Q3 2021 Eledon Pharmaceuticals Inc Earnings Call
[music].
Hello, and welcome to the Elephant in Pharmaceuticals third quarter 2021 earnings call and webcast. At this time all participants are in a listen only mode.
Sure and answer session will follow the formal presentation.
Anyone should require operator assistance. Please press star zero on your telephone keypad as a reminder, this conference is being recorded.
Now my pleasure to turn the call over to CFO Paul Little Please go ahead.
Good afternoon, and thank you for joining <unk> third quarter 2021 financial results Conference call. Joining me today is David Alexandra grow Chief Executive Officer, Steve Perrin, President and Chief Scientific Officer.
Jeff Bornstein, Chief Medical Officer earlier today, <unk> issued a press release announcing financial results for the third quarter ended September 32021.
You may access access the release under the investors tab on our company's website at <unk> Dot com.
Before we begin 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 1995 all.
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 Ela Dawn Eldar.
<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 other dogs reports filed with the U S Securities and Exchange Commission.
It is now my pleasure to pass the call to all Don CEO, Dr. David Alexandra Groh D. A.
Thank you Paul and thank you all for joining us this afternoon.
We formed what is now Ela, Don just one year ago, when we acquired and Alexis and concurrently executed a financing with leading life science investors.
Since then we have built a world class team and strove towards initiating clinical trials in three therapeutic areas.
Plantation, focusing on kidney and I, let cell transplantation auto immunity, focusing on Iga nephropathy, and neuro degeneration, focusing on a L. S.
I'm proud of the progress our team has made over the past year, and especially the past months underscoring our focus on operational execution.
Specifically.
We are nearing completion of enrollment in our phase II trial of <unk> 15 O. One in adults with a L. S. With 16 of 18 subjects enrolled in the fourth and final cohort.
We received no objection letter from health, Canada, allowing us to initiate our open label clinical trial evaluating a T 15 O. One in kidney transplantation and we are in the process of opening our first site in Canada.
We received IND clearance from the FDA to proceed with a clinical trial to assess the safety and efficacy of Fakey 15, no. One in the prevention of rejection in patients undergoing islet cell transplantation for the treatment of type one diabetes.
We initiated an 80 15 O one mono therapy kidney transplantation study.
In nonhuman primates as requested by the SBA in advance of a potential <unk> application for a <unk> 15 O one in kidney transplantation in the United States.
We announced a research collaboration with care Dx, a world leader in transplant diagnostics and services.
And we've recently announced Iga yen as the next indication for development of 2015 O one and.
And remain on track to begin opening sites for the phase two study by the end of this year.
And finally, we presented additional data at the international Pancreas, and islet transplantation World Congress from our nonhuman Primate islet transplantation study.
Focusing on the potential benefit of using a T 15 O one in transplantation versus traditional immuno suppression, including Calciner inhibitors.
Before Steven Paul dive into last quarter in more detail.
I'd like to talk about the importance of our upcoming work with care Dx as well as share some thoughts about 2022 since the new year is quickly approaching.
We recently announced a research collaboration with <unk> in October.
This multi year and multi trials collaborations enhances our capabilities for our upcoming and potential future clinical trials of <unk> 15 O. One in kidney transplantation for number of reasons.
First it gives us access to care Dx is kidney care suite, including al assure and noninvasive cell free assay that looks for donor derived a double stranded DNA in the blood as an indicator of graft rejection.
Second it gives us access to algorithms, including eye box, a predictive algorithm that provides a prognostic indication of allograft survival.
When possible we plan on integrating biomarkers and algorithms such as these into a renal transplant studies as exploratory endpoints to allow us to better characterize a T 15 O once performance and its differentiation from current standard of care and potentially allow us to do so.
So at earlier time points than whats historically possible.
Finally, as we plan and execute our trials, we will benefit from care Dx as large footprints.
Experienced with kidney transplantation clinical trials.
And its established relationship with both key medical institutions and opinion leaders.
I'll end by talking about 2022.
With our E. L. S phase two study enrollment nearly completed.
Enrollment in the other trials expected to begin in the near term.
Starting with a L. S. In the first half of 2022, we are approaching a very busy year of sequential clinical data readouts from a L. S. Renal transplantation again, an islet cell transplantation.
With that I'll turn the call over to Steve Perrin, Our President and Chief Scientific Officer to review our lead asset in clinical indications.
Steve.
Thank you D a.
As a brief reminder of our lead asset <unk> T 15, no one cares and ITG, one anti CD 40 ligand antibody locking FC effector function.
Physiologically the interaction of CD 40, ligand and CD 40 results and team B cell clonal expansion antibody production and secretion of pro inflammatory cytokines that amplified immune response.
The C. D 40 city 40 ligand pathway is an attractive drug development target because of the engagement of these receptors plays a pivotal role in immune system activation by immediate hitting both antibody and cellular immune responses.
Our programs are centered around development of antagonistic antibodies that target the ligand rather than a receptor inhibition of the law again has shown greater efficacy in preclinical models of autoimmunity is wrong as well as in the prevention of acute and long term allograph transplant rejection and animal models.
I'll begin my program updates what they owe us our most advanced indication.
Previous research has found the co stimulatory pathway to be an overactive pathway involved in more than half of people with I O us pre.
Preclinical work has demonstrated that stopping or delaying immune system activation by inhibition of C. D 40, why again can improve muscle function slow disease progression and improve survival and in a L. S animal model. This.
This provides strong scientific rationale for the development of $18 15, no one in this challenging indication.
We're in the midst of a 12 week open label dose escalating study enrolling up to 54 patients at 13 sites in the United States and Canada.
Enrollment in the fourth and final cohort is nearly complete with 16 of 18 patients enrolled and we remain on track to report data from this study in the first half of next year.
Data that we are looking to obtain include safety and tolerability as well as multiple categories of biomarker endpoints with each subject serving as their own control by comparing changes from baseline.
And the first category of Biomarkers will assess CD 40 ligand target engagement.
<unk> inhibiting CD 40 ligand function has profound effects on b cell maturation antibody production and antibody class switching.
We anticipate we'll be able to assess the inhibition of C. D 40 ligand target engagement by a T 15, no one with Biomarkers of B cell function such as <unk>.
The second category of Biomarkers or changes in pro inflammatory chemo kinds of cytokines up regulated in people living with a loss. There was a long history of AOS data describing increases a pro inflammatory signals in circulation, including TNF Alpha M. C. P. One IL six and enraged as examples we ain't.
Dissipate the inhibition of C. D 40 wagon will result in an overall decrease of these pro inflammatory markers.
Finally, we will also have sex the exploratory endpoints, including changes in the ALS functional rating scale already also for us.
Respiratory function and levels of newer filament light chain in circulation.
We consider these endpoints exploratory since we do not know if 12 weeks of therapy, a sufficient time to see an effect of note seeing an effect on <unk> light chain would be particularly exciting because of this Biomarkers association with nor in health and May allow us to be the first company to both show that a therapeutic and lower <unk>.
Preliminary biomarkers of AOS as well as lower neuro from like train and patients where they are elevated.
We're in the process of opening our first site in a phase one b Genova transplant study in Canada enrolling up to 12 subjects undergoing renal transplant. Our goal in this study is to demonstrate that 80, if you don't want a safe.
Cheese predictable drug levels and can prevent allograft rejection when used as a preclinical replacement for C&I says components of an immunosuppressive regimen in this patient population.
As <unk> mentioned, we will also be looking at exploratory endpoints, including Biomarkers the.
The reason, we're looking to replace Eni's with E. T 15, no one is the backbone of transplant immunosuppression.
N ice have been shown to be beta cell toxic, thus, causing diabetes, neurotoxic, thus, causing neurological symptoms, including tremors.
Cause of hair loss.
Especially with increased risk of heart disease infection and cancer.
Moreover, the chronic utilization of C&I is to prevent graft rejection has been associated with nerve nephrotoxicity it up to 30% of patients. After one year, 50% of patients after five years and 100% of patients. After 10 years. These toxicities can ultimately shorten graft survival, while others may lead.
To dose lowering or patient, becoming less compliant thus indirectly increasing the chance of rejection.
By improving the safety and Tolerability Tolerability of first line immunosuppression, we believe that $18 15, and one has the potential to both improve patient quality of life.
And overall morbidity in the near term as well as ultimately improve cross survival rates in the longer term.
In parallel to this clinical trial, we've initiated a nonhuman primate kidney transplant study with <unk>, one as monotherapy as requested by the FDA as a prerequisite to a potential future U S kidney transplant patient IMD.
We've begun the transplants as planned and on track with our initial data from this study are expected in mid 2022.
Now turning to islet cell transplantation.
We are focusing on people living with high risk type one diabetes, who are on chronic treatment with exogenous insulin and experienced severe swings in blood glucose levels hypoglycemic on awareness and associated Comorbidities.
Clinical trials conducted by the immune tolerance network as well as islet cell transplant in all the countries have demonstrated that islet cell transplant in patients with difficult to control tough one diabetes can maintain glycemic balance reinstate metabolic control and in some cases, even eliminate the need for exhaustless insulin.
However, the current use of Calciner inhibitors or <unk> for the <unk> for the prevention of islet cell transplant rejection poses challenges of C&I or toxic towards transplanted islands potentially resulting in significant outlet saw loss post transplant, and thus potentially leading to the requirement for multiple islet cell transplant.
In order to reduce insulin dependence and improve hypoglycemic on awareness.
Earlier this year, we initiated a phase II clinical trial of <unk> 15, and one in Canada as a replacement for C&I and a single center at the University of Edmonton, which is historically the most active islet cell transplant site in North America.
Unfortunately, COVID-19 spikes in Alberta have led to the site temporarily suspending elective procedures, including Alex cell transplants twice. This year. Most recently in August. In addition, due to the Covid environment has been challenging to find patients willing to undergo the procedure considering necessity for immunosuppression as a.
<unk>, we announced last quarter that we were considering other geographies for potential expansion.
We are proud to announce that the FDA has cleared our IND and provided us with a path forward for the clinical development of <unk> 51 in islet cell transplantation in the United States.
This IND clearance is particularly important since one that covers both <unk> as well as a method to purify cared to diavik I, what's necessary for transplantation. Two it represents the same dosing level and so we are using in our Canadian transplantation studies and expect to use in future kidney transplantation.
Studies and.
And three provides us with another geography for islet cell transplantation.
Finally in Canada, we are happy to report that the site in Edmonton has recently reopened and is restarting to screen subjects for electric procedures.
In terms of data, we presented additional nonhuman primate data at the international Pancreas islet cell transplantation World Congress in October and a nonhuman primate model of islet cell transplantation animals treated with <unk> 51 versus those treated with standard of care, including C&I has demonstrated longer graft survival.
Better graft function and glycemic control and more healthier as demonstrated by post transplant weight gain.
Now I'll turn to Iga nephropathy or <unk>.
Again, it's the leading cause of Camellia nephritis 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.
Our effective treatment options available up to approximately 40% of patients progressed to end stage renal disease within 15 to 20 years with patients who have the highest levels of urine protein being at the greatest risk of progression.
The treatment for end stage renal disease is lifelong dialysis or kidney transplant, both of which bear significant patient and health care system costs. There is currently no approved therapy for the treatment of <unk>.
We believe there is a strong mechanistic rationale for pursuing CD 40, ligand inhibition and ICANN since $80 51 has the potential ability to ameliorate pathologies associated with three of the four so-called pathological hits associated with the disease.
Planned phase II study is an open label study expected to enroll up to 42 patients with a confirmed diagnosis of Iga nephropathy and significant proteinuria.
Patients will be sequentially enrolled in two different dose cohorts and receive a T 15, one by IV infusion.
The primary endpoint will be percent reduction in proteinuria 24 weeks as compared to baseline.
We will also be a continued patient dosing up to 96 weeks to assess changes in rate of disease progression as measured by the estimated glomerular filtration rate or Egfr.
We've elected to do an open label study for this proof of principle studies since historical IGN clinical trials have demonstrated that proteinuria in <unk> patients would not be expected to change in any meaningful way over a 24 week assessment period.
We anticipate having over 30 countries active and enrolling patients in multiple countries, particularly were IGN is most prevalent we.
We expect to have our first Cta approved in site opened by the end of the year, thereby allowing us to target getting initial data in late 2022.
That concludes my clinical and scientific update I will now turn the call over to Paul for our financial update.
Okay. 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 8 million.
Or <unk> 66 per share for the three months ended September 32021, compared to a net loss of $6 1 million or $5 51 per share for the same period in 2020.
Research and development expenses were $7 7 million for the three months ended September 32021, compared to 615000 for the same period in 2020, the increase in R&D costs, primarily reflect clinical and CMC activities as we advance our <unk> <unk> hundred one programs.
G&A expenses were $2 8 million for the three months ended September 32021, compared to $3 7 million for the same period of 2020. The decrease in G&A reflects prior year restructuring charges totaling $2 2 million, partially offset by increased personnel and stock based compensation costs legal and other professional.
Fees in the current period.
Now turning to a few key financial metrics for the full year to date. The company reported a net loss of $25 7 million or $1 73 per share for the nine months ended September 32021, compared to a net loss of $16 9 million or $16 81 per share for the same period of 2020.
Research and development expenses were $17 6 million for the nine months ended September 32021.
Compared to $3 1 million for the same period in 2020.
The increase in R&D costs, primarily reflect clinical and CMC activities as we advance <unk> hundred one programs.
<unk> expenses were $9 9 million for the nine months ended September 32021, compared to $6 7 million for the same period last year. The increase in G&A spend primarily reflects increased personnel cost stock based compensation expenses legal and other professional fees the company had $94 million in cash and cash equivalents.
As of September 30, compared to $101 million in cash and cash equivalents as of June 32021, we expect our financial resources to be sufficient to fund operations as currently planned well into 2023, thereby allowing us to generate data across all of our currently planned trials and still have a year.
Of cash on hand.
With that financial update let me turn the call back over to D. A.
Thank you Paul we have made significant progress during the third quarter advancing our lead molecule <unk> hundred one.
With our nearly completing enrollment in our ALS phase III study and are receiving regulatory clearances to begin clinical trials for kidney transplantation in Canada, and I'll, let cell transplantation in the United States.
We are now approaching what should be a very busy year of sequential clinical data readouts in 2022, including our phase two ALS study followed by interim data Readouts for our I'll, let cell transplantation, kidney transplantation and Iga yet in trials.
With that I will now ask the operator to begin our Q&A session.
Operator, thank you.
You will now be conducting a question and answer session if you'd like to be placed in the question queue. Please press star one on your telephone keypad, a confirmation tone will indicate your line is in the question queue. You May press star two if you'd 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.
One moment, please when we pull for questions.
First question today is coming from our VP of young from Cantor Fitzgerald. Your line is now live.
Hey, guys. Thanks for taking my questions and congrats on the.
While we progress here.
I guess on the L. S night I'm curious about.
What do you think.
Light chain could potentially be like a biomarker that you know maybe a regulatory body recognizes and then to that point kind of what kind of can you frame kind of what kind of levels and what might be interesting, but baseline level people have and how you think about that kind of information related to that and then.
I again I guess.
Obviously, there's some some medicines in development there.
I guess I kind of wanted to talk about how you think Sydney 40 mechanism might be.
Differentiated versus some of the other plays out there in the universe.
Alicia Thank you for the questions, let me turn it over to Steve.
Talk about AOS and <unk>.
Yes.
Great question on the referral of mental Lithia.
As you know <unk> light chain as a fairly new biomarker in Nordic generation, not just a loss, but multiple sclerosis, and all timers and others as well.
Historically, we know from lots of studies that <unk> light chain is elevated in adults with AOS, but the levels are very variable and they tend to correlate with prognosis more than anything at this point. We're at time of diagnosis. If you have high levels of <unk> light chain, you tend to be a fast progress.
Or and if you have lower levels of neuro filament light chain, you tend to be a slower progressing.
The only data we have with therapeutic intervention at this point is the recent data from Biogen with their antisense oligonucleotide.
That's been in phase two studies in adults with ALS and their they showed decreases in <unk> light chain, but they didnt necessarily correlate.
With clinical outcomes or survival.
So we all agree I think in the community and neuro degeneration that <unk> light chain as a marker of nor on health and ends up in CSF in circulation, but therapeutically.
We need to demonstrate that that does correlate with other biomarkers such as pro inflammatory markers as well as clinical outcomes and that's one of the goal of the exploratory component of our study.
Did that answer your first question on AOS.
Yeah. That's helpful. It seems like you did with the correlations and it's not really a hard fast number isn't that simply doesn't have to.
See what he sees as the Biogen data kind of a little bit confusing.
Yeah, I mean, it's where we're doing a 12 week study, which may not be a long enough duration of treatment to impact <unk> light chain or clinical outcomes in I O us, but it would be an incredible finding if there was a correlation between reduction in pro inflammatory markers <unk> light.
As well as disease progression, we'd be the first company to really show.
A change in pro inflammatory markers with therapeutic intervention could correlate with a change of <unk> light chain level, so that would be a very big finding if we ended up hitting that one.
Okay. That's helpful.
And your question about <unk> again with mechanisms. So I'll just review the scientific part of that answer so.
As far as differentiation goes I mean, there is a pretty well validated model of Iga nephropathy as far as the pathophysiology, it's a multiple hit model, where the first hit as deficiencies in the enzymes that actually put appropriate triggers on Iga and those deficiencies result in a.
Improperly.
Quite cost related Iga that is recognized by the immune system because it's foreign.
And that's really step two in the process, where antibodies are mead and recognizing made by b cells.
<unk> that improper sugared Iga.
Ultimately that results in immune complex formation in circulation you get complexes that have recognized that that protein that's not normal and those end up getting to positive in the kidney overtime and that's what results in kidney damage.
Proteinuria being present in the urine and then progressive fibrosis and further damage to the kidney are chronically over time.
So other therapeutics through clinical therapies that are in clinical development that are targeting various aspects are not hitting all aspects of that multiple hit for hip process and blocking C. D 40 logging in theory should hit three out of the four it should because it inhibits class switching.
At the AGM level, it should lower overall production of Iga, So there's not as much around to be missed quite cost related.
Secondly, because blocking CD 40 ligand.
Blocks B cell maturation germinal cell formation in antibody production. It will ultimately result in less immune complex formation in circulation, because you're not going to make antibodies youre not going to recognize that that misquote, possibly with Iga is four and so there'll be less immune complex formation in circulation and then ultimately even.
After deposition in the kidney blocking CD 40 ligand has been showing because it blocks pro inflammatory differentiation of T cells and cell. So the monocyte lineage, you'll get less immune cell infiltrate into the kidney industrial get less progressive damage and fibrosis as the result of deposition.
Of immune complexes that might be there. So we think that blocking CD 40, <unk> compare to <unk>.
Other modalities in the clinic block three of the four hits.
Okay. That's helpful and then just another one on.
The Primate study have you guys say, how many primary role or anything about that or where youre at now.
So we said.
Is that the guidance, we received was that we needed a minimum of four nonhuman primates.
And as we've we just announced today, we have begun the trial. So we have begun doing.
Kidney Transplantations primates.
Okay.
Thank you. Our next question is coming from Thomas Smith from SVP Leerink. Your line is now live.
Hey, guys. Thanks for taking the questions.
That's on all the progress.
A couple of questions I guess first just on AOS.
And it sounds like Youre, making some good progress there on enrolment.
In thinking about some of the efficacy markers you're measuring in the study obviously you called out a film that light chain and I. Appreciate the color on that in terms of some of the other exploratory endpoints and I think by change in ALS FRS respiratory function can.
Can you just help frame I guess, what you'd be looking for within the 12 week treatment period understand it.
Short treatment period, but it does is it essentially any signal on those functional endpoints would be considered a positive signal in your view and then maybe secondly.
Turning to the islet cell program in the U S and equally can you just give us a little more color on how you're thinking about it.
Enrollment in the U S.
Obviously islet cells still considered an experimental procedure in the U S.
Wanted to get your sense for how many study sites.
You could target and I guess your sense of expectations relative.
To your expectations for enrollment in Canada.
Sure. So maybe let me let me start by turning it over to.
Steve.
Talk about a L S.
And then I can take over and talk about <unk>.
Thanks, a lot for your question Tom It's a.
Good to talk to you.
Tom a question on AOS for the exploratory endpoints of clinical endpoints as you know a 12 week study and they owe us is fairly.
Sure.
This is a really heterogeneous disease as far as disease progression and at time of diagnosis, it's very difficult to understand the differences in progression rates. So in a 12 week study, we probably be surprised to see.
Significant changes in Alsace alysa for us across the cohort or respiratory function or muscle function typically those types of clinical endpoints are looked at as as endpoints in longer studies six months 12 months 18 months, our study durations, where typically we'd be looking.
At those types of clinical endpoints for a loss. So if we saw something it would be incredibly exciting, especially for correlated with any of the biomarkers that we've described but in such a short study.
It would be I'd be surprised if we see something there.
Does that answer your question Tom the primary focus here is going to be obviously around safety and tolerability.
But then looking for changes in terms of the inflammatory biomarkers.
And maybe Steve do you want to add some color on the inflammatory biomarkers, we're looking at.
And what's been historically found in ALS.
Yes, so the two types of markers that we're looking for that's directly related to immune cell function. One is targeting key instrument as I mentioned on the call blocking C. D. 40 ligand has a very profound effect on b cell development in Germinal cell formation and can really block many of the key mccain's that.
Associated with that aspect of an antibody response.
We can measure target engagement by looking at.
B cell markers, including <unk>.
<unk> 13, which is a potent key mackay associated with B cell activation.
For the pro inflammatory markers and I mentioned TNF Alpha IL six MCP one as examples there is a long long history going back decades of people measuring pro inflammatory markers in patients with ALS in not only the clinical setting, but just in general studies and most of them very well.
Right so.
Because of the fact that those are elevated and their pro inflammatory if we block C. D 40 law against signaling and block pro inflammatory differentiation of T cells and B cells, we should see a decrease in pro inflammatory markers like TNF Alpha IL, six MCP, one and others.
Got it got it okay Super helpful color on on ALS, and then on Lasalle.
Lasalle.
Great and so on islet cell and as you mentioned.
I'll, let cell transplant is considered experimental here in the U S.
And so a path forward for a clinical trial in this country is a big step forward for us.
In terms of the design will start and right now the plan will be to start with a single site in the states.
In terms of enrollment.
As you've seen with us and as we've seen with some other ICT trials that are being done enrollment has been.
It has been relatively slow.
Good here is that we need a few patients.
In order to be able to have some data that could be meaningful.
And that data can come relatively quickly.
So.
We're looking forward to getting our first patients.
Hopefully enrolled and in the U S and Canada.
And once they get enrolled once they get transplanted whats nice is that within about 90 days, we'd be able to see how well the grafts are doing and so the impact that <unk> might be having in terms of protecting that graft.
And potentially allowing patients to be in.
So on independent.
Okay.
In terms of opening the U S side.
We just recently got the feedback from the agency so we.
We would expect.
At site.
To open probably towards the middle of next year.
Understood Alright, Thank you guys for taking the questions and thanks for the thanks for the color.
Thank you I just a reminder that is star one to be placed in the question queue, if you'd like to be placed in the question queue. Please press star one at this time. Our next question is coming from Matt Kaplan from Ladenburg Thalmann. Your line is now live.
Yeah.
Hi, guys. This is Raymond in for Matt. Thanks for taking my question Congrats on all the progress.
Just I guess.
Me too.
Quick question on the islet cell Transportation program I was wondering I guess.
You have U S site and the Canadian side with the data readout, we kind of.
Combined or would it be.
Similar to the initial Clinique line on a U S trial.
Let me turn first Raymond Thank you very much for the question.
Yes.
Let me turn that over to Steve.
Or Jeff just talking about the similarities between the programs.
Chuck Chuck here on the call. The protocols are slightly different so why don't you explain the nuances.
Yeah sure. Thank you. Thanks, Thanks, Steve Hi, Jeff Bornstein.
They are separate trials.
So the trial in Canada.
It has been open for some time now, but as Steve talked about earlier, we ran into issues with COVID-19.
Optimistic, but now that that seems to be behind them. They can start recruiting.
The U S trial as a separate protocol quite.
Quite similar in design.
No.
Really.
Recruiting very similar patient populations. So all those are separate protocols. When they are meant to be managed and analyzed separately.
Totality of the data we can look at comprehensively to give us an overview of how well <unk> is performing population.
So we will be able to look at the comprehensive set of the data.
Even though they are separate studies.
Okay. Thanks, that's very helpful.
Follow up I was wondering.
You mentioned the dosing is similar and I was wondering can you characterize kind of the interaction with the FDA and thinking on how the style itself might.
It might be any any additional color would be helpful. Thanks.
What do you mean, sorry, what do you mean by by that question.
Sorry, I'm more like you mentioned that it's kind of the clinical trial path in the U S kind of.
The experimental I was wondering if perhaps the FDA had changes in thinking or something kind of.
And that line or some such.
Yeah, so that has to do.
With the.
The procedure itself and the purification of the cells is considered experimental here in the U S and so the FDA has taken a different approach than some other regulatory agencies around the world.
And Thats less.
That's not specific to.
Our drug.
That's more specific to do the procedure.
In terms of.
In terms of <unk>, one we are using the same.
<unk> regimen.
And schedule.
In in both Canada and the U S.
And in Canada.
It's the.
The schedule and dose.
Is the same that we're using for kidney transplantation as well as our lead cell transplant.
Okay. Thanks.
Thank you. Our next question today is coming from Rami Cal Kudos from lifestyle capital. Your line is now live.
Hey, guys. Thanks for taking my questions as well I guess first can you walk us through how you're thinking about dosing of <unk> 15, and one in the Iga nephropathy trial comparative studies in AOS of transplantation.
And then secondly is there a potential for the FDA to consider Alisher anti bot is approvable endpoints in future renal transplant studies or has there been no indication at that.
So rami thanks for the question.
So maybe I can I can tackle both of them.
So.
In terms of your second question with regards to it.
The FDA guidance on.
The use of other endpoints right now the current guidance from the agency.
Is to to look at non inferiority.
In terms of biopsy proven rejection.
So we don't know whether the agency will allow other endpoints in the future.
Yeah.
But right now.
That is what we're considering to be the <unk>.
Primary endpoint.
But what we can do is use now.
Novel, Biomarkers and all of our algorithms.
On an exploratory perspective in order to learn more about our asset.
And potentially in order to be able to help predict how well our asset might be doing or might be able to do.
<unk> standard of care.
In terms of.
Again dosing.
We haven't.
We haven't disclosed specifically how will be how we'll be dosing in all again.
But at a high level.
The dose will be.
Slightly higher about the same in the same range.
As for AOS and as you know at that dose level is lower.
Then we are using for.
Then we're using for transplant.
Got it that makes a lot of time.
Thank you.
Thank you we reached end of our question and answer session I'd like to turn the floor back over to management for any further or closing comments.
Thank you very much to everyone for joining us today, and we look forward to talking to you in the future as we continue to make progress as a company and with a $2 51.
Thank you that does conclude today's teleconference and webcast you may disconnect. Your lines at this time and have a wonderful day, we thank you for your participation today.
Okay.