced <unk> into the global phase, one and phase II clinical trials.

Paul Little: General and administrative expenses were $3.2 million for the three months ended 31 March 2022, compared to $3.3 million for the comparable period in 2021, a decrease of $100,000. As of 31 March 2022, Eledon had $76.7 million in cash and cash equivalents, which we expect to be sufficient to fund all clinical trial operations as currently planned into 2024. With that financial update, let me turn the call back over to DA.

General and administrative expenses were $3 2 million for the three months ended March 31, 2022, compared to $3 3 million for the comparable period in 2021.

General and administrative expenses were $3.2 million for the three months ended March 31st, 2022 compared to $3.3 million for the comparable period in 2021, a decrease of $100,000.

A decrease of 100000.

As of March 31, 2022, Eladon had $76.7 million in cash and cash equivalents, which we expect to be sufficient to fund all clinical trial operations as currently planned into 2024. With that financial update, let me turn the call back over to DA.

As of March 31, 2022, <unk> had $76 7 million in cash and cash equivalents, which we expect to be sufficient to fund all clinical trial operations as currently planned into 2024.

With that financial update let me turn the call back over to D. A.

David-Alexandre Gros: Thanks, Paul. We remain focused on executing our trials, including generating our ALS data and opening more clinical sites to facilitate quicker patient recruitment to help us generate meaningful initial data in our trials this year. Our goal remains to develop a best-in-class therapeutic targeting the CD40 ligand pathway, which we believe can transform treatment options for patients living with ALS or IgAN or undergoing organ or cellular transplantation. We are proud of the progress across our clinical development programs, and as we enter a potentially transformational period for Eledon, we look forward to the multiple potential value-creating milestones ahead of us. With that, I will now ask the operator to begin our Q&A session. Operator?

Thanks, Paul.

We remain focused on executing our trials, including generating AOS data and opening more clinical sites to facilitate quicker patient recruitment to help us generate meaningful initial data in our trials this year.

We remain focused on executing our trials, including generating our ALS data and opening more clinical sites to facilitate quicker patient recruitment to help us generate meaningful initial data in our trials this year.

Our goal remains to develop the best in class therapeutic targeting the CD 40 ligand pathway, which we believe can transform treatment options for patients living with AOS.

Our goal remains develop a best in class therapeutic targeting the CD40 ligand pathway which we believe can transform treatment options for patients living

Or again, we're undergoing oregon or cellular transplantation.

or IGAN, or undergoing organ or cellular transplantation.

We are proud of the progress across our clinical development programs and as we enter a potentially transformational period for <unk>, we look forward to the multiple potential value, creating milestones ahead of us.

We are proud of the progress across our clinical development programs, and as we enter a potentially transformational period for Elidon, we look forward to the multiple potential value-creating milestones ahead of us.

With that I will now ask the operator to begin our Q&A session. Operator?

With that I will now ask the operator to begin our Q&A session.

Operator.

Yeah.

Operator: Thank you. We will now be conducting a question and answer session. If you'd like to ask a question, please press star one on your telephone keypad, and a confirmation tone will indicate that your line is in the queue. You may press star two if you would like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment please while we poll for questions. Our first question is from Pete Stavropoulos from Cantor Fitzgerald. Please proceed.

Thank you.

We will now be conducting a question and answer session. If you'd like to ask a question. Please press star one on your telephone keypad and a confirmation tone will indicate that your line is in the Q you.

If you'd like to ask a question, please press star 1 on your telephone keypad, and a confirmation tone will indicate that your line is in the queue. You may press star 1.

You May press star two if he would like to remove your question from the queue.

participants using speaker equipment it may be necessary to pick up your handset before pressing the star keys. One moment please while we poll for questions.

For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys.

Moment, please when we poll for questions.

Our first question is from Pete.

Stavropoulos from Canterford, Gerald, please.

Stefan <unk> from Cantor Fitzgerald. Please proceed.

Pete Stavropoulos: Hi, Dave and team. Congratulations on all the progress on this past quarter. First question I have is, you know, with respect to a kidney transplant, I guess, you know, what are the next steps and, like, your thoughts on a potential interaction with the FDA and moving forward in renal transplants in the US, you know, given the initial results that you have from the non-human primate study? Will you share the ALS safety data with the agency to help support the IND?

high DAA team, congratulations on all the progress on this past quarter.

<unk> congratulations on all the progress.

This past quarter.

So first question I have is, you know, with respect to a kidney transplant, I guess, you know, what are the next steps and, like, your thoughts on a potential interaction with the FDA and moving forward in renal transplant in the U.S., you know, given the initial results that you have from the non-human primate study? And will you share the ALS safety data with the agencies that help support the INE?

So.

First question I have is with respect to our kidney transplant I guess you know what are the next steps and your thoughts on a potential interaction with the FDA and moving forward.

Renal transplant in the U S. Given the initial results that you have from and.

Non human Primate study and will you share the AOS safety data with the agency to help support the <unk>.

David-Alexandre Gros: Hey, Pete. Thank you for the question. So in terms of our immediate plans in kidney transplantation, we now have, as I mentioned, sites open in Canada and the UK. We're looking to begin enrolling patients into that trial. As you alluded to, during discussions with the U.S. FDA last year, the agency had asked us to do a non-human primate study of tegoprubart as monotherapy in kidney transplantation. So we've successfully completed that study. The results showed efficacy consistent with what's been historically shown with anti-CD40 ligands.

Hey Pete, thank you for for the question. So in terms of our immediate plans and kitty transplantation now have, as I mentioned, sites open in cannon.

Thank you for the question.

So in terms of our immediate plans in kidney transplantation now have as I mentioned sites opened in kennan.

and the UK and so we're looking to begin enrolling patients into that trial.

In the U K and so we're looking to begin enrolling patients into that trial.

As you alluded to during discussions with the US FDA last year, the agency had asked us to do a non-human primate study up to go prubart as monotherapy in kidney transplantation. So we've successfully completed that study. The results showed efficacy consistent with what's been historically shown with anti-CD40 logants.

As you alluded to.

During discussions with the U S. FDA last year. The agency had asked us to do a non human primate study up to go prove bard as mono therapy.

In kidney transplantation.

We've successfully completed that study the.

The results showed.

Efficacy consistent.

With what's been historically shown with anti CD 40 law against.

David-Alexandre Gros: At this stage, what we'll do is look to complete the current ALS study so that we have that safety data available, and then reapproach the agency, including both the data that will be generated from ALS, as well as with the non-human primate data that they requested.

And at this stage, what we'll do is look to complete the current ALS study.

that we have that safety data available and then re-approach the agency including both the data that will be generated from ALS as well as with the non-human primate data that they request.

That we have that safety data available.

And then re approach the agency, including both the data that will be generated from AOS as well as with the nonhuman primate data that they requested.

Pete Stavropoulos: Okay, thanks for the color. You know, another question, you know, regarding ALS. You know, just asking you to speculate, you know, if you think there are different mechanisms, you know, by which the nerve cells are dying in the ALS patients with, like, elevated pro-inflammatory cytokines, you know, versus those without elevated inflammatory cytokines. You know, do you believe you may be able to see a differential response between those patients with AT-1501 or tegoprubart? Can you also speculate if there's any way that you can potentially enrich for patients that may respond to AT-1501, perhaps a certain cytokine profile or levels of soluble CD40 ligand?

Okay. Thanks for the color.

Thanks for the color so you know another question you know regarding ALS so you know just asking you to speculate you know if you think there are different mechanisms

Another question regarding AOS. So just asking you to speculate if you think there are different mechanisms by which the nerve cells are dying any Alice Ah patients with elevated pro inflammatory cytokines versus those without elevated inflammatory cytokines.

by which the nerve cells are dying in the ALS patients with like elevated pro-inflammatory cytokines, you know, versus those without elevation.

You know, and, you know, do believe, you know, you may be able to see a differential response between those patients with the 50-year-old.

And do you believe you may be able to see a differential response between those pieces with 15 zero one Ortega and.

Do.

Can you also speculate if there's any way that you can potentially enrich for patients?

Could you also speculate if there was any way that you could potentially enrich for patients that may respond to <unk> zero, one or perhaps a certain cytokine profile or levels of soluble <unk>.

perhaps a certain cytokine profile or levels of cytokine.

David-Alexandre Gros: Thank you. Let me turn that question over to Steve. Steve?

Thank you.

Thank you. Let me turn that question over to Steve.

Let me turn that question over to Steve Steve.

Steve.

Steve Perrin: That was a lot of questions, so I'll try to summarize as best I can.

I also have a lot of questions. So I'll try to summarize as best I can.

That was a lot of questions, so I'll try to summarize as best I can. I mean, clearly ALS is a very heterogeneous disease. It's a spectrum disorder, you know, all the way from people that have just motor deficits, all the way to people that just have cognitive impairment, and a mixture of everything between. And you overlap that there's also heterogeneity in the genetics associated with the disease.

Pete Stavropoulos: Okay.

Steve Perrin: I mean, clearly ALS is a very heterogeneous disease. It's a spectrum disorder, you know, all the way from people that have just motor deficits, all the way to people that just have cognitive impairment and a mixture of everything between. You overlap that there's also heterogeneity in the genetics associated with the disease. When we think about the impact of blocking inflammation, one of the common themes that's been is that inflammation is present in pretty much everybody with ALS. About 60% of people have a clear co-stimulatory signal, but most people at some point in time do show some level of pro-inflammatory chemokines or cytokines in circulation. No one's really learned how to leverage a biomarker set in inflammation to predict patient response.

I mean, clearly this is a very heterogeneous disease, it's a spectrum disorder. All the way from people that have just motor motor deficits all the way to people that just have cognitive impairment and a mixture of everything in between and overlap that Theres also heterogeneity in the genetics associated with it.

Yes.

So, when we think about the impact of blocking inflammation, one of the common themes that spend is that inflammation is present in pretty much everybody with ALS. About 60% of people have a clear co-stimulatory signal, but most people at some point in time do show some level of pro-inflammatory chemokines or cytokines in circulation.

So when we think about the impact of blocking inflammation one of the common themes that Spanish that inflammation is present.

And pretty much everybody with AOS about 60% of people have a clear co stimulatory signal, but most people at some point in time do show some level of pro inflammatory chemo kinds of cytokines in circulation.

No one's really learned how to leverage our biomarker set and inflammation to predict patient response.

No one's really learned how to leverage a biomarker set in inflammation to predict patient response.

Steve Perrin: Obviously, one of the goals of our study is because of the mechanism of action of tegoprubart as a blocking CD40 ligand, which is one of the most important mediators of pro-inflammatory signaling. Our biomarker plan is to elucidate not only target engagement, which is very specific effort, but to also look at the pro-inflammatory markers that are not only associated with ALS, but also downstream markers associated with CD40 ligand activation. It's potentially a very rich data set, but I don't know that we can speculate what we'll find out of it at this point as far as being able to predict drug response. That's part of the efforts of the data analysis plan.

Obviously, one of the goals of our study is because of the mechanism of action of take-off provide as a blocking CD40 ligand, which is one of the most important mediators of pro-inflammatory signaling.

Obviously, one of the goals of our study is because of the mechanism of action of takeover providers blocking CD 40 ligand.

One of the most important mediators of pro inflammatory signaling.

Our biomarker plan is to elucidate not only target engagement, which is very specific effort, but to also look at the pro-inflammatory markers that are not only associated with ALS, but also downstream markers associated with CD40 ligand active.

Our biomarker plan as to elucidate normally target engagement, which was very specific effort, but to also look at the pro inflammatory markers that are normally associated with AOS, but also downstream markers associated with CD 40 ligand activation.

So it's potentially a very rich dataset, but I don't know that we can speculate what we'll find out of it at this point as far as being able to predict drug response. So that's part of the efforts of the data analysis plan.

So it's potentially a very rich data set, but I don't know that we can speculate what we'll find out of it at this point as far as being able to predict drug response. That's part of the efforts of the Data Analysis Plan.

Pete Stavropoulos: All right. Thank you for the added color, and thanks for taking our question.

Alright, Thank you for the added color and thanks for taking my question.

Steve Perrin: Thank you.

Thank you.

Operator: Our next question is from Nat Charoensook with SVB. Please proceed.

Our next question is from Nat Sheroensoek with SBB. Please proceed.

Our next question is from that show and stuck with SBB. Please proceed.

Nat Charoensook: Hi, this is Nat Charoensook on for Tom Smith. I have one quick question on the ALS data coming out in June. Do you expect to see significant or complete target engagement with doses used in the Phase 2a trial? Do you think whether you need complete, only a complete target engagement to see clinical benefits such as a reduction in pro-inflammatory biomarkers?

Hi, This is natural decline for Tom Smith.

Hi, this is Nancy Ransouk-Anne for Tom Smith. So I have one quick question on the LS data coming out in June . Do you expect to see significant or complete target engagement with doses used in the phase two A trial? And do you think whether you need complete or near complete target engagement to see clinical benefits such as reduction in inflammatory phytoma?

One quick question on the <unk> data coming out in June do you expect to see significant or complete target engagement with doses used in the phase Iia trial, how do you think whether you'd need complete or near complete target engagement.

The clinical benefits such as reduction in Portland biomarker.

Sure.

David-Alexandre Gros: Thank you for the question, Matt. Let me turn that over to Steve, please.

Thank you for the question Matt.

Thank you for the question, Matt. Let me turn that over to Steve.

Let me turn that over to Steve Please.

Steve Perrin: In the dose ranging that we're doing in the study and based on what we know about target engagement, with tegoprubart, we should hit full target engagement in our study, over that dose range that we're looking at. I think ultimately that the answer to your question is yes, we anticipate that we would. We won't know, of course, until we actually have database lock, look at exposure level, pharmacokinetics, and other aspects of the trial that are part of the safety tolerability goals. All right. Thank you.

So when the dose ranging that we're doing in the study and based on what we know about target engagement.

So in the dose ranging that we're doing in the study, and based on what we know about target engagement with Tegoprobar, we should hit full target engagement in our study over that dose range that we're looking at. So I think ultimately the answer to your question is yes, we anticipate that we will

With take hold we should we should hit full target engagement in our study over that dose range that were looking at so I think ultimately the answer to your question is yes, we anticipate that we would but we won't know of course until we actually have database lock look at exposure level pharmacokinetics and other aspects of the trial that are part of.

But we won't know, of course, until we actually have database lock, look at exposure level, pharmacokinetics, and other aspects of the trial that are part of the safety tolerability goals.

Safety Tolerability goals.

Alright, thank you.

David-Alexandre Gros: Ultimately, what we'll look to do is to show both target engagement, and as we mentioned, the win would be able to then associate that with changes of inflammatory biomarkers.

But ultimately what we'll look to do is to show both target engagement and as we mentioned.

But ultimately what we'll look to do is to show both target engagement and as we mentioned the wind would be able to then associate that with changes of inflammatory biomarkers.

The win would be able to then associate that with changes in inflammatory biomarkers.

Okay.

Operator: Our next question is from Rami Katkhuda with LifeSci Capital. Please proceed.

Our next question is from Remy Cuda with box.

<unk> capital. Please proceed.

[Analyst] (LifeSci Capital): Hi, guys. Thanks for taking our question. This is Miriam on for Rami. Just two quick questions for us. With regards to the upcoming data in ALS, how large of a decrease from baseline are you hoping to see in these pro-inflammatory biomarkers to classify the study as a win? Quickly, Horizon recently announced positive data with their anti-CD40 ligand and rheumatoid arthritis. Is this an indication you could envision pursuing with tegoprubart in the future?

Hi guys, thanks for taking our question. This is Miriam on for just a quick question for us.

Hi, guys, thanks for taking that.

Just two quick questions right.

With regards to the upcoming data in ALS, how large of a decrease on the sign are you hoping to see in these pro-inflammatory biomarkers to classify the study of the wind?

With regard to the upcoming data and analyze how large of a decrease and they find that you're hoping to CND.

Inventory.

Bio migrate to classify this study of the win.

And quickly, Horizon recently announced positive data with their anti-CD40 ligand and rheumatoid arthritis. Is this an indication you could envision pursuing with the group provided in the future?

And.

Quickly Verizon recently announced positive data with their I'm, sorry for the light on and the rheumatoid arthritis.

The indication you could envision pursuing as it provided in the future.

David-Alexandre Gros: Thank you very much for the questions. Maybe in terms of your question with regards to ALS, I'll turn that over to Steve, but I'll start as a result by answering your second question in terms of the positive data in RA that was demonstrated by Horizon. I think in the long term, there are many indications that we could consider using an anti-CD40 ligand. As we go back to when we first merged the companies to create what is now Eledon, RA was a natural potential use of an anti-CD40 ligand like ours.

Thank you very much for the questions. So maybe in terms of the.

Thank you very much for the questions. So maybe in terms of your question with regards to ALS, I'll turn that over to Steve. But I'll start as a result by answering your second question in terms of the positive data in RA that was demonstrated by Horizon.

Your question with regards to Alice I'll turn that over to Steve, but I will start as a result by answering your second question in terms of.

Yeah.

Thanks.

The positive data NRA.

That was demonstrated by horizon.

I think in the long term, there are many indications that we could consider using an anti-CD40 log-in. As we go back to when we first merged the companies to create what is now Eladon, RA was a natural

I think in the long term there are many indications.

That we could consider using an anti CD 40 ligand and as we go going back to when we first merged the companies to create what is now I'll, let Don.

<unk> was a.

Natural.

potential use of an anti-CD40 ligand like ours. What we've done since was to really focus on indications where we felt that a smaller biotech could succeed in, both in terms of clinical development

The potential use of an anti CD 40 law again like ours.

David-Alexandre Gros: What we've done since was to really focus on indications where we felt that a smaller biotech could succeed in both in terms of clinical development as well as commercially, because we'd be able to potentially build the sales force that would be necessary. In order to do that, when we're thinking about our indications, we really focused on three things. We started by focusing on the biology and thinking about indications where the biology was well understood and the potential role of an anti-CD40 ligand therapeutic was well understood as well, so that we would have as high a likelihood of success as possible.

What we've done since <unk> was to really focus on indications.

We felt that a smaller biotech could succeeded.

Both in terms of.

Clinical development.

As well as commercially because we'd be able to potentially build the sales force that would be necessary.

as well as commercially because we'd be able to potentially build the sales force that would be necessary.

So in order to do that, when we're thinking about our indications, we really focused on three things. We started by focusing on the biology.

So in order to do that.

When we're thinking about our indications, we really focused on three things.

We started by focusing on the biology.

And in thinking about indications, where the biology was well understood and the potential role of an anti CD 40 ligand therapeutic was well understood as well as.

and thinking about indications where the biology was well understood and the potential role of an anti-CD40 ligand therapeutic was well understood as well, so that we would have as high a likelihood of success as possible. We also focused on indications where there was a clear regulatory pathway.

We would.

We would have a higher likelihood of success as possible. We also focused on indications where there was a clear regulatory pathway.

David-Alexandre Gros: We also focused on indications where there was a clear regulatory pathway, so that we could feel comfortable that the data we could generate would be supportive, if we had positive data of potential approval. We prioritized indications, as I mentioned, that could be commercialized by a smaller company, so typically, orphan indications like the ones we're looking at, since these wouldn't require a large sales and marketing organization. We think RA is a good indication for a drug like ours and one in which our drug might have a good chance of succeeding. From a strategic perspective, RA is not an indication that to date we focused on.

So that we could feel comfortable that the data would.

so that we could feel comfortable that the data we could generate would be supportive if we had positive data potential approval. And then we prioritized indications, as I mentioned, that could be commercialized by smaller company, so typically orphan indications like the ones we're looking at, since these wouldn't require a large sale.

We could generate would be supportive.

If we had positive data potential approval.

Then we prioritized indications as I mentioned that could be commercialized by smaller company.

Typically orphan indications like the one like the ones, where we're looking at.

These wouldn't require a.

A large sales and marketing organization.

So, we think RA is a good indication for a drug like ours, and one in which our drug might have a good chance of succeeding, but from a strategic perspective, RA is not indication that to date we focused on.

So we think our array is a good indication for a drug like ours and one in which.

Our drug might might have a good chance of succeeding but from a strategic perspective.

Ray is not indication that to date.

We focused on.

[Analyst] (LifeSci Capital): Thank you. Makes sense.

Thank you makes sense.

David-Alexandre Gros: Thank you.

Thank you.

Yes.

Steve Perrin: For your second question, this is Steve. A great question on how we're thinking about changes in the biomarkers that we're looking at. When you visualize what the data analysis plan looks like for this study, it's multidimensional, and we've alluded to that, so I'll try to describe it in a little bit more detail. You know, obviously, we're looking at target engagement. We're looking at multiple downstream pro-inflammatory markers that have been well described not only being present in people with ALS, but also related to CD40 ligand and inflammatory activation that would, if you block CD40 ligand signaling, you should mediate those. Also looking across dose response. It's a multidimensional analysis plan because there is going to be variability across doses, across patients, we've mentioned it's a heterogeneous disease, and across markers.

So for your second question. This is Steve Great question on on how we're thinking about.

So for your second question, this is Steve, a great question on how we're thinking about changes in the biomarkers that we're looking at. When you visualize what the data analysis plan looks like for this study, it's multi-dimensional and we've alluded to that, so I'll try to describe it in a little bit more detail. But obviously we're looking at target engagement.

Changes in the Biomarkers that we're looking at when you visualize what the data analysis plan looks like for the study.

It's multi dimensional and we've alluded to that so I'll try to describe in a little bit more detail, but obviously, we're looking at target engagement. We're looking at multiple downstream pro inflammatory markers that had been well described not only being present in people with AOS, but also related to CD 40 ligand and inflammatory.

We're looking at multiple downstream pro-inflammatory markers that have been well-described not only being present in people with ALS, but also related to CD40 ligand inflammatory activation that would, if you block CD40 ligand signaling, you should mediate those.

Reactivation that would if you block CD 40 ligand signaling you should mediate those.

And also looking across dose response, so it's a multiple multi dimensional analysis plan because there is going to be variability across the doses across patients. We've mentioned, it's a heterogeneous Janet heterogeneous disease and across markers. So I don't think it's as easy as saying.

and also looking across dose response. So it's a multi-dimensional analysis plan because there's going to be variability across doses, across patients. We've mentioned it's a heterogeneous disease and across markers. So I don't think it's as easy as saying what would be anticipated or what is the percent change we're looking for. It's more of a series of outcomes that we're looking for downstream of target

Steve Perrin: I don't think it's as easy as saying what will we anticipate or what is the percent change we're looking for. It's more of a series of outcomes that we're looking for downstream of target engagement. We wanna see target engagement, which we can measure in circulation. We wanna see changes in the pro-inflammatory biomarkers that are downstream of CD40 ligand signaling, and some of them have been characterized in ALS. Then we wanna look at individual dose response across each patient cohort. Does that answer your question?

We anticipate or what is the percent change we're looking for it's more of a series of outcomes that we're looking for downstream of target engagement, we want to see target engagement, which we can measure in circulation, we want to see changes in the pro inflammatory biomarkers that are downstream of CD 40 ligand Cigna.

We want to see target engagement, which we can measure in circulation. We want to see changes in the pro-inflammatory biomarkers that are downstream of CD40 ligand signaling, and some of them have been characterized in ALS. And then we want to look at individual dose response across each patient cohort.

And some of them have been characterized and AOS and then we want to look at individual dose response across each each patient cohort.

Does that answer your question.

Operator: She has exited the queue, and our next question comes from Matt Kaplan with Ladenburg Thalmann. Please proceed.

Oh, she has exited the queue and our next question comes from Matt Kaplan with Ladenburg Thalmann. Please proceed.

Matt Kaplan: Hi. Steve, thanks for that explanation. Just to follow up on the prior question, can you help us understand potential read-through for the ALS results to other indications that you're looking at? I guess obviously the kidney transplant and transplant and IgAN as well.

Hi Steve, thanks for that explanation. Just a follow-up on the prior question. Can you help us understand potential need-through for the ALS results to other indications that you're looking at? I guess obviously the kidney transplant and transplant and IGAN as well.

Alright.

Thanks for that explanation.

Just a follow up on on the part of your question.

Can you help us understand potential eat through for the AOS results are two other indications that youre looking at I guess, obviously.

Kidney transplant and transplant.

And.

Again as well.

David-Alexandre Gros: Thanks, Matt. That is a terrific question and quite insightful. To your point, since we are looking at a range of biomarkers, inflammatory biomarkers associated with ALS, some of those are also seen in some other diseases. For example, both MCP-1 as well as soluble CD40 ligand have been associated with proteinuria in IgAN. There are other biomarkers that are associated with transplant rejection. We would look at the beginning, of course, safety and tolerability. There may be some other biomarkers that could help us understand how tegoprubart is impacting cytokines and chemokines that have been associated with other indications as well.

Thanks, Matt that is a that is a terrific question and quite insightful.

Thanks, Matt. That is a terrific question and quite insightful.

So, to your point, since we are looking at a range of biomarkers, inflammatory biomarkers associated with ALS, some of those are also seen in some of the other areas.

So.

Your point is since we are looking at.

At a range of Biomarkers inflammatory biomarkers associated with ALS.

Some of those are also seen.

And in some other diseases. So for example, both MCP one as well as solid bowls CD 40 ligand has been associated with proteinuria.

So for example, both MCP1 as well as soluble CD40 ligand have been associated with protnurea in ligand.

Again.

And there are other biomarkers that are associated with transplant rejection.

And there are other biomarkers that are associated.

With transfer with transplant rejection.

So we would look at.

So, we would look at the beginning at, of course, safety and tolerability, but there may be some other biomarkers that could help.

At the beginning at.

Of course safety and Tolerability.

There may be some other biomarkers that could help.

that could help us understand how to go prove art is impacting.

That could help us understand.

How to go for Bard is impacting.

is impacting cytokines and chemokines that have been associated with other indications as well.

Is impacting cytokines and chemokines that are.

I have been associated with other indications as well.

Matt Kaplan: Okay. Okay, great. No, that's helpful. Just one question on the IgAN study. I guess with you're looking at the percentage decrease in proteinuria as the primary endpoint, would you expect to see a corresponding impact on eGFR if you see a reduction in proteinuria as well?

Okay. Okay, great. That's helpful. And then and then just one question on the <unk> study I guess with.

Great, no, that's helpful. And then just one question on the IGN study. I guess with that you're looking at the percentage decrease in proteinuria as the primary endpoint, would you expect to see your corresponding impact on EGFR if you see a reduction in proteinuria as well?

And Youre looking at the percentage decrease in proteinuria.

Primary endpoint would you expect to see a corresponding.

Impact on Egfr.

If you see a reduction in coronary.

Yes.

David-Alexandre Gros: Let me turn that over to Jeff. Jeff?

Let me turn that over to Jeff Jeff.

Jeff Bornstein: Yeah. Thank you, DA. Hi, Matt. It's complicated because the proteinuria predicts a slowing of the decline in eGFR. If you reduce proteinuria, you would expect to see less decline in eGFR, but not at the same time. The proteinuria predicts it in the future. Our study is designed to look at change in urine protein at 24 weeks, but we continue to dose the patients and follow them up for 96 weeks, and we'll be looking at the eGFR at the end of the trial.

Yeah, thank you, D.A. Hi, Matt. So it's complicated because the protein area predicts a slowing of the decline

Yes. Thank you.

So.

It's complicated because the prudent area predicts.

The slowing of the decline in Egfr.

So if you reduce protein area, you would expect to see less decline in the GFR, but not at the same.

So if you reduce proteinuria you would expect to see less decline in egfr, but not at the same time that the proteinuria predicted in the future. So our study is designed to look at change in urine protein at 24 weeks, but we continue to dose the patients and follow them for 96 weeks and we'll be looking at.

So the prognore predicts it in the future. So our study is designed to look at change in urine protein at 24 weeks, but we continue to dose the patients and follow them up for 96 weeks, and we'll be looking at the EGFR at the end of the day.

ETF AUM at the end of the trial.

Matt Kaplan: All right. Okay, great. Thanks. Thanks for taking the questions.

All right. Okay. Great. Thanks. Thanks for taking the question.

Alright, okay, great. Thanks, Thanks for taking the questions.

Jeff Bornstein: Sure.

Yes.

David-Alexandre Gros: Thank you.

Operator: Thank you. Ladies and gentlemen, this concludes our question and answer session. I'd like to turn the call back to D.A. Gros for any closing remarks.

Thank you ladies and gentlemen, this concludes our question and answer session I would like to turn the call back to Dr. Rowe for any closing remarks.

Thank you. Ladies and gentlemen, this concludes our question and answer session. I would like to turn the call back to DAGrow for any questions.

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

Thank you operator, and thank you all for joining us on today's call.

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

Great evening.

Operator: This concludes today's conference. Thank you for your participation. You may now disconnect.

This concludes today's conference. Thank you for your participation. You may now just come in.

This concludes today's conference. Thank you for your participation you may now disconnect.

Okay.

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