Q2 2021 Eledon Pharmaceuticals Inc Earnings Call
[music].
Greetings welcome to the Ela Dawn Pharmaceuticals reports second quarter 2021 financial results Conference call.
At this time all participants are in a listen only mode. A question and answer session will follow the formal presentation.
If anyone should require operator assistance during the conference. Please press star zero on your telephone keypad. Please note that this conference is being recorded.
I will now turn the conference over to your host Paul Little Chief Financial Officer, you May begin.
Good afternoon, and thank you for joining <unk> Pharmaceuticals second quarter 2021 financial results conference call joining.
Joining me today is David Alexandra grow Chief Executive Officer, Steven Perrin.
And Chief Scientific Officer, and Jeff Bernstein, Chief Medical Officer.
Today <unk> issued a press release announcing financial results for the second quarter ended June 32021, you may access the release under the investors tab on our company website Amazon Dot com.
Before we begin I would like to remind everyone that statements made today during this call related to <unk> expected future performance future.
<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.
Actual outcomes and results could differ materially from these forecasts due to the impact of many factors beyond the control of <unk>.
<unk> expressly disclaims any duty to provide updates to its forward looking statements whether as a result of new information future events or otherwise participants directed to the risk factors set forth in <unk> reports filed with the SEC on our website under the Investor Tab. We encourage you to review these documents carefully.
It's now my pleasure to pass the call over to our CEO, Dr. David Alexandra Groh D. A.
Thank you Paul and good afternoon, everyone.
We continue to make significant progress during the second quarter advancing our lead molecule <unk> hundred one.
I am excited by the promise offered to us by <unk> 15, O one as a potential therapeutic for Oregon or seller transplantation.
S and serious immunological diseases, where patients face limited treatment options.
We plan to advance <unk> 15, O, one and up to four clinical trials.
A L S to the prevention of kidney allograft transplant rejection, three autoimmune nephritis, starting with Iga nephropathy or again and for the prevention of islet cell allograft transplant rejection for the treatment of type one diabetes.
We selected these indications based on preclinical data that was generated with both our molecule as well as historical anti CD 40 ligand molecules.
Steve will give more details about each of these but at a high level. Our recent progress is as follows.
And the a L. S phase III biomarker study our trial is progressing according to plan. We are completing enrollment of our third or four cohorts and top line data is expected in the first half of 2022.
And renal transplantation, we previously communicated that the U S. FDA requested that we provide 80.15 O. One specific renal transplant data in nonhuman primates prior to initiating a clinical trial in renal transplantation into United States and that.
As a result, we would both look to complete the FDA requirements as quickly as possible as well as look to initiate a clinical trial outside of the United States.
In terms of our U S regulatory requirements, we reached alignment with the FDA to conduct a preclinical renal transplant study evaluating <unk> as monotherapy and for non human primates.
We anticipate initiating this nonhuman primate study in collaboration with an academic collaborator with vast transplant experience next quarter with completion of the study in mid 2022.
With regards to our ex U S. Clinical trial, we received a no objection letter from health, Canada in response to our clinical trial application proposing to evaluate <unk> hundred one.
Replacing <unk> as an immunosuppressive regimen components in patients undergoing kidney transplantation.
The trial is expected to be initiated in the last quarter of 2021 with interim data readouts expected to begin in late 2022.
In autoimmune nephritis, we will be targeting Iga nephropathy there.
There is a long history of preclinical and clinical data demonstrating that blocking CD 40, la gamma signaling ameliorate disease progression modifies biomarkers of disease and improves renal function in autoimmune diseases of the kidney.
Such as again we.
We selected a again because of <unk> approach that an anti CD 40 ligand brings and going after both the seller and the Andy eight body mediated portions of disease pathophysiology.
In islet transplantation for type one diabetes earlier.
Earlier this year, we initiated a phase II clinical trial of <unk> hundred one as a replacement for Tac alignments.
As we announced previously we learned in early January that our study site in Canada voluntarily stopped performing islet cell transplants on a temporary basis because of COVID-19, before allowing for the resumption of these procedures.
Unfortunately until late June vaccination rates in Canada remains far behind those in the United States and the number of islands cell transplant procedures performed remains much lower than pre COVID-19.
As a result, we are still waiting for our first patient to be enrolled Steve.
Steve will discuss the steps, we're taking to address the pace of this study, including making it easier for patients to enroll and looking at additional geographies, where islet cell transplants are performed.
Steve will also provide an update on <unk> hundred one.
In nonhuman primate islet cell data that was presented at the American transplant Congress in June.
I will now turn over the call to Steve Perrin, our President and Chief Scientific officer to discuss our clinical programs.
Afterwards, Paul Little will provide the financial update.
Steve. Please go ahead.
Thank you D a.
A brief reminder, our lead asset <unk>. One is an IGT won anti CD 40 ligand antibody blocking FC effector function.
Physiologically the interaction of CD 40, ligand and CD 40 results in clonal expansion antibody production and secretion of pro inflammatory cytokines that amplify an immune response. The CD 40, CD 40 ligand pathway is an attractive drug development target because the engagement of these receptors plays a.
Is it a role in immune system activation by meeting mediating, both antibody and cellular immune responses.
We are focusing our efforts on the development of an antagonist antibody targeting the ligand rather than the receptor <unk> targeting the ligand has been shown to be more efficacious in preclinical models of autoimmunity and as well as in the prevention of acute and long term allograft transplant rejection.
I'll now dive into four targeted indications AOS kidney transplant autoimmune nephritis and E Bay and in particular, and finally I'll tell transplant for the treatment of type one diabetes.
I would answer AOS, Charles a 12 week open label dose escalating study enrolling at 13 sites in the United States and Canada.
Our enrollment continues to be on track and we've now enrolled 17 of 18 patients in the third cohort with the last patient in this cohort currently completing the screening assessments we.
We expect to complete enrollment of the fourth and final cohort by the end of the year, enabling the reporting of top line data in the first half of 2022.
This data will consist of safety and Tolerability data as well as multiple categories of biomarker endpoints with each subject surfing as their own control by comparing changes from baseline.
And the first category of Biomarkers will assess biomarker to CD 40 ligand target engagement.
Mechanistically blocking CD 40 ligand has profound effects on b cell maturation antibody production and antibody class switching.
We anticipate that we'll be able to assess CD 40 logging target engagement <unk> with markers of B cell function such as <unk> <unk>.
The second category of Biomarkers or changes in pro inflammatory <unk> cytokines up regulated in people living with ALS.
There's a long history of AOS data, describing increases a pro inflammatory signals in circulation, including TNF Alpha MCP, one IL six and then reached we.
We anticipate blocking of CD 41, and will result in an overall decrease of these AOS related pro inflammatory markers.
Finally, we will also assess other exploratory endpoints, including changes in ALS functional rating scale or <unk> for us.
<unk> function and the levels of neuro filament light chain in circulation. We consider these exploratory since with short duration of the study of 12 weeks may not provide sufficient time to see changes in clinical endpoints or changes in <unk> light chain.
Moving onto renal transplant, we recently announced that we received a no objection letter from health, Canada to proceed with our first safety pharmacokinetics and efficacy study of <unk>, one and $6.12 subjects undergoing renal transplant.
This is an important study to demonstrate that <unk> can safely be utilized to replace callison earn inhibitors as part of first line immunosuppressive immunosuppressive therapy in solid organ transplantation and prevent acute and long term solid organ transplant rejection we.
We expect that replacing kelson earn inhibitors resorts on a measurable improvements in the quality of life for people undergoing organ transplants and eliminate them effort nephrotoxicity cardio toxicity neurotoxicity induction of type one diabetes that associated with chronic exposure to C&I.
The study will be an open label multiple site study, which we anticipate initiating by the end of the year with initial interim data expected in late 2022.
Endpoints will include biopsy proven acute rejection antibody mediated rejection in biomarkers of rejection as well as safety and PK PK PD endpoints.
And the terms of starting a trial in United States, We announced in April that the FDA requested that we provide <unk> one drug specific renal transplant data in nonhuman primates prior to potentially initiating a clinical trial in renal transplantation in the United States. We have now reached agreement with the U S. FDA that this study would consist of.
Evaluating <unk> as monotherapy and for non human primates to do this we will be collaborating with a world renowned expert in the development of new treatments and protocols for the prevention of allograft transplant rejection we.
We anticipate starting this study in the fourth quarter with the completion in mid 2022.
These data will continue to build on the strong foundation that has already been established for <unk> 51, and over 60, nonhuman primates across multiple species, including preclinical efficacy data in a nonhuman primate model of violence cell transplant.
Moreover, multiple historical anti CD 40 ligand molecule similar to <unk> have demonstrated preclinical safety and efficacy and hundreds of nonhuman primates, including specifically in a nonhuman primate model of renal transplantation.
And autoimmunity, we will initially focus on Iga nephropathy, one of several autoimmune nephritis, which are autoimmune diseases of the kidney there.
A long history of preclinical and clinical data demonstrating the blocking <unk> signaling ameliorate disease progression modifies biomarkers of disease, and improved renal function and diseases, such as focal segmental glomerular sclerosis, lupus nephritis and Iga nephropathy Mauro.
Moreover, a soluble CD 40 wagon offering correlates with disease flares and autoimmunity autoimmune diseases such as these.
Iga nephropathy or <unk> is the leading cause of gomel nephritis disease manifestation and clinical presents presentation involves renal dysfunction characterized by proteinuria with a slow relentless course with approximately 30% to 40% of patients ultimately reaching end stage renal disease.
The standard of care for and stage renal diseases dialysis or kidney transplant, which represents a significant economic burden as well as a major impact on the patient's quality of life.
IGN is diagnosed via a renal biopsy and the presence of Iga containing immune complex deposition in the kidney.
At time of diagnosis renal dysfunction is highly variable with proteinuria levels greater than one gram per day.
The formation of <unk>, Iga, one immune complexes on the kidney side.
Papa size to be a multi hit pathogenic cross pathological process.
Hit one is the aberrant quite constellation of Iga due to errors in the enzymatic Galactic <unk> of <unk> one.
Hit too is the recognition by the immune system that theres some bearing form of Iga, one called G. D. Iga, one is foreign and auto antibodies our generator in circulating <unk>.
<unk> three is the formation of Gd Iga, one immune complexes in circulation.
And hit for us the deposition of these immune complexes and the <unk> of the kidney, resulting in immune cell infiltration cytokine production complement activation leads to chronic loss of kidney function kidney damage proteinuria and end stage renal disease.
There is no FDA approved therapies for IGN guidelines for current standard of care for people with IGN suggests the use of certain classes of anti hypertension medications to modulate hemodynamic stresses on the kidney, resulting in improved familiar filtration rate and reduce proteinuria.
Treatment with either angiotensin converting enzyme or aces or angiotensin receptor blockade arbs and standard of care of proteinuria is greater than one gram per day and suggest that if it is greater than 0.5 grams per day.
The treatment with Aces and arbs as well as several molecules in clinical development are focusing on hit four but downstream pathological mechanism of disease after immune complex formation in the kidney and decrease kidney function.
The exciting opportunity for <unk> 51 in Iga nephropathy is at <unk> 50 on one has the potential ability to ameliorate pathologies associated loop hits, two three and 480.
<unk> hundred one can prevent the production of auto antibody towards the Gd Iga one referred to as hit too. This is due to the ability of <unk> to inhibit b cell maturation, thus decreasing antibody production and preventing antibody class switching.
The inhibition of antibody class switching at the AGM stage will not only decrease the amount of Iga synthesize that would be available for improper galactic <unk>, but it all also prevents the production of high affinity IGT want antibodies that form the immune complexes.
Blocking CD 40 ligand has the ability to decrease immune complex being complex formation has been hasnt been shown in multiple animal models of autoimmunity as well as in the clinic plus $80.51 has the potential to reduce pathogenesis associated with hit three immune complex formation.
Finally, blocking city 40, <unk> inhibits pro inflammatory polarization of T cells, and macrophages and has been shown to decrease immune cell infiltrate in infiltration inflammation in the kidney hit for income.
In conclusion, when <unk> pathophysiology is taken as a whole $80.51 has the potential to ameliorate immune cell infiltration subsequent complement activation in the kidney and improve kidney function.
We plan to launch an international Phase two study by the end of this year and we'll provide more details including trial design when we enrolled the first patient.
Finally in diabetes, 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 clinical islets transplantation consortium.
As well as islet cell transplants and other countries have demonstrated the islet cell transplantation in patients with difficult to control type one diabetes maintains glycemic balance.
Reinstate some metabolic control and in some cases, even eliminates the need for exogenous insulin. However, the current use of <unk> inhibitors for C&I for the prevention of violence cell transplant rejection poses to issues.
First C&I are toxic towards transplanted islets potentially resulting in significant outlet so loss post transplant and may lead to the requirement for multiple islet cell transplants.
Indeed in published trials islet cell transplant recipient recipients typically require multiple transplants with the need for a second transplant often apparent within approximately 90 days after the first transplant.
At the American transplant Congress in June this year, Dr. Enormous Kenyan director of the diabetes Research Institute at the University of Miami presented data comparing an avid aggregated group analysis of animals, receiving <unk> as either monotherapy or in conduction with induction therapy to animals onto Korlym us.
In conjunction with an induction therapy in a nonhuman primate model of violets cell transplant.
Her findings indicated the animals on a $50 <unk> have significantly longer rejection free survival significantly longer overall islet cell graft survival and maintain greater body weight compared to animals onto Korlym us.
In addition, C peptide levels were four times higher for animals treated with <unk> compared to animals treated with <unk>.
And one group of animals, receiving <unk> hundred one monotherapy at 10 Meg per kg every 14 days.
<unk> decreased the dosing frequency by half starting on day $2.24, and one of these animals continued with graft function well over 400 days, which according to her represented a functional cure of type one diabetes in this animal.
Finally, she reported that animals onto chroma. So we're more susceptible to life threatening CMV infections covenants toxicity associated with C&I.
As a result of data such as this we believe that replacing C&I is with <unk> may improve I'll, let cell survival and clinical outcomes associated with islet cell transplant, thus potentially allowing for islet cell transplant to become a viable treatment option and even a potential functional cure for persons living with high risk type one diabetes.
We currently have an active clinical site in Alberta, Canada seeking to enroll a single arm open label study.
Primary endpoints include safety and Tolerability glucose control insulin independence reduction of HBA, when see graft survival and function. We will also be assessing hypoglycemic awareness events as well as renal function.
Unfortunately, Canada in the province of Alberta were significantly impacted by Covid in the first half of this year and the rollout of vaccinations in Canada, where it was it wasn't until recently far behind the U S. This significantly impacted the ability of the staff to work on site and maintain a normal process of patient screening and enrollment for our cell transplant procedures.
Moreover, travel between provinces in Canada were seriously impacted as well as the willingness of patients to take the immersive presence necessary for an elective transplant procedure.
Taken together the effect has been to very significantly reduced the number of islet cell transplants procedures being performed so far this year compared to pre COVID-19.
We are working with the site to facilitate patient recruitment into the study included by reaching out to more endocrinologists across the province in Canada as well as by beginning to work on ways to allow patients to receive drug closer to home, thus decreasing their need to travel.
Separately, we have assessed the ability to expand the study to sites in Europe, but a pharma to date they have experienced similar issues with COVID-19 is Canada.
The Covid situation continues to evolve we will reassess the potential for international expansion.
We are still targeting to enroll this trial as soon as possible, which would allow us to meet our goal of generating interim data and I'll tell transplant in the first half of 2022. This is based on the timing to assess graft function in acute transplant rejection is 90 days post transplant on a patient by patient basis.
With that I'll turn the call over to Paul for our financial update.
Thank you Steve in addition to the financial results summarized in our press release, you can find additional information in our Form 10-Q, which we will file later today the.
The company reported a net loss of $7.4 million or <unk> 50 per share for the three months ended June 32021, compared to a net loss of $2.6 million or $2.74 per share for the same period in 2020.
Research and development expenses were $4.2 million for the three months ended June 32021, compared to 800000 for the same period in 2020, the increase in R&D costs, primarily reflects clinical and CMC activities as we advance our 18.81 programs.
G&A expenses were $3.7 million for the three months ended June 32021, compared to $1.3 million for the same period of 2020.
The increase in G&A spend primarily reflects increased personnel and stock based compensation costs legal and other professional fees.
Turning to a few key financial metrics for the full year to date.
The company reported a net loss of $15.9 million.
<unk> per share for the six months ended June 32021, compared to a net loss of $10.8 million or $11.31 per share for the same period of 2020 R&D expenses were $9.9 million for the six months ended June 32021, compared to $2.5 million for the same period of 2020 the <unk>.
Kris and R&D cost, primarily reflects clinical and CMC activities as we advance our <unk> programs.
G&A expenses were $7.1 million for the six months ended June 32021, compared to $3 million for the same period last year. The increase in G&A spend primarily reflects increased personnel and stock based compensation costs legal and other professional fees the.
The company had $101.1 million cash and cash equivalents as of June 30.
<unk> $108.6 million in cash and cash equivalents as of March 31, 2021, we expect our financial resources to be sufficient to fund operations. As currently planned well into 2023 finally subsequent to our acquisition of <unk> in 2020, we undertook a strategic review of <unk> pharmaceutical.
As legacy assets for Otis Media. We recently concluded this review and determined that the best path forward was to terminate license agreements associated with these assets and return the rights to the original license holders. We did this in July there.
There was no financial impact with the return of these assets.
With that financial update let me turn the call back over to D. A.
Thank you Paul.
We made significant progress during the second quarter advancing our lead molecule <unk> hundred one and.
And look forward to multiple potential upcoming milestones.
This year, we expect to present ATI 501, nonhuman primate data at the international Pancreas, and islet cell transplantation World Congress annual meeting in October.
To initiate clinical trials and clinical trial in the prevention of kidney transplant rejection and a trial in again and to initiate a nonhuman primate kidney transplant study.
We then expect to begin reporting data readouts from these trials starting in the first half of 2022 with AOS and I'll, let cell transplantation for type one diabetes as well as the non human primate kidney transplant study.
With that I will now ask the operator to begin our Q&A session.
Operator.
Thank you.
At this time, we will be conducting a question and answer session. If you would like to ask a question. Please press star one on your telephone keypad a.
A confirmation tone will indicate your line is in the question queue. You may remove your question by pressing star too. 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, while we poll for questions.
Our first question comes from Alicia Young with Cantor Fitzgerald You May proceed with your question.
Hi, This is neena on for <unk>, Thanks for taking our question.
We were wondering for Xeljanz.
Transportation program.
Any idea.
One the first patient enrolled and.
And if you think that will be in Canada outstanding yet.
And how quickly do you think you can line of patients and also if you can just remind us how many patients.
Thanks.
Sure.
Thank you for the question.
We are looking to enroll our first patients as soon as possible. Currently the trial is only opened in Canada and so that's that.
Where we are focused.
But as you heard as we discussed we will look, especially as COVID-19 progresses to see whether there are ways to add additional countries to to the trial as well what's nice here is that we can begin to get data quickly.
Since patients often need second transplant procedures within 90 days after the first transplant when they received current standard of care.
Which could allow us to.
To quickly see the fact that ATI 501 is having.
Well, we'll what's nice here is that we can get significant.
Learnings with just a few patients and so we plan on reporting.
The data that we have on the totality of patients that we'll be able to have enrolled in the first half of next year.
Steve Let me see if you have anything you'd like to add.
Yes, yes.
Again, I mean, we're working hard with the site to.
To get back up and running they've had challenges with COVID-19 is a summary body.
The important thing about the islet cell transplant procedure is.
You mentioned is the ability to.
Fairly rapidly assess graft function on a subject by subject basis, which could still yield exciting data next year.
Okay. Thank you.
Our next question comes from Matt Kaplan with Ladenburg Thalmann. You May proceed with your question.
Hey, guys. Thanks for taking my questions I apologize if there's some background noise there just getting hit with a thunderstorm right now.
Okay.
Wanted to just dig in a little bit more to the renal transplant program I guess given the.
The Readouts that you expect for the nonhuman primates and middle of next year and and clinical data.
Late next year.
When do you think youll be able to start a U S focused study.
Thanks, Matt.
Thanks.
Thanks, Matt.
Why don't I turn that.
Over to Steve to go through to go through the plan.
So I think that there was two questions here, Matt one was about the nonhuman primate study and the other was about anticipation on moving into the U S. Correct.
Correct, yes.
So for the non human Primate study is as we indicated we had very specific guidance from the agency on what they wanted their which was monotherapy <unk> in a nonhuman primate renal transplant model because of that guidance, we can reach out and start to work with an excellent collaborator on that regard.
We know based on lots of historical data that we've mentioned hundreds and hundreds of animals, who have undergone.
Renal transplant studies with monotherapy for various <unk>.
Anti CD 40 ligand antibodies in the absence of any treatment animals reject them very very quickly within a few days to a week.
Even on monotherapy there is some variability in the durability of preventing rejection.
But typically you know average survival times, which suggests that we can conduct the experiment fairly quickly.
Monotherapy treatment.
Standard depending upon the types of primates.
And the types of treatments can go anywhere from 14 days to 30 days with some standard deviations with animals surviving longer than that but a fairly straightforward study given that theyre looking for.
Just to demonstrate that <unk> can move out the timeframe towards from acute rejection in untreated animals.
As far as the clinical plans in the U S. I think that that's just very dependent on what the data looks like from Canada, I mean, we're <unk>.
Really excited for the study to initiate in Canada by the end of the year as.
As we know transplant studies are a little bit more complicated in humans and they are in animals, but really I think the decision to get back to the agency with not only their request for the nonhuman primate data, but with also some human data from that Canadian study is key.
So I think we need to wait until we see.
What that Canadian data looks like.
So we will have Ken so so we'll look at.
When we begin to have human data as well as.
Complete the study to return and re initiate discussions.
With FDA, which could be obviously as soon as in.
In the second half of next year.
Okay makes sense, Thanks, and then a second question.
For all the detail on Iga nephropathy, and potential kind of nodes of impact that 15 out one can have can you give us a little bit more color on the study that you plan. The phase two that you plan to start.
And also what kind of read through do you think the study will give to potential other etiologies of autoimmune.
That property.
I don't know profit that Friday, I should say.
And so in terms of specific color on.
On trial design will give more color as we.
As we begin to initiate the trial and enroll and enrolled patients.
As you can.
Understand we'd like to finish our discussions.
With the various regulatory bodies.
Our Cta is approved.
Four we go into before we go into full detail.
With regards to the potential read through in autoimmune nephritis overall and the overlap between the various autoimmune Fridays.
Let me turn that over to Steve.
Yes, it's a great question, Matt about read through because as you know one of the common themes, even though these diseases are different I mean, I'm thinking of lupus nephritis, SGS again, and others I mean, there's differences within each of these indications, but a common theme here is kidney dysfunction proteinuria ultimately egfr.
Our improving improving all of the above so there is some crossover if you will once you get some data points in one of these indications that if youre improving <unk>.
Downstream kidney function by ameliorated.
Union filtration complement activation.
Most of other pathophysiology as that could easily read through to other indications. So so the data and IGN I think is very important to help us understand mechanistically, how the drug is working but also if we're improving kidney function.
Okay, great. Thanks, Thanks, Steven.
Yeah.
Our next question comes from Thomas Smith with S. VB earlier, Nick you May proceed with your question.
Hey, guys. Good afternoon, thanks for the.
Jason Thanks for taking the questions.
Just on the autoimmune arthritis, I mean, you've previously talked about.
ESG and lupus nephritis as potential initial indications can you just walk us through how you thought about again relative to those other two indications and how you ended up.
Settling on again.
Yes, so we've historically spoken about autoimmune Friday is covering the three S. GFS lupus nephritis.
And again.
We ultimately selected all again, because as we thought about both our understanding of the disease.
As well as the way.
As a way of using an anti CD 40 ligand that impact the disease.
That's where we felt that we had the greatest chance of success.
Let me turn it over to Steve to just provide some more color.
On the use of <unk> potential use of CD 40 ligand and <unk>.
Yes.
Certainly hit the highlights there I mean, we think that there's opportunities and unmet need in <unk> lupus nephritis.
And even other autoimmune nephritis.
But really the disease mechanisms for some of these indications are still a little unclear there were significant heterogeneity.
In patient stratification can be a problem in the context of <unk> in particular I'm.
I'm thinking about all of the above I mean, mechanistically, we were still trying to elucidate what are the real mechanisms leading to.
Kidney dysfunction in <unk> and when we compare and contrast that to the pathophysiology of what we know about <unk>, we just understand more of of.
What caused us to season ITM and the fact that blocking CBD 40, <unk> can play a very significant role in multiple parts of that process really makes it an exciting opportunity to really understand if blocking immune complex formation downstream, if moving upstream in actually eliminating immune complex.
Formation by eliminating antibody production.
Moving even further upstream from that is really modulating ultimately the production of Iga by knocking down b cell production of antibodies and blocking class switching.
851 has the potential to do all of those things. So it really is an exciting opportunity to look and see if blocking.
<unk> 40, <unk> function can have a dramatic impact on the upstream processes of kidney dysfunction.
Got it Okay. That's helpful and then.
Just to follow up on an earlier question I understand you're still working through the.
Details of the study design and Youre waiting to hear Steve.
Feedback from some of the regulators, but I guess do you have any initial sense of when we could see a first look at data from this program.
So this will look.
Two.
It's a construct that trial to be able to begin to get some data readouts next year.
Okay.
Okay. That's helpful. And then maybe just one last question just on.
Islet cell and the presentation at the transplant World Congress coming up here in October.
What should we be looking for in terms of new datasets in that presentation.
Yeah. So the presentation, we'll be again done by normally Kenyan.
The University of Miami, and so she'll continue to give.
To give more details on all of the work that he has done to date.
With our nonhuman primates and $80.501.
Steve Okay got it.
Let me say I mean normal continues to be really excited about the data that she has generated thus far and given her long history going back over.
20 years mean normal has had her fingers on a lot of different potential treatments to prevent transplant rejection in her.
Non human Primate model. So she continues to to look at the data and we will continue to build on her story, if mechanistically how blocking the ligand.
How has the potential to prevent short long term reduction and even induce tolerance in a functional cure and some animals. So we're really excited to be working with normally and her team.
Okay got it.
Got it thanks, guys looking forward to the presentation and thanks for taking the questions.
Thank you.
As a reminder, if you would like to ask a question. Please press star one on your telephone keypad, a confirmation tone will indicate your line is in the queue.
Our next question comes from Rami Kakuta from lifestyle capital you May proceed with your question.
Hey, guys. Congrats on all the updates and thanks again for taking my questions.
I know you've touched upon this briefly but can you guys provide a little more insight on the differentiation between $8.51 in some of these b cell modulating therapies in development for Iga nephropathy, specifically.
Sure Ravi.
Rami Thanks for the question.
Let me turn that over to Steve.
Yes, so you probably specifically talking about April Bath <unk> inhibitors.
Yep exactly.
So the very targeted therapies much like CD 40, ligand theyre targeting the upstream processes of.
Antibody formation of production so the second and third hits, if you will that I was talking about and the strategies. There are probably fairly similar to how we think CD 40 ligand.
Would inhibit those two processes Europe, modulating b cell function b cell maturation antibody production.
Class switching downstream of AGM, which is critical.
I think one of the potential differentiation points is more on the downstream process. The one thing that blocking CD 40 ligand does.
But the Baffin April inhibitors.
Not specifically do is modulating immune cell infiltrate into the kidney post to mean complex deposition and.
And that's one of the things the blocking the ligand may do that's a little bit mechanistically different blocking April or Bath.
Got it that makes a lot of sense.
Then I guess switching gears a little.
Said another way.
I think back to what Steve had described which is anything about the forehead hypothesis.
This allows us to do is to potentially have an impact and more hits than other approaches.
Mhm.
Got it.
And then looking at the open label kidney transplant trial I know this is somewhat hypothetical but is there potential for positive data from that program to kind of expedite the development pathway with regards to that yet.
So.
So.
That's what we're.
We're looking to do is to see how quickly we can move the program forward and we will do it in a way that's as expeditious as possible.
While also of course, respecting our regulatory requirements and making sure we do what's right for patients.
The idea.
Is two to meet the Fda's requests in terms of the nonhuman Primate study and then.
Use the data that we are looking to generate in patients.
To see what is the.
Assuming that data is positive.
It is the fastest.
Next step in terms of the development of <unk> hundred one in kidney transplantation.
No that's great. Thank you guys.
Our next question comes from Vernon Bernardino You May proceed with your question.
Hi.
J C.
Steve and Paul Thanks for the update and thanks for taking my question.
Most of my questions were related to the choice of ICANN.
<unk>.
Therefore asked and answered and then.
What to expect at the <unk>.
Conference in October.
I know you briefly mentioned.
Private work, but we'll some of that work.
Also be related to the <unk> again.
Search.
So the the work in first thank you very much Vernon for the question.
The work that we'll present is.
Is going to be primarily focused on enormous work in in islet cell.
But let me turn that over to Steve.
To talk about how that work could impact or could read through other immune conditions as well.
I mean, the work that we're doing with enormous fairly focused on islet cell transplants, mechanistically, there's probably not a lot of read through there for.
Understanding mechanistically, how it could work out or impact autoimmune nephritis indications now the animals that were talking about doing for monotherapy for.
The renal transplant study in non human primates, we will be looking obviously out not only rejection, but also.
Immune cell infiltrate and other downstream parameters associated with transplant rejection and function that could be informative in the context of autoimmune nephritis. So that could provide that study could provide.
Some information and information on Mechanistically, how blocking city 40 log in modulating the immune system and may mitigate improvements in renal function in the context of a transplant. So that one that one could have some read through downstream.
Okay.
That's perfect and then therefore with the against study I just want to confirm is that going to be a phase II study I know youre going to look at.
Different doses.
So.
It's going to be to your point this will be a human clinical trials. So we'll look to do a.
A phase II.
The.
The specific trial design and the potential to use multiple doses will give more color on <unk>.
Further down the line.
Okay.
The one in Q okay.
Thanks for taking my question everything else was already asked and answered so I appreciate the update and all the answers. Thank you.
Okay.
At this time, we have reached the end of the question and answer session. I will now turn the call over back to management for closing remarks.
Okay.
Thank you operator, and thank you everyone for joining us today on the call. We are pleased you could join us to hear our progress during the second quarter and we look forward to keeping you updated on our company and programs.
This concludes today's conference you may disconnect your lines at this time. Thank you for your participation.
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